title: Routes, dynamics, and correlates of cochlear inflammation in terminal and recovering experimental meningitis.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
authors.affiliation: Department of Otorhinolaryngology, Head and Neck Surgery, Copenhagen University Hospital Gentofte, Denmark. peca@geh.regionh.dk
authors.forename: Per
authors.initials: P
authors.lastname: Cayé-Thomasen
authors.forename: Lise
authors.initials: L
authors.lastname: Worsøe
authors.forename: Christian Thomas
authors.initials: CT
authors.lastname: Brandt
authors.forename: Hidemi
authors.initials: H
authors.lastname: Miyazaki
authors.forename: Christian
authors.initials: C
authors.lastname: Ostergaard
authors.forename: Niels
authors.initials: N
authors.lastname: Frimodt-Møller
authors.forename: Jens
authors.initials: J
authors.lastname: Thomsen
mesh_terms: D000818:Animals; D001707:Biopsy, Needle; D002443:Ceftriaxone / Q000494:pharmacology*; D002555:Cerebrospinal Fluid / Q000166:cytology / Q000382:microbiology; D015834:Cochlear Diseases / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology*; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D007249:Inflammation / Q000209:etiology / Q000473:pathology*; D007958:Leukocyte Count; D008297:Male; D008586:Meningitis, Pneumococcal / Q000150:complications* / Q000188:drug therapy / Q000473:pathology*; D008854:Microscopy, Electron; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012680:Sensitivity and Specificity
chemical_list: D002443:Ceftriaxone