CLEVELAND, October 4, 2019--Wenquan Zou, MD, PhD, an expert in degenerative neurological diseases, along with his collaborators Shu G. Chen, PhD also from the Case Western Reserve University School of Medicine, Jiyan Ma, MD, PhD, from Van Andel Institute in Grand Rapids, Michigan, and Thomas Beach, MD, PhD, from Banner Sun Health Research Institute, Sun City, Arizona, have received a five-year, $3.6 million grant from the National Institutes of Health for diagnosing Parkinson's disease (PD) via an innovative skin testing approach. Also part of the team is Steven Gunzler, MD, a neurologist at the University Hospitals Cleveland Medical Center and the School of Medicine.

The methodology uses highly sensitive technology to detect the presence in the skin of "misfolded" alpha-synuclein (α-Syn) proteins that are the cause of nerve cell dysfunction and death in PD.


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Novel Spiroplasma sp. Isolated From CWD Is an Extreme Bacterial Thermoacidophile That Survives Autoclaving, Boiling, Formalin Treatment, and Significant Gamma Irradiation


Rapid spreading of chronic wasting disease (CWD) in wildlife and captive cervid populations has exposed lack of progress in deal- ing with the transmissible spongiform encephalopathies (TSE) of man and animals. Since the TSE transmissible agent was resistant to extremes in environmental and chemical treatments, focus was on an unconventional agent including the prion theory. Recent break- through research has revealed consistent isolation of a novel Spiro- plasma sp. from TSE-affected tissues that propagates in cell-free media and on agar. Here, we developed a live culture assay to test whether the CWD spiroplasma isolate possessed unconventional bi- ologic properties akin to those of the transmissible agent of TSE.


View the online abstract HERE. 

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After much deliberation and after years of working as a gratis professor at LSU Agricultural Center, I recently decided to resign. As my research continues to move forward at an exciting pace, I decided to explore other exciting opportunities and partnerships during this next phase of my research that are more conducive to completing my long term goals. I have been in discussions with collaborators at Unified Sportsmen of Pennsylvania, inter alia, about a joint venture and will let you know once more details are confirmed. I am in the process of moving my laboratory to New Orleans and have included new e-mail contact information: bastianfrank87 AT gmail DOT com (Phone 504-610-9177). Thanks for your continued support with my research.

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Dr. Frank Bastian, formerly of the Louisiana State University (LSU), has promoted a theory since about 2003 that Chronic Wasting Disease (CWD) is caused by spiroplasma bacteria. Nearly every other researcher has determined that CWD is caused by misfolded prions, which are protein materials. According to Dr. James Kroll and others, Bastian's theory has been discredited because no other researcher has been able to replicate Bastian's findings. Because of his controversial theory, Bastian lost his privilege to do research at LSU.

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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).


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