flounder9
Member
Research claiming that bacteria are the causative agents of transmissible spongiform encephalopathies has never been reproduced despite extremely rigorous attempts to do so.
In blind studies done by the University of Maryland School of Medicine, samples of brain material infected with scrapie, along with uninfected samples, were searched for Spiroplasma spp. and other common bacteria and bacteria-like structures using Polymerase Chain Reaction (PCR) amplification (PCR is a method widely used in molecular biology to make many copies of specific DNA segments). Researchers found no evidence that any eubacterium, including Spiroplasma or any other bacteria type, was consistently associated with scrapie-infected brain tissue, thus concluding that the “agent responsible for TSE disease cannot be a spiroplasma or any other eubacterial species.”
Source:
Absence of Spiroplasma or Other Bacterial 16S rRNA Genes in Brain Tissue of Hamsters with ScrapieIrina Alexeeva, Ellen J. Elliott, Sandra Rollins, Gail E. Gasparich, Jozef Lazar, Robert G. RohwerJournal of Clinical Microbiology Jan 2006, 44 (1) 91-97; DOI: 10.1128/JCM.44.1.91-97.2006
An extensive research project completed at Louisiana State University on the potential roles of Spiroplasmain transmissible spongiform encephalopathies found that following inoculation of Spiroplasma mirum into neonatal goats and five month-old white-tailed deer, none of the animals developed clinical signs or pathology seen in transmissible spongiform encephalopathies. In this study, the bacteria were introduced to the animals intracerebrally, intravenous, or intradermally. Additionally, researchers conducting this study tested three species of Spiroplasma and found that they were susceptible to minimal dilutions of common laboratory disinfectants as well as heat sterilization of only 250°F for 15 minutes. In a wide array of other studies, samples of transmissible spongiform encephalopathy-infected material treated with similar sterilization methods were shown to remain infectious; thus indicating that other factors not related to bacteria result in the transmission and/or persistence of the disease.
Source:
French, Hilari Maree, "Characterization of Spiroplasma mirum and its role in transmissible spongiform encephalopathies" (2011).
LSU Doctoral Dissertations. 3012.
Nearly all experimental examination of TSE-causing agents point to proteins at the infectious agent.
The hallmark study of the prions’ role in transmissible spongiform encephalopathies was conducted by Dr. Stanley Prusiner who demonstrated that after adding enzymes that destroyed DNA and RNA to scrapie-infected brain material, the material remained infections. These enzymes would have damaged or destroyed bacteria present in the samples. However, when he adding protein-neutralizing enzymes to the scrapie-infected brain material, it’s infectivity plummeted. Thus, he demonstrated that the causative agent of the disease was most likely protein based, not bacterial-based. It should be noted that Prusiner’s work earned a Nobel Prize due to its rigor and reproducibility by other researchers.
Source:
Prusiner SB. (1982). Novel proteinaceous infectious particles cause scrapie. Science. 9;216(4542):136-44.
Artificially synthesized prions have shown to be capable of causing prion disease.
To rule out the role of unidentified substances as disease causative agents in samples of infectious tissues, researchers successfully created a “clean” synthetic version of the scrapie prion that was capable of infecting mice.
Source:
Legname G, Baskakov IV, Nguyen HB, et al. (2004). Synthetic Mammalian Prions. Science. 7;305:673-676.
https://nationaldeeralliance.com/ed...vKK4AHmka-0E8Q1mQiOWDJkWA1d7unBBhqGKrKT5X5-kg
In blind studies done by the University of Maryland School of Medicine, samples of brain material infected with scrapie, along with uninfected samples, were searched for Spiroplasma spp. and other common bacteria and bacteria-like structures using Polymerase Chain Reaction (PCR) amplification (PCR is a method widely used in molecular biology to make many copies of specific DNA segments). Researchers found no evidence that any eubacterium, including Spiroplasma or any other bacteria type, was consistently associated with scrapie-infected brain tissue, thus concluding that the “agent responsible for TSE disease cannot be a spiroplasma or any other eubacterial species.”
Source:
Absence of Spiroplasma or Other Bacterial 16S rRNA Genes in Brain Tissue of Hamsters with ScrapieIrina Alexeeva, Ellen J. Elliott, Sandra Rollins, Gail E. Gasparich, Jozef Lazar, Robert G. RohwerJournal of Clinical Microbiology Jan 2006, 44 (1) 91-97; DOI: 10.1128/JCM.44.1.91-97.2006
An extensive research project completed at Louisiana State University on the potential roles of Spiroplasmain transmissible spongiform encephalopathies found that following inoculation of Spiroplasma mirum into neonatal goats and five month-old white-tailed deer, none of the animals developed clinical signs or pathology seen in transmissible spongiform encephalopathies. In this study, the bacteria were introduced to the animals intracerebrally, intravenous, or intradermally. Additionally, researchers conducting this study tested three species of Spiroplasma and found that they were susceptible to minimal dilutions of common laboratory disinfectants as well as heat sterilization of only 250°F for 15 minutes. In a wide array of other studies, samples of transmissible spongiform encephalopathy-infected material treated with similar sterilization methods were shown to remain infectious; thus indicating that other factors not related to bacteria result in the transmission and/or persistence of the disease.
Source:
French, Hilari Maree, "Characterization of Spiroplasma mirum and its role in transmissible spongiform encephalopathies" (2011).
LSU Doctoral Dissertations. 3012.
Nearly all experimental examination of TSE-causing agents point to proteins at the infectious agent.
The hallmark study of the prions’ role in transmissible spongiform encephalopathies was conducted by Dr. Stanley Prusiner who demonstrated that after adding enzymes that destroyed DNA and RNA to scrapie-infected brain material, the material remained infections. These enzymes would have damaged or destroyed bacteria present in the samples. However, when he adding protein-neutralizing enzymes to the scrapie-infected brain material, it’s infectivity plummeted. Thus, he demonstrated that the causative agent of the disease was most likely protein based, not bacterial-based. It should be noted that Prusiner’s work earned a Nobel Prize due to its rigor and reproducibility by other researchers.
Source:
Prusiner SB. (1982). Novel proteinaceous infectious particles cause scrapie. Science. 9;216(4542):136-44.
Artificially synthesized prions have shown to be capable of causing prion disease.
To rule out the role of unidentified substances as disease causative agents in samples of infectious tissues, researchers successfully created a “clean” synthetic version of the scrapie prion that was capable of infecting mice.
Source:
Legname G, Baskakov IV, Nguyen HB, et al. (2004). Synthetic Mammalian Prions. Science. 7;305:673-676.
https://nationaldeeralliance.com/ed...vKK4AHmka-0E8Q1mQiOWDJkWA1d7unBBhqGKrKT5X5-kg