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Published in final edited form as: Am J Otolaryngol. 2023 Nov 5;45(1):104104. doi: 10.1016/j.amjoto.2023.104104

Postmeningitic pediatric hearing loss from non-type b Haemophilus influenzae

Brian W Herrmann a,b, Salina H Goff c, Juri Boguniewicz b,d, Sarah A Gitomer a,b
PMCID: PMC10841718  NIHMSID: NIHMS1943564  PMID: 37948823

Abstract

Background:

Postmeningitic hearing loss from Haemophilus influenzae (H. influenzae) is increasingly due to encapsulated serotypes other than type b (Hib) and nontypeable strains (collectively, nHiB H. influenzae). Pediatric hearing loss after nHib H. influenzae meningitis remains poorly described.

Methods:

Retrospecive case series of nHiB H. influenzae meningitis cases identified from a microbiologic database at Children’s Hospital Colorado from 2000 to 2020. Literature regarding nHiB H. influenzae and H. influenzae postmeningitic hearing loss was also reviewed.

Results:

Eleven cases of nHib H. influenzae meningitis (median age 15.9 months) were identified due to serotype f (36%), serotype a (27%), and nontypable strains (36%). Seven (64%) patients were male, 55% were white and 18% were Hispanic or Latino. Hearing loss was initially identified in 4 children (40%), with two patients with moderate conductive hearing loss (CHL) and one child with unilateral moderate sensorineural (SNHL) hearing loss patients recovering normal hearing. One patient with bilateral profound sensorineural hearing loss and associated labyrinthitis ossificans required cochlear implantation. All children (4) with identified hearing loss were noted to have additional intracranial sequelae, which included empyema (2), sinus thrombosis (2), and seizures (2). Of patients receiving steroids, 25% had hearing loss on initial testing, compared to 66% of those who did not receive steroids.

Conclusions:

nHib H. influenzae can cause both transient and permanent postmeningitic hearing loss. Steroids may offer otoprotection in nHib H. influenzae meningitis similar to Hib meningitis. Given the limited literature, further study is needed to better characterize hearing outcomes after nHib H. influenzae meningitis.

Keywords: pediatric, Haemophilus, influenzae, hearing loss, meningitis, SNHL

1. INTRODUCTION

H. influenzae is a gram negative coccobacilli commonly found within the the upper respiratory tract of children. Subdivided into encapsulated (serotypes a-f) and nonencapsulated (nontypeable) forms, it is associated with acute otitis media, sinusitis, and invasive disease such as pneumonia, meningitis, and septicemia, predominantly affecting children and the elderly.[1] The dramatic reduction in invasive Hib disease after introduction of the Hib conjugate vaccine in 1990 has been tempered by the rise of other encapsulated serotypes (Hia-f) and nontypeable strains (NTHi), potentially as a result of serotype replacement.[2-6] Numerous studies have also noted rates of invasive H. influenzae disease have persisted despite the reduction of Hib, and suggested that previous assumptions regarding the lower virulence of nHib H. influenzae compared to Hib may be incorrect. [7-10]

Despite increasing recognition of nHib H. influenzae as a cause of pediatric bacterial meningitis, knowledge regarding neurological outcomes including hearing loss remains limited. A recent case series by Antony et al. of invasive nHib H. influenzae disease, identified 13 children (77%) presenting with meningitis, of which two (15%) patients developed postmeningitic SHNL.[10] This single institutional review provides a 20 year experience with hearing loss after nHib H. influenzae meningitis.

2. MATERIALS & METHODS

A retrospective chart review was performed for patients 18 years and younger with nHib H. influenzae meningitis diagnosed between January 2000 to December 2020, spanning the extent of a microbiologic database of clinical cerebrospinal fluid (CSF) samples at Children’s Hospital Colorado. Postmeningitic pediatric survivors with positive CSF culture or FilmArray Meningitis/Encephalitis Panel (MEP) assay (BioMerieux, Marcy-l’Étoile, France) for nHib H. influenzae were included. Patients over 18 years of age, without a positive CSF bacterial culture or MEP assay, with concurrent viral meningoencephalitis, or recurrent meningitis were excluded. Patients with preexisting conditions requiring exclusion included those with meningitis due to trauma or neurosurgical procedures (e.g. ventriculoperitoneal shunt), preexisting hearing loss, known underlying immunodeficiency, conditions requiring treatment with biologic agents, neurological disorder, congenital cytomegalovirus infection, or preexisting perinatal insult. For surviving patients lacking previous audiological testing, premeningitic hearing status was based on initial history and newborn hearing screen.

Relevant clinical data including demographics, hospital course including medical evaluations and treatments, audiologic testing, and any otologic evaluations for nHib H. influenzae meningitis patients was collected and managed through Research Electronic Data Capture (REDCap), a HIPPA-compliant electronic data tool.[11] Postmeningitic audiologic data was collected through age-appropriate evaluations or sedated automated brainstem response testing (ABR) by a pediatric audiologist. Testing was performed during initial hospitalization and those demonstrating hearing loss recommended for follow up testing in three month intervals over the first year. Middle ear status was determined by tympanometry and/or otoscopic findings. Hearing loss was declared if audiological thresholds exceeded 20dB. Long term hearing status was determined by the last available audiometric evaluation for each patient. Descriptive statistics were used where appropriate, however, the small number of patients in this series precluded further inferential statistical analysis.

The relevant literature identified through PubMed, Medline, and Cochrane library from 200-2022 searches was also reviewed. This study was reviewed and approved by the Colorado Multiple Institutional Review Board (Protocol # 19-2670).

3. RESULTS

Eleven children surviving nHib H. influenzae meningitis were identified by positive CSF culture or MEP at our center during the study period, of which ten also possessed audiometric data. (Table 1) Median age was 15.9 months (range 4.3-176.4 months), the majority of patients were male (64%), Caucasian (55%), and non-Hispanic/Latino (82%). None of the identified patients were found to have a documented history of congenital CMV or preexisting hearing loss. Serotyping identified three cases of H. influenzae serotype a, four cases of serotype f, and four cases of non-typeable H. influenzae. All children were up to date on Hib and PCV13 vaccinations for their age. None of the patients required mechanical ventilation. Eight children (73%) received dexamethasone before or within 8 hours of first antibiotics, while three did not receive steroids. Of those receiving steroids, 25% demonstrated hearing loss on initial audiometric testing. In contrast, 66% of patients who did not receive steroids in this series were identified to have hearing loss.

Table 1.

Haemophilus influenzae meningitis patient characteristics

Participant Age
(months)		 Sex nHiB
serotype		 Antibiotics used
(after LP)		 Duration of
antibiotics
(days)		 Received
steroids		 Duration
of
steroids
(days)		 Length of
admission
(days)		 Duration
between LP
and
audiologic
evaluation
(days)		 Hearing
loss		 Seizure Other complications
1 9 M A Ceftriaxone, Vancomycin 9 Yes 5 6 5.8 No Yes Re-admitted 3 months later with subdural hematoma & seizure thought to be related to recent meningitis
2 56 M F Ceftriaxone, Vancomycin, Acyclovir 10 Yes 5 6 14.0 No No No
3 4 M A Ceftriaxone, Cefotaxime, Vancomycin, Gentamicin, Meropenem 14 Yes 5 15 8.3 No No No
4 17 M F Ceftriaxone, Vancomycin, Gentamicin 15 Yes 4 17 7.1 Unilateral SNHL No Cerebral venous sinus thrombosis
5 13 M A Ceftriaxone, Vancomycin, Cefepime, Levofloxacin 34 Yes 5 27 4.1 CHL No Subdural empyema, septic arthritis
6 177 F Non-typeable Ceftriaxone, Cefotaxime, Vancomycin 9 Yes 5 5 4.4 No No No
7 16 F F Ceftriaxone, Vancomycin 9 Yes 5 10 6.7 No No No
8 12 M Non-typeable Ceftriaxone, Vancomycin 9 Yes 3 11 -- No No DIC, small thromboses cortical vein along superior left cerebellar hemisphere
9 20 F F Ceftriaxone, Vancomycin, Metronidazole 9 No -- 9 4.0 No No Bronchiolitis, Sinusitis, Otitis Media (mastoiditis)
10 169 M Non-typeable Ampicillin, Ceftriaxone, Vancomycin 10 No -- 5 3.3 CHL No No
11 6 F Non-typeable Ceftriaxone 58 No -- 18 3.5 Bilateral SNHL Yes DIC, purpura fulminans, sepsis, seizures
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nHiB: nHib H. influenzae; LP: lumbar puncture; SNHL: sensorineural hearing loss; DIC: diffuse intravascular coagulation; CHL: conductive hearing loss; CSF:cerebrospinal fluid

Hearing loss was the most common major neurologic sequelae of meningitis within this series, followed by seizures (18%) and intracranial thrombosis (9%). Of the ten patients with audiologic data, 90% were tested during their admission (one patient completed initial testing within one month after discharge). Two patients demonstrated sensorineural hearing loss during initial testing. The first patient was a 6-month-old female diagnosed with bilateral profound SNHL by auditory brainstem response (ABR), which ultimately progressed labyrinthitis ossificans (LO) on imaging. She underwent bilateral cochlear implantation within two months of meningitis diagnosis. Her hospital course was complicated by thrombocytopenia causing delay in lumbar puncture, disseminated intravascular coagulation with purpura fulminans, sepsis, and seizures during her admission. This patient also did not receive steroids as part of her treatment. The second patient was a 16-month-old male who was diagnosed with mild right-sided SNHL by ABR testing during his admission. His hospital course was complicated by cerebral venous sinus thrombosis. His SNHL was ultimately transient, demonstrating resolution through two years of follow up audiological testing. He received steroids and aminoglycoside antibiotics during the course of his treatment. Two cases of transient postmeningitic mild to moderate bilateral conductive hearing loss were identified on audiologic evaluation during admission, which resolved on follow up testing within the first few months after discharge. No patients developed delayed-onset hearing loss.

A literature review initially identified 162 articles, of which 60 included postmeningitic hearing loss. Additional screening for pediatric articles and nHib H. influenzae meningitis resulted in 20 articles for review. From these, 7 articles provided hearing outcomes related to nHib H. influenzae meningitis in children, and one article with a mixed age cohort.

4. DISCUSSION

Despite the dramatic reduction in nHib H. influenzae over the last 30 years, the presence of H. influenzae as a commensal upper airway inhabitant or source of infection has not dramatically changed, but rather shifted to nHib H. influenzae isolates. [12,13] Our study was consistent with other reviews of invasive H. influenzae in Europe and the United States reporting NTHi, Hia, and Hif as the predominant isolates in the post Hib vaccination era.[13,14-16] (Table 2) Our results were consistent with the literature identifiying Hif and Hia as the most frequent encapsulated sources of pediatric nHib H. influenzae meningitis and noting both may produce postmeningitic neurological sequelae.[17-19]

Table 2:

Summary of relevant literature for nHib H. influenzae postmeningitic SNHL

Study Publication
year		 Total nHib
invasive
infection		 Total nHib
meningitis		 Meningitis pathogen SNHL
(%)
NTHi
(%)		 Hia
(%)		 Hif
(%)
Vallejo et al (0-18 years) 2019 61 12 8% 58% 17% 58%
Cleland et al (0-18 years) 2018 125 13 15% 23% 15% 8%
Antony et al (0-18 years) 2017 17 13 77% 15% 8% 15%
McConnell et al (0-18 years) 2007 89 28 29% 46% 14% 20%
Russo et al (0-12 years) 2022 35 12 0 100% 0 0%
Abou-Hanna et al (0-18 years) 2019 1 1 0 0 100% 100%
Roaa et al (0-18 years) 2016 2 2 0 100% 0 0%
Bozio et al (all ages) 2021 169 43 0 100% 0 23%
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nHiB: nHib H. influenzae; SNHL: sensorineural hearing loss

Sensorineural hearing loss (SNHL) has been consistently reported as the most common neurological morbidity from pediatric bacterial meningitis, with prevalence varying by bacterial etiology: Streptococcus pneumoniae (14–52%), Haemophilus influenzae serotype B (20-58%), and Neisseria meningitidis (4–23%).[4,20-26] Hearing loss may develop from both the direct spread of bacterial products into the inner ear as well as the host inflammatory response, resulting in a suppurative labyrinthitis with resultant cochlear end organ damage. Although this was a widely recognized sequelae of meningitis prior to introduction of vaccines for Hib, recent literature evaluating impacts of nHib H. influenzae meningitis on hearing is more limited. As summarized in Table 2, the literature is quite limited regarding hearing loss related to nHib H. influenzae meningitis in children, suggesting additional multi-institutional investigation or meta-analysis is needed.

While use of corticosteroids has been shown to reduce hearing loss risk from Hib meningitis, this benefit may be reduced if initiated after the first antibiotic dose.[26,27] Although transient hearing loss after pneumococcal meningitis has been noted, the frequency of hearing recovery after nHib H. influenzae meningitis remains unclear.[23,28] The literature reporting neurological outcomes including SNHL from nHib H. influenzae meningitis is sparse regariding use and timing of steroids. Early identification and intervention in postmeningitic children with hearing loss is critical, as this population is at risk for developing speech delay, gait disturbances, and behavioral problems.[29,30] Because the literature is limited to small case series, additional investigation with a larger multi-institutional cohort is needed to draw any statistical conclusions regarding the efficacy of steroid administration in reducing SNHL in nHib H. influenzae meningitis,

Postmeningitic SNHL due to nHib H. influenzae was initially identified in 20% of patients within this series, similar to rates described in Hib meningitis (20-58%).[3,11] One patient in our study demonstrated long term SNHL from nHib H. influenzae, similar to Antony, et al.[10] Vallejo et al documented postmeningitic nHib H. influenzae hearing loss in 58.3% of surviving children, with 86% of those presenting with bilateral loss.[4] Transient loss was noted in three patients in our study, with two CHL and one SNHL patients resolving deficits on follow up audiometric testing. While transient postmeningitic hearing loss has been reported after pneumococcal meningitis, our results suggest that this can also occur after nHib H. influenzae meningitis.[9,28] Although progressive hearing loss has been reported in H. influenzae meningitis, no patients in this study demonstrated this finding through their latest audiometric evaluation.[31] Despite the relative rarity of nHib H. influenzae limiting the number of patients in our series, this study suggested that steroids may provide an otoprotective effect for nHib H. influenzae similar to Hib meningitis. Patients not receiving steroids were more likely to demonstrate hearing loss on initial testing (66% vs 25%).

This study also demonstrated the severe damage nHib H. influenzae meningitis can inflict upon the inner ear, with one patient developing labyrinthitis ossification (LO) related to the infection and subsequent inflammatory response. Fibrous and bony deposition within the cochlea from the inflammatory response has been shown to begin within the first week after infection, and can rapidly progress to obliteration of basal turn of the cochlea, making cochlear implantation problematic.[32] Although early corticosteroid administration has been shown to improve hearing outcomes in Hib meningitis, delays in administration are common, and can negatively impact its effectiveness.[13,33] A small case-series also suggested early steroid administration may help reduce potential LO development.[34] As in our patient with LO, MRI demonstrated value in observing early LO changes and expedited cochlear implantation, as recommended in postmeningitic implant candidates when early signs of LO are encountered.[35,36]

This study is limited by its retrospective single-center design, which may predispose to identifying severe cases more than a population-based approach. The relative rarity of pediatric nHib H. influenzae meningitis with appropriate audiometric data may have limited the generalizability of these findings. Although we utilized multiple methods to identify all nHib meningitis patients, we may have underreported the true number and/or burden of disease. The varying lengths of long term audiometric follow up may have also inadvertently limited identification of delayed onset or progressive hearing loss. The small sample size and retrospective nature of the study also precluded determining whether steroids are truly beneficial at preventing hearing loss in nHib H. influenzae meningitis similar to Hib meningitis, and warrants further investigation. This study reflects the relatively sparse literature regarding postmeningitic SNHL in children from nHib H. influenzae, and suggests additional, larger studies are needed.

5. CONCLUSION

Hearing loss remains a common morbidity after nHib H. influenzae meningitis. Despite the potential otoprotective effects of early corticosteroid administration in H. influenzae meningitis, significant hearing loss and progression to LO can occur. Close audiometric follow up and neuroimaging can help determine if a nHib H. influenzae postmeningitic child demonstrates transient loss, progressive loss, or will need expedited cochlear implantation. Further study is required to better understand the postmeningitic risk for SNHL from nHib H. influenzae, and to determine if steroids provide an otoprotective effect in nHib H. influenzae meningitis similar to Hib meningitis.

Highlights.

  1. Although rare, nHib H. influenzae is increasing common in pediatric meningitis

  2. nHib H. influenzae is associated with all forms of postmeningitic hearing loss

  3. Pediatric hearing loss after nHib H. influenzae meningitis is poorly described

ACKNOWLEGEMENTS:

Shilpa Tummala for her assistance in data collection.

Funding sources:

Supported by NIH/NCATS Colorado CTSA Grant Number UL1 TR002535. Contents are the authors’ sole responsibility and do not necessarily represent official NIH views.

Footnotes

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Financial Disclosure: The authors have no financial relationships relevant to this manuscript.

Other Disclosures not relevant to study: None

Conflict of Interest: The authors have no conflicts of interest.

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