Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well established that sensorineural hearing loss (SNHL) is an important sequela of acute bacterial meningitis. Previous human temporal bone histopathologic studies have suggested that such hearing loss is due to labyrinthitis. This study involved a detailed and systematic evaluation of the auditory and vestibular end-organs in 41 human temporal bones from patients with acute bacterial meningitis, aimed at describing the spectrum of histopathologic changes within the labyrinth, ascertaining likely routes for spread of infection from the meninges to the inner ear, and comparing the data from humans with those described in a rabbit model of meningogenic labyrinthitis. Our study revealed the following: (a) Suppurative labyrinthitis occurred in 20 (49%) bones. Of these 20 bones, the cochlea was affected in all, whereas the vestibular organs were involved in 10. Eosinophilic staining of inner ear fluids without the presence of inflammatory cells (so-called "serous" labyrinthitis) occurred in 14 of the remaining 21 bones. This staining occurred primarily within the vestibular system. Its significance and pathogenesis remains unknown; (b) Sensory and neural structures of the inner ear appeared intact in the majority of specimens, including bones with suppurative labyrinthitis and those with eosinophilic staining of inner ear fluids. This finding raises the possibility of preventing or reversing SNHL by therapeutic intervention. Spiral ganglion cells were severely degenerated in 12% of bones, indicating a retrocochlear site of hearing loss in addition to the cochlea. This subset of patients may perform poorly after cochlear implantation; (c) It has been traditionally assumed that irreversible and permanent SNHL is caused by suppurative labyrinthitis, whereas reversible SNHL is caused by serous labyrinthitis. Our findings question the validity of these assumptions; (d) The data were consistent with the hypothesis that both the cochlear modiolus and cochlear aqueduct can serve as potential pathways for spread of infection from the meninges to the inner ear; (e) There were many similarities in the histopathology of the inner ear in humans when compared with the rabbit model of meningogenic labyrinthitis. A notable difference was that the cochlear aqueduct appeared to be the sole pathway for spread of infection in the rabbit, whereas in the human, both the modiolus and aqueduct were possible pathways.
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PMID:A human temporal bone study of acute bacterial meningogenic labyrinthitis. 881 13

In patients with acute bacterial meningitis, hearing loss can be transient but is often permanent. The mechanisms underlying meningitis-associated hearing loss are not fully understood. Therefore, we investigated the morphological correlates of hearing loss in a rat model of pneumococcal meningitis. Transcutaneous intracisternal injection of Streptococcus pneumoniae resulted in a dose-dependent hearing loss (determined by auditory brainstem response audiometry), which was partially reversible during the acute stage. Nevertheless, a severe permanent hearing loss persisted until 2 weeks after infection. Suppurative labyrinthitis was accompanied by blood-labyrinth barrier disruption (determined by cochlear Evans blue extravasation), which correlated closely with hearing loss during the acute stage but not after recovery. Two weeks after infection, spiral ganglion neuronal density was markedly decreased and correlated with the severity of permanent hearing loss. Neuronal loss can be explained by the new finding of meningitis-associated spiral ganglion neuronal necrosis rather than apoptosis (determined by morphology, TUNEL staining, and immunohistochemistry).
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PMID:Morphological correlates of acute and permanent hearing loss during experimental pneumococcal meningitis. 1274 66