Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/8859
Full metadata record
DC FieldValueLanguage
dc.contributor.authorHirst, Robert A.-
dc.contributor.authorGosai, Bejal-
dc.contributor.authorRutman, Andrew-
dc.contributor.authorGuerin, Christopher J.-
dc.contributor.authorNicotera, Pierluigi-
dc.contributor.authorAndrew, Peter W.-
dc.contributor.authorO'Callaghan, Christopher L.-
dc.date.accessioned2010-12-10T12:42:52Z-
dc.date.available2010-12-10T12:42:52Z-
dc.date.issued2008-03-01-
dc.identifier.citationJournal of Infectious Diseases, 2008, 197 (5), pp. 744-751en_GB
dc.identifier.issn0022-1899-
dc.identifier.urihttp://jid.oxfordjournals.org/content/197/5/744en_GB
dc.identifier.urihttp://hdl.handle.net/2381/8859-
dc.description.abstractBackground: The role played by pneumolysin and autolysin in pneumococcal meningitis is poorly understood. Method: A rat model was used to investigate the disease, in which surgical implantation of a cisternal catheter allowed bacterial instillation and cerebrospinal fluid (CSF) sampling. Results: CSF infection of rats with wild-type pneumococci caused meningitis within 26 h, whereas isogenic mutants that do not express pneumolysin (∆Ply) or autolysin (LytA ¯) caused very mild or no disease. Wild-type infections resulted in pneumococci in the CSF and cortical homogenates, but a minority of the rats infected with ∆Ply or LytA ¯had bacteria in these locations at 26 h. Leukocyte numbers in the CSF were similar after infection with all pneumococci; however, neutrophils and monocytes predominated after wild-type infection, whereas lymphocytes and atypical lymphocytes predominated after infection with the mutants. Wild-type pneumococci caused disruption to the ependyma, but this was not observed in rats infected with ∆Ply or LytA ¯. Cells surrounding the ventricles in wild type–infected animals expressed caspase 3, and astrocytes had hypertrophy; both findings were absent in rats infected with the mutants. Conclusions: This study provides strong in vivo evidence that pneumolysin and autolysin play crucial roles in the pathogenesis of pneumococcal meningitis.en_GB
dc.language.isoenen_GB
dc.publisherUniversity of Chicago Pressen_GB
dc.rightsCopyright © 2010. University of Chicago Press. All rights reserved.-
dc.rightsThis is the final publisher edited version of the paper published as Journal of Infectious Diseases, 2008, 197 (5), pp. 744-751. This version was first published at http://www.journals.uchicago.edu/doi/abs/10.1086/527322, Doi: 10.1086/527322.-
dc.titleStreptococcus pneumoniae Deficient in Pneumolysin or Autolysin Has Reduced Virulence in Meningitisen_GB
dc.typeArticleen_GB
dc.identifier.doi10.1086/527322-
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

Files in This Item:
File Description SizeFormat 
527322.web[1].pdf525.04 kBAdobe PDFView/Open


Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.