Do we or should we test?? [Archive] - The Michigan Sportsman Forums

Fierkej

03-08-2002, 10:31 AM

Tom, You beat me to it!

Hello,
There have been no deer or elk (wild or captive) with CWD in Michigan.
452 deer were tested for CWD in 1998. All tested negative.
Prevention measures are being finalized. I will post them as soon as they are avialable.
Here are two CWD links for more information:
http://wildlife.state.co.us/hunt/HunterEducation/chronic.asp
http://www.aphis.usda.gov/oa/pubs/fscwd.html

Here is our MDNR Chronic Wasting Disease Full Report prepared by biologists Tom Cooley and Elaine Carlson. It is also available on the DNR website at:
http://www.dnr.state.mi.us/Wildlife.asp?sublinkid=157&Link=Sub&Linkid=90&imageID=4

Chronic Wasting Disease (CWD) belongs to a group of fatal neurodegenerative diseases known as transmissible spongiform encephalopathy(ies) (TSE) or prion (pronounced pree-on) diseases. CWD is an emerging TSE that naturally occurs in both captive (research) and free-ranging white-tailed deer (Odocoileus virginianus) and mule deer (O. hemionus) and elk (Cervus elaphus nelsoni) in north-central Colorado and SE Wyoming, in free-ranging mule deer in SW Nebraska and Saskatchewan, in free-ranging white-tailed deer in NW Nebraska, south central Wisconsin, and SW South Dakota, in elk from captive cervid ranches in Colorado, South Dakota, Nebraska, Oklahoma, Montana, Kansas, and Saskatchewan and from deer in a captive cervid ranch in NW Nebraska. Endemic CWD has been sustained in free-ranging cervid populations for decades. Other TSE that have been identified worldwide are:
1. Bovine Spongiform Encephalopathy (BSE) or Mad Cow Disease of cattle
2. Creutzfeld-Jacob Disease (CJD) of humans
3. Scrapie of sheep and goat
4. Fatal Familial Insomnia of humans
5. Gerstmann-Staussler-Sheinker Disease of humans
6. Kuru of humans (New Guinea tribesmen)
7. New Variant CJD of humans
8. Transmissible Mink Encephalopathy of mink
9. Feline Spongiform Encephalopathy (FSE) of cats
All of these TSE's are separate diseases although they may cause similar clinical signs in their hosts. Symptoms consistent with CWD were first observed in deer in 1967 in captive research facilities in Colorado. Within 10 years, the disease was also observed at the Sybille Research Unit in Wyoming. In 1977, it was diagnosed as a TSE and characteristic brain lesions were first detected in 1978 in captive deer and elk from these facilities. Also in 1978 a captive mule deer that originated from a captive herd in a park in Colorado died due to CWD at the Metro Toronto Zoo. In 1981 in North Eastern Colorado a sick free-ranging elk was detected with the disease. In 1985 the disease was detected in free-ranging mule deer in Colorado. In 1986 in Wyoming, an elk became the first free-ranging big game animal in that state to be diagnosed with the disease. By 1990 it was detected in free-ranging white-tailed deer and mule deer in Colorado and Wyoming. In 2000, CWD was detected in one mule deer in southwestern Nebraska. This was the first case of CWD in a free-ranging cervid outside of the known endemic areas in Colorado and Wyoming. In 2001 and 2002, another free-ranging mule deer in southwestern Nebraska, a free ranging mule deer in Saskatchewan, in free-ranging white-tailed deer in NW Nebraska, south central Wisconsin, and SW South Dakota were diagnosed with CWD.
It is unclear where CWD may have originated. Captive herds with CWD were comprised of wild deer. Prior to diagnosis of the disease, some of these captive animals were released back to the wild.
Prevalence
Since free-ranging deer and elk in northcentral Colorado and southeast Wyoming have been surveyed for CWD, the annual prevalence rates have ranged from 1 to 15%. The overall prevalence rate of CWD in the endemic areas is approximately 5% in mule deer and less than 1% in elk. Prevalence in some mule deer hunt areas is as high as 15%. The prevalence rate is greater in deer 2 ½ years and older and in elk 1 ½ years and older. There does not appear to be a gender prevalence difference.
Between 1996 and 2000, the level of infection hadn't changed appreciably over that period of time. The pathogen was firmly established in the endemic area but transmission was not accelerating.
Prion Organism
Prions (Proteinaceous Infectious Particles) are the disease-causing agents associated with CWD and all of the TSE diseases. Prions are mutant versions of proteins that occur normally in the body. The mutant proteins are found on the membranes of nerve cells (neurons) and have the capabilities of transforming other proteins into their own image.
The mutant proteins (the alpha-helical form) do this by twisting into forms that resist the attack of enzymes. The protein molecules stick together in microscopic mutated mats (beta-sheet formation). As the twisted molecules contact normal protein, the normal molecules twist as well, forming a new generation of dangerous prions. The mutated forms accumulate in lysosomes (a space in the brain tissue where damaged tissue is segregated and disposed of). These filled lysosomes burst and damage other cells. Sheets of the molecules collected are not broken down or removed by the body , and eventually kill the nerve cell. Accumulation of the abnormal proteins in nerve cells appears to account for the brain dysfunction that characterizes TSE's. As a result of the nerve cells dying, holes are created in the brain tissue forming the diagnostic lesions seen with a spongiform disease. Prions that were present within the nerve cells are released and go on to attack more cells.
Prions are not sensitive to routine sterilization techniques. The only effective techniques are those used to break down proteins such as incineration (at least 1500 degrees F). They are not destroyed by cooking, formaldehyde, alcohol, or UV light.
They can be inactivated by strong sodium hydroxide (Lye), undiluted chlorine bleach, and autoclaving at 132°C for 1 to 4.5 hours.
Clinical Signs
There are a variety of clinical signs seen in deer and elk with CWD. Emaciation is the main clinical sign observed. This weight loss and poor body condition may be due to brain damage, especially to the part that controls rumination. Other clinical signs observed are:
1. Excessive salvation
2. Increased drinking and urination
3. Depression
4. Dehydration
5. Rough, dull hair coat
6. General weakness
7. Reduced fear of humans
8. Drooped head and ears
9. Decreased interactions with other animals in the pen
10. Listlessness
11. Ataxia (lack of coordination)
12. Blank facial expression
13. Repetitive walking in set patterns within the pen, walking in circles
14. Grinding of the teeth
15. Disorientation
16. Loss of control of bodily functions, inability to stand
17. Paralysis
18. Difficulty swallowing
19. Twitching and trembling
20. Chronic pneumonia
21. Hyperexcitability and nervousness (elk)
22. Death-weeks to months after first symptoms
Gross Examination
Gross lesions observed on post mortem examination are:
1. Emaciation-generalized absence or serious atrophy of subcutaneous and visceral fat tissue and yellow gelatinous bone marrow
2. Aspiration pneumonia (due to the rumen contents)
3. A rumen full of excess frothy fluid mixed with large amounts of sand or gravel
4. Abomasal and omasal ulcers
5. An enteritis (inflammation of the intestinal tract)
6. Abscesses
Histopathological (Microscopic) Examination
The predominant lesions seen with CWD in deer and elk are found in the brain (parasympathetic vagal nucleus, thalamus, hypothalamus, and olfactory tubercle and gyri) and the spinal cord. While the lesions are similar in deer and elk, they are more severe in deer.
The lesions seen are the result of microscopic changes in the brain tissue. Spongiform encephalopathy results in the microcavitation of the gray matter of the brain, intraneuronal vacuolation, and neuronal degeneration. Nerve cells and the brain or spinal cord substance around them develop small holes or larger vacuoles that give the tissue a sponge-like appearance. Patches of protein build-up between some neurons (brain cells) and cause degeneration of others. An inflaminatory response by the animal's immune system does not occur.
Testing
There is currently no laboratory test available for the disease in a live animal therefore CWD is diagnosed through various techniques on dead animals. Histopathological examination of the affected area of the brain will allow for the tissue changes to be seen. The brain needs to be fresh and preserved in formalin. Immunohistochemistry (IHC) consistently demonstrates protease-resistant prion protein (PrP res) in the brain. The brain can be fresh or frozen, and this examination can still occur when an animal has been dead for a longer period of time.
The Western Blot Test can be performed on unfixed fresh brain tissue but it is applicable even if the brain has undergone considerable postmortem autolysis. It can not be performed on formalin-fixed tissue. Other tests that have been used are Capillary Immunoelectrophoresis (PrP test) and the Enzyme-linked immunosorbent assay (ELISA) test.
Treatment
There is no treatment for a deer or elk that has CWD. An animal displaying clinical signs consistent with CWD should be euthanized. Removing the animal may help prevent the spread of the disease.
Transmission: Animal to Animal
Transmission of CWD is possible in species with closely related proteins, thereby being able to exchange prions and cause disease. It is not likely to jump the species barrier. There is no evidence at this time that CWD can be naturally transmitted to livestock or animals other than deer and elk.
In deer and elk, the causal agent of CWD is transmissible from infected to uninfected individuals. Both circumstantial and experimental evidence implicates an animal to animal form of transmission. This can occur in two manners; horizontal or lateral (contact between adult animal and adult animal, contamination of feed or water sources with saliva, urine, and/or feces, or contact with an infected facility or area) and vertical or maternal (adult animal (dam) to offspring via contact). Research has determined that the prevalence levels that are observed could not be attained without horizontal or lateral transmission but could be sustained without vertical or maternal transmission. Transmission via feed contaminated with animal protein is not considered to be a contributing factor. When animals are confined, more intensive transmission occurs than is seen in wild populations. In wild deer the disease spreads very slowly and affects a small proportion of the herd. Horizontal transmission among deer and elk most likely has occurred from mule deer to white-tailed deer and elk.
Once natural transmission occurs, a minimum incubation period (the time from infection to observance of clinical signs) of 18 months is required between exposure to the causal agent and development of the disease. In captive cervid herds a minimal incubation period of 18 to 20 months for mule deer and 18 to 36 months for elk was observed.
The transmission route of the CWD prion protein is probably from the alimentary tract to the central nervous system. Research has found that by 42 days post oral inoculation, CWD prions were detected in the lymphoid tissues draining the alimentary tract. This horizontal transmission may reflect the initial pathway for CWD infection in deer. Transport along ganglia or nerve fibers in the alimentary tract to the brain is a possible route taken by the prion protein.
Research has shown that mule deer fed brains of mule deer that died from CWD have abnormal prions in the cervical lymph nodes at 3 months postinoculation and spongiform encephalopathy in the brain at 16 months postinoculation.
Research on cattle has shown that the only way cattle have been infected is by direct injection of CWD tissues into the brain. Cattle in close association with infected deer or that have ingested the pathogen have not developed the disease. There appears to be a biological barrier between cattle and deer and/or elk transmission. It is possible that prions are not transmitted but arise from a spontaneous change in a protein molecule.
Transmission: Animal to Human
To date, there is no evidence that CWD can be naturally transmitted to humans or to animals other than deer and elk. There is no evidence that the agent that causes CWD occurs in the meat. Proteins differ from one species to another therefore prions are unlikely to prosper in a new species. There is a "substantial barrier" to CWD transmission between animals and people.
By the end of 2000, the World Health Organization, the Transmissible Spongiform Encephalopathy Advisory Committee of the Food and Drug Administration, and public health officials have stated that there currently was no evidence that CWD in Cervidae is transmitted to humans. They encouraged awareness and surveillance for CWD and as a prudent precaution, stated that no part or product of an animal with evidence of CWD or any other TSE be fed to humans or any species of domestic or captive animal. They also stated that it was necessary to prevent introduction and spread of CWD when allowing for the translocation of wild or domestic cervids.
To date, BSE is the only TSE known to cross over from animals and infect humans. A National Institute of Health Study by Dr. Byron Caughey showed that CWD-infected materials (from an elk) were capable of infecting human tissue invitro (in a lab situation) and that although CWD doesn't transmit easily, it is possible. Dr. Thomas Pringle, a molecular biologist at the Sperling Biomedical Foundation in Oregon concluded that this was evidence that there is a definite risk of transmission.
Colorado and Wyoming authorities believe that CWD has been in the free-ranging deer and elk population in isolated locations for at least 30 years and there have been no human cases to date.
Captive Cervid Ranches
Since 1989, Captive Cervid Ranches with positive elk have been diagnosed in Colorado, South Dakota, Nebraska, Oklahoma, Montana, Kansas, and Saskatchewan. All of the positive captive elk in Canada have been traced back to a single Canadian herd that received diseased elk prior to 1990 from a U.S. herd in which CWD was subsequently diagnosed. In many states and Canadian provinces there is concern for close contact between captive and wild animals along fence lines, where fences are broken by storms and accidents, and where gates are left open. Many states and provinces prohibit importation from herds where CWD has been diagnosed and have either set in place or are proposing management plans to monitor captive herds for CWD. It is feared that movement of captive cervids in North America could provide a mechanism whereby the time and distance normally required to spread the disease naturally could be reduced significantly and result in animals in a state far from the endemic wild areas in Colorado and Wyoming becoming infected.
Supplemental Feeding
Providing a supplemental food or water source could increase the likelihood of transmitting this as well as other diseases. It is suspected if CWD is transmitted horizontally (animal to animal) either by direct contact or environmental contamination then artificial feeding stations for wild cervids could be accelerating the problem on a local level. In Colorado, the disease is most prevalent in areas where residents placed feeders to attract deer and elk.
Precautions
In areas where CWD occurs, governmental agencies have made the following precautionary recommendations:
1. Avoid sick animals; don't handle them or shoot them, instead contact local wildlife agency personnel.
2. Don't consume animals that appear to be diseased or are diagnosed with CWD.
3. Wear rubber/latex gloves when field dressing deer or elk.
4. Minimize handling the brain, spinal cord, and lymph nodes.
5. Bone out the carcass.
6. Avoid consuming the brain, spinal cord, eyes, spleen, and lymph nodes of any animal.
7. Wash hands, knives, and other tools used to field dress the animal.
8. Dispose of the hide and bones in a sanitary landfill or incinerator.
Common Policies, Management Practices and Surveillance Techniques in States and Provinces with CWD
The policies and management practices utilized in Colorado, Wyoming, and other states and provinces with CWD are aimed at preventing the spread of CWD and to reduce its occurrence in affected deer and/or elk herds. These practices are:
1. Limit the number of deer and elk in infected populations by utilizing management strategies such as late season hunts.
2. Prohibit relocation of free-ranging deer and elk from the affected area.
3. Enforce regulations that prohibit the feeding of deer and elk.
4. Aggressive and prompt elimination of any deer or elk exhibiting clinical signs consistent with CWD. This involves recognition, collection, and submission of suspect CWD animals. The usual profile for a CWD deer or elk is one that is at least 18 months of age, emaciated, exhibiting abnormal behavior, increased salivation and/or trembling, stumbling, incoordination, and difficulty in swallowing.
5. Active surveillance of deer and elk from affected areas through the collection of heads (brain stems and tonsils).
Routine CWD Surveillance in States and Provinces
Surveillance for CWD in free-ranging deer has occurred since 1998 in numerous states and provinces.
In 1998, 452 Michigan white-tailed deer were tested from DMU 452 and all were negative for CWD. The surveys in all of the other states and provinces except Colorado, Wyoming, Nebraska and Saskatchewan were negative also.
If a hunter harvests a deer or elk from an endemic area in Colorado or Wyoming, they should have the head tested for CWD. There are no additional precautions involved with transporting the carcass).
Policies, Management Practices, and Surveillance for CWD to be used in Michigan if the disease occurs here
If chronic wasting disease is found in free-ranging deer or elk in Michigan, the Department of Natural Resources will implement management strategies that will be aimed at preventing its spread and reducing its occurrence in affected deer and elk herds.
1. Surveillance of hunter killed deer and elk to determine distribution and prevalence rates.
2. Prompt elimination of deer and elk showing signs of chronic wasting disease.
3. Seek regulations prohibiting deer and elk feeding in affected areas.
4. Seek policies that preclude relocation of deer or elk from affected areas.
5. Collaborate on research to enhance both understanding and management efforts.