Behavioral changes, weight loss, decreased interactions with other animals, tremors, repetitive walking in set patterns, increased drinking and urination, excessive salivation and grinding of the teeth, loss of fear of humans, confusion
Chronic wasting disease (CWD), sometimes called zombie deer disease, is a transmissible spongiform cephalopathy (TSE) affecting deer. TSEs are a family of diseases thought to be caused by misfolded proteins called prions and include similar diseases such as BSE (mad cow disease) in cattle, Creutzfeldt–Jakob disease (CJD) in humans and scrapie in sheep.
Natural infection causing CWD affects members of the deer family. In the United States, CWD affects mule deer, white-tailed deer, red deer, sika deer, elk, caribou, and moose.
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It was initially recognized as a clinical wasting syndrome and th in 1978, it was idtified more specifically as a TSE disease. Since th, CWD has be found in free-ranging and captive animal populations in 30 US states and four Canadian provinces.
In addition, CWD has be found in one Minnesota red deer farm, one wild reindeer herd in Norway (March 2016) as well as in wild moose. Single cases of CWD in moose have be found in Finland (March 2018) and in Swed (March and May 2019, September 2020). CWD was found in South Korea in some deer imported from Canada.
CWD is typified by chronic weight loss and clinical signs compatible with brain lesions, aggravated over time, always leading to death. No relationship is known betwe CWD and any other TSEs of animals or people.
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Although reports in the popular press have be made of humans being affected by CWD, by 2004 a study for the Cters for Disease Control and Prevtion (CDC) suggested, [m]ore epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.
The epidemiological study further concluded, [a]s a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agt (e.g., brain, spinal cord, eyes, sple, tonsils, lymph nodes) from areas where CWD has be idtified.
Chronic wasting disease was first discovered by American wildlife veterinarian Beth S. Williams. Williams performed necropsies on deer and elk that had died of an unknown syndrome. She recognized that the brain lesions in these animals were consistt with transmissible spongiform cephalopathy (TSE).
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In 1978, she and neuropathologist Stuart Young cowrote the first scitific paper that named the disease and described it as a TSE.
In February 2003, the Cters for Disease Control published a report of Fatal degerative neurologic illnesses in m who participated in wild game feasts--Wisconsin, 2002. It read in conclusion that Although no association betwe CWD and CJD was found, continued surveillance of both diseases remains important to assess the possible risk for CWD transmission to humans.
In September 2003, Hoey pointed out that one of the three patits (the 55 year-old) prested with a 3-month history of difficulty in writing and unsteadiness of gait, followed by demtia, speech abnormalities and myoclonic jerking. Pathologic examination of the brain at autopsy 3 months later revealed widespread subcortical spongiform lesions consistt with CJD.
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As of 2013 Patrice Klein the CWD Program Manager at USDA/APHIS rejected the somewhat inconclusive findings of Hoey and stated that no evidce had be found of transmission to humans from deer, nor by eating animals in the deer family, but both channels remain a subject of public health surveillance and research.
The MFFP ministry in Quebec practiced 9500 tests in the period betwe 2007 and autumn 2018 before they detected a seropositive case in September 2018.
The September 2018 discovery of CWD on a managed operation in Grville-sur-la-Rouge Quebec prompted a wholesale slaughter of 3500 animals in two months before the terprise shut down permantly.
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The CFIA ordered the cull, as well as the decontamination of 25 ctimetres (9.8 in) of soil in certain places on the 400-hectare (990-acre) operation.
Post-discovery, each animal was tested for CWD by the CFIA before it was released onto the market. Other Quebec producers lamted the glut of supply.
The governmt slaughtered hundreds of wild animals over a two-month period. The routine cull for market was betwe 70 and 100 animals per week. Wh the producer was forced to close, the weekly slaughter neared 500 animals per week.
Chronic Wasting Disease
It came to light in August 2019 that prior to 2014 in Canada, all animals on CWD-infected farms were buried or incinerated. Since 2014, however, the CFIA has allowed animals from CWD-infected farms to ter the food chain because there is no national requiremt to have animals tested for the disease.
For the fall 2019 hunting season in western Quebec, the provincial ministry relaxed the rules for the annual white-tailed deer (WTD) hunt, in an effort to curb the spread of CWD. Any WTD can be hunted with any weapon in certain municipalities in the Outaouais valley and the Laurtides. The MFFP hopes thereby to receive more samples to test for CWD.
The quarantine around Grville was still in place, and the ministry specifically prohibited (only) the removal from the quarantine hanced monitoring area zone of the head, more specifically any part of the brain, the eyes, the retropharyngeal lymph nodes and the tonsils, any part of the spinal column, the internal organs (including the liver and the heart), and the testicles.
Zombie Deer Disease
Due to CWD taking 18–24 months after initial exposure to onset, most cases of CWD occur in adult animals; the youngest animal to exhibit clinical symptoms of the disease was 15 months.
The disease is progressive and always fatal. The first signs are difficulties in movemt. The most obvious and consistt clinical sign of CWD is weight loss over time. Behavioral changes also occur in the majority of cases, including decreased interactions with other animals, listlessness, lowering of the head, tremors, repetitive walking in set patterns, and nervousness. Excessive salivation and grinding of the teeth also are observed. Most deer show increased drinking and urination; the increased drinking and salivation may contribute to the spread of the disease.
The cause of CWD (like other TSEs, such as scrapie and bovine spongiform cephalopathy) is a prion, a misfolded form of a normal protein, known as prion protein (PrP), that is most commonly found in the ctral nervous system (CNS) and peripheral nervous system (PNS). The misfolded form has be shown to be capable of converting normally folded prion protein, PrP
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(Sc for scrapie), thus leading to a chain reaction. CWD is thought to be transmitted by this mechanism. The abnormality in PrP has its getic basis in a particular variant of the protein-coding ge PRNP that is highly conserved among mammals and has be found and sequced in deer. The build-up of PrP
The allele which codes leucine, codon 132 in the family of Elks, is either homozygous LL, homozygous MM, or heterozygous ML. Individuals with the first coding seem to resist clinical signs of CWD, whereas individuals with either of the other two codings have much shorter incubation periods.
In white-tailed deer, polymorphisms at codons 95 (Q->H) and 96 (G->S) dramatically affect CWD progression and prion strain specification. Deer containing the 96S allele have delayed progression to clinical disease onset.
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Researchers in July 2019 stated that with all the research on the malignity of prions, and the permance of prions in the wider vironmt, and their resistance to destruction and degradation, it is necessary to reduce the pottial sources of exposure to CWD.
In fact an APHIS scitist observed that, while the longevity of CWD prion is unknown, the scrapie prion has be measured to dure for 16 years.
In the prion diseases, the initial formation of PrPSc leads to an expontial increase in the protein, which can be readily transmitted to another host
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How the prions that cause CWD spread is unknown, but rect research indicates that prions can be excreted by deer and elk, and are transmitted by eating grass growing in contaminated soil.
Animals born in captivity and those born in the wild have be affected with the disease. Transmission of CWD is thought to be lateral (from animal to animal). Maternal transmission may occur, although it appears to be relatively unimportant in maintaining epidemics. An infected deer's saliva is able to spread the CWD prions.
Rect research on Rocky Mountain elk found that with CWD-infected females, many subclinical, a high rate (80%) of maternal-to-offspring transmission of CWD prions occurred, regardless of gestational period.
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While not dispositive relative to disease developmt in the fetus, this does suggest that maternal transmission may be yet another important route of direct CWD transmission.
Modern news stories and anecdotal evidce from treating physicians suggest that a human may have contracted Creutzfeldt–Jakob disease via the consumption of squirrel brains infected with CWD.
In addition to the cervid species in which CWD is known to naturally occur, black-tailed deer and European red deer have be demonstrated to be naturally susceptible to CWD.
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An experimtal case study of oral transmission of CWD to reindeer shows certain reindeer breeds may be susceptible to CWD, while other subpopulations may be protective against CWD in free-ranging populations. None of the reindeer in the study showed symptoms of CWD, pottially signifying resistance to differt CWD strains.
Vironmtal transmission has be linked to contact with infected bodily fluids and tissues, as well as contact
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