Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant Health Inspection Service Veterinary Services
Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant
Health Inspection Service Veterinary Services
snip...
c. Funding sources
Cervid Health Programs are funded through the equine, cervid, small
ruminant health (ECSR) line. The total APHIS FY 2014 ECSR budget is $19. 5
million. Congressional language accompanying the FY 2014 appropriations
specifies that APHIS should spend $3. 0 million for cervid health
activities.
III. Value of Program Objectives:
In 2007, the cervid industry in the United States included 5,600 deer farms
and 1,900 elk farms with an economic value of $894 million that supported nearly
30,000 jobs. The recently conducted 2012 National Agricultural Statistics
Service (NASS) census will provide important updates on cervid industry
statistics.
The Cervid Health Program protects the health of cervids and improves the
quality, productivity and economic viability of the cervid industry. CWD, TB,
and brucellosis remain important disease threats to cervid populations.
Outbreaks of these diseases could have serious consequences for the cervid
industry and allied stakeholders. APHIS’ CWD HCP, cervid TB herd accreditation,
and proposed brucellosis herd certification programs are essential to reducing
and mitigating those consequences.
A key value of the cervid health programs is to reduce losses to the cervid
industry and to reduce the overall cost to the Federal government to respond to
outbreaks. In the past 10 years, many CWD infected and exposed cervid farms were
depopulated with Federal indemnity at a significant cost to the industry,
States, and Federal government. The cervid TB herd accreditation program has
reduced disease transmission in cervid populations and in other domestic species
that could have resulted in larger and more serious disease outbreaks.
An additional value of the cervid health program is to promote and
facilitate domestic and international trade of animals and cervid-derived
products. Since the identification of CWD, many international markets have
refused farmed cervids or cervid-derived products from the United States. The
U.S. cervid industry cannot expand its markets without USDA animal health
programs to certify their animals to have low disease risk and/or disease
freedom. The Cervid Health Program promotes the opportunity for the cervid
industry to start competing in international trade again.
Lastly, TB and brucellosis are zoonotic diseases which can be transmitted
from farmed cervids to other livestock, wildlife, and people. Although CWD has
not been recognized as a prion disease transmissible to people, it can be
transmitted between farmed cervids to wild cervid populations and it persists in
the environment. A direct benefit of the Cervid Health Program is to safeguard
public health, prevent transmission at the domestic animal-wildlife interface,
and reduce environmental contamination.
IV. FY 2014 – FY 2018 Implementation
Objective 1: Prevent and control CWD in farmed cervid populations
Strategy 1: Implement CWD rule and CWD Program Standards.
FY 2014 Activities:
1. 1 Affirm CWD final rule and publish in FY 2014.
1. 2 Finalize CWD Program Standards revision (consider public comments) and
publish new version in FY 2014.
1. 3 Prepare and submit information collection documents for renewal by FY
2015.
FY 2015- FY 2018 Activities
1. 4 CWD Program Standards (2nd edition) to be reviewed for further
updates.
1. 5 Information collection renewal to be completed in FY 2015 (triennial
cycle).
Strategy 2: Maintain Approved State CWD HCPs.
FY 2014 Activities:
2. 1 Finalize annual report template and guidance for Approved States
renewal process, and collect annual reports from Approved States.
2. 2 Complete Approved State status for remaining six Provisional Approved
States.
FY 2015 – FY 2018 Activities
2. 3 Review annual reports and evaluate compliance of Approved
States.
2. 4 Administer the national CWD HCP, subject to the availability of
appropriated funds, for herd owners in States that do not have an approved State
HCP.
June 19, 2014 6
2. 5 Develop metrics for Approved State program administration
reviews.
2. 6 Conduct Consistent State Reviews of Approved State CWD HCPs based on
requests for review by States or observation of deficiencies in State
programs.
Strategy 4: Complete official CWD, cervid TB, and cervid brucellosis
testing.
FY 2014 Activities:
4. 1 Monitor NAHLN approved laboratories for proficiency and accuracy in
lab testing and reporting in defined timeframes.
4. 2 Establish list of approved laboratories to conduct IHC and/or ELISA
testing for CWD.
4. 3 Approve new laboratories as needed as outlined in the NAHLN SOP and
CWD Program Standards.
FY 2015 – FY 2018 Activities
4.4 Continue activities 4. 1 – 4. 3.
Strategy 5: National Program Reporting/ Data Management.
FY 2014 Activities:
5. 1 Develop and implement cervid health indemnity database on indemnity
SharePoint site.
5. 2 Assess use of SCS/national CWD instance by Approved States.
5. 3 Develop SCS data entry guidance for national CWD instance (if
warranted).
5. 4 Prepare national annual summary report from Approved States’
reports.
5. 5 Receive quarterly tallies of CWD testing surveillance in farmed
cervids and prepare annual summary surveillance report.
5. 6 Encourage VS personnel and stakeholders regarding the use of
electronic identification of animals, electronic data collection and reporting,
e. g. MIMS, of program surveillance and disease control activities, collection
and use of data and test results from outside sources. Tools that support this
type of data handling also need to be improved so the process is streamlined,
easily accessible and user friendly to VS employees, States and Federally
accredited veterinarians.
FY 2015 – FY 2018 Activities
5. 6 Continue activities 5. 1 – 5. 5 (with or without SCS/national CWD
instance). Strategy 6: Interstate and International Cervid Movement.
FY 2014 Activities:
6. 1 Address import/export issues for cervids and cervid products.
6. 2 Facilitate requests for interstate movement (translocation) of
free-ranging cervids based on CWD rule requirements. Refine interstate movement
agreement protocols as needed. Complete guidance.
June 19, 2014 7
FY 2015 – FY 2018 Activities:
6. 3 Continue work on import/export issues.
6. 4 Continue facilitation of requests for interstate movement
(translocation) of wild cervids.
6. 5 Develop risk assessment and surveillance templates for interstate
movement of cervids.
June 19, 2014
Monday, June 18, 2012
natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red
deer crossbreeds captive Korea and Experimental oral transmission to red deer
(Cervus elaphus elaphus)
spreading cwd around...tss
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...tss
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea Chronic Wasting Disease (CWD) outbreaks and surveillance
program in the Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
: Corresponding author: Dr. Hyun-Joo Sohn (+82-31-467-1867, E-mail:
shonhj@korea.kr) 2011 Pre-congress Workshop: TSEs in animals and their
environment 5
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
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
Sunday, August 24, 2014
*** USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program
Goals TSE PRION October 17 – 23, 2013
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...
Saturday, August 02, 2014
*** Structural effects of PrP polymorphisms on intra- and inter-species
prion transmission
In contrast, the scrapie prions used in the deer transmission studies of
Greenlee and colleagues were isolated from a sheep encoding A136, ***raising the
possibility that deer may be susceptible to multiple scrapie strains.
snip...
Significance
The unpredictable recurrences of prion epidemics, their incurable
lethality, and the capacity of animal prions to infect humans, provide
significant motivation to ascertain the parameters governing disease
transmission. The unprecedented spread, and uncertain zoonotic potential of
chronic wasting disease (CWD), a contagious epidemic among deer, elk, and other
cervids, is of particular concern. Here we demonstrate that naturally occurring
primary structural differences in cervid PrPs differentially impact the
efficiency of intra- and interspecies prion transmission. Our results not only
deliver new information about the role of primary structural variation on prion
susceptibility, but also provide functional support to a mechanism in which
plasticity of a tertiary structural epitope governs prion protein conversion and
intra- and inter-species susceptibility to prions.-
snip...
Friday, September 05, 2014
*** CFIA CWD and Grain Screenings due to potential risk factor of spreading
via contamination of grain, oil seeds, etc.
>>>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. <<<
Draft Guidance on Use of Material From Deer and Elk in Animal Feed; CVM
Updates on Deer and Elk Withdrawn FDA Veterinarian Newsletter July/August 2003
Volume XVIII, No 4
FDA has announced the availability of a draft guidance for industry
entitled “Use of Material from Deer and Elk in Animal Feed.” This draft guidance
document (GFI #158), when finalized, will describe FDA’s current thinking
regarding the use in animal feed of material from deer and elk that are positive
for Chronic Wasting Disease (CWD) or that are at high risk for CWD.
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the cervidae animal family (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). TSEs are very rare, but are
always fatal.
This draft Level 1 guidance, when finalized, will represent the Agency’s
current thinking on the topic. It does not create or confer any rights for or on
any person and does not operate to bind FDA or the public. An alternate method
may be used as long as it satisfies the requirements of applicable statutes and
regulations.
Draft guidance #158 is posted on the FDA/Center for Veterinary Medicine
Home Page. Single copies of the draft guidance may be obtained from the FDA
Veterinarian.
- - Page Last Updated: 04/16/2013
CONTAINS NON-BINDING RECOMMENDATIONS
158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
Comments and suggestions regarding the document should be submitted to
Division of Dockets Management (HFA-305), Food and Drug Administration, 5630
Fishers Lane, Rm. 1061, Rockville, MD 20852. Submit electronic comments to http://www.regulations.gov. All comments
should be identified with the Docket No. 03D-0186.
For questions regarding this guidance, contact Burt Pritchett, Center for
Veterinary Medicine (HFV- 222), Food and Drug Administration, 7519 Standish
Place, Rockville, MD 20855, 240-453-6860, E-mail: burt.pritchett@fda.hhs.gov.
Additional copies of this guidance document may be requested from the
Communications Staff (HFV-12), Center for Veterinary Medicine, Food and Drug
Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed on
the Internet at http://www.fda.gov/AnimalVeterinary/GuidanceComplianceEnforcement/GuidanceforIndustry/default.htm.
U.S. Department of Health and Human Services
Food and Drug Administration Center for Veterinary Medicine September 15,
2003
CONTAINS NON-BINDING RECOMMENDATIONS
158
Guidance for Industry1
Use of Material from Deer and Elk in Animal Feed
This guidance represents the Food and Drug Administration’s current
thinking on the use of material from deer and elk in animal feed. It does not
create or confer any rights for or on any person and does not operate to bind
FDA or the public. You can use an alternative approach if the approach satisfies
the requirements of applicable statutes or regulations. If you want to discuss
an alternative approach, contact the FDA staff responsible for implementing this
guidance. If you cannot identify the appropriate FDA staff, call the appropriate
number listed on the title page of this guidance.
I. Introduction
FDA’s guidance documents, including this guidance, do not establish legally
enforceable responsibilities. Instead, guidances describe the Agency’s current
thinking on a topic and should be viewed only as recommendations, unless
specific regulatory or statutory requirements are cited. The use of the word
“should” in Agency guidances means that something is suggested or recommended,
but not required.
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer
and elk is prohibited for use in feed for ruminant animals. This guidance
document describes FDA’s recommendations regarding the use in all animal feed of
all material from deer and elk that are positive for Chronic Wasting Disease
(CWD) or are considered at high risk for CWD. The potential risks from CWD to
humans or non-cervid animals such as poultry and swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer, and because CWD’s route of transmission is poorly understood,
FDA is making recommendations regarding the use in animal feed of rendered
materials from deer and elk that are CWD-positive or that are at high risk for
CWD.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer,
1 This guidance has been prepared by the Division of Animal Feeds in the
Center for Veterinary Medicine (CVM) at the Food and Drug Administration.
CONTAINS NON-BINDING RECOMMENDATIONS
2
white-tailed deer, North American elk, and in farmed black-tailed deer. CWD
belongs to a family of animal and human diseases called transmissible spongiform
encephalopathies (TSEs). These include bovine spongiform encephalopathy (BSE or
“mad cow” disease) in cattle; scrapie in sheep and goats; and classical and
variant Creutzfeldt-Jakob diseases (CJD and vCJD) in humans. There is no known
treatment for these diseases, and there is no vaccine to prevent them. In
addition, although validated postmortem diagnostic tests are available, there
are no validated diagnostic tests for CWD that can be used to test for the
disease in live animals.
III.
Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV.
Use in animal feed of material from deer and elk considered at high risk
for CWD
Deer and elk considered at high risk for CWD include: (1) animals from
areas declared by State officials 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 immediately before the time of slaughter were in a captive herd that
contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal. V. Use in animal feed of material from deer
and elk NOT considered at high risk for CWD
FDA continues to consider materials from deer and elk NOT considered at
high risk for CWD to be acceptable for use in NON-RUMINANT animal feeds in
accordance with current agency regulations, 21 CFR 589.2000. Deer and elk not
considered at high risk include: (1) deer and elk from areas not declared by
State officials to be endemic for CWD and/or to be CWD eradication zones; and
(2) deer and elk that were not at some time during the 60-month period
immediately before the time of slaughter in a captive herd that contained a
CWD-positive animal.
that voluntary mad cow feed ban that became law, how did that work out for
us $
ENFORCEMENT REPORT FOR AUGUST 2, 2006
please note, considering .005 grams is lethal, 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
###
Rangen, Inc,
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI ___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 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-LTo: 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...
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 ;
Sunday, December 15, 2013
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
*** Susceptibility of UK red deer (Cervus alaphus elaphus) to oral BSE
transmission Project Code: M03024 ***
02/08/2011
The project confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42 months post inoculation) i.c inoculated and one (56 months post
inoculation) orally dosed deer that tested positive for TSE by
immunohistochemistry and Western blotting using several primary antibodies
demonstrated widespread accumulation of disease specific prion protein in the
central nervous system, peripheral nervous system and enteric nervous system but
none in lymphoreticular system. All showed several brain sites positive for
disease specific prion protein and presented immunohistochemistry and Western
blotting phenotypes with similarities to BSE in sheep, goats and cattle but
unlike those seen in chronic wasting disease (CWD) in elk or scrapie in sheep.
The vacuolar pathology and distribution of disease specific prion protein in red
deer resembled that of CWD in most major respects however we have shown that BSE
can be clearly differentiated from CWD by existing immunohistochemical and
biochemical methods that are in routine use.
The knowledge gained as a result of this work will permit rapid and
accurate diagnosis should a TSE ever be detected in European red deer and will
also enable effective disease control methods to be quickly put in place.
Results
No pre-clinically diseased orally infected animals were identified at the 6
months and 12 months post infection cull points. Intra-cerebrally infected
animals were maintained until all 6 developed clinical disease. Only one out of
six orally dosed deer developed clinical disease before termination of the
project.
We confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42mpi) i.c inoculated and one (56mpi) orally dosed deer that tested
positive for TSE by IHC and WB using several primary antibodies demonstrated
widespread accumulation of disease specific PrP in CNS, PNS and ENS but none in
LRS. All showed several brain sites positive for disease specific PrP and
presented IHC and WB phenotypes with similarities to BSE in sheep, goats and
cattle but unlike those seen in CWD in elk or scrapie in sheep. The vacuolar
pathology and distribution of PrPd BSE in red deer resembled that of CWD in most
major respects however we have shown that BSE can be clearly differentiated from
CWD by existing immunohistochemical and biochemical methods that are in routine
use.
Final technical report MO3024 01/04/2003 – 31/03/2010 Susceptibility of UK
red deer (Cervus elaphus elaphus) to oral BSE transmission. Stuart Martin - VLA
Lasswade Pentlands Science Park Bush Loan Penicuik EH26 0PZ Page 2 of 21 Further
work undertaken August 2009 – March 2010. Genetic analysis - Wilfred Goldmann;
Roslin NPD.
Negative controls and the remaining 5 orally dosed deer culled at 72mpi
tested negative by IHC and Western blot however analysis of the PrP ORF of these
deer (kindly carried out by Wilfred Goldmann of the Roslin NPD) identified a Q
to E polymorphism at codon 226 that may influence the efficiency of oral
transmission (not published).
In the experimental BSE challenge of red deer six out of six deer succumbed
to BSE when challenged by intracerebral routes but only one of six deer
challenged by the oral route succumbed to infection. Deer killed at 190 days or
365 days post oral challenge showed no evidence of abnormal PrP accumulation
when tested by immunocytochemistry. The PrP gene of red deer includes a Q to E
polymorphism at codon 226. The table shows the distribution of these codon 226
polymorphisms within experimental challenge groups.
Deer ID R No. Challenge Death
codon
226 IHC Deer ID R No. Challenge Death
codon
226 IHC
020 1791
int. death
210 QE N 323 2160 oral seq. kill 365 QE N
322 1820 seq. kill 190 QQ N 337 2161 oral seq. kill 365 EE N
319 2137 seq. kill 365 QE N 314 2162 oral seq. kill 365 QQ N
334 2138 seq. kill 365 EE N 318 2163 oral seq. kill 365 QE N
022 4173 ic saline
seq. kill
1017 EE N 310 2164 oral seq. kill 365 QE N
029 4644 ic saline
seq. kill
1290 QE N 028 2165 oral seq. kill 365 QQ N
032 5863 cull 2320 QQ N
034 5861 cull 2320 QE N 312 3991 ic TSE 794 EE P
039 5864 cull 2320 EE N 332 4140 ic TSE 929 QE P
014 5862 cull 2320 EE N 329 4174 ic TSE 996 QE P
331 4175 ic TSE 996 QE P
327 1813 oral seq. kill 190 QE N 025 4279 ic TSE 1059 QQ P
309 1821 oral seq. kill 190 EE N 315 4643 ic TSE 1289 QE P
031 1822 oral seq. kill 190 QQ N
320 1823 oral seq. kill 190 QE N 009 4987 oral TSE 1727 QQ P
324 1824 oral seq. kill 190 QQ N 015 5866 oral cull 2320 QE N
326 1825 oral seq. kill 190 QQ N 033 5867 oral cull 2320 EE N
016 5868 oral cull 2320 EE N
Death: numbers indicate age (oral controls) or time 023 5869 oral cull 2320
QE N
post-inoculation in days 037 5870 oral cull 2320 EE N
Within the intracerebral challenge experiment QQ (n=1), QE (n=4) and EE
(n=1) deer all succumbed to clinical BSE infection which was confirmed by
histology and immunocytochemistry. These data show that the codon 226
polymorphism does not provide absolute resistance to infection. Although the
first deer to succumb to infection was the only EE genotype it had to be killed
early because of intercurrent health problems and had substantially less
abnormal PrP in brain than the remainder of the group. Overall, the small number
of deer within each genotype group does not permit any meaningful analysis of
attack rates or incubation periods.
Final technical report MO3024 01/04/2003 – 31/03/2010
Susceptibility of UK red deer (Cervus elaphus elaphus) to oral BSE
transmission. Stuart Martin - VLA Lasswade Pentlands Science Park Bush Loan
Penicuik EH26 0PZ Page 3 of 21
Of the oral challenged deer only one QQ deer succumbed to infection at 58
months post challenge while QE (n=2) and EE (n=3) deer did not show clinical
signs of disease when the experiment was terminated at 72 months post challenge.
The five deer that lived to the end of the experiment did not show histological
or immunocytochemical evidence of disease.
These data are summarised in the table. There is insufficient information
on which to draw unambiguous conclusions regarding the impact of the 226
polymorphism on susceptibility of red deer to BSE challenge, but the possibility
that this codon may influence the efficiency of oral transmission cannot be
dismissed. It would be prudent to take the frequency distribution of this
polymorphism into consideration when performing critical analysis of deer
surveys and possible interpretations of the incidence of deer TSEs within
Europe.
Transgenic mouse bioassay - Marion Simmons/John Spiropoulos; VLA
Weybridge.
2 BSE infected red deer plus the BSE source that was used to inoculate the
deer were inoculated into a panel of 20 Tg(CervinePrP)1536+/- mice – not
published. The deer passaged BSE bioassays have been completed and the bovine
BSE source passage is ongoing.
For deer 1 the attack rate was 18/20=90%. The incubation period varied from
202-274 days post inoculation (dpi) or 240+22 mean+standard deviation (M+SD).
For deer 2 the attack rate was 19/20=95%. Incubation periods varied from
207-298 (dpi) or 254+28 (M+SD). A T-test analysis between the 2 groups showed no
significance (p=0.096).
The panel that was inoculated with the bovine BSE has surviving mice (n=12)
590 dpi.
Seven of the mice died due to intercurrent deaths. Data analysis will be
completed when the bioassays finish. It is however interesting that the deer
succumbed to bovine BSE while the cervid mice show such prolonged incubation
period.
Research article Open Access
Immunohistochemical and biochemical characteristics of BSE and CWD in
experimentally infected European red deer (Cervus elaphus elaphus)
Stuart Martin*1, Martin Jeffrey1, Lorenzo González1, Sílvia Sisó1, Hugh W
Reid2, Philip Steele2, Mark P Dagleish2, Michael J Stack3, Melanie J Chaplin3
and Aru Balachandran4 Address: 1Veterinary Laboratories Agency (VLA-Lasswade),
Pentlands Science Park, Bush Loan, Penicuik, Midlothian, EH26 0PZ, UK, 2Moredun
Research Institute, Pentlands Science Park, Bush Loan, Penicuik, Midlothian,
EH26 0PZ, UK, 3VLA-Weybridge, Addlestone, Surrey, KT15 3NB, UK and 4Animal
Diseases Research Institute, Canadian Food Inspection Agency, Ottawa, Ontario,
K2H 8P9, Canada Email: Stuart Martin* - s.f.martin@vla.defra.gsi.gov.uk; Martin
Jeffrey - m.jeffrey@vla.defra.gsi.gov.uk; Lorenzo González -
l.gonzalez@vla.defra.gsi.gov.uk; Sílvia Sisó - s.siso@vla.defra.gsi.gov.uk; Hugh
W Reid - hugh.reid@moredun.ac.uk; Philip Steele - philip.steele@moredun.ac.uk;
Mark P Dagleish - mark.dagleish@moredun.ac.uk; Michael J Stack -
m.j.stack@vla.defra.gsi.gov.uk; Melanie J Chaplin -
m.j.chaplin@vla.defra.gsi.gov.uk; Aru Balachandran -
aru.balachandran@inspection.gc.ca * Corresponding author
Abstract
Background: The cause of the bovine spongiform encephalopathy (BSE)
epidemic in the United Kingdom (UK) was the inclusion of contaminated meat and
bone meal in the protein rations fed to cattle. Those rations were not
restricted to cattle but were also fed to other livestock including farmed and
free living deer. Although there are no reported cases to date of natural BSE in
European deer, BSE has been shown to be naturally or experimentally
transmissible to a wide range of different ungulate species. Moreover, several
species of North America's cervids are highly susceptible to chronic wasting
disease (CWD), a transmissible spongiform encephalopathy (TSE) that has become
endemic. Should BSE infection have been introduced into the UK deer population,
the CWD precedent could suggest that there is a danger for spread and
maintenance of the disease in both free living and captive UK deer populations.
This study compares the immunohistochemical and biochemical characteristics of
BSE and CWD in experimentally-infected European red deer (Cervus elpahus
elaphus).
Results: After intracerebral or alimentary challenge, BSE in red deer more
closely resembled natural infection in cattle rather than experimental BSE in
small ruminants, due to the lack of accumulation of abnormal PrP in lymphoid
tissues. In this respect it was different from CWD, and although the
neuropathological features of both diseases were similar, BSE could be clearly
differentiated from CWD by immunohistochemical and Western blotting methods
currently in routine use.
Conclusion: Red deer are susceptible to both BSE and CWD infection, but the
resulting disease phenotypes are distinct and clearly distinguishable. SNIP...
Results
Clinical disease
All six deer challenged i.c. with BSE developed clinical disease between
794 and 1260 days post-inoculation with a mean incubation period of 1027 days. A
detailed description of the clinical signs was provided in an earlier report
[8]. Briefly, affected deer showed variable degrees of ataxia, anorexia,
circling and apparent blindness, together with failure of seasonal change of
coat, weight loss and 'panic attacks'. In addition, one of six red deer orally
dosed with BSE developed clinical disease 1740 days after challenge, and this
animal presented with a short clinical duration of two days; the other five deer
from this group remain healthy at the time of writing (65 months after
challenge). Sequential rectal biopsies taken at five different time points from
orally and i.c. inoculated deer were negative for PrPd.
All four deer orally challenged with CWD started to show behavioural
changes between 577 and 586 days post challenge;
these progressed to definite neurological disease between 742 and 760 days
post-challenge (Table 1).
Clinical signs were similar to the BSE challenged deer and included
nervousness, weight loss, excessive salivation, roughness of coat, and
progressive ataxia. All these CWD inoculated deer showed PrPd accumulation in
the secondary follicles of rectal biopsies taken at 7 months post
infection.
Conclusion
European red deer are susceptible to infection with the cattle BSE agent,
not only by the intra-cerebral but also by the oral route, and although the
clinical signs and spong- iform change are similar to those of CWD in the same
species, these two infections can be easily differentiated. The lack of lymphoid
involvement, the PrPd truncation pattern both "in vivo" and "in vitro", and the
predominantly intracellular accumulation of PrPd are features of deer BSE that
are in contrast with those of deer CWD. However, only one of six deer developed
disease after alimentary exposure to 25 g of a BSE brain pool homogenate after
an incubation period of nearly 5 years; this suggests a strong species barrier
but if a TSE in European red deer should ever be identified then BSE/CWD
discrimination would be an urgent priority. To determine whether there are
potential naturally occurring BSE-like strains and to determine the degree to
which there is strain variation, it would be necessary to examine many more
naturally occurring CWD cases. These results will support the ongoing European
surveillance for natural TSEs in red deer and the further assessment of
potential risk to human health.
Published: 27 July 2009 BMC Veterinary Research 2009, 5:26
doi:10.1186/1746-6148-5-26 Received: 12 February 2009 Accepted: 27 July 2009
This article is available from: http://www.biomedcentral.com/1746-6148/5/26
© 2009 Martin et al; licensee BioMed Central Ltd. This is an Open Access article
distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing ***
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).
as I said, 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. ***
===========================================
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
WHAT IF ?
Saturday, April 19, 2014
Exploring the zoonotic potential of animal prion diseases: In vivo and in
vitro approaches
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** 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.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** 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
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
***However, they also show that there is no absolute barrier ro conversion of
human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
there is in fact evidence that the potential for cwd transmission to humans
can NOT be ruled out.
I thought your readers and hunters and those that consume the venison,
should have all the scientific facts, personally, I don’t care what you eat, but
if it effects me and my family down the road, it should then concern everyone,
and the potential of iatrogenic transmission of the TSE prion is real i.e.
‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there
from...like deer antler velvet and TSE prions and nutritional supplements there
from, all a potential risk factor that should not be ignored or silenced. ...
the prion gods at the cdc state that there is ;
''no strong evidence''
but let's see exactly what the authors of this cwd to human at the cdc
state ;
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD
transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article
and call me if you have questions or need more clarification (phone:
404-639-3091). Also, we do not claim that "no-one has ever been infected with
prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip...
full text ;
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** 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.
Wednesday, September 17, 2014
*** Cost benefit analysis of the development and use of ante-mortem tests
for transmissible spongiform encephalopathies ***
BOTTOM LINE $$$
IF YOU TEST, YOU FIND, and the more you test, the more you will find.
HUMANS ARE EXPENDABLE WITH A SLOW, LONG INCUBATING, 100% FATAL DISEASE,
ONCE CLINICAL DISEASE...tss
TSS
posted by Terry S. Singeltary Sr. at
2:57 PM
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