States need to be more proactive in stopping spread of chronic wasting disease among deer
Chronic wasting disease, which has now been reported in 24 states, is an always-fatal disease that wreaks havoc on infected deer, elk, and other cervids, and can linger for years in the environment, making it difficult to control. Photo by iStockphoto
Captive deer farms are breeding grounds for the deadly chronic wasting disease, which has now spread to 24 states. While some states have wisely banned such facilities, others have done nothing, even as the disease spreads and costs taxpayers millions of dollars in response efforts. On the blog today, I have invited Samantha Hagio, director of wildlife protection for The HSUS, to discuss how states can combat this deadly disease, including ending a war on large carnivores like wolves and mountain lions who can be key allies in stopping CWD.
Samantha Hagio, director of wildlife protection
Mississippi officials recently reported the first case of chronic wasting disease (CWD) in the state, confirming the further spread of this deadly disease that has been known to incubate among animals on captive deer farms. The news created alarm in neighboring Tennessee and Alabama, which immediately banned deer carcasses from Mississippi, and has added to the broader anxiety about CWD among wildlife and public health agencies.
CWD, which has now been reported in 24 states, is an always-fatal disease that wreaks havoc on infected deer, elk, and other cervids, and can linger for years in the environment, making it difficult to control. While it has yet to be diagnosed in a human, people risk becoming exposed to the disease through eating CWD-tainted meat. There is no cure, no vaccine, and no way to detect the disease in live deer.
Cracking down on captive deer farms and canned hunts, which are obvious breeding grounds for CWD, is essential to preventing its spread into healthy populations. While some states have wisely banned such facilities, others have done nothing, even as the disease spreads and costs taxpayers millions of dollars in response efforts.
Too many state and federal lawmakers seem determined to make the problem even worse by their relentless targeting of wolves and other native carnivores, who are significant allies in the effort to contain the disease.
Studies have shown that deer killed by large carnivores have a higher rate of CWD infection than deer killed by hunters. This is consistent with our common understanding that large carnivores like wolves, who run long distances to chase their prey, single out weak, old, and sick animals, contributing to the overall health of the population. Mountain lions, an ambush predator, also targeted CWD-infected animals, in a study conducted near Rocky Mountain National Park. Protecting native carnivores and allowing them to play their natural role in the ecosystem is a much more effective means of controlling CWD than wholesale culling of deer in an infected area. National Park Service biologist Douglas Smith states, “[w]olves are probably the single best way to stop the spread of CWD. Chronic wasting disease causes animals to act weird. Wolves kill animals like that.”
The Great Lakes states of Wisconsin, Michigan, and Minnesota (all states where CWD has been found) are waging a war on wolves, having succeeded in getting the species delisted from the Endangered Species Act (ESA) in 2011 and killing more than 1,500 gray wolves before protections were restored in 2014. The HSUS recently won a significant victory restoring federal protections for Great Lakes wolves, and we’re in the frontlines of the fight for wolves in other arenas as well. Most notably, lawmakers in Wisconsin and Michigan are currently pushing legislation to bar state officials from even enforcing laws against killing wolves.
Montana is responsible for another assault against wolves. Since ESA protections for wolves were stripped by Congress in 2011, between 200 and 250 wolves have been killed each year in Montana, including by inhumane and indiscriminate trapping. Wolves in neighboring Wyoming – where supplemental winter feeding of elk has concentrated the animals, also contributing to the spread of CWD – lost their federal protections last spring, and 44 wolves were killed in the state’s first hunting season since 2013.
Retired wolf interpreter at Yellowstone National Park, Norman Bishop, said “[w]hat we are witnessing with wolves is a battle of modern scientific data against entrenched Old West dogma and we are in a time in which data doesn’t appear to matter to those who cling to dogma. It is disheartening to realize how the states have abandoned good sense.” Former Montana wildlife commissioner and former CEO/president of the Rocky Mountain Elk Foundation, biologist Gary Wolfe, noted that the unlimited killing of wolves “is probably not the best ecological strategy for containing CWD…I believe wolf predation is an important tool that needs to be recognized and effectively utilized, along with other tools, as part of Montana’s CWD management plan.”
Now more than ever, it’s critical that we protect the large carnivores whose ecological role can help control CWD’s spread. State wildlife agencies and lawmakers should end their war on wolves and other large carnivores and allow these creatures to serve their natural function in maintaining a healthy ecosystem. We must urge members of Congress to acknowledge the foolishness of killing native carnivores, and cease the politically misguided and ecologically reckless backroom efforts to strip protections for wolves.
CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW TYPE DISEASE ROUNDUP
WEDNESDAY, FEBRUARY 21, 2018
TEXAS TPWD CWD TSE PRION 2 MORE FROM BREEDER RELEASE SITE TOTALS 81 CASES TO DATE
http://chronic-wasting-disease.blogspot.com/2018/02/texas-tpwd-cwd-tse-prion-2-more-from.html
WEDNESDAY, FEBRUARY 21, 2018
Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties
http://chronic-wasting-disease.blogspot.com/2018/02/maryland-chronic-wasting-disease-cwd.html
FRIDAY, FEBRUARY 09, 2018
Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer
http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-chronic-wasting-disease.html
TUESDAY, FEBRUARY 13, 2018
*** MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations ***
http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-state-department-of-health.html
SUNDAY, FEBRUARY 18, 2018
Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018
http://chronic-wasting-disease.blogspot.com/2018/02/chronic-wasting-disease-cwd-tse-prion.html
Terry S. Singeltary Sr.
It sounds like this is a hugely under-reported story. If there’s no cure and no vaccine, I’d be interested in what medical research is being done on this. Perhaps another blog post on that topic? Also, I assume it’s not spread to wolves by eating the deer? A quick online search indicates it’s not transferable to humans by exposure or eating, but it’s “being monitored.” But no guarantees.
And, if captive deer farms are a problem, is this perhaps related to the feed? Wasn’t that the source of mad cow disease? Animals ate feed contaminated with the brains, spinal cords or digestive tracts of infected animals? The obvious question is how is the disease striking captive deer farms?
Sounds like this is a real problem that needs a lot more attention. Would be interested to read more from you.
ZOONOSIS OF TSE PRION DISEASE
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
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***thus questioning the origin of human sporadic cases***
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***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
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https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
“Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: “UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip…
R. BRADLEY
https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
http://www.nature.com/articles/srep11573
Terry S. Singeltary Sr.