Here is a non-technical explanation of my CWD-TSE theory.

The Spiroplasma theory I have presented in my paper is sufficiently different from current CWD causative theory to create a bit of a stir. Perhaps 95% of the scientific community has subscribed to "prions" as being the causative agent of all TSE diseases, which has helped spread "prion hysteria" all over the world. That hysteria has been the real problem.

After 25 years and hundreds of millions of research dollars, no one has actually proved that prions cause disease! A small group of scientists, myself included, believe prions are a symptom of the disease and do not cause the disease. Prions are to TSE diseases as cancer cells are to cancer: a result, not a cause!

Basically, for four decades, some researchers have continued to suspect bacteria or virus to be involved in TSE diseases. However, in the early 1980s some researchers were frustrated by the inability to specifically identify a bacterial or viral origin and hence proposed a non-biotic process as creating these diseases, AKA non- DNA coded prions (proteinaceous infectious particles). Through very adroit and expert PR manipulation, the theory (initially nixed by the scientific community) caught on and eventually led to a Nobel Prize for Dr. Stan Pruisner. Since then, research monies have flowed like water, but the results have been less than stellar. Prion theory has major flaws, some seemingly fatal, e.g., multiple strains of disease (21 kinds of sheep scrapie), animal-to-animal transmission but no detectable transferring agent, a suppression of the disease by tetracycline (an antibiotic), the presence of foreign DNA within diseased cells, and so on.

As such, when my own animals contracted CWD (I had 350 elk, 3 of which got the disease) I watched the disease progression very closely. Using basic scientific observation skills (I am a geologist-geochemist, a noted elk expert and national championship level elk antler grower) I tried to better understand the disease. Then, over the next year I read all I could find from the National Institute of Health library, and discovered that not everyone believes in prions. A Tulane University professor had very interesting proofs that TSE may be caused by bacteria.

The gist of this theory (actually Dr. Bastian's, as he originally proposed it some 35 years ago) is founded and explained with my disease "symptom chart" found about two-thirds of the way into the paper. There are twenty-one symptoms of TSE disease and a bacteria can cause all 21 of them! Every symptom of TSE disease can be explained by a very peculiar bacteria which is very poorly understood by most medical personnel. Sprioplasmas were only "discovered" in the mid-1970s. All my proofs are from independently documented sources. When presented in the whole (for the first time in my paper) the evidence is, in my humble opinion, overwhelming. This is the first time anyone will have seen all this information in one place. This makes a compelling case!

The most convincing individual proof is from Dr. Bastian of Tulane University who has actually found Spiroplasma bacteria in the brain of CJD and scrapie victims. He injected similar bacteria into rats (rabbits and hamsters too) and produced a TSE disease. All this evidence has been seemingly ignored by the "established" medical research community, giving us nothing of use for over two decades! NO proven cause, no preventative actions, no vaccine, no treatment, no nothing for hundreds of millions of research dollars.

Effectively, the Spiroplasma theory CAN explain why the meat animal in central Alberta was positive. It can explain what has happened in Colorado, South Dakota, Saskatchewan, New Mexico, Wisconsin and other places. It easily fits in all areas because it is so basic. A very simple bacteria with very unusual abilities lives in insects, and those insects are a secondary reservoir of disease lying in wait to newly infect.

To paraphrase the last two pages of my text: CWD is a disease caused by a deer or elk variety of parasitic Spiroplasma bacteria, most logically supplied by an insect, invading the host likely via ingestion into the digestive system. The bacteria passes through the gut membranes into the lymph and blood system. Since it consumes sterol proteins, Spiroplasma coats itself in host cholesterol to confound the host's immune system, but does initially induce the production of anti-infection chemicals which stimulate the production of defensive white blood cells.

Spiroplasma then invades the white cells without assimilation due to its chemical structure, allowing it to be transported throughout the host, including to the brain. The bacteria also gets red blood cells and brain cells to produce another anti-infection drug (TNF-alpha) which induces the creation of excess manganese in the cell structure and helps induce star-shaped defense cells (astrocyts) found in TSE diseased brain tissue. Once in the brain, Spiroplasma cloaks itself in brain tissue as shape-shifting blebs, or dense sugar-coated capsules entirely emplaced within individual brain cells, escaping detection, immune response and drug therapy.

During its reproduction state, Spiroplasma changes shape but does have a short-lived, but distinctive helical shape. To reproduce, it steals the necessary proteins, and in particular, the requisite metallic building blocks, to convey host-immune defenses to its bacterial offspring. The bacteria steals copper and zinc from normal cellular prion protein and internal cell components, basically killing the cell by robbing it of its own defense mechanisms, and additionally inducing the emplacement of more manganese leading to cell destruction. All the while the bacteria digest its host cell membrane walls with secretions of hydrogen peroxide.

The newly created Spiroplasma cells (carrying the scavenged copper and proteins) are available to attack new cells. They can also be excreted by the host into the environment and subsequently picked up by insects to repeat the cycle. The host animal then looks like it has a copper deficiency, and it yet has extra manganese in the brain.

The extra brain manganese creates the positive test results on the poorly understood testing procedures (western blot and ELISA). The bacteria yield the distinctive tiny helical protein fibrils found in all TSE-infected tissue. And the dead brain cells give the sponge- like texture to the brain. All three diagnostic criteria are met!

To my knowledge, only three researchers in the USA (I am one) are pursuing this most logical causal agent. My goal is to show the fallibility of the current testing routines, and to prove that a more reasonable solution is out there. I am sure I will be ridiculed for what I propose, but 25 years as a gold mine scam debunker has put me face to face with controversy before. And while I am not a "trained" medical researcher, I have spent over thirty years logically and successfully figuring out Mother Nature's puzzles and man's theoretical baloney. As such, my forensic abilities, my scientific BS detector, and my basic scientific investigative skills are very well-developed.

If someone wants to shoot me down, I welcome the chance to respond to valid theory criticism after thoughtful deliberation. But I must say that, this theory is very difficult to knock down.

Here are some of my answers, based on my theory, to specific questions that have been asked.

1. Is there a more specific way now to identify the disease, i.e., an early live animal test?

Yes the bacteria should be directly detectable in the blood within a short time after infection, and their byproducts should show up in the urine. This makes for an easy screening test for humans, but maybe not so easy for an elk (unless you can get them to pee in a cup!) I will be addressing the possible solutions in Part 3 of my paper.

2. With the ability to cloak itself, is there the possibility for a) a cure, b) a vaccine potential c) eradication, and d) disease treatment? What management techniques can we incorporate to minimize risk, in both farmed and wild animals?

A cure is a matter of finding the proper combination of spiroplasmacidal antibiotics in a cocktail and treating animals over an extended period of time to kill the dormant or cloaked bacteria. Right now, we know that tetracycline slows them down, but we need to try all the variants of tetra, as well as other bacteriastats. If the agent can be identified, then a live-attenuated vaccine may be possible as well. The host immune system is important in the first stage of infection. Kill it quick or you may be toast! Once it is ensconced, the bugs will be difficult to root out. CWD will be a management disease, and culling may still be necessary for overall domestic control.

Wild control is very problematic. Part 3 will present a more complete picture, but personally, if I were facing a CWD risk and NOT making meat animals, I would feed a tetra medicated pellet with extra copper and some immune system vitamins. If you can keep the buggers out of the animal or if you can weaken the bugs when they first show up, plus additionally boost the host immune system, why not? Even the alien-like "prions" seem to be subject to the host immune defenses.

3. Can you culture the specific agents and infect healthy animals and create the disease? Can this be done without using an already infected cervid, i.e., insect to cervid?

Yes, I would think so, once you isolate the specific organism. Mouse infection studies followed by cervid studies will "prove" the hypothesis, but many months will be necessary, along with big bucks!

4. Can you isolate the specific organism from diseased animals?

Yes. I would expect that through the use of PCR (polymer chain reaction) amplification and DNA sequencing very specific strains should be identifiable, followed up by very discriminating culturing procedures. The buggers are parasitic and very difficult to cultivate outside of live mammalian tissue. Fortunately, tissue could even be well deteriorated and still harbour these rotten little buggers, munching away!

5. Can you find the disease agent on site after an eradication of positive animals?

Yes. I would expect the possibility of somebody creating a live animal screening test either using blood or urine, maybe even saliva. Right now, I want to try some urine byproduct tests with some off-the-shelf products. I'm ready to go to work, but alas! All this research takes people, time and money, and we are not exactly an army.