Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry
TAHC TPWD CWD TSE PRION
83R30157 BPG-D By: Kuempel H.R. No. 2597
R E S O L U T I O N
WHEREAS, Texas is home to the largest population of white-tailed deer in
the nation, and deer breeding and hunting make important contributions to the
state's economy; and
WHEREAS, A Texas A&M University study conducted in 2007 found that
deer breeding and ranching generated over $650 million annually and supported
more than 7,300 jobs; as land ownership becomes increasingly fragmented, deer
breeding is particularly well suited to the utilization of smaller tracts, and
the industry is now one of the fastest growing in rural America; by 2012, Texas
had permitted over 1,200 breeder facilities containing over 100,000 breeder deer
in nearly 200 counties; and
WHEREAS, Disease issues that arise in the deer industry are handled by the
Texas Animal Health Commission, but most industry activities fall under the
purview of the wildlife division of the Texas Parks and Wildlife Department;
although TPWD is noted for its vast knowledge of wildlife biology, it is the
TAHC that maintains expertise in agriculture, animal husbandry, and related
matters of genetics, health, nutrition, breeding, and marketability;
moreover, the TAHC manages certain breeds of cervid animals, including red
deer and sika deer; and
WHEREAS, Properly managing this growing industry is of long-term
importance, and an in-depth consideration of relevant issues would be beneficial
to this state; now, therefore, be it
RESOLVED, That the House of Representatives of the 83rd Texas Legislature
hereby request the speaker of the house to create a select interim committee to
study regulatory oversight of the deer breeding industry in order to ensure that
the industry is served by the state agency tasked with promoting and ensuring
animal health and productivity; and, be it further
RESOLVED, That the study include recommendations on measures to ensure the
vitality of the industry and encompass assurances that the Texas Parks and
Wildlife Department will remain involved in the industry through its
responsibility for issuing hunting licenses and providing game wardens; and, be
it further
RESOLVED, That the committee submit a full report, including findings and
recommendations for legislation, to the speaker and the members of the house of
the 84th Texas Legislature when it convenes in January 2015.
By:AAKuempel H.B.ANo.A2092
A BILL TO BE ENTITLED
AN ACT
relating to the transfer of responsibility for regulating deer breeding
from the Parks and Wildlife Department to the Texas Animal Health
Commission.
BE IT ENACTED BY THE LEGISLATURE OF THE STATE OF TEXAS:
SECTIONA1.AASubchapter L, Chapter 43, Parks and Wildlife Code, is
transferred to Subtitle A, Title 6, Agriculture Code, redesignated as Chapter
135, Agriculture Code, and amended to read as follows:
By:AAHinojosa S.B.ANo.A1444
A BILL TO BE ENTITLED
AN ACT
relating to the transfer of responsibility for regulating deer breeding
from the Parks and Wildlife Department to the Texas Animal Health
Commission.
BE IT ENACTED BY THE LEGISLATURE OF THE STATE OF TEXAS:
SECTIONA1.AASubchapter L, Chapter 43, Parks and Wildlife Code, is
transferred to Subtitle A, Title 6, Agriculture Code, redesignated as Chapter
135, Agriculture Code, and amended to read as follows:
CWD tested venison?
83R1094 SLB-D By: Phillips H.B. No. 1616
A BILL TO BE ENTITLED
AN ACT
relating to allowing a deer breeder to transfer and sell for processing as
venison certain breeder deer.
BE IT ENACTED BY THE LEGISLATURE OF THE STATE OF TEXAS:
SECTION 1. Sections 43.357(a) and (b), Parks and Wildlife Code, are
amended to read as follows:
(a) The holder of a valid deer breeder's permit may:
(1) engage in the business of breeding breeder deer in the immediate
locality for which the permit was issued; [and]
(2) sell, transfer to another person, or hold in captivity live breeder
deer for the purpose of propagation or sale; and
(3) transfer and sell live breeder deer not needed for propagation for the
purpose of processing and sale as venison.
(b) The commission may make regulations governing:
(1) the possession of breeder deer held under the authority of this
subchapter;
(2) the recapture of lawfully possessed breeder deer that have escaped
from the facility of a deer breeder;
(3) permit applications and fees;
(4) reporting requirements;
(5) procedures and requirements for the purchase, transfer, sale, or
shipment of breeder deer;
(6) the endorsement of a deer breeder facility by a certified wildlife
biologist;
(7) the number of breeder deer that a deer breeder may possess; [and]
(8) the dates for which a deer breeder permit is valid; and
(9) procedures for the identification, transfer, and sale of live breeder
deer not needed for propagation for the purpose of processing and sale as
venison.
SECTION 2. Section 43.364, Parks and Wildlife Code, is amended to read as
follows:
Sec. 43.364. USE OF BREEDER DEER. (a) Except as provided by Subsection
(b), breeder [Breeder] deer may be purchased, sold, transferred, or received in
this state only for the purposes of liberation or holding for propagation. All
breeder deer and increase from breeder deer are under the full force of the laws
of this state pertaining to deer, and those breeder deer may be held in
captivity for propagation in this state only after a deer breeder's permit is
issued by the department under this subchapter.
(b) Live breeder deer not needed for propagation may be transferred,
processed, and sold as venison only in accordance with Section 43.357 and
either:
(1) Chapter 433, Health and Safety Code, and rules adopted under that
chapter; or
(2) 9 C.F.R. Part 352, as authorized by the federal Agricultural Marketing
Act of 1946 (7 U.S.C. Section 1621 et seq.).
SECTION 3. Subchapter A, Chapter 433, Health and Safety Code, is amended
by adding Section 433.010 to read as follows: Sec. 433.010. APPLICABILITY OF
CHAPTER TO BREEDER DEER.
(a) In this section, "breeder deer" has the meaning assigned by Section
43.351, Parks and Wildlife Code.
(b) This chapter applies to breeder deer, identified by the Parks and
Wildlife Department for the purpose of processing and sale as venison, in the
same manner that the chapter applies to an exotic animal.
SECTION 4. This Act takes effect September 1, 2013.
HB 1616 (83rd Legislature (2013) Relating to allowing a deer breeder to
transfer and sell for processing as venison certain breeder deer.
see more bills here on captive industry in Texas;
see history of CWD in Texas here ;
Sunday, December 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected
to advocate for bills that will seek to further deregulate their industry
Greetings Texas Hunters et al,
I tried telling the TAHC about mad cow disease and mad deer disease aka
Transmissible Spongiform Encephalopathy TSE prion disease aka Bovine Spongiform
Encephalopathy BSE and Chronic Wasting Disease CWD since 1997. I told the TAHC
even where to find CWD in cervids in 2002 i.e. waltzing across the border from
New Mexico WSMR area. IT TOOK TEN YEARS for the TAHC to finally test there at
the NM border in any significant numbers to find CWD, or they just got lucky,
and you guessed it, 6 cases were finally detected in Texas, in the area right
where I told them to look 10 years previously. wonder how many positive CWD
infected deer they missed waltzing across Texas over that 10 year period? now,
all these CWD postive cervids have exposed our wild and very possibly some of
the captive cervids, by commingling along fence line, or flat out getting inside
the fence line and exposing the farm. I would think this is possible in some
cases, but the deer farming industry has been a problem with CWD in many states,
on their own. they are not the only cause in my opinion, but have played a big
part, if you look at past history. some of the CWD infection rates were
extremely high in these captive facilities. Environmental factors and the risk
to our wild cervid herds are too great to start deregulating the cervid farming
industry any further. USDA vs TAHC vs TPWD vs ... it’s big business now$
also, I remember, the TAHC tried to cover up two cases of mad cow disease,
and this proven via the OIG and the GAO, (see my correspondence with TAHC trying
to confirm this madcow for 7 months), and only after the tissue sample of said
2nd mad cow case sat up on a shelf for 7+ months (all the while the BSE MRR was
being set in motion by the USDA and OIE et al, the legal trading of all strains
of TSE prion disease as a legal trading commodity), only after this act of
Congress and the Honorable Fong of the OIG, letters from me and Scientist around
the globe, did they finally send said sample to Weybridge, England, for another
opinion, where mad cow disease was finally CONFIRMED in Texas, the first case
was indeed covered up, and rendered without testing. also, look at the
surveillance, breaches there from, and those trace back efforts for the mad cow
cases they did happen to stumble across. so my point, I think the TPWD has done
a good job, and that with the TAHC, it will just be business as usual. again,
just my opinion. ...
please see reference materials as follows ;
”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.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
*** CWD TSE PRION AND ENVIRONMENTAL FACTORS ***
***Given that scrapie prions are widespread on the surfaces of affected
farms (Maddison and others 2010a), irrespective of the source of the infectious
prions in the pens, this study clearly highlights the difficulties that are
faced with the effective removal of environmentally associated scrapie
infectivity.
***This is likely to be paralleled in CWD which shows strong similarities
to scrapie in terms of both the dissemination of prions into the environment and
the facile mode of disease transmission. These data further contribute to the
understanding that prion diseases can be highly transmissible between
susceptible individuals not just by direct contact but through highly stable
environmental reservoirs that are refractory to decontamination.
***The presence of these environmentally associated prions in farm
buildings make the control of these diseases a considerable challenge,
especially in animal species such as goats where there is lack of genetic
resistance to scrapie and, therefore, no scope to re-stock farms with animals
that are resistant to scrapie.
***These data suggest that recommended current guidelines for the
decontamination of farm buildings following outbreaks of scrapie do little to
reduce the titre of infectious scrapie material and that environmental
recontamination could also be an issue associated with these premises.
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE)
Accepted October 12, 2014. Published Online First 31 October 2014
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
*** 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.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep. ...
also, see where even decades back, the USDA had the same thought as they do
today with CWD, not their problem...see page 27 below as well, where USDA stated
back then, the same thing they stated in the state of Pennsylvania, not their
damn business, once they escape, and they said the same thing about CWD in
general back then ;
”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.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature. Acknowledgments.
Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal
Foundation.
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
Sunday, November 3, 2013
*** Environmental Impact Statements; Availability, etc.: Animal Carcass
Management [Docket No. APHIS-2013-0044]
Friday, October 17, 2014
Missouri Final action on Orders of Rule making Breeders and Big Game
Hunting Preserves
Saturday, October 18, 2014
Chronic wasting disease threatens Canadian agriculture, Alberta MLA
says
Thursday, October 23, 2014
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Tuesday, October 21, 2014
*** Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer
Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
”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.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD
index herd in Pennsylvania Great Escape
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN
INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the
loose in Pennsylvania
Wednesday, September 04, 2013
***cwd - cervid captive livestock escapes, loose and on the run in the
wild...
Tuesday, October 07, 2014
*** Wisconsin white-tailed deer tested positive for CWD on a Richland
County breeding farm, and a case of CWD has been discovered on a Marathon County
hunting preserve
Thursday, October 02, 2014
*** IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
Saturday, October 25, 2014
118th USAHA Annual Meeting CWD and Captive Cerivds
Sunday, December 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected
to advocate for bills that will seek to further deregulate their industry
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program
Standards
>>>The CWD herd certification program is a voluntary, cooperative
program that establishes minimum requirements for the interstate movement of
farmed or captive cervids, provisions for participating States to administer
Approved State CWD Herd Certification Programs, and provisions for participating
herds to become certified as having a low risk of being infected with
CWD<<<
Greetings USDA/APHIS et al,
I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting
Disease Herd Certification Program and Interstate Movement of Farmed or Captive
Deer, Elk, and Moose; Program Standards.
I believe, and in my opinion, and this has been proven by scientific facts,
that without a validated and certified test for chronic wasting disease cwd,
that is 100% sensitive, and in use, any voluntary effort will be futile. the
voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow
surveillance program has failed terribly, as well as the testing for bse tse
prion in cattle, this too has failed terrible. all this has been proven time and
time again via OIG reports and GOA reports.
I believe that until this happens, 100% cwd testing with validated test,
ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO
INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.
In my opinion, and the opinions of many scientists and DNR officials, that
these so called game farms are the cause of the spreading of chronic wasting
disease cwd through much negligence. the game farms in my opinion are not the
only cause, but a big factor. I kindly wish to submit the following to show what
these factors are, and why interstate movement of cervids must be banned.
...
snip...see full text and PDF ATTACHMENT HERE ;
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper
(Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE PRION
disease in cervids
***SINGELTARY SUBMISSION
The Scottish Parliament’s Rural Affairs, Climate Change and Environment
Committee has been looking into deer management, as you can see from the
following press release,
***and your email has been forwarded to the committee for information:
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
Sunday, July 21, 2013
Welsh Government and Food Standards Agency Wales Joint Public Consultation
on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations
2013
*** Singeltary Submission WG18417
Sunday, November 10, 2013
*** LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER
ANTLER VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $
Sunday, July 07, 2013
*** Could avian scavengers translocate infectious prions to disease-free
areas initiating new foci of chronic wasting disease? Prion. 2013 Jul 3;7(4).
[Epub ahead of print]
Monday, February 14, 2011
*** THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND
NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease
Association 2011
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an
unrecognized sporadic or genetic case of bovine prion disease incorporated into
cattle feed or even cattle feed contaminated with prion-infected human remains.1
However, strong support for a genetic origin of BSE has recently been
demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2
Furthermore, a specific prion protein strain causing BSE in cattle is believed
to be the etiological agent responsible for the novel human prion disease,
variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in
a number countries, including France, Italy, Ireland, the Netherlands, Canada,
Japan, US and the UK with the largest number of cases. Naturally occurring
feline spongiform encephalopathy of domestic cats4 and spongiform
encephalopathies of a number of zoo animals so-called exotic ungulate
encephalopathies5,6 are also recognized as animal prion diseases, and are
thought to have resulted from the same BSE-contaminated food given to cattle and
humans, although and at least in some of these cases, a sporadic and/or genetic
etiology cannot be ruled out. The canine species seems to display resistance to
prion disease and no single case has so far been reported.7,8 Here, we describe
a case of a 9 week old male Rottweiler puppy presenting neurological deficits;
and histological examination revealed spongiform vacuolation characteristic of
those associated with prion diseases.9 Initial biochemical studies using
anti-PrP antibodies revealed the presence of partially proteinase K-resistant
fragment by western blotting. Furthermore, immunohistochemistry revealed
spongiform degeneration consistent with those found in prion disease and
displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross
the species barrier transmitted to hamster in vitro with PMCA and in vivo (one
hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100%
attack rate (n = 4) and animals displayed untypical lesional profile and shorter
incubation period.
In this study, we show that the canine species might be sensitive to prion
disease and that PrPSc isolated from a dog can be transmitted to dogs and
hamsters in vitro using PMCA and in vivo to hamsters.
If our preliminary results are confirmed, the proposal will have a major
impact on animal and public health and would certainly lead to implementing new
control measures for ‘canine spongiform encephalopathy’ (CSE).
References 1. Colchester AC, Colchester NT. The origin of bovine spongiform
encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61;
PMID:16139661; http://
dx.doi.org/10.1016/S0140-6736(05)67218-2.
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation.
PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal.
ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy
(BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/
hmg/6.10.1699.
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith
JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic
cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus
angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI.
Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu
(Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink
encephalopathy species barrier effect between ferret and mink: PrP gene and
protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317-
75-11-2947.
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et
al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad
Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30;
PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904
6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long
delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform
Encephalopathy Advisory Committee (SEAC), the UK Government's independent
Advisory Committee on all aspects related to BSE-like disease, gave the hound
study detailed consideration at their meeting in January 1994. As a summary of
this meeting published in the BSE inquiry noted, the Committee were clearly
concerned about the work that had been carried out, concluding that there had
clearly been problems with it, particularly the control on the histology, and
that it was more or less inconclusive. However was agreed that there should be a
re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound
study to see if any useful results could be gained from it. The Chairman
concluded that there were varying opinions within the Committee on further work.
It did not suggest any further transmission studies and thought that the lack of
clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as
conducted. As a result it is likely that the authors felt that it would not
stand up to r~eer review and hence it was never published. As noted above, and
in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether
additional work should be performed to examine dogs for evidence of TSE
infection. Although the Committee had mixed views about the merits of conducting
further work, the Chairman noted that when the Southwood Committee made their
recommendation to complete an assessment of possible spongiform disease in dogs,
no TSEs had been identified in other species and hence dogs were perceived as a
high risk population and worthy of study. However subsequent to the original
recommendation, made in 1990, a number of other species had been identified with
TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry,
gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership
of the data essentially remains with the original researchers. Thus
unfortunately, I am unable to help with your request to supply information on
the hound survey directly. My only suggestion is that you contact one of the
researchers originally involved in the project, such as Gerald Wells. He can be
contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases
of spongiform encephalopathy in animals and poultry were made notifiable. Hence
since that date there has been a requirement for vets to report any suspect SE
in dogs for further investigation. To date there has never been positive
identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's
minute.
I do NOT think that we can justify devoting any resources to this study,
especially as larger and more important projects such as the pathogenesis study
will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound
brains then it should be passed entirely to the VI Service.
J W WILESMITH Epidemiology Unit 18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would
by the end of the year, indentify the three brains that were from the
''POSITIVE'' end of the lesion spectrum.
TSE in dogs have not been documented simply because OF THE ONLY STUDY,
those brain tissue samples were screwed up too. see my investigation of this
here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS
BRAIN TISSUE SAF's. ...TSS
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to
other species will invariably present pathology typical of a scrapie-like
disease.
snip...
76 pages on hound study;
snip...
The spongiform changes were not pathognomonic (ie. conclusive proof) for
prion disease, as they were atypical, being largely present in white matter
rather than grey matter in the brain and spinal cord. However, Tony Scott, then
head of electron microscopy work on TSEs, had no doubt that these SAFs were
genuine and that these hounds therefore must have had a scrapie-like disease. I
reviewed all the sections myself (original notes appended) and although the
pathology was not typical, I could not exclude the possibility that this was a
scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian
degeneration was also present in the white matter of the hounds, another feature
of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that
micrographs and descriptive neuropathology from papers on 'hound ataxia'
mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer
(Cambridge) had done much of this work, and I obtained original sections from
hound ataxia cases from him. This enabled me provisionally to conclude that
Robert Higgins had in all probability detected hound ataxia, but also that hound
ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination
of single restricted microscopic fields that there was no distinction between
the white matter vacuolation present in BSE and scrapie cases, and that
occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known
risk factor for its development was the feeding to hounds of downer cows, and
particularly bovine offal. Circumstantial evidence suggests that bovine offal
may also be causal in FSE, and TME in mink. Despite the inconclusive nature of
the neuropathology, it was clearly evident that this putative canine spongiform
encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the
link with hound ataxia pursued. I telephoned Robert Higgins six years after he
first sent the slides to CVL. I was informed that despite his submitting a
yearly report to the CVO including the suggestion that the hound work be
continued, no further work had been done since 1991. This was surprising, to say
the very least.
41.The hound work could have provided valuable evidence that a scrapie-like
agent may have been present in cattle offal long before the BSE epidemic was
recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from
experiments studying the attempted transmission of BSE to chickens and pigs (CVL
1991) and to mice (RVC 1994).
It was thought likely that at least some, and probably all, of the cases in
zoo animals were caused by the BSE agent. Strong support for this hypothesis
came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A.,
McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of
bovine spongiform encephalopathy and scrapie to mice: strain variation and
species barrier. Philosophical Transactions of the Royal Society B 343, 405-411:
J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation
period and lesion profile in six strains of mice inoculated with brain
homogenates from an affected kudu and the nyala, was similar to that seen when
this panel of mouse strains was inoculated with brain from cattle with BSE. The
affected zoo bovids were all from herds that were exposed to feeds that were
likely to have contained contaminated ruminant-derived protein and the zoo
felids had been exposed, if only occasionally in some cases, to tissues from
cattle unfit for human consumption.
snip...
NEW URL ;
Friday, March 8, 2013
Dogs may have been used to make Petfood and animal feed
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents
that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
Singeltary Submission TAHC on CWD rule proposal
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting
Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and
Hueco Mountains of New Mexico, CWD may be well established in the population and
in the environment in Texas at this time.
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and
behavioural changes that can span weeks or months (Williams, 2005). In addition,
signs might include excessive salivation, behavioural alterations including a
fixed stare and changes in interaction with other animals in the herd, and an
altered stance (Williams, 2005). These signs are indistinguishable from cervids
experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB,
for example, infected deer populations would need to be tested to differentiate
if they were infected with CWD or BSE to minimise the risk of BSE entering the
human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
NEW URL LINK ;
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
*** 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.
cwd exposure, and iatrogenic CJD, what if ???
*** our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions. ***
snip...see full text ;
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
*** We hypothesize that both BSE prions and CWD prions passaged through
felines will seed human recPrP more efficiently than BSE or CWD from the
original hosts, evidence that the new host will dampen the species barrier
between humans and BSE or CWD. The new host effect is particularly relevant as
we investigate potential means of trans-species transmission of prion disease.
CWD TO HUMANS, AND RISK FACTORS THERE FROM (see latest science)
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated
venison in an Upstate New York community: risk behaviours and health outcomes
2005–2011
Tuesday, November 04, 2014
Towards an Age-Dependent Transmission Model of Acquired and Sporadic
Creutzfeldt-Jakob Disease
Friday, December 5, 2014
SPECIAL ALERT The OIE recommends strengthening animal disease surveillance
worldwide
OIE BSE TSE PRION AKA MAD COW DISEASE ?
‘’the silence was deafening’’ ...tss
Wednesday, December 3, 2014
Over 200 Groups Urge Congress to Continue Supporting COOL
For Immediate Release
Tuesday, December 2, 2014
UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion
aka Mad Cow Disease
USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE
WORLD (?) [protected by the BSE MRR policy] $$$
Terry S. Singeltary Sr.
Sunday, December 14, 2014
ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report
Saturday, December 13, 2014
Terry S. Singeltary Sr. Publications TSE prion disease
for my files...tss
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
snip...
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
10:21 PM
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