Chronic Wasting Disease (CWD)

 
C
hronic
 
W
asting
 
D
isease
 
NREC March 1
st
, 2018
 
Transmissible Spongiform Encephalopathy
 
Cattle – BSE
Sheep – Scrapie
CWD – some Cervids
Others in Mink, Cats, etc.
 
History of CWD
 
• First identified in elk of wild origin in the mid
1960’s at Colorado State University
• The origin of CWD is unknown
• Hypotheses:
1.
a natural disease of elk and deer
2.
from scrapie infected sheep
3.
deer/elk fed pelleted feed with TSE in it
4.
spontaneous genetic mutation deer prion
 
History of CWD
 
2002 – CWD Response Plan developed
2008 – first captive deer found positive for CWD in
Michigan (Kent County). Lower Peninsula baiting ban
initiated.
2012 – CWD Response plan revised
2015 – First free ranging deer positive for CWD
(Ingham County). Core and management zones
created.  CWD later identified in Clinton county deer
also.
2015-16: 4 positive deer in Clinton Cty, 5 positive in
Ingham
 
2017 – CWD found in Mecosta County cervid
facility (
may have been wild deer heads
)
2017 – CWD identified in Montcalm and Kent Co
free ranging deer (36 positives in Montcalm
County in 2017).  No positives in these counties
prior to 2017.
2017 – CWD identified in second Mecosta cervid
facility
Feb. 7 2018 – Latest update on CWD numbers is
57 deer.  No new suspect/positive deer since
mid-January update.
What is “CWD”
Pr
ion 
P
rotein (
PrP
) – A normal protein found
in most cells, but more frequent in nervous
system.
PrP
cwd
 
– Mutated version of protein.
Mutation causes protein to mutate other
normal PrP it encounters.  
 
Ingestion of infectious prions via close contact, contaminated
food/environment, or in-vitro (mother to offspring)
Tonsils-lymph-PNS-CNS
Infectious prions mutate “normal” prions (
PrP to PrP
cwd 
)
Infectious prions build up and destroy cells, leaving “holes” in
brain
2-4 years between infection of animal and clinical symptoms
 
Transmissibility of CWD
 
No evidence that CWD is transmissible to humans
despite the frequent and long term (30+ years)
consumption of venison
Increases in CJS in Wisconsin likely not related
Macaques study inconclusive
Absence of evidence does not indicate safety,
merely suggests there is no acute effect
Further mutations possible (how Mad Cow formed)
 
Transmissibility of CWD to Humans
 
• Direct: (animal to animal)
• Indirect: (animal to environment to animal)
• Direct probably more important early, indirect late
• Role of dose
 
Variability in Transmission
 
Genetic Resistance to CWD
• Naturally occurring genetic variation (PRNP gene)
exists within deer and elk populations
• Natural resistance does not appear to be complete.
 
Genetic Component
Clinical Signs of CWD 
 
Reduced appetite
Loss of body weight (poor condition)
Excessive drinking and urination
Increased salivation/slobbering/drooling
Incoordination, ataxia, head tremors
 
Clinical Signs of CWD
 
Change of behavior
Head tremors
May carry head and ears lowered
Wide body stance
Walking repetitive path
Pneumonia is commonly found in
antemortem testing
 
Facts on CWD
 
Effects adults 17 months to 15+ years
Most 3-5 years old, or >15 years
Both sexes
No seasonality
17 month minimum incubation period
 
Infected individuals more likely to be hit by
cars, killed by predators/hunters.
 
ELISA-based tests (enzyme linked immunosorbent assay)
Approximately $30-$40/test
Antemortem Test: Tonsillar and rectal biopsy test using IHC
technology
Others in development
 
Diagnostic Tests for CWD
 
No vaccines currently available
Preventing spread/concentration of environmental contamination
Can’t stop natural migration of deer
Prevention of CWD 
 
Populations in Colorado and Wyoming infected for 30+ years
40-50% prevalence rate
Some seem fine, others are on decline
 
Learning from Neighbors?
 
Coordinating with MDNR/MDARD 
(at technical and leadership levels)
Testing/Monitoring
Management Strategies (comment on NRC Recs)
Funding
 
Education of Membership
CWD
Need for management
How to have deer tested
How to help limit the spread
 
Next Steps Forward
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Chronic Wasting Disease (CWD) is a transmissible spongiform encephalopathy affecting cervids and other animals. The disease was first identified in the mid-1960s and has since been a concern in wildlife populations. CWD is caused by a mutated prion protein that leads to neurological degeneration. While there is no evidence of CWD transmission to humans, precautions are taken to manage and monitor the disease in animal populations.

  • Chronic Wasting Disease
  • CWD
  • Transmissible Spongiform Encephalopathy
  • Prion Protein
  • Wildlife Disease

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  1. Chronic Wasting Disease NREC March 1st, 2018

  2. Transmissible Spongiform Encephalopathy Cattle BSE Sheep Scrapie CWD some Cervids Others in Mink, Cats, etc.

  3. History of CWD First identified in elk of wild origin in the mid 1960 s at Colorado State University The origin of CWD is unknown Hypotheses: 1. a natural disease of elk and deer 2. from scrapie infected sheep 3. deer/elk fed pelleted feed with TSE in it 4. spontaneous genetic mutation deer prion

  4. History of CWD 2002 CWD Response Plan developed 2008 first captive deer found positive for CWD in Michigan (Kent County). Lower Peninsula baiting ban initiated. 2012 CWD Response plan revised 2015 First free ranging deer positive for CWD (Ingham County). Core and management zones created. CWD later identified in Clinton county deer also. 2015-16: 4 positive deer in Clinton Cty, 5 positive in Ingham 2017 CWD found in Mecosta County cervid facility (may have been wild deer heads) 2017 CWD identified in Montcalm and Kent Co free ranging deer (36 positives in Montcalm County in 2017). No positives in these counties prior to 2017. 2017 CWD identified in second Mecosta cervid facility Feb. 7 2018 Latest update on CWD numbers is 57 deer. No new suspect/positive deer since mid-January update.

  5. What is CWD Prion Protein (PrP) A normal protein found in most cells, but more frequent in nervous system. NOT LIVING CAN T KILL PrPcwd Mutated version of protein. Mutation causes protein to mutate other normal PrP it encounters.

  6. Transmissibility of CWD Ingestion of infectious prions via close contact, contaminated food/environment, or in-vitro (mother to offspring) Tonsils-lymph-PNS-CNS Infectious prions mutate normal prions (PrP to PrPcwd ) Infectious prions build up and destroy cells, leaving holes in brain 2-4 years between infection of animal and clinical symptoms

  7. Transmissibility of CWD to Humans No evidence that CWD is transmissible to humans despite the frequent and long term (30+ years) consumption of venison Increases in CJS in Wisconsin likely not related Macaques study inconclusive Absence of evidence does not indicate safety, merely suggests there is no acute effect Further mutations possible (how Mad Cow formed)

  8. Variability in Transmission Direct: (animal to animal) Indirect: (animal to environment to animal) Direct probably more important early, indirect late Role of dose

  9. Genetic Component Genetic Resistance to CWD Naturally occurring genetic variation (PRNP gene) exists within deer and elk populations Natural resistance does not appear to be complete.

  10. Clinical Signs of CWD

  11. Clinical Signs of CWD Change of behavior Head tremors May carry head and ears lowered Wide body stance Walking repetitive path Pneumonia is commonly found in antemortem testing Reduced appetite Loss of body weight (poor condition) Excessive drinking and urination Increased salivation/slobbering/drooling Incoordination, ataxia, head tremors

  12. Facts on CWD Effects adults 17 months to 15+ years Most 3-5 years old, or >15 years Both sexes No seasonality 17 month minimum incubation period Infected individuals more likely to be hit by cars, killed by predators/hunters.

  13. Diagnostic Tests for CWD ELISA-based tests (enzyme linked immunosorbent assay) Approximately $30-$40/test Antemortem Test: Tonsillar and rectal biopsy test using IHC technology Others in development

  14. Prevention of CWD No vaccines currently available Preventing spread/concentration of environmental contamination Can t stop natural migration of deer

  15. Learning from Neighbors? Populations in Colorado and Wyoming infected for 30+ years 40-50% prevalence rate Some seem fine, others are on decline

  16. Next Steps Forward Coordinating with MDNR/MDARD (at technical and leadership levels) Testing/Monitoring Management Strategies (comment on NRC Recs) Funding Education of Membership CWD Need for management How to have deer tested How to help limit the spread

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