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Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/8859

Title: Streptococcus pneumoniae Deficient in Pneumolysin or Autolysin Has Reduced Virulence in Meningitis
Authors: Hirst, Robert A.
Gosai, Bejal
Rutman, Andrew
Guerin, Christopher J.
Nicotera, Pierluigi
Andrew, Peter W.
O'Callaghan, Christopher L.
Issue Date: 1-Mar-2008
Publisher: University of Chicago Press
Citation: Journal of Infectious Diseases, 2008, 197 (5), pp. 744-751
Abstract: Background: 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.
ISSN: 0022-1899
Links: http://www.journals.uchicago.edu/doi/abs/(...)
http://dx.doi.org/10.1086/527322
http://hdl.handle.net/2381/8859
Type: Article
Rights: Copyright © 2010. University of Chicago Press. All rights reserved.
Description: This 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.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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