Chronic Wasting Disease CWD TEXAS UPDATE ON REGULATION RULES
Texas Administrative Code
TITLE 4 AGRICULTURE PART 2 TEXAS ANIMAL HEALTH COMMISSION CHAPTER 40
CHRONIC WASTING DISEASE
Rules
§40.1 Definitions §40.2 General Requirements §40.3 Herd Status Plans for
Cervidae §40.4 Entry Requirements §40.5 Movement Requirements for CWD
Susceptible Species §40.6 CWD Movement Restriction Zone §40.7 Executive Director
Declaration of a CWD Movement Restriction Zone
Instructions — CWD Susceptible Species Movement Record
This form was created to facilitate the reporting of movements of CWD
Susceptible Species as required by TAHC regulation 40.5. A copy of this
regulation may be viewed here or by visiting the Statutes & Rules page of
the TAHC website and clicking on the Texas Administrative Code link.
Slaughter: Provide name of slaughter facility.
Movements to slaughter are exempt from the 20% testing requirement but
animals 16 months of age and older that are slaughtered do count as eligible
mortalities for any other future movements.
Species: Enter the appropriate CWD susceptible species (red deer, sika,
elk, or moose).
snip...see full text ;
Instructions —CWD Susceptible Species Inventory
This form was created to facilitate the reporting of movements of CWD
Susceptible Species as required by TAHC regulation 40.5. A copy of this
regulation may be viewed here or by visiting the Statutes & Rules page of
the TAHC website and clicking on the Texas Administrative Code link.
snip...see full text ;
Oral Transmission of Chronic Wasting Disease in Captive Shira’s Moose
Terry J. Kreeger1,3, D. L. Montgomery2, Jean E. Jewell2, Will Schultz1 and
Elizabeth S. Williams2 + Author Affiliations 1Wyoming Game and Fish Department,
2362 Highway 34, Wheatland, Wyoming 82201, USA; 2Department of Veterinary
Sciences, University of Wyoming, Laramie, Wyoming 82071, USA ↵3Corresponding
author (email: tkreeger@wildblue.net)
Next Section Abstract
Three captive Shira’s moose (Alces alces shirasi) were orally inoculated
with a single dose (5 g) of whole-brain homogenate prepared from chronic wasting
disease (CWD)–affected mule deer (Odocoileus hemionus). All moose died of causes
thought to be other than CWD. Histologic examination of one female moose dying
465 days postinoculation revealed spongiform change in the neuropil, typical of
transmissible spongiform encephalopathy. Immunohistochemistry staining for the
proteinase-resistant isoform of the prion protein was observed in multiple
lymphoid and nervous tissues. Western blot and enzyme-linked immunosorbent
assays provided additional confirmation of CWD. These results represent the
first report of experimental CWD in moose.
SNIP...
It is unknown whether moose can die from PrPCWD infection and whether CWD
presents a threat to free-ranging moose populations. Nonetheless, this
experiment did confirm that 1) moose can become orally infected with mule
deer–derived CWD, 2) PrPCWD propagated and accumulated in multiple lymphoid and
nervous tissues similar to deer and elk (Spraker et al., 1997), and 3) PrPCWD
caused spongiform changes in the central nervous system considered
characteristic for CWD in cervids (Williams and Young, 1992). Thus, this is the
first report of experimental CWD in moose. Subsequent to these findings, a
hunter-killed wild moose was diagnosed with CWD in Colorado in September 2005
(M. Miller, unpubl. data). Although CWD has now been established in moose, cases
in moose probably will be a rare occurrence because their social habits differ
from elk and deer. Nonetheless, wildlife managers should be aware of this
possibility and increase their surveillance efforts for naturally occurring CWD
in moose.
SNIP...see full text ;
Because of their close taxonomic relationship and similarities in DNA
sequences of the prion protein (PrP) coding region to deer and wapiti, it had
been hypothesized that moose (Alces alces shirasi) would be naturally
susceptible to infection if sufficient exposure to the CWD agent occurred
(Williams, 2005). A recent experiment using oral exposure to infectious brain
tissue in captive moose confirmed that this species is susceptible to CWD
(Kreeger et al., 2006). Here, we report a natural case of CWD in a free-ranging
moose from north central Colorado.
BANNED RUMINANT FEED AND CERVIDS
please note, I do not know how much of this 125 TONS of banned mad cow
protein was part of the ;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
bbbut, this was about 10 years post mad cow feed ban from 1997. 10 years
later, and still feeding banned mad cow protein to cervids???
considering that .005 gram is lethal to several bovines, and we know that
the oral consumption of CWD tainted products is very efficient mode of
transmission of CWD.
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall #
V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
***e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50
lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%,
Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to
20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall #
V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall #
V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email
and visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
10,000,000 lbs banned blood laced meat and bone meal mbm 2007
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on; Docket 03D-0186FDA Issues Draft Guidance
on Use of Material From Deer and Elk in Animal Feed; Availability Several
factors on this apparent voluntary proposal disturbs me greatly, please allow me
to point them out;
snip...
Oral transmission and early lymphoid tropism of chronic wasting
diseasePrPres in mule deer fawns (Odocoileus hemionus ) These results indicate
that CWD PrP res can be detected in lymphoid tissues draining the alimentary
tract within a few weeks after oral exposure to infectious prions and may
reflect the initial pathway of CWD infection in deer. The rapid infection of
deer fawns following exposure by the most plausible natural route is consistent
with the efficient horizontal transmission of CWD in nature and enables
accelerated studies of transmission and pathogenesis in the native
species.
snip...
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 –0700
From: "Terry S. Singeltary Sr." Reply-To: BSE-L
To: BSE-L
8420-20.5% Antler DeveloperFor Deer and Game in the wildGuaranteed Analysis
Ingredients / Products Feeding Directions
snip...
_animal protein_
snip...
DEPARTMENT OF HEALTH & HUMAN SERVICESPUBLIC HEALTH SERVICEFOOD AND DRUG
ADMINISTRATIONApril 9, 2001 WARNING LETTER01-PHI-12CERTIFIED MAILRETURN RECEIPT
REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy
Lake, PA 16145
PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:Food and Drug Administration Investigator Gregory E.
Beichner conducted an inspection of your animal feed manufacturing operation,
located in Sandy Lake, Pennsylvania, on March 23,2001, and determined that your
firm manufactures animal feeds including feeds containing prohibited materials.
The inspection found significant deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such
deviations cause products being manufactured at this facility to be misbranded
within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic
Act (the Act).Our investigation found failure to label your swine feed with the
required cautionary statement "Do Not Feed to cattleor other Ruminants" The FDA
suggests that the statement be distinguished by different type-size or color or
other means of highlighting the statement so that it is easily noticed by a
purchaser.
In addition, we note that you are using approximately 140 pounds of cracked
corn to flush your mixer used in the manufacture of animal feeds containing
prohibited material. This flushed material is fed to wild game including deer, a
ruminant animal.Feed material which may potentially contain prohibited material
should not be fed to ruminant animals which may become part of the food
chain.The above is not intended to be an all-inclusive list of deviations
fromthe regulations. As a manufacturer of materials intended for animalfeed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance withthe law. We have enclosed a
copy of FDA's Small Entity Compliance Guideto assist you with complying with the
regulation... blah, blah, blah...
snip...end...full text ;
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
see my full text submission here ;
Tuesday, June 11, 2013
Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant
deviations from requirements in FDA regulations that are intended to reduce the
risk of bovine spongiform encephalopathy (BSE) within the United States
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI
ratings as at June 5, 2013
Greetings,
since our fine federal friends have decided not to give out any more
reports on the USA breaches of the feed ban and surveillance etc. for the BSE
TSE prion mad cow type disease in the USDA livestock, I thought I might attempt
it. I swear, I just don’t understand the logic of the SSS policy, and that
includes all of it. I assure you, it would be much easier, and probably better
for the FDA and the USDA INC., if they would simply put some kind of report out
for Pete’s sake, instead of me doing it after I get mad, because I am going to
put it all out there. the truth.
PLEASE BE ADVISED, any breach of any of the above classifications OAI, VAI,
RTS, CAN lead to breaches into the feed BSE TSE prion protocols, and CAN lead to
the eventual suspect tainted feed reaching livestock. please, if any USDA
official out there disputes this, please explain then how they could not.
paperwork errors can eventually lead to breaches of the BSE TSE prion mad cow
feed ban reaching livestock, or contamination and exposure there from, as well.
I would sure like to see the full reports of just these ;
4018 CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL
61044-9605 OPR FR, OF HP 11/26/2012 OAI Y
9367 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO
81067 OPR RE, TH HP 2/27/2013 OAI N
9446 DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley
CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N
9447 DEN-DO 3002857110 Weld County Bi-Products dba Fort Morgan Pet Foods
13553 County Road 19 Fort Morgan CO 80701-7506 OPR RE HP 12/7/2011 OAI N
see full list of the fda mad cow bse feed follies, toward the bottom, after
a short brief update on the mad cow bse follies, and our good friend Lester
Crawford that was at the FDA.
ALSO, I would kindly like to comment on this FDA BSE/Ruminant Feed
Inspections Firms Inventory (excel format)4 format, for reporting these breaches
of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters
the fda use to put out for each violations. simply put, this excel format sucks,
and the FDA et al intentionally made it this difficult to follow the usda fda
mad cow follies. this is an intentional format to make it as difficult as
possible to follow these breaches of the mad cow TSE prion safety feed
protocols. to have absolutely no chronological or numerical order, and to format
such violations in a way that they are almost impossible to find, says a lot
about just how far the FDA and our fine federal friends will go through to hide
these continued violations of the BSE TSE prion mad cow feed ban, and any
breaches of protocols there from. once again, the wolf guarding the henhouse $$$
NAI = NO ACTION INDICATED
OAI = OFFICIAL ACTION INDICATED
VAI = VOLUNTARY ACTION INDICATED
RTS = REFERRED TO STATE
Inspections conducted by State and FDA investigators are classified to
reflect the compliance status at the time of the inspection, based upon whether
objectionable conditions were documented. Based on the conditions found,
inspection results are recorded in one of three classifications:
OAI (Official Action Indicated) when inspectors find significant
objectionable conditions or practices and believe that regulatory sanctions are
warranted to address the establishment’s lack of compliance with the regulation.
An example of an OAI classification would be findings of manufacturing
procedures insufficient to ensure that ruminant feed is not contaminated with
prohibited material. Inspectors will promptly re-inspect facilities classified
OAI after regulatory sanctions have been applied to determine whether the
corrective actions are adequate to address the objectionable conditions.
VAI (Voluntary Action Indicated) when inspectors find objectionable
conditions or practices that do not meet the threshold of regulatory
significance, but warrant an advisory to inform the establishment that
inspectors found conditions or practices that should be voluntarily corrected.
VAI violations are typically technical violations of the 1997 BSE Feed Rule.
These violations include minor recordkeeping lapses or conditions involving
non-ruminant feeds.
NAI (No Action Indicated) when inspectors find no objectionable conditions
or practices or, if they find objectionable conditions, those conditions are of
a minor nature and do not justify further actions.
when sound science was bought off by junk science, in regards to the BSE
TSE prion mad cow type disease, by the USDA, CFIA, WHO, OIE, et al. $$$
when the infamous, and fraudulently USDA, FSIS, APHIS, FDA, gold card was
taken away that infamous day in December of 2003, all cards were off the table,
it was time to change the science, and change they did. ...tss
snip. ...please see full text ;
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI
ratings as at June 5, 2013
please see what the U.K. DEFRA recently said ABOUT CWD RISK FACTORS ;
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
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...
see full text report here ;
see much more here ;
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
> Species: Enter the appropriate CWD susceptible species (red deer,
sika, elk, or moose).
*** 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.
The chances of a person or domestic animal contracting CWD are “extremely
remote,” Richards said. The possibility can’t be ruled out, however. “One could
look at it like a game of chance,” he explained. “The odds (of infection)
increase over time because of repeated exposure. That’s one of the downsides of
having CWD in free-ranging herds: We’ve got this infectious agent out there that
we can never say never to in terms of (infecting) people and domestic
livestock.”
P35
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A
WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of
Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5
The identification and characterization of prion strains is increasingly
important for the diagnosis and biological definition of these infectious
pathogens. Although well-established in scrapie and, more recently, in BSE,
comparatively little is known about the possibility of prion strains in chronic
wasting disease (CWD), a disease affecting free ranging and captive cervids,
primarily in North America. We have identified prion protein variants in the
white-tailed deer population and demonstrated that Prnp genotype affects the
susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic region.
PPo3-7:
Prion Transmission from Cervids to Humans is Strain-dependent
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi
Gambetti and Liuting Qing Department of Pathology; Case western Reserve
University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial
Sloan-Kettering Cancer Center; New York, NY USA
Key words: CWD, strain, human transmission
Chronic wasting disease (CWD) is a widespread prion disease in cervids
(deer and elk) in North America where significant human exposure to CWD is
likely and zoonotic transmission of CWD is a concern. Current evidence indicates
a strong barrier for transmission of the classical CWD strain to humans with the
PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD
strains. What remain unknown is whether individuals with the PrP-129VV/MV
genotypes are also resistant to the classical CWD strain and whether humans are
resistant to all natural or adapted cervid prion strains. Here we report that a
human prion strain that had adopted the cervid prion protein (PrP) sequence
through passage in cervidized transgenic mice efficiently infected transgenic
mice expressing human PrP, indicating that the species barrier from cervid to
humans is prion strain-dependent and humans can be vulnerable to novel cervid
prion strains. Preliminary results on CWD transmission in transgenic mice
expressing human PrP-129V will also be discussed.
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A.
Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and
related Brain disorders; Dept of Neurology; University of Texas Houston Medical
School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular
Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky
Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve
University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago;
Chicago, IL USA
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of
cervids is a prion disorder of increasing prevalence within the United States
that affects a large population of wild and captive deer and elk. CWD is highly
contagious and its origin, mechanism of transmission and exact prevalence are
currently unclear. The risk of transmission of CWD to humans is unknown.
Defining that risk is of utmost importance, considering that people have been
infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the infectious form by CWD
PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification
(PMCA) technique, which mimic in vitro the process of prion replication. Our
results show that cervid PrPSc can induce the pathological conversion of human
PrPC, but only after the CWD prion strain has been stabilized by successive
passages in vitro or in vivo. Interestingly, this newly generated human PrPSc
exhibits a distinct biochemical pattern that differs from any of the currently
known forms of human PrPSc, indicating that it corresponds to a novel human
prion strain. Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD
Isolates
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin,
Germany
Key words: CWD, strains, FT-IR, AFM
Chronic wasting disease (CWD) is one of three naturally occurring forms of
prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie
in sheep. CWD is contagious and affects captive as well as free ranging cervids.
As long as there is no definite answer of whether CWD can breach the species
barrier to humans precautionary measures especially for the protection of
consumers need to be considered. In principle, different strains of CWD may be
associated with different risks of transmission to humans. Sophisticated strain
differentiation as accomplished for other prion diseases has not yet been
established for CWD. However, several different findings indicate that there
exists more than one strain of CWD agent in cervids. We have analysed a set of
CWD isolates from white-tailed deer and could detect at least two biochemically
different forms of disease-associated prion protein PrPTSE. Limited proteolysis
with different concentrations of proteinase K and/or after exposure of PrPTSE to
different pH-values or concentrations of Guanidinium hydrochloride resulted in
distinct isolate-specific digestion patterns. Our CWD isolates were also
examined in protein misfolding cyclic amplification studies. This showed
different conversion activities for those isolates that had displayed
significantly different sensitivities to limited proteolysis by PK in the
biochemical experiments described above. We further applied Fourier transform
infrared spectroscopy in combination with atomic force microscopy. This
confirmed structural differences in the PrPTSE of at least two disinct CWD
isolates. The data presented here substantiate and expand previous reports on
the existence of different CWD strains.
2012
Envt.06:
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2
Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6
and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food
Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS
USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa,
ON Canada
†Presenting author; Email: emmanuel.comoy@cea.fr
The constant increase of chronic wasting disease (CWD) incidence in North
America raises a question about their zoonotic potential. A recent publication
showed their transmissibility to new-world monkeys, but no transmission to
old-world monkeys, which are phylogenetically closer to humans, has so far been
reported. Moreover, several studies have failed to transmit CWD to transgenic
mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the
only animal prion disease for which a zoonotic potential has been proven. We
described the transmission of the atypical BSE-L strain of BSE to cynomolgus
monkeys, suggesting a weak cattle-to-primate species barrier. We observed the
same phenomenon with a cattleadapted strain of TME (Transmissible Mink
Encephalopathy). Since cattle experimentally exposed to CWD strains have also
developed spongiform encephalopathies, we inoculated brain tissue from
CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice
overexpressing bovine or human PrP. Since CWD prion strains are highly
lymphotropic, suggesting an adaptation of these agents after peripheral
exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid
brains using the oral route. Nearly four years post-exposure, monkeys exposed to
CWD-related prion strains remain asymptomatic. In contrast, bovinized and
humanized transgenic mice showed signs of infection, suggesting that CWD-related
prion strains may be capable of crossing the cattle-to-primate species barrier.
Comparisons with transmission results and incubation periods obtained after
exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted
TME) will also be presented, in order to evaluate the respective risks of each
strain.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes. 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.
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
*** Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans
2005 - December 14, 2012
Saturday, March 09, 2013
Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest
Incubation Time Model for Prion Diseases
> Movements to slaughter are exempt from the 20% testing requirement but
animals 16 months of age and older that are slaughtered do count as eligible
mortalities for any other future movements.
Chronic Wasting Disease CWD, has been documented in many cervids (when
tested), much younger than the 12 month rule now proposed. AS I so much
appreciate the TAHC decreasing the age from 16 months to 12 months, I believe
this rule to still leave a risk factor, due to the fact fawns as young as 4 or 5
months old have been documented with CWD.
*** I propose that ALL farmed cervids should be tested for CWD. going into
a farm, leaving a farm, and or at death. ...TSS
Wisconsin : Six White-Tailed Deer Fawns Test Positive for CWD
Date: May 13, 2003 Source: Wisconsin Department of Natural Resources
Contacts: Julie Langenberg Wildlife Veterinarian 608-266-3143 Tom Hauge
Director, Bureau of Wildlife Management 608-266-2193
MADISON -- Six fawns in the area of south central Wisconsin where chronic
wasting disease has been found in white-tailed deer have tested positive for the
disease, according to Department of Natural Resources wildlife health officials.
These are the youngest wild white-tailed deer detected with chronic wasting
disease (CWD) to date.
Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of fawns
sampled were between the ages of 5 to 9 months, though some were as young as 1
month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of
the positive fawns were taken from the core area of the CWD eradication zone
where the highest numbers of positive deer have been identified.
"This is the first intensive sampling for CWD in fawns anywhere," said Dr.
Julie Langenberg, Department of Natural Resources wildlife veterinarian, "and we
are trying to learn as much as we can from these data".
"One noteworthy finding is simply the fact that we found positive fawns,"
Dr. Langenberg said. "These results do show us that CWD transmission can happen
at a very young age in wild white-tailed deer populations. However, we found
that the percentage of fawns infected with CWD is very low, in the area of 0.14
percent. If there was a higher rate of infection in fawns, then fawns dispersing
in the spring could be much more worrisome for disease spread."
Dr. Langenberg noted that while the youngest CWD-positive fawns had
evidence of disease-causing prions only in lymph node tissue, several of the
older CWD-positive fawns had evidence of CWD prions in both lymph node and brain
tissues -- suggesting further progression of the disease.
"Finding CWD prions in both lymph and brain tissues of deer this young is
slightly surprising," said Langenberg, "and provides information that CWD
infection and illness may progress more rapidly in a white-tailed deer than
previously suspected. Published literature suggests that CWD doesn't cause
illness in a deer until approximately 16 months of age. Our fawn data shows that
a few wild white-tailed deer may become sick from CWD or may transmit the
disease before they reach that age of 16 months."
One of the positive fawns was shot with a doe that was also CWD positive.
Information about these fawn cases combined with will help researchers who are
studying the age and routes of CWD transmission in wild deer populations. "More
data analysis and ongoing deer movement studies should give us an even better
understanding of how this disease moves across the landscape", said Langenberg.
"Thanks to eradication zone hunters who submitted deer of all ages for
sampling, we have a valuable set of fawn data that is contributing to our
state's and the nation's understanding about CWD," Langenberg said.
> > > Two of the six fawns with CWD detected were 5 to 6 months
old. < < <
Why doesn't the Wisconsin DNR want to routinely test fawns ?
The DNR highly discourages the testing of any fawns regardless of where
they were harvested. Of the more than 15,000 fawns from the CWD-MZ that have
been tested, only 23 were test positive, and most of those were nearly one year
old. It is exceedingly unlikely that a deer less than one year old would test
positive for CWD, even in the higher CWD prevalence areas of southern Wisconsin.
Few fawns will have been exposed to CWD, and because this disease spreads
through the deer's body very slowly, it is very rare in a fawn that the disease
has progressed to a level that is detectable. This means that testing a fawn
provides almost no information valuable to understanding CWD in Wisconsin's deer
herd and does not provide information of great value to the hunter in making a
decision about venison consumption.
> > > It is exceedingly unlikely that a deer less than one year
old would test positive for CWD < < < ???
Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm
and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.
specific susceptibility?
194. It is probable, based on age-class specific prevalence data from wild
cervids and epidemiological evidence from captive cervids in affected research
centres, that both adults and fawns may become infected with CWD (Miller, Wild
& Williams, 1998; Miller et al., 2000).
198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed
deer which had become enclosed by an elk farm fence, in Sioux County,
northwestern Nebraska, four fawns only eight months old were among the 50% of
CWD-positive animals; these fawns were not showing any clinical signs of CWD
(Davidson, 2002).
Research Article
Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with
Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay
Tracy A. Nichols mail, Terry R. Spraker, Tara D. Rigg, Crystal
Meyerett-Reid, Clare Hoover, Brady Michel, Jifeng Bian, Edward Hoover, Thomas
Gidlewski, Aru Balachandran, Katherine O'Rourke, Glenn C. Telling, Richard
Bowen, [ ... ], Kurt C. VerCauteren equal contributor
Abstract
Chronic wasting disease (CWD), the only known prion disease endemic in
wildlife, is a persistent problem in both wild and captive North American cervid
populations. This disease continues to spread and cases are found in new areas
each year. Indirect transmission can occur via the environment and is thought to
occur by the oral and/or intranasal route. Oral transmission has been
experimentally demonstrated and although intranasal transmission has been
postulated, it has not been tested in a natural host until recently. Prions have
been shown to adsorb strongly to clay particles and upon oral inoculation the
prion/clay combination exhibits increased infectivity in rodent models. Deer and
elk undoubtedly and chronically inhale dust particles routinely while living in
the landscape while foraging and rutting. We therefore hypothesized that dust
represents a viable vehicle for intranasal CWD prion exposure. To test this
hypothesis, CWD-positive brain homogenate was mixed with montmorillonite clay
(Mte), lyophilized, pulverized and inoculated intranasally into white-tailed
deer once a week for 6 weeks. Deer were euthanized at 95, 105, 120 and 175 days
post final inoculation and tissues examined for CWD-associated prion proteins by
immunohistochemistry. Our results demonstrate that CWD can be efficiently
transmitted utilizing Mte particles as a prion carrier and intranasal exposure.
snip...
The results of this study confirm that CWD can be successfully transmitted
IN as a lyophilized prion particulate adsorbed to Mte and that genotype at codon
96 affects the lymphoid distribution of CWD within the body. Additionally, two
novel intranasal tracking methods were employed that provided insight into CWD
translocation within the nasal cavity. The data collected in this study may also
shed light on why there is a higher prevalence of CWD in males, as males
participate in more behaviors that generate dust. We propose chronic, long-term
exposure to CWD prions adsorbed to dust particles to be a natural CWD infection
route in addition to chronic oral and nasal contact exposure.
Citation: Nichols TA, Spraker TR, Rigg TD, Meyerett-Reid C, Hoover C, et
al. (2013) Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus)
with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay. PLoS ONE 8(5): e62455.
doi:10.1371/journal.pone.0062455
Editor: Anthony E. Kincaid, Creighton University, United States of America
Received: November 30, 2012; Accepted: March 21, 2013; Published: May 9,
2013
This is an open-access article, free of all copyright, and may be freely
reproduced, distributed, transmitted, modified, built upon, or otherwise used by
anyone for any lawful purpose. The work is made available under the Creative
Commons CC0 public domain dedication.
Funding: Funding was provided by U.S. Department of Agriculture, Animal and
Plant Health Inspection Service, Veterinary Services (VS). The funders had no
role in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
Competing interests: The authors have declared that no competing interests
exist.
see full text ;
Thanks again to PLOS et al for full text access to this scientific research
on the CWD TSE prion disease...tss
see more here ;
Wednesday, May 15, 2013
Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with
Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay
Research Article
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Friday, February 25, 2011
Soil clay content underlies prion infection odds Soil clay content
underlies prion infection odds
see full text ;
Saturday, February 04, 2012
Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Thursday, June 13, 2013
WISCONSIN DEER FARMING Chronic Wasting Disease CWD DATCP
Tuesday, June 11, 2013
CWD GONE WILD, More cervid escapees from more shooting pens on the loose in
Pennsylvania
Sunday, June 09, 2013
Missouri House forms 13-member Interim Committee on the Cause and Spread of
Chronic Wasting Disease CWD
Saturday, June 01, 2013
Texas Animal Health Commission (TAHC) Proposes Modifications to Chronic
Wasting Disease (CWD), Brucellosis, and Other Rules
Thursday, May 02, 2013
Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans
Pecos
Wednesday, June 12, 2013
CWD now waltzing into Texas from Pennsylvania CWD index herd, via Louisiana, or Missouri now ?
TSS
posted by Terry S. Singeltary Sr. at
10:32 AM
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