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WOW, i am shocked, this came from the PORK farm journal...

Chronic Wasting Disease A Time Bomb For Agriculture?

Chris Bennett, Farm Journal Media
January 30, 2018 11:25 AM

“Everyone at least needs to wake up to the potential of CWD to move in crops because it would shake up agriculture as we know it,” says David Clausen. ( © Herbert Lange, WDNR )
Is chronic wasting disease (CWD) a potential time bomb for the agriculture industry? A silent killer stalking deer and elk, CWD continues to move quietly across the U.S., with 22 states currently reporting CWD presence in free-ranging cervids.

CWD is a neural malady with devastating final-stage symptoms akin to mad cow disease. There is no direct proof of transmission via contaminated grain or feedstuffs, but researchers say accumulating evidence warrants a closer look at the possibility for potential disruption of multiple facets of the agriculture industry.

CWD is a guarantee of protracted death. Without exception, host deer slowly enter a zombie-like state characterized by extreme thirst, lack of mobility, loss of balance and near-total disorientation. CWD plays by a unique set of disease rules and does not spread by the common modes of infection (bacteria or virus), but is transmitted by a corrupted prion, essentially a misfolded protein. The corrupted prions multiply until the infection reaches the brain, destroying cells and attacking the central nervous system. Brain cells die in response to the presence of prions, creating holes in the brain.

“It’s a bad way to die. The animals are emaciated and waste away, and ultimately die from aspiration pneumonia because the swallowing reflex is affected and saliva gets into the lungs, or they freeze to death because they have no more body fat,” says Tracy Nichols, a molecular biologist and staff officer with USDA’s Veterinary Services Cervid Health Program in Fort Collins, Co.


There are no known cases of natural transmission of CWD to domestic livestock. However, in laboratory conditions, CWD has been reproduced experimentally in cattle and swine, and research studies continue to examine crossover possibilities. There is no evidence of human crossover of CWD, although a 2017 studydocumented oral transmission of CWD to macaque monkeys. (Conducted in Canada, the study awaits peer review and publication.) Since 1997, the World Health Organization (WHO) has called for the exclusion of all prion disease material from the human and animal food chains.

“Mad cow disease crossed the species barrier to humans, but we haven’t seen evidence of CWD crossover. We can’t say crossover won’t happen in time, and as a precautionary measure WHO doesn’t want infected prions in the human or animal food chains,” says Bryan Richards, chronic wasting disease project leader for the U.S. Geological Survey (USGS) National Wildlife Health Center in Madison, Wis.

The possibility of CWD transmission beyond cervid populations remains an unanswered question, partly because different strains of CWD behave distinctly. “There is so much about CWD transmission we don’t know and so much yet to be studied. There are so many CWD unknowns related to brain matter, infectivity, prion stage, lymph nodes and more,” says David Clausen, a retired Wisconsin veterinarian, farmer, and former chair of the Wisconsin Natural Resources Board. Clausen presently serves as board president of Midwest Environmental Advocates.

The infectivity range of CWD is another significant unknown. When one species door is closed, another may serve as a Trojan horse. Hamsters were originally thought to be immune to CWD, while ferrets were easily infected. “Take deer CWD and infect the ferret. Take the ferret CWD and infect the hamster. Boom. The hamster can’t be infected by the deer, but is susceptible to the ferret. These prions are constantly evolving and changing,” Clausen explains.

“The question is sitting there: If CWD is able to get into livestock or swine, could it be transmitted in feedstuffs?” he adds.

Echoing Clausen’s query, is CWD passed along in agricultural plant matter exposed to urine, feces or carcass material? Prions form a chemical bond with plant surfaces and also bind to some soil particles, according to Richards. “After dipping plant leaves in prion proteins, researchers haven’t been able to wash off the prions. There isn’t enough science yet, but it’s been shown that plants can pick up proteins in the soil matrix through their roots and deposit those proteins in shoots and leaves, likely in flowers as well,” he explains. “Is the infectivity still there and is the concentration enough to transmit disease?”

CWD has infected cervid populations in 181 counties across 22 states, according to the Centers for Disease Control and Prevention.


Uptake in a laboratory isn’t real-world confirmation, but Richards finds the implications disturbing. In addition, CWD expansion across the U.S. compounds the infectivity issue. “With the geographic footprint of CWD greatly expanded, we have to ask if plant material really moves infectious material. We have to contemplate the question because agriculture would be such a huge mechanism for disease movement,” he says.

In theory, take a county with a 40% CWD rate in a whitetail population. If 20 whitetail typically feed in-and-out of a given wheat field, eight of those deer are CWD-positive. An adult deer defecates roughly 12 times per day and urinates at a higher frequency. After harvest, if the wheat straw is rolled, statistical probability places a good deal of fecal material in the bales. “It’s not a far-fetched idea for infectious material to move in agricultural commodities,” Richards says. “This is not really on the ag industry radar, but it comes up regularly in conversations among scientists. We don’t know if transmission happens, but it must be kept on the radar screen.”

“There was once a time when people said mad cow disease could never cross the species barrier. Almost 300 human deaths and an industry disaster later, it’s pretty simple to see why we keep on conducting the science and relying strictly on what the evidence shows,” he adds.

Nichols cites several studies where plant roots grown in hydroponic or spiked soil solutions were exposed to CWD material. The stem and leaf tissue subsequently tested positive for infected prions, despite no contact with the CWD material. However, high levels of laboratory exposure don’t necessarily equate with field environments. “The results are disconcerting, but what really matters is what happens in the real world. The next level of inquiry is to find out if there is any threat via agriculture crops,” Nichols says.

“There is no scientific conclusion, but the questions raised could impact international trade. Right now, we don’t know what, if any, threat exists,” she continues.

Clausen takes a dim view of CWD containment and believes the disease will continue to creep into additional states: “I’m a country boy. Basic epidemiology of disease control is to contain and quarantine. Deer farm or deer carcass, we have to prevent the movement of all CWD material, dead or alive.”

“With the geographic footprint of CWD greatly expanded, we have to ask if plant material really moves infectious material. We have to contemplate the question because agriculture would be such a huge mechanism for disease movement,” says Bryan Richards, USGS.


It is incumbent on the agriculture industry to consider the ramifications of CWD spread through agricultural commodities, according to Clausen. “Sometimes we just seem to bounce from crisis to crisis without enough preparation or foresight. Corn or alfalfa, CWD uptake has been demonstrated in plants. Whether the uptake is infectious, that research hasn’t been done.”

“Everyone at least needs to wake up to the potential of CWD to move in crops because it would shake up agriculture as we know it,” Clausen says. “We’re all responsible to take a precautionary approach and consider what could happen.”


kind regards, terry

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It already could be a AG issue. Majority of new cases of CWD are found in fenced areas. Thus they are fed with several forms of feed grain, pellets, etc., or AG products. Or the food is not adequate to provide minerals needed to prevent CWD from evolving?

Basically they still do not know how it starts or evolves. They also do not know how it keeps popping up in new areas. The kicker is they also do not know how to get rid of it or eradicate it.

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I wonder if anyone investigated the deer farms and preserves that have CWD were diagnosed. Look at what feed were used and if any use the same manufactured feed. It could be as simple as the processor added or induced an additive or meat by product into it's manufacturing process.

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I wonder if anyone investigated the deer farms and preserves that have CWD were diagnosed. Look at what feed were used and if any use the same manufactured feed. It could be as simple as the processor added or induced an additive or meat by product into it's manufacturing process.
At this point no one has a clue .Baiting takes the brunt of the blame but widespread CWD in area's with little to no baiting have large out breaks .My thoughts are a lot of variables contribute to its spread .Its freaky stuff .

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Discussion Starter · #6 ·
I wonder if anyone investigated the deer farms and preserves that have CWD were diagnosed. Look at what feed were used and if any use the same manufactured feed. It could be as simple as the processor added or induced an additive or meat by product into it's manufacturing process.

Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012


In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.


36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.


The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).


In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.


In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.


Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.



i am thinking of that 10,000,000 POUNDS OF BLOOD LACED MEAT AND BONE MEAL IN COMMERCE WARNING LETTER back in 2007, see;

FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006




''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''




Location: Virus and Prion Research

Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:

Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.

Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.

Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:

This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.

CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.


Price of prion poker goes up...

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