Electron microscopic temporal bone histopathology in experimental pneumococcal meningitis

Citation
Jm. Rappaport et al., Electron microscopic temporal bone histopathology in experimental pneumococcal meningitis, ANN OTOL RH, 108(6), 1999, pp. 537-547
Citations number
43
Categorie Soggetti
Otolaryngology,"da verificare
Journal title
ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY
ISSN journal
00034894 → ACNP
Volume
108
Issue
6
Year of publication
1999
Pages
537 - 547
Database
ISI
SICI code
0003-4894(199906)108:6<537:EMTBHI>2.0.ZU;2-8
Abstract
Bacterial meningitis is one of the most common causes of acquired profound sensorineural deafness in children. Measurement of hearing and examination of the cochlea is limited in patients suffering from acute meningitis. A ra bbit model of pneumococcal meningitis was developed to identify the tempora l bone histopathologic changes that occur in meningogenic labyrinthitis cau sed by Streptococcus pneumoniae. Light microscopy was previously performed on temporal bones from acutely meningitic rabbits with profound hearing los s as determined electrophysiologically. Extensive inflammation of the cochl ea with endolymphatic hydrops was observed. The organ of Corti, however, sh owed preserved architecture in the majority of these animals. In order to f urther investigate these findings, a protocol was used to create meningitic rabbits with hearing loss ranging from early high-frequency loss to profou nd deafness. The temporal bones from 7 rabbits were examined by transmissio n electron microscopy. In cases of mild hearing loss, partial degeneration of the inner row of outer hair cells, as well as edema of efferent cochlear nerve endings and marginal cells of the stria vascularis, was seen. With i ncreasing degrees of hearing loss, the remainder of the organ of Corti and intermediate cells of the stria showed ultrastructural abnormalities. Spira l ganglion cells and basal cells of the stria vascularis remained intact in all subjects. This study provides unique information regarding the histolo gy and pathophysiology of meningogenic dearness. The clinical implications of these findings are discussed, with an emphasis on potentially reversible changes and therapeutic intervention.