Linking chronic wasting disease to scrapie by comparison of Spiroplasma mirum ribosomal DNA sequences

Frank O Bastian1, Srikanta Dash, Robert F Garry

  • 1Department of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. fbastian@tulane.edu

Insights

Spiroplasma bacteria DNA was detected in animal and human transmissible spongiform encephalopathies (TSE) cases, suggesting its involvement in these fatal neurodegenerative diseases. This finding offers a new perspective on the cause of TSE, including scrapie, chronic wasting disease, and Creutzfeldt-Jakob disease.

Area of Science:

  • Neuroscience
  • Microbiology
  • Pathogen Discovery

Background:

  • Transmissible spongiform encephalopathies (TSE) are fatal neurodegenerative diseases affecting humans and animals.
  • The causative agent of TSE remains unidentified, though it is known to be filterable.

Purpose of the Study:

  • To investigate the potential role of Spiroplasma, a wall-less bacterium, in the pathogenesis of TSE.
  • To detect Spiroplasma ribosomal gene sequences in animal and human TSE-affected tissues.

Main Methods:

  • DNA extraction from sheep (scrapie) and cervid (chronic wasting disease - CWD) brain samples, as well as human (Creutzfeldt-Jakob disease - CJD) brain samples.
  • Polymerase chain reaction (PCR) amplification using Spiroplasma-specific 16S rDNA primers.
  • Southern blotting and DNA sequence analysis to confirm amplicon specificity and homology.

Main Results:

  • Spiroplasma 16S rDNA was detected in 80% of scrapie-infected sheep brains and 86% of CWD-infected cervid samples.
  • Spiroplasma 16S rDNA was also identified in 2 out of 2 human CJD brains, but not in any normal control tissues.
  • Sequence analysis showed >99% homology between the detected Spiroplasma DNA and Spiroplasma mirum.

Conclusions:

  • The presence of Spiroplasma DNA in TSE-infected tissues supports the hypothesis that Spiroplasma is involved in the pathogenesis of these diseases.
  • This study provides evidence for a potential bacterial etiology in TSE, challenging the traditional prion-only hypothesis.

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