Factors associated with the occurrence of hearing loss after pneumococcal meningitis.

BACKGROUND: On the basis of a nationwide registration during a 5-year period (1999-2003), the frequency and severity of hearing loss was investigated retrospectively in 343 consecutive Danish patients who survived pneumococcal meningitis, to identify important risk factors (including the pneumococcal serotype) for development of hearing loss. METHODS: Results of blood and cerebrospinal fluid (CSF) biochemistry, bacterial serotyping, follow-up audiological examinations, and medical records were collected, and disease-related risk factors for hearing loss were identified. The mean pure-tone hearing threshold levels were compared with normative data. RESULTS: Of 240 patients examined by use of audiometry, 129 (54%) had a hearing deficit, and 50 (39%) of these 129 patients were not suspected of hearing loss at discharge from hospital. Of the 240 patients, 16 (7%) had profound unilateral hearing loss, and another 16 (7%) had bilateral profound hearing loss. Significant risk factors for hearing loss were advanced age, the presence of comorbidity, severity of meningitis, a low CSF glucose level, a high CSF protein level, and a certain pneumococcal serotype (P < .05). By applying multivariate logistic regression analysis, we found that advanced age, female sex, and a certain serotype were significant risk factors, because fewer patients with serotype 6B had hearing loss than did patients with serotype 12F (P = .03), which was the most commonly occurring serotype. CONCLUSION: Hearing loss is common after pneumococcal meningitis, and audiometry should be performed on all those who survive pneumococcal meningitis. Important risk factors for hearing loss are advanced age, female sex, severity of meningitis, and bacterial serotype.

Systemic steroid reduces long-term hearing loss in experimental pneumococcal meningitis.

OBJECTIVES/HYPOTHESIS: Sensorineural hearing loss is a common complication of pneumococcal meningitis. Treatment with corticosteroids reduces inflammatory response and may thereby reduce hearing loss. However, both experimental studies and clinical trials investigating the effect of corticosteroids on hearing loss have generated conflicting results. The objective of the present study was to determine whether systemic steroid treatment had an effect on hearing loss and cochlear damage in a rat model of pneumococcal meningitis. STUDY DESIGN: Controlled animal study of acute bacterial meningitis. METHODS: Adult rats were randomly assigned to two experimental treatment groups: a group treated with systemic steroid (n = 13) and a control group treated with saline (n = 13). Treatment was initiated 21 hours after infection and repeated once a day for three days. Hearing loss and cochlear damage were assessed by distortion product otoacoustic emissions (DPOAE), auditory brainstem response (ABR) at 16 kHz, and spiral ganglion neuron density. RESULTS: Fifty-six days after infection, steroid treatment significantly reduced hearing loss assessed by DPOAE (P < .05; Mann-Whitney) and showed a trend toward reducing loss of viable neurons in the spiral ganglion (P = .0513; Mann-Whitney). After pooling data from day 22 with data from day 56, we found that systemic steroid treatment significantly reduced loss of spiral ganglion neurons (P = .0098; Mann-Whitney test). CONCLUSIONS: Systemic steroid treatment reduces long-term hearing loss and loss of spiral ganglion neurons in experimental pneumococcal meningitis in adult rats. The findings support a beneficial role of anti-inflammatory agents in reducing hearing loss and cochlear damage in meningitis.

Intratympanic steroid prevents long-term spiral ganglion neuron loss in experimental meningitis.

HYPOTHESIS: Intratympanic steroid treatment prevents hearing loss and cochlear damage in a rat model of pneumococcal meningitis. BACKGROUND: Sensorineural hearing loss is a long-term complication of meningitis affecting up to a third of survivors. Streptococcus pneumoniae is the bacterial species most often associated with a hearing loss. METHODS: Rats were randomly assigned to 3 treatment groups: a group treated with intratympanic betamethasone and 2 control groups treated with either intratympanic or systemic saline. Treatment was initiated 21 hours after infection and repeated once a day for 3 days. Hearing loss and cochlear damage were assessed by distortion product otoacoustic emissions, auditory brainstem response at 16 kHz, and spiral ganglion neuron density. RESULTS: Fifty-six days after infection, auditory brainstem response showed no significant differences between groups, and distortion product otoacoustic emissions showed significant hearing loss at the low frequencies in animals treated with intratympanic steroid compared with animals treated with systemic saline (p < 0.05; Mann-Whitney test). However, intratympanic steroid significantly increased the number of viable neurons in the spiral ganglion compared with both intratympanic and systemic saline (p = 0.0082 and p = 0.0089; Mann-Whitney test). Histology revealed fibrosis of the tympanic membrane and cavity in steroid-treated animals, which plausibly caused the low-frequency hearing loss. CONCLUSION: Intratympanic betamethasone treatment prevents long-term spiral ganglion neuron loss in experimental pneumococcal meningitis. This finding is clinically relevant in relation to post-meningitic hearing rehabilitation by cochlear implantation. However, the drug instillation in the middle ear induced local fibrosis and a concurrent low-frequency hearing loss.

Routes, dynamics, and correlates of cochlear inflammation in terminal and recovering experimental meningitis.

OBJECTIVES/HYPOTHESIS: To examine the routes, dynamics and correlates of cochlear inflammation in meningitis to provide information on the pathogenesis of the associated hearing loss and indications for rational pharmacotherapeutical intervention. STUDY DESIGN: A well-established rat model of Streptococcus pneumoniae meningitis was employed. METHODS: Eight rats were inoculated intrathecally and not treated, whereas 26 were inoculated and treated with ceftriaxone. Six rats were sham-inoculated, making a total of 40 rats. The rats were sacrificed when reaching terminal illness or after 7 days, followed by light microscopy. Routes of cochlear inflammatory infiltration were examined. The volume fraction of inflammatory infiltration was estimated and correlated to bacterial and leukocyte counts in cerebrospinal fluid (CSF) and blood. RESULTS: The perilymphatic space was infiltrated with inflammatory cells via cochlear aqueduct, whereas the endolymphatic space was infiltrated from the spiral ligament. Rosenthal's canal was infiltrated through osseous spiral lamina canaliculi. In the untreated group, the degree of inflammation correlated with time of death, whereas antibiotic treatment reversed this development. Perilymphatic inflammation correlated significantly with the CSF leukocyte count, whereas endolymphatic inflammation correlated with spiral ligament inflammation. CONCLUSIONS: Meningogenic inflammation of the rat cochlea occurs via the cochlear aqueduct and the spiral ligament capillary bed. The spiral ganglion is infiltrated through the osseous spiral lamina. The degree of inflammation correlates positively with time of death in untreated meningitis, whereas antibiotic treatment leads to subsiding infiltration during recovery.