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Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In Vitro Prion Protein Conversion Assay
Published on: March 10, 2015
Spiroplasma as a candidate agent for the transmissible spongiform encephalopathies
1Department of Pathology, Tulane Health Science Center, New Orleans, Louisiana 70112, USA. fbastian@tulane.edu
Journal of Neuropathology and Experimental Neurology
|October 11, 2005
Summary
A novel Spiroplasma species was recovered from animals and humans with transmissible spongiform encephalopathies (TSEs). This review presents evidence suggesting Spiroplasma infection may be the cause of TSEs, warranting further investigation.
Area of Science:
- Veterinary Neurology
- Infectious Diseases
- Microbiology
Background:
- Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases affecting various animal species and humans.
- Diseases include scrapie in sheep, chronic wasting disease in cervids, and Creutzfeldt-Jakob disease in humans.
- The etiology of TSEs remains a subject of intense research and debate.
Purpose of the Study:
- To review and synthesize evidence supporting the hypothesis that Spiroplasma infection is involved in the pathogenesis of TSEs.
- To evaluate the role of a novel Spiroplasma species in the context of an epidemiologic infection model for TSEs.
- To address the potential of Spiroplasma as the causal agent of TSEs.
Main Methods:
- Review of accumulated evidence over 30 years regarding Spiroplasma infection and TSEs.
- Analysis of data within an established epidemiologic infection model.
- Consideration of Koch's postulates in relation to Spiroplasma and TSEs.
Main Results:
- A novel Spiroplasma species was successfully isolated from brain tissues of sheep with scrapie, cervids with chronic wasting disease, and patients with Creutzfeldt-Jakob disease.
- Evidence suggests a consistent involvement of Spiroplasma infection in TSE cases across different species.
- The findings support the hypothesis linking Spiroplasma sp. to the development of TSEs.
Conclusions:
- The recovery of Spiroplasma sp. from TSE-affected hosts raises significant questions about its role in disease causation.
- Accumulated evidence supports the hypothesis that Spiroplasma sp. is the causal agent of TSEs.
- Fulfillment of Koch's postulates is necessary to definitively establish Spiroplasma as the causative agent of TSEs.
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