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Spiroplasma sp. 16S rDNA in Creutzfeldt-Jakob disease and scrapie as shown by PCR and DNA sequence analysis
1Department of Pathology, College of Medicine, University of South Alabama, Mobile 36617, USA.
Abstract:
The pathogenesis of the transmissible spongiform encephalopathies (TSE), which include Creutzfeldt-Jakob disease (CJD) in humans and scrapie in sheep, remains an enigma. In this paper we present evidence for the association of Spiroplasma sp., a wall-less prokaryote, with TSE. We have shown PCR amplification of Spiroplasma 16S rDNA in TSE-infected brain tissues (13 of 13 CJD cases and 5 of 9 scrapie cases) and not in control brains (0 of 50). Direct sequencing of the amplified PCR products has confirmed the presence of Spiroplasma-like DNA in all 5 of the TSE brains tested. Our evidence is not necessarily in conflict with involvement of a PrPres--a protease-resistant host-derived protein referred to as the prion--in the pathogenesis of TSE, since there is evidence that another factor is involved. We propose a bacterium, namely Spiroplasma, as this associated factor although the role of Spiroplasma in TSE cannot be determined from these experiments. The presence of the nucleic acid sequence of this microbe in all cases of TSE in our laboratory and not in controls provides direct evidence of the association of Spiroplasma sp. with TSE.
Insights
Researchers found Spiroplasma bacteria in transmissible spongiform encephalopathies (TSE) brain tissue, including Creutzfeldt-Jakob disease (CJD) and scrapie. This microbe
Area of Science:
- Neuroscience
- Microbiology
- Infectious Diseases
Background:
- Transmissible spongiform encephalopathies (TSE) pathogenesis, including Creutzfeldt-Jakob disease (CJD) and scrapie, is not fully understood.
- The role of prions (PrPres) in TSE is established, but evidence suggests other factors may be involved.
Purpose of the Study:
- To investigate the potential association of Spiroplasma sp., a wall-less prokaryote, with TSE.
- To identify potential novel etiological factors in TSE pathogenesis.
Main Methods:
- Polymerase Chain Reaction (PCR) amplification of Spiroplasma 16S rDNA was performed on brain tissues from TSE cases and controls.
- Direct sequencing of PCR products was used to confirm the presence of Spiroplasma-like DNA.
Main Results:
- Spiroplasma 16S rDNA was detected in 13 of 13 CJD cases and 5 of 9 scrapie cases.
- No Spiroplasma 16S rDNA was found in 50 control brain samples.
- Direct sequencing confirmed Spiroplasma-like DNA in all tested TSE brains.
Conclusions:
- The study provides direct evidence for the association of Spiroplasma sp. with TSE.
- Spiroplasma is proposed as a potential associated factor in TSE pathogenesis, although its exact role requires further investigation.
