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Streptococcus pneumoniae deficient in pneumolysin or autolysin has reduced virulence in meningitis

Robert A Hirst1, Bejal Gosai, Andrew Rutman

  • 1Department of Infection, Immunity, and Inflammation, University of Leicester, Leicester, United Kingdom. rah9@le.ac.uk

The Journal of Infectious Diseases
|February 12, 2008
PubMed
Abstract

Insights

Pneumolysin and autolysin are key virulence factors in pneumococcal meningitis. Deleting these genes in bacteria significantly reduced disease severity and pathological changes in a rat model.

Area of Science:

  • Microbiology
  • Pathogenesis
  • Neuroscience

Background:

  • The role of pneumolysin and autolysin in pneumococcal meningitis pathogenesis remains unclear.
  • Understanding these factors is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the in vivo roles of pneumolysin and autolysin in the development of pneumococcal meningitis.
  • To elucidate the specific contributions of these bacterial factors to disease progression and host response.

Main Methods:

  • A rat model of pneumococcal meningitis was established using a cisternal catheter for bacterial instillation and cerebrospinal fluid (CSF) sampling.
  • Isogenic mutants of Streptococcus pneumoniae lacking pneumolysin (DeltaPly) or autolysin (LytA(-)) were compared to wild-type strains.

Main Results:

  • Wild-type pneumococci rapidly induced meningitis, while DeltaPly and LytA(-) mutants caused significantly milder or no disease.
  • Infections with wild-type bacteria led to bacterial presence in CSF and cortical tissue, ependymal disruption, and caspase 3 expression/astrocyte hypertrophy, which were absent or reduced in mutant infections.
  • While overall leukocyte counts were similar, differential cell populations varied, with neutrophils/monocytes dominating wild-type infections and lymphocytes predominating in mutant infections.

Conclusions:

  • Pneumolysin and autolysin are critical virulence factors essential for the development of severe pneumococcal meningitis.
  • These bacterial toxins directly contribute to meningitis pathogenesis and associated neuropathological changes in vivo.

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