# CWD & Spiroplasma



## Ed Gehrman (Aug 20, 2002)

Sportsmen,
I wonder if you'd spare me a few minutes and examine some 
evidence that indicates the infective agent in CWD is a conventional organism, a Spiroplasma. I believe Prions are a 
result of the infection and while important, not the main factor to consider.
We are able to diagnose TSE/CWD (under certain circumstances), 
but we will never understand the dynamics of CWD until we understand the 
nature of the infective agent, and we cannot develop a diagnostic test until we 
know what we're testing for. If the agent is a spiroplasma, then a simple saliva 
test could be developed since spiroplasma migrate to the salivary glands 
( a symptom of CWD is excessive drooling). Also tetracycline, which is 
effective in limiting the growth of Spiroplasma, (and now known to affect the disease agent)
could be a possible intervention, if the disease were spotted sooner with a 
validated test procedure. 
Could you review the following information and 
perhaps briefly discuss Dr. Bastian's research with me. Please don't consider this argumentative. 
I really want to know what you think.

(I'm a teacher and part time writer and researcher on environmental contaminants)

Ed Gehrman
[email protected]

PS
It's difficult to understand why the scientific establishment has ignored spiroplasma as the agent. Science has become so specialized that it's very difficult
for most practicing scientists, MDs included, to venture very far from their specialties and keep abreast of the new developments.
But in the case of the prion, there's something else going on. The prion is some kind of a red herring, a distraction, that keeps most of the scientific community 
and the general public, including the press, from understanding the true nature of this disease (TSE & probably including Alzheimer's). Why is there such a resistance to bacteria as the causal agent? One bit of history I found interesting while researching spiroplasma (FASTIDIOUS ENDOPHYTES)
is that for over 70 years the plant pathologists studying various plant diseases resisted (in spite of overwhelming evidence to the contrary) the notion that many of the diseases they were examining were the result of spiroplasma infection. It turned out they were wrong. We now know that Spiroplasma are/were involved in the vast majority of the serious plant infestations. We don't have 70 years. The Brown's story should soon become quite common
if we don't begin to understand these diseases.
Please contact Dr. Bastian if you have any questions. He's THE authority on CJD in this country. 

http://www.mcl.tulane.edu/departments/pathology/faculty/bastian/bastian.html

From Dr. Frank Bastian MD

This note is written in regard to the controversy over the nature of the transmissible agent of CJD and the other transmissible spongiform encephalopathies (TSE includes CJD, BSE, wasting disease, transmissible mink encephalopathy, kuru). Little is known about the pathogenesis of these diseases for the following reasons.

1) The identity of the agent is not known.

2) The epidemiology of TSE is not known.

3) There is no workable test.

4) Susceptibility to TSE is unknown.


The reasons that we have accumulated so little information in this regard is that the research efforts have been hampered for twenty years by investigations limited to the 'prion'. This altered host protein , in my opinion, is a reaction product of the infection; yet, most monies committed to research on TSE has essentially been limited to studies of this protein. This course of action by funding agencies has continued even though:

1) Numerous studies have shown that the 'prion' can be separated from TSE infectivity.

2) The prion in purified form is not infectious.

3) Prion researchers have admitted that another factor is involved.


The prion concept is based upon some false premises, exemplified by the following:

a) There is no nucleic acid component*

This concept is based on experiments wherein Psoralin, which binds and cross-links nucleic acids thereby making them more susceptible to destruction by UV radiation, causes no loss of infectivity when added to scrapie tissues. It is noteworthy that two conventional pathogens, polio virus and Bacillus subtilis are resistant to these treatments. In other words, if the chemical cannot penetrate into the microbe, it can't cause a problem. These data do not rule out the presence of a nucleic acid component in the TSE agent.

b) The scrapie agent is resistant to irradiation, fixatives and extremes in heat unlike any conventional pathogen.

This conclusion does not take into account that 99.99% of the agent is killed by these treatments. We have shown that Spiroplasma are able to withstand boiling temperature (100oC). We have seen Spiroplasma swim in culture tube filled with 50% glutaraldehyde, a potent tissue fixative used normally at 3% concentration. Radiodurans, a radiation resistant microbe, survives irradiation because of an efficient DNA repair mechanism, which may be operative in the TSE agent. There is nothing in experimental data obtained so far that eliminates the possibility of a conventional pathogen being involved in the pathogenesis of TSE.

Spiroplasma are also resistant to wide shifts in pH, from 3 to 11. I would suspect that the prion protein would be susceptible to destruction by passage through the acidity of the stomach. This is important since the oral route is an important source of TSE infection in both animals and man.

My data, accumulated over the past 25 years, supports the role of a bacterium (Spiroplasma) in the pathogenesis of TSE. This concept is based on the following:

1) Spiroplasma-like inclusions were found by myself in a brain biopsy and necropsy tissue by electron microscopic study of CJD patients. I reported these findings in Archives of Pathology and Laboratory Medicine, 1979 and Lancet, 1981.

2) Experimental spiroplasma infection in the rodent induces a spongiform encephalopathy. I reported those findings in American Journal of Pathology, 1984.

3) Fibril proteins within Spiroplasma and unique to this microbe are identical morphologically to scrapie-associated fibrils that are seen consistently in TSE.

Furthermore, scrapie antibody shares antigenic determinants with spiroplasma proteins. I reported the comparison between scrapie and spiroplasma proteins in Journal of Clinical Microbiology, 1987.

4) Spiroplasma DNA (the 16S ribosomal gene specific to this microbe) has been found in all TSE brains tested (18 brains) and not in controls (50 brains). This has been documented by polymerase chain reaction using probes specific to Spiroplasma 16S rDNA. The PCR product has been directly sequenced and reveals 99% homology with Spiroplasma DNA. Preliminary studies have been reported in Journal of Neuropathology and Experimental Neurology, 1999.

Another important observation that appears to support the bacterial concept is that experimental scrapie can be prevented by tetracycline therapy. Although the authors try to explain these results by some effect on the folding of the prion protein, a strong consideration has to be the involvement of a bacterium in TSE.

CONCLUSION:

Currently, our scientific community is floundering regarding this problem. There is a great deal of anxiety out there among the public and the medical community with regard to safety of food (meat), the blood supply (for transfusions) and the safety of medical personnel involved in the care of CJD patients. I propose that these concerns would be alleviated if there was evidence of a conventional microbe which would be accessible to treatment regimens. I believe that the prion is likely a reaction product in that the bacterium may coat itself with this host protein to hide from the immune system (a common phenomenon with other bacterial infections). Therefore, it is essential that a broader base of funding be provided by government agencies to provide for all possible explanations and to involve more diversified and unbiased research laboratories in this field.


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## sadocf1 (Mar 10, 2002)

Thanks to Ed- something different from the PR propoganda concerning TSE'S DISTRIBUTED SO FREELY BY THE "SCIENTIFIC COMMUMITY''
When the prion theory was advanced it was greeted by much disbelief and criticism by the "SCIENTIFIC COMMUNITY'' but gradually accepted.
Dr. Bastians credentials are excellent. His findings and conclusions will also be greeted by disbelief and criticism.
Research will eventually find the answers to the transmissable spongiform encephalopathies, lets give it the funding to do the job instead of spending our time and money eradicating the host animals.


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## Steve (Jan 15, 2000)

Very interesting indeed.


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## Huntnut (Jan 21, 2000)

Mr Gehrman,

First of all, let me say welcome to the site. It's nice to see new members post such comprehensive threads. I hope you will stay, and discuss some of these issues.

Are you a deer hunter? Or is your interest in TSE's only proffesional? We have a mix of both here, and it adds insight.

I have researched some of Dr. Bastians stuff, but it is difficult to locate under the mounds of prion cause and effect theory.
I stumbled across the spiroplasma research about 6 months ago. 
I recall reading that the spiroplasma was evident whenever the mutated prions were evident in this specific study (sorry no reference). The article was wrapped around the protien being a by-product of the spiroplasma, and how difficult it is to have this theory researched.
With the prion cause theory, I could never understand the gap in reasoning on how an inanimate protien prion could cause normal inanimate protiens to mutate. (Wildlife Bio major! Not Bio Chem!!) 

The spiroplasma agent theory seems much more plausible, but much less supported, and I haven't seen any studies specifically disproving this theory. I remember thinking this might be a crack in the CWD armor. Basically, if spiroplasma IS the agent, it is a living bacteria, and if living, it can be killed.

Actually, I came across this while searching for evidence of a reported individual host having a natural immunity to TSE's. I wanted to understand if TSE's were 100% fatal or 99.9999% fatal when contracted. I want to understand whether this was capable of species extinction, or whether we are witnessing natural selection in action.

I also agree with Sadocf1,
Right now our time is well spent writing our favorite politicians lobbying for research money. We need to trust our Pres that he will release those locked up CWD research funds once the pork barrell fat has been trimmed.
But I disagree about eradication. I feel that until we do develop tests, vaccines, and knowledge, it is imperative that states work to limit prevalence. I agree with the eradication efforts of many states in areas where CWD has been found. 
I also believe that the bulging deer herds east of the Mississippi river need to be significantly trimmed..not only for CWD but Bovine TB as well.
I will never believe that it is safe for our state to host 2 million deer pinched between 2 diseases.(Any diseases) I also cannot believe that the exploding deer herd did not aid Bovine TB into becoming deeply entrenched in our wild herd.
The prevalence level has steadied these recent years in direct correlation to the lower deer herd. 
Colorado has dealt with CWD for 30 years. They have also maintained a low prevalence by removing a significant portion of hosts.

I believe that CWD will arrive in Michigan before science arrives at a vaccine or cure.

I can see tests becoming cheap and effective, offering quick results as soon as the private sector gets their market operating.

I think we will see deer hunting in the future with CWD. I can see a state herd that maintains a low prevalence (2%-7%?) of CWD, and hunters submitting tissue for testing, with quick online accessible results. 
Unless science eliminates CWD soon, I believe this is a best case scenario.

However, I am watching Wyoming to see the conclusion on their no action CWD plan.

Lastly, it truly sucks that we are even sitting here talking about disease right before deer season. I wish this bug would just go away and let me enjoy my deer.

Hunt


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## Fierkej (Dec 21, 2001)

Hi,
I emailed Dr. Mike Miller, Colorado Division of Wildlife, this morning with this question:

"What do you know about spiroplasma being a possible TSE disease agent?"

His reply was:

No evidence that spiroplasma is involved -- this resurfaces every few years, but so far hasn't borne out...

Jean


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## Ed Gehrman (Aug 20, 2002)

*No evidence that spiroplasma is involved -- this resurfaces every few years, but so far hasn't borne out...*

It's this type of reply that is so frustrating. There are mounds of evidence that support spiroplasma as the agent. The question you need to ask is what evidence is there that spiroplasma
are not the agent. How have they refuted Bastian's research?
Have they replicated his experiments? no!
Ask the DOW why spirolpasma DNA is found in TSE tissue samples
and not in controls. 
We need to pin them down so a discussion can begin.
Dr. Bastian's research has ALL been published in respected,
peer reviewed journals. I have not found a single refutation.
Until now his work has been soundly ignored, so how would anyone know
if "so far (it) hasn't borne out". 
One simple experiment they could try is to check the saliva of CWD infected animals for spiroplasma. ( they should find spiroplasma but no prions)
Ed


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