Fierkej
02-04-2003, 01:17 PM
Hello,
Below is the abstract from the Bastian article on spiroplasma, CJD and scrapie, taken from http://www.ncbi.nlm.nih.gov
J Neuropathol Exp Neurol 2001 Jun;60(6):613-20
Spiroplasma sp. 16S rDNA in Creutzfeldt-Jakob disease and scrapie as shown by PCR and DNA sequence analysis.
Bastian FO, Foster JW.
Department of Pathology, College of Medicine, University of South Alabama, Mobile 36617, USA.
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.
PMID: 11398837 [PubMed - indexed for MEDLINE]
Also, at the end of the article was this statement:
"Notwithstanding the controversy raised by our presentation of these data, the most immediate need in research efforts regarding TSE is the development of a means to identify TSE cases, preferably preclinically. We propose that the DNA sequences reported here could be used short term to identify TSE cases. Long-term studies evolving from these data would give new insight into the pathogenic mechanisms involved in TSE. In summary, while it cannot be determined from this study what the role of Spiroplasma sp. may be in the pathogenesis of TSE, the reproducible presence of Spiroplasma-like 16S rDNA in TSE tissues could prove, at the very least, to become the basis for a workable diagnostic test for this group of diseases."
Jean
Below is the abstract from the Bastian article on spiroplasma, CJD and scrapie, taken from http://www.ncbi.nlm.nih.gov
J Neuropathol Exp Neurol 2001 Jun;60(6):613-20
Spiroplasma sp. 16S rDNA in Creutzfeldt-Jakob disease and scrapie as shown by PCR and DNA sequence analysis.
Bastian FO, Foster JW.
Department of Pathology, College of Medicine, University of South Alabama, Mobile 36617, USA.
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.
PMID: 11398837 [PubMed - indexed for MEDLINE]
Also, at the end of the article was this statement:
"Notwithstanding the controversy raised by our presentation of these data, the most immediate need in research efforts regarding TSE is the development of a means to identify TSE cases, preferably preclinically. We propose that the DNA sequences reported here could be used short term to identify TSE cases. Long-term studies evolving from these data would give new insight into the pathogenic mechanisms involved in TSE. In summary, while it cannot be determined from this study what the role of Spiroplasma sp. may be in the pathogenesis of TSE, the reproducible presence of Spiroplasma-like 16S rDNA in TSE tissues could prove, at the very least, to become the basis for a workable diagnostic test for this group of diseases."
Jean