To read part one of this article, click here.
Where Did CWD Come From?
One of the problems in figuring out where CWD originally came from is that the exact cause of TSE’s, and the means of transmission of TSE’s from one animal or person to another are still relatively unknown. Other TSE’s appear to:
- occur sporadically (like cancer),
- be inherited,
- be passed from mother to offspring,
- be contracted by coming into contact with diseased tissue from infected animals or humans
- be contracted by coming into contaminated soil or other surfaces,
- be contracted by coming into contact with infected surgical equipment,
- or be contracted by being injected with material from a disease-infected animal or person.
It has been theorized that CWD has been around in wild deer and elk for years, but I know of no scientific evidence to support that theory. In light of the low number of occurrences of CWD in the wild, and the relatively higher number of occurrences in commercial deer and elk herds, and the fact that CWD was first reported in a research facility in Fort Collins, Colorado (where both sheep and deer were kept) it is likely that CWD, like Mad Cow Disease, is a result of deer coming into contact with either scrapie infected sheep or scrapie-contaminated soil or other surfaces (providing that CWD is caused by a prion, bacteria, virus or virino). Alternatively, CWD may be the result of a copper deficiency, or something entirely different.
Other TSE Theories
According to a paper on the USDA’s website dated November 2002, “The agent responsible for CWD (and other animal TSE’s, such as scrapie and bovine sponigorm encephalopathy) has not been completely characterized. There are three main theories on the nature of the agent that causes CWD:
- the agent is a prion, an abnormal form of a normal protein, known as a cellular prion protein, most commonly found in the central nervous system. The abnormal protein “infects” the host animal by promoting conversion of normal cellular prion proteins to the abnormal form.
- the agent is an unconventional virus;
- the agent is a virino, or “incomplete” virus composed of nucleic acid protected by host proteins.
The CWD agent is smaller than most viral particles and does not evoke any detectable immune response or inflammatory reaction in the host animal. Based on experience with other TSE agents, the CWD agent is assumed to be resistant to enzymes and chemicals that normally break down proteins, as well as resistant to heat and normal disinfection procedures.” If a virus causes CWD scientists may be able to produce a vaccine that would make both animals and humans immune to CWD.
Dr. Frank Bastian, a research professor of neuropathology at Tulane University in New Orleans questions the prion protein theory. He is quoted as saying, “A protein has never been known to be the causative agent for a disease.” Bastian feels that CWD may be caused by a bacterium known as a Spiroplasma. His research has shown that Spiroplasma is associated with CJD and scrapies. To make itself unnoticed by the immune system as it enters a host, Spiroplasma bacteria may cloak itself with host proteins such as prions.
Bastian believes that if bacteria cause CWD it may be spread through some type of vector, such as mites or other insects. Drs. Henryk Wisniewski, Sigurdur Sigurdarson, Richard Rubenstein, Richard Kascsak and Richard Carp found that their preliminary results presented the prospect that mites may serve as a vector for scrapie, and that mites may “represent a self-sustaining reservoir for scrapie-like agents.” If a bacteria cause CWD, and mites transmit it, it may be treatable with antibiotics.
British organic farmer Mark Purdey has presented the hypothesis that a nutritional copper deficiency may result in cows being susceptible to Mad Cow Disease. It has been found that the number of Mad Cow Diseases per 1000 head of cattle was not evenly or randomly distributed throughout the United Kingdom, but the highest concentrations occur in southern and eastern counties known to have widespread copper deficiencies in the soils and crops. Purdey believes that a copper deficiency (with a manganese replacement for copper in the prion protein), which was initially a result of repeated applications of high doses of phosmet (an organophosphate insecticide), and the use of manganese-rich chicken manure-based feed supplements, are the key to the origin of Mad Cow Disease in British cattle.
Dr. Murray McBride, of Cornell University, notes that Mad Cow Disease in Britain is also linked to the feeding of concentrated meat bone meal to dairy calves, and that one impact of high meat bone meal diets could induce copper deficiencies in ruminants such as cattle (and deer). Copper deficiencies have been found in cattle, moose, red deer, Sika deer, elk, muskoxen and goats. Confined or farmed elk and red deer are particularly susceptible to copper deficiencies, because they may have copper supplements available to them in their feed or mineral supplements. One reason why wild deer and elk may not exhibit TSE’s as frequently as cattle is because they appear to need less copper in their diets.
As I checked the web I found that there are at least 32 different hypotheses on the cause of Mad Cow Diseases/CWD. But, in spite of these other theories/hypotheses, the wildlife management community and other researchers may be ignoring the possibility that CWD may be caused by a bacteria, virus, or virino or that a nutritional copper deficiency may result in animals being susceptible to CWD. Many people within the scientific community don’t support the bacteria, virus, virino or copper theories because they have chosen to accept the prion theory. As a result of this, many of them are looking for answers on how CWD is transmitted, and ways to prevent or cure it based on their acceptance that prions are the causative agent of CWD.
In my dealings with the scientific community over the last 20 years I have found that many research scientists fail to look beyond their own area of expertise. And I’ve found this to be true when it comes to CWD. After corresponding with several of the scientists mentioned in this article by e-mail, I found that many of them did not know of the others work, and had not read their research, theories or hypothesis. In an effort to advance the research into the causative agent of CWD, and find possible ways to innoculate against, treat cure, or stop the spread of CWD, I have provided the top CWD scientists (many of who are only looking into prions) with the web sites and e-mail addresses of several non-prion scientists. And I have sent copies of some of the research abstracts of the non-prion scientists to the CWD scientists, in the hopes that they can work together. Fortunately, at least two of these scientists (who I consider to be very important), have agreed that they should keep an open mind when it comes to CWD.
To continue on to part three of this article, click here.