Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases mounting
2015-2016 CWD Surveillance Summary to Date
CWD surveillance in Missouri includes two distinct sampling areas: CWD
Management Zones and Statewide. CWD Management Zones include counties within
approximately 25-miles of confirmed CWD detections in free-ranging deer.
Statewide surveillance focuses on counties outside of established CWD Management
Zones, and is designed to detect new areas of infection in the state. To date,
CWD Management Zones include the following counties:
North Management Zone: Adair, Chariton, Knox, Linn, Macon, Putnam,
Randolph, Schuyler, Scotland, Shelby and Sullivan counties
Central Management Zone: Boone, Callaway, Cole, Cooper, Miller, Moniteau,
Morgan and Osage counties
Total CWD Samples Taken To Date Area CWD Not Detected CWD Positive Results
Pending Total
Central CWD Management Zone CWD Management Zone 2162 0 39 2201
North CWD Management Zone CWD Management Zone 2499 6 120 2625
Statewide (Outside of Zone) 2621 1 36 2658
TOTAL 7282 7 195 7484
A CWD surveillance season runs from July 1 through June 30 the following
year.
Surveillance Maps
Can I Get It?
As of 2014, there is no evidence that humans can be infected with CWD.
However, research is ongoing to determine any public health impacts.
HOW BAD CAN IT GET?
As of 2014, no human health risk has been reported.
SYMPTOMS IN HUMANS Currently, CWD is not known to infect people.
Safe for Pets? There is no evidence that CWD can be naturally transmitted
to pets but, to be safe, animals that have tested positive for CWD should not be
fed to pets.
Assessing Transmissible Spongiform Encephalopathy Species Barriers with an
In Vitro Prion Protein Conversion Assay
Christopher J. Johnson1, Christina M. Carlson2, Aaron R. Morawski3, Alyson
Manthei4, Neil R. Cashman5
1USGS National Wildlife Health Center, 2Department of Soil Science,
University of Wisconsin–Madison, 3Laboratory of Immunology, National Institute
of Allergy and Infectious Diseases, National Institutes of Health, 4Merial
Veterinary Scholars Program, School of Veterinary Medicine, University of
Wisconsin–Madison, 5Department of Neurology, University of British Columbia
Summary
Measuring the barrier to the interspecies transmission of prion diseases is
challenging and typically involves animal challenges or biochemical assays.
Here, we present an in vitro prion protein conversion assay with the ability to
predict species barriers.
Date Published: 3/10/2015, Issue 97; doi: 10.3791/52522
Keywords: Medicine, Issue 97, Prion, species barrier, conversion,
immunoblotting, transmissible spongiform encephalopathy, interspecies
transmission Cite this Article
Johnson, C. J., Carlson, C. M., Morawski, A. R., Manthei, A., Cashman, N.
R. Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In
Vitro Prion Protein Conversion Assay. J. Vis. Exp. (97), e52522,
doi:10.3791/52522 (2015). Abstract
Studies to understanding interspecies transmission of transmissible
spongiform encephalopathies (TSEs, prion diseases) are challenging in that they
typically rely upon lengthy and costly in vivo animal challenge studies. A
number of in vitro assays have been developed to aid in measuring prion species
barriers, thereby reducing animal use and providing quicker results than animal
bioassays. Here, we present the protocol for a rapid in vitro prion conversion
assay called the conversion efficiency ratio (CER) assay. In this assay cellular
prion protein (PrPC) from an uninfected host brain is denatured at both pH 7.4
and 3.5 to produce two substrates. When the pH 7.4 substrate is incubated with
TSE agent, the amount of PrPC that converts to a proteinase K (PK)-resistant
state is modulated by the original host’s species barrier to the TSE agent. In
contrast, PrPC in the pH 3.5 substrate is misfolded by any TSE agent. By
comparing the amount of PK-resistant prion protein in the two substrates, an
assessment of the host’s species barrier can be made. We show that the CER assay
correctly predicts known prion species barriers of laboratory mice and, as an
example, show some preliminary results suggesting that bobcats (Lynx rufus) may
be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting
disease agent.
>>> show some preliminary results suggesting that bobcats (Lynx
rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic
wasting disease agent.
AD.63: Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1
1Colorado State University; Fort Collins, CO USA; 2University of Minnesota;
Saint Paul, MN USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD. These results demonstrate that
CWD can be transmitted and adapted to the domestic cat, thus raising the issue
of potential cervid-to- feline transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Monday, August 8, 2011
Susceptibility of Domestic Cats to CWD Infection
Sunday, August 25, 2013
Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats,
blood, and mother to offspring transmission
Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK
in 1990. Most cases have been reported in the UK, where the epidemic has been
consistent with that of the BSE epidemic. Some other countries (e.g. Norway,
Liechtenstein and France) have also reported cases.
Most cases have been reported in domestic cats but there have also been
cases in captive exotic cats (e.g. Cheetah, Lion, Asian leopard cat, Ocelot,
Puma and Tiger). The disease is characterised by progressive nervous signs,
including ataxia, hyper-reactivity and behavioural changes and is fatal.
The chemical and biological properties of the infectious agent are
identical to those of the BSE and vCJD agents. These findings support the
hypothesis that the FSE epidemic resulted from the consumption of food
contaminated with the BSE agent.
The FSE epidemic has declined as a result of tight controls on the disposal
of specified risk material and other animal by-products.
References: Leggett, M.M. et al.(1990) A spongiform encephalopathy in a
cat. Veterinary Record. 127. 586-588
Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat.
Veterinary Record. 129. 320
Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform
encephalopathy in five domestic cats. Veterinary Record. 129. 233.
Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J.
Small Animal Practice. 33. 471-476.
Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and
PrP studies. Veterinary Record. 131. 307-310.
Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma
(Felis concolor). Veterinary Record. 131. 431-434.
Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy
to mice. Veterinary Record 134. 449.
Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in
Norway. Veterinary Record 136. 444
Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in
France. Veterinary Record 141. 270-271
Zanusso, G et al. (1998) Simultaneous occurrence of spongiform
encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp
1116-1117.
Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural
tissues of cats with feline spongiform encephalopathy. Veterinary Record 146.
437-441
Kelly, D.F. et al. (2005) Neuropathological findings in cats with
clinically suspect but histologically unconfirmed feline spongiform
encephalopathy. Veterinary Record 156. 472-477.
3 further cheetah cases have occured, plus 1 lion, plus all the primates,
and 20 additional house cats. Nothing has been published on any of these UK
cases either. One supposes the problem here with publishing is that many
unpublished cases were _born_ long after the feed "ban". Caught between a rock
and a hard place: leaky ban or horizontal transmission (or both).
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
Thursday, December 03, 2015
Missouri MDC reports CWD found in Franklin County
Saturday, September 05, 2015
Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for
Money, while mad deer and elk disease silently spreads
Tuesday, June 16, 2015
Missouri MDC changes deer hunting regs to help slow CWD
Wednesday, March 11, 2015
MDC reports 11 new cases of Chronic Wasting Disease CWD in Missouri deer
Monday, January 26, 2015
Missouri MDC reports two new cases of CWD found in Adair and Macon counties
Tuesday, December 09, 2014
Missouri MDC reports one new case of CWD, found in Adair County
Friday, October 17, 2014
Missouri Final action on Orders of Rule making Breeders and Big Game
Hunting Preserves
Thursday, September 11, 2014
Missouri Nixon's Veto Stands Overide Fails on Agriculture Legislation
How they voted: attempt to override veto of ag bill fails in the House
Thursday, May 01, 2014
Missouri DNR CWD prevention and captive cervid farming Update
Tuesday, March 26, 2013
CWD Missouri remains confined to Linn-Macon-County Core Area with four new
cases
Wednesday, January 23, 2013
Missouri sixth case CWD documented northwest Macon County
Tuesday, January 24, 2012
CWD found in two free-ranging deer from Macon County Missouri
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer
Sunday, March 25, 2012
Three more cases of CWD found in free-ranging deer in Macon County
From: Terry S. Singeltary Sr.
Sent: Thursday, March 29, 2012 6:26 PM
To: warhovert@missouri.edu
Cc: abbottjm@missouri.edu ; waltermr@missouri.edu ;
John.McLaughlin@missouri.edu ; connerek@missouri.edu ; contact@dnr.mo.gov ;
Shelly.Witt@mda.mo.gov ; Animal.Health@mda.mo.gov ; acfa@mda.mo.gov ;
animalid@mda.mo.gov ; Linda.Hickam@mda.mo.gov
Subject: re-Missouri officials seek states' advice on chronic wasting
disease in deer
Thursday, May 31, 2012
Missouri MDC staff will provide information on five recently found cases of
CWD in free-ranging deer in northwest Macon County June 2, 2012
Wednesday, September 05, 2012
Missouri MDC seeks hunters’ help when processing harvested deer and
preventing CWD
Thursday, December 20, 2012
MISSOURI Initial CWD sampling test results available online from MDC so far
one adult buck has tested positive for the disease
Friday, October 21, 2011
Chronic Wasting Disease Found in Captive Deer Missouri
The Missouri Department of Agriculture discovers the state's first case of
CWD in a captive white-tailed deer.
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer February 25, 2010
Chronic Wasting Disease Found in Captive Deer
The Missouri Departments of Agriculture, Conservation and Health and Senior
Services and the U.S. Department of Agriculture announced today that a captive
white-tailed deer in Linn County, Missouri has tested positive for Chronic
Wasting Disease (CWD). CWD is a neurological disease found in deer, elk and
moose.
"There is no evidence that CWD poses a risk to domestic animals or humans,"
said State Veterinarian Dr. Taylor Woods. "We have protocols in place to quickly
and effectively handle these situations."
The animal that tested positive for CWD was a white-tailed deer inspected
as part of the State's CWD surveillance and testing program. Preliminary tests
were conducted by the USDA National Veterinary Services Laboratory in Ames,
Iowa.
Upon receiving the confirmed CWD positive, Missouri's departments of
Agriculture, Conservation and Health and Senior Services initiated their CWD
Contingency Plan. The plan was developed in 2002 by the Cervid Health Committee,
a task force comprised of veterinarians, animal health officers and conservation
officers from USDA, MDA, MDC and DHSS working together to mitigate challenges
associated with CWD.
CWD is transmitted by live animal to animal contact or soil to animal
contact. The disease was first recognized in 1967 in captive mule deer in the
Colorado Division of Wildlife captive wildlife research facility in Fort
Collins, Colorado. CWD has been documented in deer and/or elk in Colorado,
Illinois, Kansas, Michigan, Minnesota, Montana, Nebraska, New Mexico, New York,
Oklahoma, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and the
Canadian Provinces of Alberta and Saskatchewan. There has been no evidence that
the disease can be transmitted to humans.
"Missouri's proactive steps to put a testing protocol in place and create a
contingency plan years ago is proving beneficial. We are in a solid position to
follow pre-established steps to ensure Missouri's valuable whitetail deer
resource remains healthy and strong," said Jason Sumners Missouri's Deer
Biologist.
For more information regarding CWD, please contact Dr. Taylor Woods at
(573) 751-3377.
Friday, September 20, 2013
*** Missouri State records show gaps in oversight of captive deer farms,
ranches ***
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation ***
Friday, February 05, 2016
Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
1:02 PM
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