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Chronic Wasting Disease (CWD)

In 1967, a syndrome known as chronic wasting disease was first described in several wildlife facilities in Colorado and Wyoming.  These facilities used deer from captive does, captured pregnant does, and orphaned fawns for nutritional, metabolic and disease studies.  In a 12 year period, 53 mule deer and one blacktail deer in these facilities showed signs of chronic wasting disease. The affected animals were young adults that had been within captivity for 2.5-4 years.  These animals had minimal contact with wild ruminants, domestic ruminants or free ranging small mammals such as rodents and small furbearers.

  Chronic wasting disease is now found in captive and wild elk and deer in both the United States and Canada.  The disease has been demonstrated in RockyMountain elk, mule deer, white-tailed deer, and black-tailed deer.  On many occasions, affected cervids have been in direct or indirect contact with other ruminants such as cattle, sheep, and goats, with no evidence of disease transmission to these other ruminant species.  There is also no evidence of CWD being related to Transmissible Spongiform Encephalopathies in humans.  For years, the disease has  occurred endemically in free ranging elk and deer in northern Colorado, southern Wyoming, and southwestern Nebraska.  No animals in these areas are permitted to be moved to other research facilities or translocated for repopulation.  Recently, the disease has also been found in free ranging deer and/or elk in Wisconsin, South Dakota, and New Mexico.  Numerous positive animals have also been identified on farm raised elk herds.  They include farms located in South Dakota, Nebraska, Colorado, Oklahoma, Montana, Kansas and the Canadian province of Saskatchewan.  These farms were quarantined and many have been depopulated, slaughtered and tested.

  The signs of CWD are numerous and vary in severity and time of onset.  Males, females and castrates are affected equally.  The onset of signs can occur during any season of the year.  The signs may start with listlessness, progressive weight loss, and depression that lasts over a 2 week – 8 month period of time.  Many deer develop signs of polyuria, polydipsia, excess salivation, odontoprisis, flaccid facial muscles, drooping ears, lowering of the head, and terminal anorexia.  Many animals have changes in behavior which may include a lack of awareness that is seen by a lowered head and fixed stare for a period of minutes, followed by a return to a normal state of consciousness.  These signs progress until the animal develops secondary complications, such as pneumonia, that lead to the death or euthanasia of the animal.  Clinical pathological findings are non-specific and are generally related to the secondary infections.

  Many pathologic changes are seen on necropsy.  Gross pathological changes are varied and often non-specific.  The most common gross finding is severe emaciation; however, some animals show no abnormalities at all.  Many other findings are due to secondary complications such as pneumonia, abscesses, enteritis, and parasitism.  Histopathologic changes of the central nervous system are the most specific finding in affected animals.  These changes include microcavitation (spongiform transformation) of the neuropil, intracytoplasmic vacuoles in neuronal perikaryons and neuronal degeneration.  The spongiform transformation was seen in the gray matter of the spinal cord, medulla oblongata, pons, mesencephalon, thalamus, hypothalamus and cerebral cortex.  The histologic lesions are most consistently found in the “obex” region of the medulla oblongata (caudal brain stem), and it is this portion of the brain that is routinely tested for CWD.

  Because of the similar lesions, CWD was linked to a category of other transmissible spongiform encephalopathies including scrapie, bovine spongiform encephalopathy, transmissible mink encephalopathy, Kuru and Creutzfeldt-Jakob disease.  These diseases are caused by unique agents called prions.  The incubation period of the prions is from weeks to years; for this reason, they are known as a “slow virus” disease. However, prions are an unconventional agent in that they differ from viruses in many ways.  They facilitate the use of normal cellular pathways for replication.  However, no evidence of nucleic acid has been found in conjunction with any prions.  They are very resistant to many agents that are used to neutralize many viruses  such as ultraviolet radiation, ionizing radiation, ultrasonication, proteases, nucleases, heat, formaldehyde, chloroform and ether.  It is believed that prions are an abnormal protein made from a normal protein-making gene.  The normal gene, PrP gene, encodes the formula for the production of a normal protein called the “prion protein”, PrP.  The protein attaches to the outer layer of the plasma membrane lipid bilayer.  The function of the “prion protein” is not known.  The “prion protein” is normally in an a-helix formation.  The abnormal isoform forms a b-pleated sheet that is protease resistant and, therefore, forms the characteristic protein plaques that are often seen ultrastructurally in many of these diseases.  How the ingestion of an abnormal protein can facilitate the transformation of a normal gene to make an abnormal protein is not yet known.

  Because of its similarity to bovine spongiform encephalopathy and its apparent spread to wild deer populations outside of the endemic area, there is increasing public concern about CWD.  Because of this concern, Indiana now requires all captive elk herds to be registered with the state and a number of restrictions have been placed on the movement of captive elk.  If you have any questions about the management or transport of elk you are encouraged to contact the State Veterinarian’s office (317-227-0300).  To date, there is no evidence that CWD exists in Indiana.  To give us greater confidence that Indiana is free of CWD, the ADDL will cooperate with the State Veterinarian’s office and the Indiana DNR this fall in a survey of hunter-killed deer.  It is hoped that we will continue to find no evidence of CWD in Indiana; however, if we do, it is important to keep in mind that this disease is not known to pose a threat to domestic cattle or humans. 

  If you have questions about the fall deer survey, you are again encouraged to contact the Office of the State Veterinarian.  If you would like to learn more about chronic wasting disease, an excellent review has been made available by the Southeastern Cooperative Wildlife Disease Study (SCWDS) on the internet at www.uga.edu/scwds/briefs.htm.  After accessing the site, click on Volume 18, issue 1.

-by Jill Rietdorf, Class of 2002
-edited by Dr. Duane Murphy,   ADDL Pathologist

 

References:

1.  Cotran R, Kumar V, Collins T: 1999.  Transmissible spongiform encephalopathies (prion diseases). Robbins Pathologic Basis of Disease pp 1323-1326.

2.  Jones TC, Hunt RD, King NW: 1997.  Prions.  Vet Path pp 360-366.

3.  USDA, APHIS.  October, 2001.   www.aphis.usda.gov/pa/pubs/fscwd.html

4. Williams ES, Young S: 1980. Chronic wasting disease of captive mule deer; a spongiform encephalopathy. J Wildl Dis 16:89-98.

5.  Williams ES, Young S: 1982. Spongiform encephalopathy of RockyMountain elk. J Wildl Dis 18:465.471.

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