title: Bacterial meningitis causes two distinct forms of cellular damage in the hippocampal dentate gyrus in infant rats.
abstract: Bacterial meningitis causes neurological sequelae in up to 50% of survivors. Two pathogens known for their propensity to cause severe neurological damage are Streptococcus pneumoniae and group B streptococci. Some forms of neuronal sequelae, such as learning and memory deficits, have been associated with neuronal injury in the hippocampus. To learn more about hippocampal injury in meningitis, we performed a comparative study in bacterial meningitis due to S. pneumoniae and group B streptococcus, in which 11-day-old infant rats were infected intracisternally with either of the two pathogens. Histopathological examination of the neuronal injury in the dentate gyrus of the hippocampus showed that S. pneumoniae caused predominantly classical apoptotic cell death. Cells undergoing apoptosis were located only in the subgranular zone and stained positive for activated caspase-3 and TUNEL. Furthermore, dividing progenitor cells seemed particularly sensitive to this form of cell death. Group B streptococcus was mainly responsible for a caspase-3-independent (and TUNEL-negative) form of cell death. Compared with the morphological features found in apoptosis (e.g., apoptotic bodies), this form of neuronal death was characterized by clusters of uniformly shrunken cells. It affected the dentate gyrus throughout the blade, showing no preferences for immature or mature neurons. Thus, depending on the infecting agent, bacterial meningitis causes two distinct forms of cell injury in the dentate gyrus.
authors.affiliation: Institute for Infectious Diseases, University of Bern, Bern, Switzerland.
authors.forename: Yoeng-Delphine
authors.initials: YD
authors.lastname: Bifrare
authors.forename: Christian
authors.initials: C
authors.lastname: Gianinazzi
authors.forename: Hans
authors.initials: H
authors.lastname: Imboden
authors.forename: Stephen L
authors.initials: SL
authors.lastname: Leib
authors.forename: Martin G
authors.initials: MG
authors.lastname: Täuber
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000494:pharmacology; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D003497:Cyclic N-Oxides; D018891:Dentate Gyrus / Q000382:microbiology* / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D020287:In Situ Nick-End Labeling; D008586:Meningitis, Pneumococcal / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D009336:Necrosis; D009410:Nerve Degeneration / Q000188:drug therapy / Q000382:microbiology* / Q000473:pathology*; D009474:Neurons / Q000382:microbiology* / Q000473:pathology*; D009589:Nitrogen Oxides / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013292:Streptococcus agalactiae / Q000472:pathogenicity; D013296:Streptococcus pneumoniae / Q000472:pathogenicity; D016896:Treatment Outcome
chemical_list: D000975:Antioxidants; D003497:Cyclic N-Oxides; D009589:Nitrogen Oxides; C029217:phenyl-N-tert-butylnitrone; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases