chronic wasting disease
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IdentityTop of page
Preferred Scientific Name
- chronic wasting disease
International Common Names
- Spanish: la enfermedad de emaciacion cronica
OverviewTop of page
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of deer and elk in USA and Canada. To date, this disease has been found only in cervids (members of the deer family). First recognized as a clinical "wasting" syndrome in 1967 in mule deer in a wildlife research facility in northern Colorado, it was identified as a TSE in 1978, and was described by Williams and Young (1980, 1982). The disease CWD is typified by chronic weight loss leading to death. There is no known relationship between CWD and any other TSE of animals or people.
The disease has no connection with 'chronic wasting disease' in cattle, which appears to be a multifactorial disease of high yielding dairy cattle in the Netherlands (Kruif, 2001), nor any connection with a chronic wasting disease of cattle in the Sudan (Catley et al., 2001). Also it does not appear to be connected with a wasting syndrome in Swedish moose (Broman et al., 2002).
In the mid-1980s, CWD was detected in free-ranging deer and elk in contiguous portions of northeastern Colorado and southeastern Wyoming. In May 2001, CWD was found in free-ranging deer in the southwestern corner of Nebraska (adjacent to Colorado and Wyoming) and later in additional areas in western Nebraska. The limited area of northern Colorado, southern Wyoming, and western Nebraska in which free-ranging deer and/or elk positive for CWD have been found is referred to as the endemic area. Soon after diagnosis of the disease as a TSE, Colorado and Wyoming wildlife management agencies stopped the movement of deer and elk from their research facilities; wild cervids have not been translocated from the endemic area. In 2002, CWD was detected in wild deer in south-central Wisconsin, southwestern South Dakota, the western slope of Colorado, southern New Mexico, and northern Illinois. The number of States in the USA with positive animals detected in wild populations had risen to 15 by 2011 (in an additional four States, CWD had been detected in one or more captive animals). A map of the current situation is available from the Chronic Wasting Disease Alliance at: http://www.cwd-info.org/index.php/fuseaction/about.map.
The first positive farmed elk herd in the USA was detected in 1997 in South Dakota. By 2011, CWD had been diagnosed in farmed elk and deer herds in eleven States of the USA.
CWD has also been found in farmed elk in the Canadian provinces of Saskatchewan and Alberta and in free-ranging mule deer in Saskatchewan. For more information on CWD in Canada, visit the Canadian Food Inspection Agency Web site at www.inspection.gc.ca/english/anima/disemala/cwdmdc/cwdmdce.shtml
Hosts/Species AffectedTop of page
Species that have been affected with CWD include Rocky Mountain elk (Cervus elaphus nelsoni), mule deer [black tailed deer] (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus) and moose (Alces alces shirasi) (Baeten et al., 2007). Other ruminant species, including wild ruminants and domestic cattle, sheep, and goats, have been housed in wildlife facilities in direct or indirect contact with CWD-affected deer and elk without evidence of disease transmission. There is ongoing research to further explore the possibility of transmission of CWD to other species. Evidence has been found indicating that conversion of human and bovine PrP by the PrP of CWD was much less efficient than for other cervid species. This would suggest a species barrier for CWD (Raymond, GJ, 2000).
Analysis of the PrP gene sequence genotypes of CWD-affected elk and of unaffected elk in free-ranging and captive populations was shown to be highly conserved, encoding a single amino acid polymorphism (Met to Leu) at cervid codon 132. Homozygosity for Met at the corresponding polymorphic site (Met to Val) in humans (human codon 129) predisposes exposed individuals to some forms of Creutzfeldt-Jakob disease. Rocky Mountain elk homozygous for PrP codon 132 Met were over-represented in both free-ranging and farm-reared CWD-affected elk (O'Rourke et al., 1999).
An examination of the glycoform patterns failed to identify patterns capable of reliably distinguishing these transmissible spongiform encephalopathy diseases. However, PrP-res patterns sometimes differed among individual animals, suggesting infection by different or multiple CWD strains in some species (Race et al., 2002).
Cattle may be susceptible to experimental infection with CWD (Hamir, 2001). 13 calves were inoculated intracerebrally with brain suspension from mule deer with CWD. Between 24 and 27 months after inoculation, 3 animals became recumbent and were killed. Microscopic lesions in the brain were subtle in 2 animals and absent in the third case. However, all 3 animals were positive for PrPres by immunohistochemistry and Western blot, and scrapie-associated fibrils (SAFs) were detected in 2 of the animals. Three years after the CWD challenge, the 10 remaining inoculated cattle were alive and apparently healthy. These preliminary findings demonstrate that diagnostic techniques currently used for bovine spongiform encephalopathy surveillance would also detect CWD in cattle should it occur naturally.
DistributionTop of page
In the mid-1980s, CWD was detected in free-ranging deer and elk in contiguous portions of northeastern Colorado and southeastern Wyoming. In May 2001, CWD was also found in free-ranging deer in the southwestern corner of Nebraska (adjacent to Colorado and Wyoming) and later in additional areas in western Nebraska. The limited area of northern Colorado, southern Wyoming, and western Nebraska in which free-ranging deer and/or elk positive for CWD have been found is referred to as the endemic area. Soon after diagnosis of the disease as a TSE, Colorado and Wyoming wildlife management agencies stopped the movement of deer and elk from their research facilities; wild cervids have not been translocated from the endemic area. In 2002, CWD was detected in wild deer in south-central Wisconsin, southwestern South Dakota, the western slope of Colorado, southern New Mexico, and northern Illinois. The number of States in the USA with positive animals detected in wild populations had risen to 15 by 2011 (in an additional four States, CWD had been detected in one or more captive animals). For current information on prevalence of the disease, see the Chronic Wasting Disease Alliance map at: http://www.cwd-info.org/index.php/fuseaction/about.map
CWD has also been diagnosed in farmed elk and deer herds in a number of US States (11 as of 2011 - Colorado, Kansas, Michigan, Minnesota, Missouri, Montana, Nebraska, New York, Oklahoma, South Dakota and Wisconsin). The first positive farmed elk herd in the USA was detected in 1997 in South Dakota. Most of the herds with CWD positive animals have been depopulated and tested. CWD also has been found in farmed elk in the Canadian provinces of Saskatchewan and Alberta and in free-ranging mule deer in Saskatchewan. For more information on CWD in Canada, visit the Canadian Food Inspection Agency Web site at: http://www.inspection.gc.ca/english/anima/disemala/cwdmdc/cwdmdce.shtml
The disease was also recorded in seven-year-old male elk (Cervus elaphus nelsoni) imported into Korea from Canada on March 9, 1997. This appears to be the only report of the disease outside of North America (Sohn et al., 2002).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Korea, Republic of||Present||Sohn et al., 2002|
|Canada||Present||Present based on regional distribution.|
|USA||Present||CAB ABSTRACTS Data Mining 2001|
|-Michigan||Present only in captivity/cultivation|
|-Missouri||Present only in captivity/cultivation|
|-Montana||Present only in captivity/cultivation|
|-Oklahoma||Present only in captivity/cultivation|
PathologyTop of page
Examination of white tailed deer, mule deer and Rocky Mountain elk from Colorado showed clinical signs included emaciation, excessive salivation, behavioral changes, ataxia, and weakness (Spraker et al., 1997). Emaciation with total loss of subcutaneous and abdominal adipose tissue, and serous atrophy of remaining fat depots were the only consistent gross findings. Clinical signs, gross and microscopic lesions and ancillary test findings in affected deer and elk were indistinguishable from those reported in chronic wasting disease of captive cervids.
Amyloid plaques were identified in the brains of affected deer (Bahmanyar et al., 1985), and the distribution of the plaques using antibodies to scrapie plaques were described by Guiroy et al. (1991, 1993). The pathological similarities between CWD and scrapie and BSE confirmed that the disease was a TSE (Williams et al., 1993)
The pathology of CWD did not differ between farmed and wild cervids (Spraker et al., 1997).
In a comparison of the central nervous system of 9 mule deer and 6 elk with CWD studied by light microscopy, lesions were similar in both species and were characterized by spongiform transformation of grey matter, intracytoplasmic vacuolation of neurons, neuronal degeneration and loss, astrocytic hypertrophy and hyperplasia, occurrence of amyloid plaques, and absence of significant inflammatory response (Williams, 1993). There were only minor differences in the distribution and severity of lesions between deer and elk. Consistent, severe lesions occurred in olfactory tubercle and cortex, hypothalamus, and the parasympathetic vagal nucleus of deer, and sections examined from these regions would be sufficient to establish a diagnosis of CWD. Lesions were milder in these locations in elk but were sufficiently apparent to be of diagnostic value. Other differences included increased severity of lesions in some thalamic nuclei in elk in contrast to deer, the occurrence of amyloid plaques demonstrable by histochemical stains in deer in contrast to elk, and the presence of mild white matter lesions in elk but not in deer. Topographic distribution and lesion severity of chronic wasting disease were most similar to those of scrapie and bovine spongiform encephalopathy, than to transmissible mink encephalopathy. The duration of clinical disease does not significantly influence lesion distribution or severity in either species.
DiagnosisTop of page
The most obvious and consistent 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, blank facial expression and repetitive walking in set patterns. In elk, behavioral changes may also include hyperexcitability and nervousness. Affected animals continue to eat grain but may show decreased interest in hay. Excessive salivation and grinding of the teeth also are observed. Most deer show increased drinking and urination.
Research is being conducted to develop live-animal diagnostic tests for CWD. Currently, definitive diagnosis is based on postmortem examination (necropsy) and testing. Gross lesions seen at necropsy reflect the clinical signs of CWD, primarily emaciation. Aspiration pneumonia, which may be the actual cause of death, also is a common finding in animals affected with CWD. On microscopic examination, lesions of CWD in the central nervous system resemble those of other TSEs. In addition, an immunohistochemical (IHC) test can be used to test brain tissue for the presence of the abnormal prion protein to diagnose CWD. The test has been shown to detect the disease before the animals displayed clinical signs (Peters et al., 2000). In this study the most consistently IHC-positive tissue was medulla oblongata, especially the obex.
Immunohistochemical staining (IHC) using monoclonal antibody F89/160.1.5 for detecting protease-resistant prion protein (PrP(res)) of brain and tonsil tissue found that dorsal motor nucleus of the vagus nerve was the most consistent single neuroanatomic site of detectable PrP(res) (Spraker et al., 2002).
A new monoclonal antibody (MAb F99/97.6.1) demonstrated excellent properties for detection of PrPres in fresh, frozen or mildly to moderately autolytic samples of brain and tonsils of mule deer. This immunohistochemistry assay is a sensitive, specific, readily standardized diagnostic test for CWD in deer (Spraker et al., 2002). Tonsil biopsies (Wild et al., 2002) and rectoanal mucosa-associated lymphoid tissue (Keane et al., 2009) have also been shown as useful methods for preclinical diagnosis.
To assess whether alimentary-associated neural pathways may play a role in prion-spread, neural and endocrine tissues from mule deer naturally infected with CWD were examined by immunohistochemistry. PrPCWD was detected in the myenteric plexus, vagosympathetic trunk, nodose ganglion, pituitary, adrenal medulla and pancreatic islets. Little or no PrPCWD staining was detected in other nerves or ganglia (brachial plexus, sciatic nerve, gasserian ganglion, coeliac ganglion, cranial cervical ganglion, spinal nerve roots) of CWD-positive deer. These findings suggest that the transit of PrPCWD in nerves, either centrifugally or centripetally, is one route of prion spread and organ invasion and endocrine organs may also be targets for pathogenic prion accumulation in CWD (Sigurdson et al., 2001).
Disease CourseTop of page
Most cases of CWD occur in adult animals. The disease is progressive and always fatal.
EpidemiologyTop of page
In a study of the epidemiology of CWD, between June 1986 and May 1997, CWD was the only natural cause of adult mortality among captive Rocky Mountain elk held at a wildlife research facility in Colorado (Miller et al 1998). Of 23 elk that remained in this herd for more than15 months, 4 (17%) developed CWD. All affected elk were unrelated females from the founding cohort, captured as neonates and reared in 1986. The index case was diagnosed in 1989; time intervals between subsequent cases ranged from 13 to 32 months. Initial age at onset of clinical signs ranged from about 2.9 to 8.1 years; duration of clinical disease ranged from 5 to 12 months (mean = 7.5 months) before death. Intraspecific lateral transmission of CWD seemed the most plausible explanation for the epidemic pattern observed; neither periparturient nor maternal transmission appeared necessary to sustain this outbreak. It is suggested that early detection and elimination of incubating or clinical individuals may have aided in reducing exposure or infection rates as compared to a previous outbreak in the same facility.
Surveillance and epidemic modeling of the disease in deer and elk in Colorado and Wyoming showed that prevalence varied widely among biologically- or geographically-segregated subpopulations within a 38137 km2 endemic area but appeared stable over a 3-year period (Miller et al., 2000). Using plausible transmission assumptions that mimicked field data, prevalence in epidemic models reached about 1% in 15 to 20 years and about 15% in 37 to 50 years. Models forecast population declines once prevalence exceeded about 5%. Both field and model data supported the importance of lateral transmission in CWD dynamics. Based on prevalence, spatial distribution, and modeling, Miller et al. (2000) suggest that CWD has been occurring in northeastern Colorado and southeastern Wyoming for more than 30 years, and may be best represented as an epizootic with a protracted time-scale.
Little is known about the natural transmission of CWD. In tests on six mule deer fawns inoculated orally with a brain homogenate prepared from mule deer with naturally occurring CWD, PrPres was detected in alimentary-tract-associated lymphoid tissues in all fawns from 42-80 days after inoculation (Sigurdson et al., 1999). The fact that CWD PrPres could be detected in lymphoid tissues draining the alimentary tract within a few weeks of oral exposure to infectious prions and may reflect the initial pathway of the disease in deer.
Impact: EconomicTop of page
Cervids are important game species throughout North America and are also farmed for meat. The importance of the chronic wasting disease is due to its similarity with bovine spongiform encephalopathy and the human disease Creutfzfeldt-Jakob disease (CJD) and its potential to spread to other species. Because of the uncertainties surrounding CWD it greatly diminishes the value of the wild cervid population as a resource. Because of the concern over the possible links between CWD and other TSEs in other species, in May 2002, the US Congress requested that USDA and the Department of Interior develop a plan to assist State wildlife management and agriculture agencies with CWD management [See Disease Prevention and Control].
Zoonoses and Food SafetyTop of page
There is no evidence that CWD can be transmitted to humans or other non-cervid species.
However, with the emergence of variant CJD and its links to BSE, certain precautions should be followed. In Colorado, where most cases of CWD have been found, the Colorado Division of Wildlife recommends the following:
When pursuing or handling deer and elk in infected units:
1. Do not shoot, handle or consume any animal that appears sick; contact the Division of Wildlife in Fort Collins at (970) 472-4300 if you see or harvest an animal that appears sick.
2. Wear rubber gloves when field dressing carcasses.
3. Bone out the meat from your animal.
4. Minimize the handling of brain and spinal tissues.
5. Wash hands and instruments thoroughly after field dressing is completed.
6. Avoid consuming brain, spinal cord, eyes, spleen, tonsils and lymph nodes of harvested animals. (Normal field dressing coupled with boning out a carcass will remove most, if not all, of these body parts. Cutting away all fatty tissue will remove remaining lymph nodes.)
7. Avoid consuming the meat from any animal that tests positive for the disease.
8. Knives, saws and cutting table surfaces can be disinfected by soaking in a solution of 50 percent unscented household bleach and 50 percent water for an hour. Thoroughly rinse all utensils in water to remove the bleach. Afterwards, allow them to air dry.
9. Request that your animal be processed individually, without meat from other animals being added to meat from your animal.
Disease TreatmentTop of page
There is no treatment for the disease; animals suspected of having the disease should be destroyed and tested.
Prevention and ControlTop of page
Surveillance for CWD in free-ranging deer and elk in Colorado and Wyoming has been continuing since 1983 and has helped define the core endemic areas for the disease in those States. CWD in free-ranging deer in Nebraska was detected in 2000/2001; more intensive surveillance to better define the prevalence and distribution of the disease in free-ranging deer in Nebraska is underway. In addition, an extensive nationwide surveillance effort was started in 1997-98 to better define the geographic distribution of CWD in free-ranging cervids in USA. This surveillance effort is a two-pronged approach consisting of hunter-harvest cervid surveys conducted in many States, as well as surveillance throughout the entire country targeting deer and elk exhibiting clinical signs suggestive of CWD. As of March 2010, approximately 775,000 wild cervids had been sampled and tested for CWD in the USA. The finding of CWD in wild deer in areas far removed from the known endemic area has resulted in the development of plans for intensive surveillance in many states during their hunting seasons to better define distribution of the disease in wildlife in the USA.
Surveillance for CWD in farmed elk began in 1997 and has been a cooperative effort involving State agriculture and wildlife agencies and the US Department of Agriculture’s (USDA) Animal and Plant Health Inspection Service (APHIS). Farmed cervid surveillance has been increasing each year since 1997 and will be an integral part of the USDA program to eliminate CWD from farmed elk. As of October 2010, approximately 150,000 farmed cervids had been sampled for CWD testing.
A model has been developed by Connor et al. (2000) to show how prevalence estimates of the disease could be affected bias in sampling techniques. Most diseased deer are found during the autumn hunting season.
In each State where CWD has been detected in wildlife, State wildlife agencies have enacted response and/or management plans. APHIS has provided assistance to State officials in diagnosing CWD and in monitoring international and interstate movements of animals to help prevent further spread of CWD. Also, APHIS is developing a program to eliminate CWD from farmed elk. In addition, many State animal health regulatory agencies have instituted CWD programs for farmed elk. All of these agencies are committed to limiting the distribution of the disease in free-ranging deer and elk to the current localized area and decreasing its occurrence in both the free-ranging and farmed deer and elk populations.
Using a mechanistic model to simulate dynamics of CWD, simulated selective culling programmes revealed the importance of starting control while CWD prevalence was low < 0.01). Low selective culling rates (less than 20% of infected populations) effectively eliminated CWD if started when the prevalence was low, but the likelihood of control diminished rapidly as prevalence increased. Management programmes will likely require an effort sustained over many decades to eliminate CWD (Gross et al., 2001).
In May 2002, the US Congress requested that USDA and the Department of Interior develop a plan to assist State wildlife management and agriculture agencies with CWD management. A CWD task force was formed to ensure that Federal and State agencies cooperate in the development and implementation of an effective national CWD programme. The task force delivered the Plan for Assisting States, Federal Agencies, and Tribes in Managing Chronic Wasting Disease in Wild and Captive Cervids to Congress in June 2002 and is currently developing an implementation document for the plan. The plan addresses CWD diagnostics, communication, information dissemination, management, research, and surveillance. For more information about the plan and the task force see: http://www.aphis.usda.gov/animal_health/animal_diseases/cwd.
ReferencesTop of page
Asante EA et al., 2002. BSE prions propogate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO Journal, 21(23):6358-6366.
Baeten LA, Powers BE, Jewell JE, Spraker TR, Miller MW, 2007. A natural case of chronic wasting disease in a free-ranging moose (Alces alces shirasi). Journal of Wildlife Diseases, 43(2):309-314. http://www.wildlifedisease.org
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Catley A, Okoth S, Osman J, Fison T, Njiru Z, Mwangi J, Jones BA, Leyland TJ, 2001. Participatory diagnosis of a chronic wasting disease in cattle in southern Sudan. Preventive Veterinary Medicine, 51(3/4):161-181; 38 ref.
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Conner MM, McCarty CW, Miller MW, 2000. Detection of bias in harvest-based estimates of chronic wasting disease prevalence in mule deer. Journal of Wildlife Diseases, 36(4):691-699.
Gross JE, Miller MW, 2001. Chronic wasting disease in mule deer: disease dynamics and control. Journal of Wildlife Management, 65(2):205-215.
Guiroy DC et al., 1993. Ultrastructural neuropathology of chronic wasting disease in captive mule deer. Acta Neuropathologica, 85(4):437-444.
Guiroy DC, Williams ES, Song KJ, Yanagihara R, Gajdusek DC, 1993. Fibrils in brains of Rocky Mountain elk with chronic wasting disease contain scrapie amyloid. Acta Neuropathologica, 86(1):77-80; 21 ref.
Guiroy DC, Williams ES, Yanagihara R, Gajdusek DC, 1991. Topographic distribution of scrapie amyloid-immunoreactive plaques in chronic wasting disease in captive mule deer (Odocoileus hemionus hemionus). Acta Neuropathologica, 81(5):475-478; 18 ref.
Hamir AN, Cutlip RC, Miller JM, Williams ES, Stack MJ, Miller MW, O'Rourke KI, Chaplin MJ, 2001. Preliminary findings on the experimental transmission of chronic wasting disease agent of mule deer to cattle. Journal of Veterinary Diagnostic Investigation, 13(1):91-96; 20 ref.
Keane D, Barr D, Osborn R, Langenberg J, O'Rourke K, Schneider D, Bochsler P, 2009. Validation of use of rectoanal mucosa-associated lymphoid tissue for immunohistochemical diagnosis of chronic wasting disease in white-tailed deer (Odocoileus virginianus). Journal of Clinical Microbiology, 47(5):1412-1417. http://jcm.asm.org/cgi/content/full/47/5/1412
Kruif Ade, 2001. Did vaccination with an infectious bovine rhinotracheitis (IBR) marker vaccine on thirteen cattle farms give rise to 'chronic wasting' among dairy cattle?. Tijdschrift voor Diergeneeskunde, 126(6):166-173.
Miller MW et al., 2000. Epizootiology of chronic wasting disease in free-ranging cervids in Colorado and Wyoming. Journal of Wildlife Diseases, 36(4):676-690.
O'Rourke KI, Besser TE, Miller MW, Cline TF, Spraker TR, Jenny AL, Wild MA, Zebarth GL, Williams ES, 1999. PrP genotypes of captive and free-ranging Rocky Mountain elk (Cervus elaphus nelsoni) with chronic wasting disease. Journal of General Virology, 80(10):2765-2769; 24 ref.
Peters J, Miller JM, Jenny AL, Peterson TL, Carmichael KP, 2000. Immunohistochemical diagnosis of chronic wasting disease in preclinically affected elk from a captive herd. Journal of Veterinary Diagnostic Investigation, 12(6):579-582; 11 ref.
Race RE et al., 2002. Comparison of abnormal prion protein glycoform patterns from transmissible spongiform encephalopathy agent-infected deer, elk, sheep, and cattle. Journal of Virology, 76(23):12365-12368.
Raymond GJ, Bossers A, Raymond LD, O'Rourke KI, McHolland LE, Bryant PKIII, Miller MW, Williams ES, Smits M, Caughey B, 2000. Evidence of a molecular barrier limiting susceptibility of humans, cattle and sheep to chronic wasting disease. EMBO Journal, 19(17):4425-4430; 21 ref.
Schmerr MJ, Jenny AL, Bulgin MS, Miller JM, Hamir AN, Cutlip RC, Goodwin KR, 1999. Use of capillary electrophoresis and fluorescent labeled peptides to detect the abnormal prion protein in the blood of animals that are infected with a transmissible spongiform encephalopathy. Journal of Chromatography, A, 853(1/2):207-214; 21 ref.
Sigurdson CJ, Spraker TR, Miller MW, Oesch B, Hoover EA, 2001. PrP in the myenteric plexus, vagosympathetic trunk and endocrine glands of deer with chronic wasting disease. Journal of General Virology, 82(10):2327-2334; 37 ref.
Sigurdson CJ, Williams ES, Miller MW, Spraker TR, O'Rourke KI, Hoover EA, 1999. Oral transmission and early lymphoid tropism of chronic wasting disease PrP in mule deer fawns (Odocoileus hemionus). Journal of General Virology, 80(10):2757-2764; 27 ref.
Sohn HyunJoo, Kim JaeHoon, Choi KangSeuk, Nah JinJu, Joo YiSeok, Jean YoungHwa, Ahn SooWhan, Kim OkKyung, Kim DaeYong, Balachandran A, 2002. A case of chronic wasting disease in an elk imported to Korea from Canada. Journal of Veterinary Medical Science, 64(9):855-858; 11 ref.
Spraker TR et al., 1997. Spongiform encephalopathy in free-ranging mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk (Cervus elaphus nelsoni) in northcentral Colorado. Journal of Wildlife Diseases, 33(1):1-6.
Spraker TR et al., 2002. Distribution of protease-resistant prion protein and spongiform encephalopathy in free-ranging mule deer (Odocoileus hemionus) with chronic wasting disease. Veterinary Pathology, 39 (5), 546-556.
Spraker TR, O'Rourke KI, Balachandran A, Zink RR, Cummings BA, Miller MW, Powers BE, 2002. Validation of monoclonal antibody F99/97.6.1 for immunohistochemical staining of brain and tonsil in mule deer (Odocoileus hemionus) with chronic wasting disease. Journal of Veterinary Diagnostic Investigation, 14(1):3-7; 18 ref.
Wild MA, Spraker TR, Sigurdson CJ, O'Rourke KI, Miller MW, 2002. Preclinical diagnosis of chronic wasting disease in captive mule deer (Odocoileus hemionus) and white-tailed deer (Odocoileus virginianus) using tonsillar biopsy. Journal of General Virology, 83(10):2629-2634; 14 ref.
Williams ES, Young S, 1980. Chronic wasting disease of captive mule deer: a spongiform encephalopathy. Journal of Wildlife Diseases, 16(1):89-98.
Williams ES, Young S, 1982. Spongiform encephalopathy of Rocky Mountain elk. Journal of Wildlife Diseases, 18(4):465-471.
Distribution MapsTop of page
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