This article is based on research by Rich Forrest of the Colorado-based CWD Foundation. For a series of CWD technical articles by Forrest, please visit the CWD Foundation Library at http://www.stopcwd.org]
Chronic Wasting Disease (CWD) is a Transmissible Spongiform Encephalopathy (TSE) disease affecting both wild and domestic deer and elk. All TSE diseases are now grouped under the term of "prion" diseases in recognition of the disease's destructive effect upon the protective protein particles shielding nerve cells. Prion diseases are fundamentally diseases of membrane tissue, although not necessarily of neuronal tissue.
Current scientific thinking is that an abnormal prion is the causal agent of TSE and CWD. However, after two decades of intensive research, definitive proof has yet to be established.
According to Mr. Forrest, various strains of Spiroplasma bacteria produce similar symptoms and conditions generally associated with the TSE disease and its causal agents. Here are just a few of the stunning similarities:
1. Size. Several studies have found that brain biopsy specimens from patients with Creutzfeldt-Jakob disease revealed coiled inclusions structurally similar to Spiroplasma bacteria. Scientists have also noted that Spiroplasma can range from 50 nm to over 150 nm in width and will generally pass through the same filter widths as the suspected TSE agents.
2. Resistance to disinfectants. TSE agents, especially scrapie, have several unique disinfectant-resistant properties. The agent can survive: a) 5% chloroform and 2% phenol, b) 20% formalin solutions for 18 hours, and c) treatment with less aggressive protein enzymes. Spiroplasma displays considerable resistance to these normal bactericidal disinfectants as well.
3. Resistance to heat. TSE scrapie agent can survive in boiling water for several hours and numerous freeze-thaw cycles. In fact, a small degree of infectivity still survived after a one hour exposure to temperatures as high as 360 degrees C. Similar research has not yet been done on Spiroplasma. However, viable Spiroplasma organisms have been recovered from boiling water. Wet spores of several bacterial species have survived brief exposures between 270 to 340 degrees C, while dry spores are known to persist after exposure to 370 degrees C.
4. Surface adherence. Prions can tightly bind to stainless steel surfaces, and even after washing and 10% formaldehyde submersion, can transmit scrapie to recipient mice after short exposure times. Spiroplasma can survive in dried media on smooth surfaces such as plastic, glass and ceramic for over 3 weeks and survive formaldehyde disinfection.
5. Ground contamination. Scrapie agents can survive for over 3 years in buried soil conditions. Spiroplasma are capable of surviving up to 9 years in a liquid medium, and up to 17 years in dry and farmed soils.
6. Hyperbaric oxygenation. Multiple exposures of scrapie-infected mice to hyperbaric oxygenation led to aggravation of the scrapie infection. Similarly, hyperbaric oxygen aggravated Spiroplasma-induced rat brain encelphalopathy. 7. Antibiotics. Tetracycline and its derivatives delay the onset of prion disease and can seemingly assist host immuno-reactivity against the disease. Strains of mosquito-derived Spiroplasma were highly susceptible to tetracycline and similar bacteriastat antibiotics.
8. Vaccines. Mice sequentially inoculated with two strains of CJD showed complete resistance to the last injected disease strain despite an anticipated more rapid incubation period. This suggests specific antibody production in response to the TSE agent. Similarly, sheep vaccinated with inactivated Spiroplasma-like bacteria resisted disease transmission. These results suggest that attenuated agent vaccines are effective and can limit or eliminate spiroplasma-mycoplasma infections.
9. Delayed symptoms. The detection of abnormal prions can only be done many weeks after infection. In the case of deer, prions can be detected as early as 42 days after oral inoculation. More than 12 months may be necessary before outward clinical signs appear. One can assume that the causative agent is present in the host animal from time of infection, but yet is not readily expressed in prion development.
Rats infected with Spiroplasma showed spleen infections within two days, but central nervous system affliction did not commence immediately. Fourteen days after inoculation, notable visually detectable Spiroplasma were present in the nerves. However, after 25 days, no visibly detectable Spiroplasma were found. Apparently, an intracellular stealth mode had been achieved by the bacteria.
10. Blood. Several studies show that it is possible to transmit TSE diseases using blood transfusions. However, the gastrointestinal tract appears to be the natural route of infection of TSEs in response to the oral exposure to the infectious agent. The favoured interpretation is that the agent spreads from the gut by lymph system to the spleen and on into the spinal cord via associated nerve cells. The early occurrence of abnormal prions in gut lymphoid tissue suggests that blood transport may be a more potent transportation method than the neural routes.
Spiroplasma and the larger group of mycoplasma are blood cell immune activators. Further, many mycoplasma species undergo antigenic variation by which they alter their surface protein structure so as to evade immune system recognition. Therefore, Spiroplasma bacteria can likely be spread throughout the body by the blood.
11. DNA. Spiroplasma bacteria have been directly identified using DNA tests in both CJD and scrapie brain tissue taken from divergent regional locations. This is a direct proof that Spiroplasma is in the brains of TSE diseased hosts.
If one operates under the premise that a TSE disease is classified as a prion disease, what in fact is the causative agent? Many would suggest that the prions themselves are the causative agent. However, decades of work have failed to fully or logically explain the nature of prions as it pertains to TSE. Abundant proof exists that abnormal prions are the result of TSE disease, but proofs are insufficient to assure that prions are the "cause" of TSE disease.
Upon review, one can conclude that Spiroplasma could conceivably possess the ability to infect and create disease characteristics and symptoms virtually identical to the mysterious TSE diseases. While the capacity to produce disease is not direct evidence, certainly one cannot ignore the direct DNA presence of Spiroplasma within diseased tissue.
Based on this empirical evidence, more research should be directed at Spiroplasma bacteria as the possible cause of TSEs in general, and CWD in specific.
[If Rich's hypothesis is true, and he certainly presents a good case for it, then it increases the possibility that a vaccine can be developed for CWD, and the disease can be treated with antibiotics. Ed.]