Deadly 'zombie' deer disease that rots its victims brains could be spreading to humans.

Chronic wasting disease (CWD), also known as zombie deer disease, is a disease that affects deer.TSEs are a family of diseases thought to be caused by prions and include diseases such as BSE in cattle, Creutzfeldt-Jakob disease in humans and scrapie in sheep.In the US, CWD affects mule deer, white-tailed deer and red deer.CWD affects members of the deer family.Experiments have shown that CWD can be transmitted to other species such as squirrel monkeys.[4]

The first case of CWD in a mule deer was identified in 1967.It was initially thought of as a clinical "wasting" syndrome, but in 1978 it was found to be a TSE disease.CWD has been found in free-ranging and captive animal populations in 26 US states and three Canadian provinces.One red deer farm, one wild reindeer herd in Norway, as well as wild moose have been found with CWD.There have been single cases of CWD in moose in Sweden.Some deer imported from Canada were found to have CWD.CWD is typified by chronic weight loss and clinical signs that are compatible with brain disease, always leading to death.There is no relationship between CWD and other TSEs.

Although reports in the popular press have been made of humans being affected by CWD, by 2004, a study for the Centers for Disease Control and Prevention suggested that laboratory studies are needed to monitor the possibility of such transmissions.The epidemiological study concluded that hunters should avoid eating deer and elk tissues from areas where CWD has been found.[6]

Beth S. Williams discovered chronic wasting disease.Williams performed necropsies on animals that had died.She knew that the brain damage in these animals was related to TSE.She and Stuart Young wrote the first scientific paper that named the disease and described it as a TSE.[8]

The youngest animal to show clinical symptoms of the disease was 15 months.The disease is progressive and fatal.Difficulty in movement is the first sign.Weight loss over time is the most obvious sign of CWD.In most cases, behavioral changes include decreased interactions with other animals, listlessness, lowering of the head, tremors, repetitive walking in set patterns, and nervousness.There is excessive salivation and grinding of the teeth.Increased drinking and salivation may contribute to the spread of the disease.Loss of fear of humans and appearance of confusion are common.The APHIS summarized it.

Ataxia, salivation, aspiration pneumonia, and progressive death are all related to behavioral changes.

The cause of CWD is a misfolded form of a normal proteins that is found in the central nervous system.The misfolded form has been shown to be capable of converting normally folded prion protein into an abnormal form, thus leading to a chain reaction.CWD is thought to be transmitted by this mechanism.There is a variant of the PRNP that is highly conserved among mammals and has been found in deer.There is a build-up of prPd in the brain.2, 10, and 12

There are at least three alleles in the family of Elks which contain leucine, codon 132.Individuals with the firstEncoding seem to be resistant to clinical signs of CWD, whereas individuals with either of the otherEncoding have shorter incubation periods.[3]

CWD progression and prion strain specification can be affected by codons 95(H) and 96.There is a delayed progression to clinical disease in deer with the 96S allele.It was [13].

There was no evidence of transmission to humans from deer or from eating animals in the deer family, but both channels remain a subject of public health research.It is necessary to reduce the potential sources of exposure to CWD with all the research on the malignity of prions and their resistance to destruction and degradation.According to an APHIS scientist, the scrapie prion has been measured to last 16 years.The PrPCWD is resistant to digestion by proteases and is insoluble in all but the strongest solvents.When contact is made with the normalproteinPrPC, it converts into more of itself and forms aggregates.In 2001 Prusiner noted that.

The prion diseases can be transmitted if the initial formation ofPrPSc leads to an increase in theprotein.

CWD was not transmissible to humans or cattle as of 2013).[3]

Recent research shows that deer and elk excrete prions that can be passed on to other animals.Animals born in captivity have been affected by the disease.CWD is thought to be transmitted from one animal to another.It appears to be unimportant in maintaining epidemics, although maternal transmission may occur.The deer's saliva can spread the CWD prions.Sharing food and water sources contaminated with CWD prions is associated with exposure between animals.[19]

It is possible for CWD to be transmitted directly by contact with animals and their bodily fluids.If a deer is sick, contact with it may result in the spread of the disease.[21]

There was a high rate of maternal-to-offspring transmission of CWD prions regardless of the time of year.Maternal transmission may be an important route of direct CWD transmission.

Black-tailed deer and European red deer have been shown to be susceptible to CWD.Other cervid species are also thought to be vulnerable to this disease.Many noncervid mammals have been exposed to CWD by intracerebral inoculation.The species include monkeys, sheep, cattle, prairie voles, mice, and ferrets.[23]

A case study of oral transmission of CWD to reindeer shows that certain reindeer breeds may be susceptible to the disease.The reindeer in the study did not show any symptoms of CWD.[ 24]

Environmental transmission can be linked to contact with bodily fluids and tissues.CWD prions may remain in the environment for a long time.The urine, saliva, feces, and antler velvet of people who have been exposed to CWD can be deposited in the environment.10

Researchers at the National Wildlife Research Center in Fort Collins, Colorado successfully inoculated white-tailed deer with the misfolded prion, when the prions were mixed with clay.The prions had already been shown in 2006 to bind with sand.[3]

The American crow was evaluated as a potential source of CWD.crows represent a possible mechanism for the creation of environmental reservoirs of CWD, as prions remain viable after passing through the bird's digestive tract.There are plenty of opportunities for the crows to come in contact with CWD.The population density and longevity of communal roosting sites in both urban and rural locations suggest that fecal deposits may represent a CWD environmental reservoir.Conservative estimates for crows' fecal deposits at one winter roosting site ranged from 391,552 to 599,032 kg.[26]

CWD prions adhere so tightly to soil surface particles that the ground becomes a source of infection and may be a major route of transmission due to frequent ground contact when animals in the deer family are grazed.10

APHIS published a voluntary system of control in the US Federal Register.It depended on minimum voluntary standards methodology and herd certification programs.It was based on a framework.This problem has been dealt with by the APHIS law in 9 CFR Part 55 - CONTROL OF CHRONIC WASTING DISEASE.

The ministry in Quebec practiced 9500 tests over the course of a decade before detecting a positive case in September.[28]

Thousands of animals were slaughtered in two months after the discovery of CWD in a managed operation in Quebec.The 1000-acre operation was ordered to have a cull and 10 inches of soil removed.Each animal was tested for CWD before it was released onto the market.There was a lot of supply lamented by other Quebec producers.All hunting and trapping activities were banned in a 400 km area.Over a two-month period, the government massacred hundreds of wild beasts.The market had between 70 and 100 animals per week.500 beasts were slaughtered per week when the producer was forced to close.750 wild specimens were culled in the 45 km-radius "enhanced monitoring area" one year later, and none tested positive for CWD.[31]

In August of this year, it came to light that prior to Canada's introduction of CWD, all animals were buried or incinerated.There is no national requirement to have animals tested for the disease, so the Canadian Food Inspection Agency has allowed animals from farms with CWD to enter the food chain.131 animals were sold for human consumption from one herd.[32]

In an effort to curb the spread of CWD, the provincial ministry relaxed the rules for the annual white-tailed deer hunt in western Quebec.In the Outaouais valley and the Laurentides, any WTD can be hunted with any weapon.The goal is to get more samples to test for CWD.The ministry did not allow the removal of any part of the brain, eyes, retropharyngeal, and tonsils from the enhanced monitoring area.[33]

The no-cost deer carcass-incineration program was rolled out by Crow Wing County officials hoping to stem the spread of CWD in the region.CWD was found among deer in Crow Wing County for the first time.Residents and visiting hunters are encouraged to bring deer carcasses to the county landfill for disposal.[2]

General signs of poor health and aspiration pneumonia, which may be the actual cause of death, are not definitive, as many animals die early in the course of the disease and conditions found are nonspecific.The CWD in the central nervous system resembles those of other TSEs.Positive IHC findings in the obex are considered to be the gold standard for the diagnosis of CWD.There are a number of methods for amplification of CWD prions in the lab.[34]

The prion was not detected in samples from animals younger than a year old.Strategies are being developed to allow for the quantification of prion burden in a tissue, body fluid, or environmental sample.[34]

There were no commercially feasible diagnostic tests for live animals in 2015.An antemortem test was deemed urgent as early as 2001.ethical issues exist with this and it is not feasible to run a bioassay and take fluids from animals in the deer family suspected ofinfecting them with cervid prion.10

The method of testing for CWD in live deer has been reliable, but it only works on mule deer and white-tailed deer.The rectal mucosa has been found to be effective at detecting CWD in live mule deer and white-tailed deer.38,39,40,41

There is a closed herd of captive mule deer in northeastern Colorado.The disease was determined to be a TSE in 1980.In the early 1980s, it was first found in mule deer and white-tailed deer in Colorado and Wyoming.The disease did not affect Canada until 1996.[15]

CWD was found in free-ranging deer in the southwestern corner of Nebraska in May 2001 and later in additional areas in western Nebraska.There is a limited area of northern Colorado, southern Wyoming, and western Nebraska where free-ranging deer and moose have been found positive for CWD.The area expanded in 2006 to include parts of eastern Utah, southwestern South Dakota, and northwestern Kansas.There are areas not contiguous to the endemic area in central Utah and central Nebraska.Since the disease is at a low incidence and the amount of sampling may not be enough to detect it, the limits of the affected areas are not well defined.In 2002, CWD was found in deer in south-central Wisconsin and northern Illinois, as well as in an isolated area of southern New Mexico.In 2005, it was found in deer in New York and West Virginia.The first case of CWD in Michigan was discovered in a deer on an enclosed deer-breeding facility.It is found in both provinces of Canada.

The first confirmed case of the disease in Maryland was reported in February 2011.A white-tailed deer was killed by a hunter.[42]

CWD has been found in deer herds in a number of states and Canadian provinces.In 1997 there was the first positive farmelk herd in the United States.More positive deer herds have been found in South Dakota, Nebraska, Colorado, Oklahoma, Kansas, Minnesota, Montana, Wisconsin, and New York.In the fall of 2006 there were four positive herds of animals in Colorado and one positive white-tailed deer herd in Wisconsin.All of the other herds have been slaughtered and tested, and the one herd that underwent rigorous surveillance has been free of disease.In Canada, CWD has been found in farmed animals.A study shows mule deer exported from Denver to the Toronto Zoo were affected.The disease was discovered in a white-tailed deer on a breeding ranch in Texas.State officials euthanized 34 deer because of a possible outbreak.

In February of last year, the Mississippi Department of Wildlife, Fisheries, and Parks announced that a deer had tested positive for chronic wasting disease.Another Mississippi whitetail was euthanized in Pontotoc County and tested positive for CWD.The National Veterinary Services Laboratory in Ames, Iowa confirmed the disease on October 30.[45]

White-tailed deer are one of the species that have been affected by CWD.Other ruminant species, including wild ruminants and domestic cattle, sheep, and goats, have been housed in wildlife facilities with no evidence of disease transmission.The disease that results from experimental transmission of CWD into other ruminants is likely due to a weak species barrier.The possibility of transmission of CWD to other species is being explored.

By April 2016 CWD had been found in captive animals in South Korea; the disease arrived there with live elk that were imported from Canada for farming in the late 1990s.[46]

In the summer of 2018, there were cases in the Harpur Farm herd.[28]

Over the course of last year, 12% of the mule deer that were tested had a positive result.More than 8% of deer in the province were found to be positive.[32]

The first case of CWD in Europe was in southern Norway.As the female reindeer was dying, scientists found a disease that was positive at the necropsy.Imported deer from Canada were the source of CWD cases in South Korea.Live animals and deer are not allowed into the country of Norway.While no reports of scrapie within the range of the reindeer population have been identified, sheep are herded through that region and are a potential source of infections.[47]

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