Lines of Evidence
1. There is not an immune response to CWD like other disease agents.
When a foreign virus or bacteria enters the body, the immune system starts to fight it. There is inflammation and fever. The body produces antibodies to the disease agent. We do not see these processes in CWD.
The author is not aware that Manuelidis has shown immune response in TSEs characterized by macrophage response indicative of an inflammatory activity. It is interesting in our study of eyes in experimental spiroplasma infection, collections of organisms are seen in the vitreous without inflammatory response.
Frank O. Bastian,* Charles M. Boudreaux,* Sue D. Hagius,* Marie S. Bulgin,† Sharon J. Sorensen-Melson,† Frederick M. Enright* and Philip H. Elzer*, Spiroplasma found in the eyes of scrapie affected sheep. Veterinary Ophthalmology (2011) 14, 1, 10–17
2. Prions are resistant to normal disinfection procedures that kill bacteria and viruses.
Prions can withstand high temperatures, radiation, and chemicals (including formalin) that would normally kill bacteria and viruses. Commonly used methods, such as autoclaving, decreases infectivity but does not completely eliminate it. Harsh chemicals, like bleach, must have an extended contact time to break down the protein.
Indeed the agent causing TSEs is unusually resistant to these treatments suggesting it not to be a conventional organism. That resulted in the prion theory since a mathematician suggested it had to be a protein, even though Pasteur’s well-accepted germ theory is not consistent with a ‘replicating protein’. Our latest research shows that the spiroplasma isolated from TSEs show biologic properties like the transmissible scrapie agent. That may be due to spiroplasma isolates forming biofilm and thus are resistant to such treatments.
Frank O. Bastian, Philip H. Elzer, Xiaochu Wu. Spiroplasma spp. biofilm formation is instrumental for their role in the pathogenesis of plant, insect and animal diseases. Experimental and Molecular Pathology 93 (2012) 116–128.
3. Prions can last in the environment for years.
Multiple studies looking at CWD and scrapie have attempted to “clean” pastures and then restock with animals5. This involves decontaminating all equipment or structures and leaving the area fallow for two or more years. Invariably, new animals end up becoming diseased because prions can bind to steel and soil particles, where they remain infectious. Scrapie persisted in infected sheep paddocks in Iceland for at least 16 years6.
Spiroplasma form biofilm on mica (a clay-like substance) indicating that the bacterium can bind to clay particles in soil and thus can survive for years. Ruminants eat soil therein completing the cycle. Spiroplasma biofilm also binds to stainless steel. SEE ABOVE REFERENCE.
4. Genetic studies have shown that “knock-out” animals that do not produce normal prions do not get TSEs.
Genetically engineered animals that lack the prion gene have been produced in a variety of species from mice to cattle. These animals do not produce normal cellular prion protein, and therefore, are not susceptible to TSEs7.
There is no question that certain genetic makeups may be resistant to TSE infection, and that may involve the prion gene. The association of spiroplasma with prion proteins and formation of the prion amyloid has to be studied in the future. It is of interest that many bacteria including spiroplasmas form several amyloids involved in neurological diseases in tissue culture (alpha synuclein, A beta, tau)
Frank O. Bastian. Combined Creutzfeldt-Jakob-Jacob/ Alzheimer’s Disease Cases are Important in Search for Microbes in Alzheimer’s Disease. J Alzheimer’s disease, 2016.
5. Synthetic “artificial” prions have been created and they cause TSE-like disease.
Most studies use brain material as the source of prions for infection trials, which could potentially transfer other disease agents. However, researchers created prions in E. coli bacteria and produced disease in mice, which is compelling evidence that prions are infectious proteins8.
As of now, purified recombinant prion protein has not been shown to be infectious. Laura Manuelidis at Yale has shown in multiple studies that prion protein is not associated with infectivity.
6. Bacteria have not been identified in diseased animal tissues using a variety of testing methods9,10. DNA or RNA from a virus or bacteria has not been identified consistently in diseased animals.
Examining infected tissues under a microscope has not demonstrated that bacteria are present. If spiroplasma was the cause, genetic sequencing should be able to find the DNA or RNA for that bacteria in samples. Highly sensitive tests used only to amplify proteins has generated infectious prions11. Originally, Dr. Prusiner examined scrapie and found if he inactivated all DNA or RNA in the source material, when he infected experimental animals they still ended up diseased. If he got rid of all the proteins in the source material, the disease agent was no longer infectious.
We have shown morphological and molecular evidence that spiroplasma infection is always associated with TSEs. Recently we have been able to isolate a novel spiroplasma from all forms of TSE available (scrapie, CWD, and CJD tissues). We have shown clear scientific evidence (Koch’s postulates) that a novel spiroplasma is the cause of TSEs. We have shown association of spiroplasma with TSEs; we have consistently cultured a novel spiroplasma sp. out of TSE-affected tissues into cell-free culture; we have inoculated those isolates into sheep and goats and produced the disease; and we have re-isolated spiroplasma isolate from those experimentally inoculated ruminants (KOCH’S POSTULATES CRITERIA OF CAUSALITY).
Frank O. Bastian. The Case for Involvement of Spiroplasma in the Pathogenesis of Transmissible Spongiform Encephalopathies. J Neuropathol Exp Neurol 2014; 73:104-114
Frank O. Bastian, MD, James Lynch, BSc, Sue Hagius, BSc, Xiaochu Wu, PhD, Greg McCormick, BSc, Donald G. Luther, DVM, PhD, and Philip H. Elzer, PhD. Novel Spiroplasma Spp. Cultured From Brains and Lymph Nodes From Ruminants Affected With Transmissible Spongiform Encephalopathy. J Neuropathol Exp Neurol, 2017.
Frank O. Bastian, Dearl E. Sanders,Will A. Forbes,Sue D. Hagius,Joel V. Walker,William G. Henk,Fred M. Enright, and Philip H. Elzer. Spiroplasma spp. from transmissible spongiform encephalopathy brains or ticks induce spongiform encephalopathy in ruminants. Journal of Medical Microbiology (2007), 56, 1235–1242.
This is a classic infectious disease pattern, but many prion proponents seem to have little knowledge of classic infectious diseases, including their latent sequestration for years in myeloid cells and lymph nodes, which is also the hide-out place for TSE agents," Manuelidis said.
"They don't think in terms of those fundamental established principles. They ignore facts that do not fit their belief. Scientific truth, however, is not determined by popular vote or decree."
I have known Laura for many years. She is a Neuropathologist and has spent much of her career debunking the prion theory. She has shown that the prion protein has nothing to do with TSE infectivity. She has done careful work and has thought that a virus was the cause. I asked her if she could test out the spiroplasma work and she said ‘that is your thing’. Hope she does with the new evidence that I can grow the spiroplasma from TSE tissues. She ran into some flack when she demonstrated that Alzheimer’s disease was transmissible showing spongiform encephalopathy in experimental animals. In retrospect her data was due to transmission of CJD which is associated with AD in 15% of cases (see enclosure).
HER COMMENTS ABOUT THE PRION THEORY IN THE COMMUNICATION ARE ACCURATE.