In Jackson Hole, Good News About CWD—For Now

On December 16, 2020, wildlife officials in Grand Teton National Park received word of something they had been dreading, and for years respected disease experts said was inevitable: confirmation that an elk taken by a hunter in the park had tested positive for Chronic Wasting Disease.

State and federal wildlife managers had known it wasn’t a matter of if, but when, wapiti congregating in Jackson Hole would come down with CWD. The test result 26 months ago further corroborated fears that the always fatal disease afflicting members of the cervid (or deer family) had reached the geographic middle of the Greater Yellowstone Ecosystem.

This article was written by Todd Wilkinson. Read the rest of the article HERE.

Welcome to the TSE Research Center

The PURPOSE of this website is to present information on transmissible spongiform encephalopathies (TSE) in a clear manner and to provide easy access to peer-reviewed publications for those interested in pursuing the topic in a more detailed manner. This site emphasizes the work of Dr. Frank Bastian, (Neuropathologist and Research Professor at Tulane Medical School and the University of New Orleans) with regard to the role of spiroplasma, a wall-less bacterium in the pathogenesis of TSEs.

The PROBLEM with most Government and University informational websites is that no attempt is made to critique the research reports, making it impossible for others to understand the significance of these data. There is much controversy regarding the causality of TSEs. Our research shows that prion amyloid (the TSE research focus for the past 30 years) is the result of a bacterial infection. This controversy directly reflects on Louis Pasteur's efforts to prove that replicating crystals are not the cause of infectious disease, but instead, bacteria are the culprits. Too bad we have to rehash this controversy.

The SOLUTION is to set out a new course for TSE research. Here we present data showing involvement of spiroplasma, a tiny wall-less bacterium, in the pathogenesis of TSEs. Spiroplasma are consistently associated with the TSEs, and experimental spiroplasmosis in animals shows remarkable clinical and pathological similarities to naturally occurring TSEs. A novel spiroplasma species has been isolated into cell-free media from all forms of TSE. Recent breakthrough research shows that this bacterium induces biofilm and becomes buried in a polysaccharide (complex sugar) matrix wherein the organism is resistant to physical and chemical treatments consistent with TSE.

The REWARD for our pursuing alternative research for over 30 years may be 'the TSE riddle is solvable'. Over this time there has been little progress in determining strategies for diagnosis and treatment of CJD patients because scientists have been barking up the wrong tree. If we are ever going to resolve this mystery and relieve the suffering of the many families associated with CJD cases, or the uncertainty of the health of cattle and other ruminants, then we have to go down another path of scientific investigation. This will require broader government funding to attract young researchers into TSE research.

We CONCLUDE that the scientific community must take notice of the abundant data supporting spiroplasma as a candidate causal agent of TSEs and focus on this organism for developing future strategies on handling these diseases.

Spiroplasma Presentation

 

Click HERE for a link to Dr. Bastian's latest presentation on his extensive spiroplasma research.

Data Supports Spiroplasma

It is a remarkable fact that almost all the data used to support the prion concept is conjecture. It is unfortunately the case that the wrong science is being used to address the CWD panzootic.

What follows are numerous lines of evidence supporting the role of an extreme thermo-acidophilic bacterium (spiroplasma sp.) in the pathogenesis of chronic wasting disease and the other transmissible spongiform encephalopathies (with references).

MORPHOLOGICAL

• spiroplasma identified by TEM in CJD brain tissues (Ref 1 & 2)
• spiroplasma in aqueous fluid of sheep with terminal scrapie (Ref 9) 
• experimentally spiroplasma-infected animal model (Ref 3 & 4)

RAT MODEL 

• spiroplasma induces spongiform encephalopathy (Ref 3 & 4)

DEER MODEL

• clinical evidence of brain stem lesions (Ref 8)

• morphological evidence of brain stem lesion (Ref 8)

RUMINANT MODEL- SHEEP AND GOATS

• morphological evidence of brain stem lesion (Ref 8)

• localization to eyes- retinopathy (Ref 9)

MOLECULAR DETECTION OF ORGANISM IN TSE-AFFECTED TISSUES (PCR)

• culture of spiroplasma from CWD & TSE-affected tissues (Ref 7 & 12)

• passage in embryonated eggs (Ref 7)

GROWTH IN CELL-FREE BRUCELLA SPECIAL MEDIA

• growth on agar with formation of subsurface plaques (Ref 12)

• identical biological characteristics of transmissible TSE agent as shown by enumeration of subsurface plaques on agar (Ref 13) 

IMMUNOLOGICAL

• reaction scrapie hyperimmune sera with spiroplasma fibrils (Ref 5) 

• ELISA reaction spiroplasma recombinant HSP60 with CJD sera (Ref 14) 

OTHER

• formation of alpha synuclein in spiroplasma mirum infected mammalian tissue culture

• normal prion protein isoform on cell surface is receptor for bacterium-explains interaction of prion with spiroplasma

REFERENCES

1. Bastian FO: Spiroplasma-like inclusions in Creutzfeldt-Jakob disease. Arch Pathol Lab Med l979;103:665-669.
2. Bastian FO, Hart MN, Cancilla PA: Additional evidence of Spiroplasma in Creutzfeldt-Jakob disease. Lancet l981;1(8221):660.
3. Bastian FO, Purnell DM, Tully JG: Neuropathology of spiroplasma infection in the rat brain. Amer J Pathol l984;114(3):496-514.
4. Tully JG, Bastian FO, Rose DL: Localization and Persistence of Spiroplasma in an Experimental Brain Infection in Suckling Rats. Ann Microbiol (Inst Pasteur) 84;135A:111-117.
5. Bastian FO, Jennings R, Gardner W: Antiserum to Scrapie Associated Fibril Protein Cross-Reacts with Spiroplasma mirum Fibril Proteins. J Clin Microbiol l987;25(12):2430-2431.
6. Bastian FO, Jennings R, Huff C: Neurotropic Response of Spiroplasma mirum following peripheral inoculation in the rat. Ann Microbiol (Inst Pasteur) 1987;138(6):651.
7. Bastian FO, Dash S, Garry R. Linking chronic wasting disease to scrapie by comparison of Spiroplasma mirum ribosomal DNA sequences. Exp Mol Pathol 2004;77:48-56.
8. Bastian FO, Sanders DE, Forbes WA, Hagius SD, Walker JV, Henk WG, Enright FM, Elzer PH. Spiroplasma spp. from TSE Brains or Ticks Induce Spongiform Encephalopathy in Ruminants. J Med Microbiol, 2007; 56: 1235-1242.
9. Bastian FO, Boudreaux C, Hagius SD, Sorensen S, Bulgin M, Enright FM, Elzer PH. Spiroplasma found in eyes of scrapie affected sheep. Veterinary Ophthalmology (2011) 14, 1, 10–17
10. Bastian FO, Elzer PH, Wu X (2012) Spiroplasma spp. biofilm formation is instrumental for their role in the pathogenesis of plant, insect and animal diseases. Exp Mol Pathol 93: 116-128.
11. Bastian FO. (2014) The case for involvement of spiroplasma in the pathogenesis of transmissible spongiform encephalopathies. J Neuropathol Exp Neurol 73: 104-114
12. Bastian FO, Lynch J, Hagius S, Wu X, McCormick G, Luther DG, Elzer PH.(2018) Novel Spiroplasma Spp. Cultured From Brains and Lymph NodesFrom Ruminants Affected With Transmissible Spongiform Encephalopathy. J Neuropathology & Experimental Neurology, 77: 64-73.
13. Bastian FO, Lynch J, Wang W-H. Novel Spiroplasma sp. Isolated From CWD Is an Extreme Bacterial Thermoacidophile That Survives Autoclaving, Boiling, Formalin Treatment, and Significant Gamma Irradiation. J Neuropath Exp Neurol 2019 IN PRESS
14. US 7,888,039 B2 Feb. 15, 2011

 

A Historical Note

Dr. Bastian has been researching the pathogenesis of the transmissible spongiform encephalopathies (TSE) for over four decades. He grew up in Saskatchewan, Canada (a current hotbed of the ongoing panzootic of chronic wasting disease (CWD), a rapidly spreading TSE in deer, moose, and elk populations. CWD was discovered to have spread from Fort Collins, Colorado to currently involve 29 States and four Canadian provinces). CWD has also a global presence involving deer populations in Europe and recently found in reindeer herds in Sweden and Norway. CWD is also affecting the cervid population in South Korea. Dr. Bastian is a Neuropathologist trained under Professor Steven Vogel at Duke Medical School in Durham NC (1968-1972).

In the 1960s the transmissible agent of scrapie (a TSE known for over 300 years in sheep) would not pass through a 100 nanometers filter (the size of a large virus thus the idea of a slow virus disease- a Herpes virus measures 140 nanometers in diameter and is easily visualized by Electron Microscopy [EM]).

After finishing his training at Duke, and a productive fellowship with Alan Rabson at the National Institutes of Health (NIH) in Bethesda MD, involving studies of latency of Herpes viruses in brain and spinal cord, he assumed a position of Assistant Professor of Pathology and Neuropathology at Baylor College of Medicine in Houston, TX. At this juncture, Dr. Bastian diagnosed a case of Creutzfeldt Jakob disease (CJD) which is a fatal TSE in humans by brain biopsy. Since the brain tissues in the brain biopsy were ideally prepared for ultrastructural study, he used his expertise in EM to search for morphological evidence of the TSE transmissible agent, which as mentioned above was virus-like in size. After extensive search, he found a helical bacterium in the CJD-affected brain biopsy tissues that closely resembled a group of phytopathogens (Spiroplasma spp.) recently described by Dr. Joseph Tully, Head of the Mycoplasmology Section at the NIH.

Subsequently Dr. Bastian moved to University of Maryland in Baltimore, MD and set up a close relationship with Dr. Tully at the nearby NIH to pursue his quest and study the biology of these novel organisms. He set up a Spiroplasma laboratory at University of South Alabama as Professor and Director of Neuropathology. During his tenure at USA he established a link between spiroplasma and the TSEs using molecular studies including PCR. He published a comprehensive book on CJD and the other TSEs while on faculty. Dr. Bastian moved his laboratory after Katrina to Department of Veterinary Science at the LSU Agriculture Center where he conducted experiments in small ruminants wherein he completed Koch’s postulates regarding proof of concept that a novel spiroplasma was the cause of TSEs. He then had a research breakthrough in his laboratory wherein he was able to isolate the novel spiroplasma from TSE-affected tissues including CJD, scrapie and CWD into cell-free media and as colonies on agar plates. He showed that the spiroplasma TSE isolates were resistant to boiling, radiation and formalin fixation (an extreme thermoacidophilic bacterium) consistent with the known biological properties of the TSE transmissible agent. All these studies are recorded in peer-reviewed publications. His laboratory is currently established in the AMRI business complex on the University of New Orleans (UNO) campus. Dr. Bastian is currently Research Professor at UNO and Tulane Medical School.