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The case for involvement of spiroplasma in the pathogenesis of transmissible spongiform encephalopathies

Frank O Bastian1

  • 1From the Department of Animal Science, Louisiana State University Agricultural Center, Baton Rouge, Louisiana.

Journal of Neuropathology and Experimental Neurology
|January 16, 2014
PubMed

Insights

Spiroplasma bacteria form biofilms, potentially explaining their role in transmissible spongiform encephalopathies (TSEs). This biofilm formation may explain prion amyloid development and disease transmission, suggesting new diagnostic and therapeutic targets for neurodegenerative diseases.

Area of Science:

  • Microbiology
  • Neuroscience
  • Infectious Diseases

Background:

  • Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases.
  • The exact cause and transmission mechanisms of TSEs remain incompletely understood.
  • Spiroplasma, a genus of wall-less bacteria, has been implicated in TSE pathogenesis.

Purpose of the Study:

  • To investigate the role of Spiroplasma biofilm formation in TSE pathogenesis.
  • To explore Spiroplasma's potential contribution to prion amyloid formation.
  • To identify Spiroplasma as a potential target for TSE diagnostics and therapeutics.

Main Methods:

  • Analysis of Spiroplasma biofilm structure and resistance properties.
  • Investigation of Spiroplasma's interaction with host proteins and amyloid formation.
  • Examination of Spiroplasma's role in the transmission of scrapie and chronic wasting disease.
  • Assessment of Spiroplasma's production of α-synuclein in mammalian cell cultures.

Main Results:

  • Spiroplasma biofilms exhibit resistance to physical and chemical treatments, mimicking TSE agent properties.
  • Spiroplasma biofilms bound to clay particles may facilitate the lateral transmission of scrapie and chronic wasting disease.
  • Spiroplasma biofilms on surgical instruments could contribute to iatrogenic transmission of Creutzfeldt-Jakob disease.
  • Spiroplasma's curli-like fibrils may initiate host prion amyloid formation, potentially through α-synuclein production.

Conclusions:

  • Spiroplasma biofilm formation is a plausible mechanism explaining the pathogenesis and transmission of TSEs.
  • Spiroplasma's ability to trigger prion amyloid formation warrants further investigation.
  • Developing diagnostic tests and therapeutic strategies targeting Spiroplasma is crucial for managing TSEs, including Creutzfeldt-Jakob disease.

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