• If you are having problems logging in please use the Contact Us in the lower right hand corner of the forum page for assistance.

REPORT ON THE INVESTIGATION OF THE TENTH CASE OF BSE CANADA

flounder

Well-known member
Joined
Sep 3, 2005
Messages
2,631
Location
TEXAS
REPORT ON THE INVESTIGATION OF THE TENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
BACKGROUND
On April 24, 2007, a cow on a dairy operation in the Fraser Valley area of British Columbia was destroyed following a brief illness. On April 25, 2007, the Canadian Food Inspection Agency (CFIA) sampled the animal under Canada's National BSE Surveillance Program. On April 25, 2007, brain samples were received by the British Columbia Ministry of Agriculture and Lands (BCMAL) Laboratory, where they were screened for BSE using a Prionics rapid test. The result of this preliminary test did not rule out BSE. In accordance with the prescribed testing protocol, the test was repeated and produced a second reaction that day. Samples were then forwarded to the National BSE Reference Laboratory in Lethbridge, Alberta, where rapid screening tests (Prionics-Check PrioStrip and Prionics-Check Western) to validate these results were positive on April 26, 2007. On May 2, 2007, BSE was confirmed by the immunohistochemistry procedure and the Scrapie Associated Fibril Immunoblot. The carcass was secured at the sampling site, and was subsequently transferred to the CFIA Laboratory in Lethbridge for incineration. No part of the carcass entered the human food supply or animal feed chain.

The CFIA immediately initiated an epidemiological investigation based on the most recent recommended BSE guidelines of the World Organisation for Animal Health, referred to as OIE. Specifically, the CFIA investigated:

the birth cohort (all cattle born in the same herd as, and within 12 months of the birth of the BSE-positive animal);
the feed cohort (all cattle that, during their first year of life, were reared with the BSE-positive animal during its first year of life, and that investigation showed consumed the same potentially contaminated feed during the period); and
feed to which the animal may have been exposed early in its life.
ANIMAL INVESTIGATION
The positive animal was a registered Holstein cow born on November 10, 2001, and it was 66 months of age at the time of death. The animal was born, raised and had spent its entire life on the same farm. The cow had appeared to be lame for a few weeks prior to calving. After calving, she became unsteady and then non-ambulatory (downer). The producer determined that the animal should be destroyed, and because it met the inclusion criteria of Canada's National BSE Surveillance Program, arrangements were made to forward appropriate samples for laboratory evaluation.

The birth farm was a dedicated dairy operation. The feed cohort was determined to comprise 156 animals, which, along with the case animal, were raised on the birth farm. This cohort consisted of Holstein females. Males sold at a few weeks of age for fattening and subsequent slaughter without having access to any commercially prepared feeds were excluded from the investigation, because they were not exposed to the same potentially contaminated feed as the case animal. No males were retained or raised on the farm. The trace-out investigation of the feed cohort located 41 live animals on the premises and in one other herd. Five of the animals have been humanely destroyed, for reasons unrelated to this investigation, and their carcasses and will be disposed of along with the case animal. The remaining feed cohorts are currently quarantined and agreement has been reached with the Producer to allow animals to calve out before humane destruction and disposal. This is due mainly to the operation being a purebred Holstein one and the need to retain genetics and farm production cycle. The following is the disposition of the remaining 115 animals in the feed cohort:

a total of 92 animals were traced and confirmed to have died or been slaughtered (five animals had previously been tested under Canada's National BSE Surveillance Program, with negative results); and
a total of 23 animals were determined to be untraceable because of records limitations.
FEED INVESTIGATION
The feed investigation focused on feeds to which the case animal may have had access during its first year of life and on the manufacturing practices used to produce each of these feeds.

Investigation at the farm revealed that the only non-bovine species present were one or more barn cats and a dog. Only the dog, which was fed at the house, received a commercially prepared, bagged pet food. There was no pasture use on the farm, and all forages (hay and silages) were grown on land fertilized with commercial fertilizer and harvested using farm-owned equipment. Non-forage feed products included three different commercially prepared complete feeds and mineralized salt blocks—all provided by one commercial feed manufacturer.

Two of the complete feeds (one for the lactating cows and one for young heifers) were always delivered in bulk and transferred directly into their respective bulk storage bins. The third ration, a pre-lactation ration, was delivered in 20 kg bags, or in bulk, and then transferred directly into bulk bags on the farm.

Feed mixing and handling practices described for the farm preclude feeding of the lactation or pre-lactation feeds to heifers less than 12 months of age. The lactation feed was mixed with forages in a mobile mixer wagon and fed to the milking cows. The pre-lactation ration was pail-fed directly to dry cows and bred heifers for the last two to three weeks before calving.

Consistent with management practices for all heifer calves on the farm, the case animal was housed in a single enclosed pen for approximately the first three months of life, and then moved through a series of group pens with other heifers of similar age and size. Calves were fed colostrum, followed by milk, until weaning at approximately 12 weeks of age. Heifer calves were introduced to the commercial ration beginning at approximately six weeks of age, and they were pail-fed increasing amounts until approximately six to eight months of age. From six to eight months of age through to two or three weeks pre-calving, the animals were fed forage (hay and silage) only. Therefore, the case animal's only direct exposure to a mixed ration was the heifer ration; however, incidental exposure to the lactation ration, the dry-cow ration and the mineralized salt block cannot be completely ruled out.

Investigation at the commercial feed manufacturer identified that the mineralized salt blocks were manufactured in a separate, specialized facility free of prohibited material and other rendered products. The mineralized salt block was therefore ruled out as a possible source of contamination. The three complete feeds were manufactured on-site using equipment cross-utilized between feeds for ruminants and those containing prohibited material. Procedures to prevent cross-contamination of ruminant feeds with prohibited material existed at the facility, but, for some procedures, did not include a requirement to document that the procedure was followed.

For procedures accompanied by documentation to indicate that they had been followed, no deviations were noted for the specific feed products of interest. Procedures not accompanied by documentation to indicate that they had been followed (flush of common receiving system after receipt of prohibited material and cleaning of compartments of cross-utilized trucks) cannot be assessed for specific failures. As a result, cross-contamination during the receipt of feed ingredients and/or during the transportation of prepared bulk rations cannot be ruled out. The investigation supports that the most likely source was cross-contamination of the heifer ration through ingredient receiving or transportation, but it cannot rule out other products or other steps in the manufacturing process.

Prohibited material was regularly supplied to the manufacturing facility from four different rendering facilities, one of which supplied prohibited material to each feed supplier identified in previous BSE cases.

INVESTIGATION OVERVIEW
The detection of this case does not change any of Canada's BSE risk parameters. The location and age of the animal are consistent with previous cases, and the BSE surveillance results to date, including this new case, reflect an extremely low level of BSE in Canada. In essence, the case confirms what was already known about an extremely low level of BSE infectivity having existed in Canada's feed system during the late 1990s and early 2000s.

Since the confirmation of BSE in a native-born animal in May 2003, Canada has significantly increased its targeted testing of cattle in high-risk categories advocated by the OIE (including non-ambulatory animals). This effort is directed at determining the level of BSE in Canada, while monitoring the effectiveness of the suite of risk-mitigating measures in place. Canada's National BSE Surveillance Program continues to demonstrate an extremely low level of BSE in Canada, with 10 positive animals detected among the over 169,000 targeted tests conducted since 2003.

With respect to BSE, the safety of beef produced in Canada is assured by public health measures enacted in 2003, following the first detection of BSE in a native-born animal in Canada. The removal of specified risk material (SRM)—those tissues that have been demonstrated to have the potential to harbour BSE infectivity—from all animals slaughtered for human consumption is the most effective single measure to protect consumers in Canada and importing countries from exposure to BSE infectivity in meat products.

As demonstrated by the surveillance system, the feed ban implemented in 1997 is effectively preventing the amplification of BSE in Canada's feed system. The detection of BSE in a few animals born after the 1997 feed ban is not unexpected and does not indicate a failure of those measures. Additional regulations to enhance Canada's feed ban were enacted on July 12, 2007. The most important change is the removal of SRM from all animal feeds, pet food and fertilizer. The enhancement will significantly accelerate progress toward eradicating BSE from the national cattle herd by preventing more than 99 per cent of potential BSE infectivity from entering the Canadian feed system.

On May 22, 2007, Canada was officially categorized under the OIE's science-based system as a controlled BSE risk country. This status clearly recognizes the effectiveness of Canada's surveillance, mitigation and eradication measures, and acknowledges the work done by all levels of government, the cattle industry, veterinarians and ranchers to effectively manage and eventually eradicate BSE in Canada.


http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/bccb2007/10investe.shtml


TSS
 
INVESTIGATION OVERVIEW
The detection of this case does not change any of Canada's BSE risk parameters. The location and age of the animal are consistent with previous cases, and the BSE surveillance results to date, including this new case, reflect an extremely low level of BSE in Canada. In essence, the case confirms what was already known about an extremely low level of BSE infectivity having existed in Canada's feed system during the late 1990s and early 2000s.

Every one of these releases has the same wording-- which makes me wonder what are these risk-parameters :???: What is a consistent location and age :???:

If I remember right-- these cattle have been found from age 4 to age 11 or 12-- with connections to 4 different provinces-- with 2 differing forms of BSE (typical & atypical)...

So does that mean if it is an any age bovine, within the exterior boundaries of Canada, that tests positive for any form of BSE - then it is consistent :???: :shock: :wink: :lol:
 
"In essence, the case confirms what was already known about an extremely low level of BSE infectivity having existed in Canada's feed system during the late 1990s and early 2000s."


But the same outfit who the Ninth Circuit ruled must be given deference and who the anti-RCALFers claim should not be filed on said the feed ban was effective in March, 1999. :mad: Yep, just a bunch of dang protectionists... :roll:
 
The carcass was secured at the sampling site, and was subsequently transferred to the CFIA Laboratory in Lethbridge for incineration

How long before BSE shows up down-wind of this Lethbridge incinerator.

My God, is the CFIA really this dumb. "Incineration" is part of the problem!

Metals do not disappear with incineration, they gasefy and recondense in the cooler atmosphere forming the nanoparticle spheres (Proteon nucleating centers - PNCs) spoken of in Dr. Vitaly Vodyanoy's USA patent application 20070122799.

The Swan Hills incinerator north-west of Edmonton, must be shut down.

The flaring by the oil and gas industry must be stopped. [they brag that they have reduced flaring levels by 40% of early 1990's levels] Time to take this much farther.

There was no pasture use on the farm, and all forages (hay and silages) were grown on land fertilized with commercial fertilizer

Also, time to look at the "commercial fertilizer" for levels of metals. Uranium goes hand in hand with phosphorous.

The Frazer Valley has seen uranium mining activity again, starting in 1987, after a moritorium of many years. Time to put that moritorium back in place. "Uranium Free BC" www.uraniumfreebc.org/

USA Food and Drug Administration has a draft of Potential Hazardous Contaminants in animal feed. I note that they list strontium 90 BUT NOT Cesium 137/134. www.fda.gov/cvm/DocketHazardAnimalFeed.htm

The fallout from nuclear testing and Chernobyl deposited Cesium and Strontium all over this planet (as has other nuclear incidents we are not as familiar with). Cesium decays into Barium. Mark Purdey found elevated levels of Barium and Strontium in antler material from a CWD zone in AB/Sask. with lower levels in non-CWD zones. The Barium may be the decay product of Cesium 137. IT actually makes alot of sense. With a decay half-life of 30 years, where-ever this fallout deposited (after the 1986 Chernobyl melt down), it is steadily transforming into the next decay product. Contamination of the brain - for example - with Cs137 may not cause any problems, UNTIL that transformation occurs. Millions of electron volts destroy cells within a close proximity to the decaying particles.

CFIA admits it does not examine research linked to "cause"; its' mandate is for diagnosis, transmission etc.... Well, it is very hard to stop the disease, when you won't admit what is causing it!
 
Kathy said:
The carcass was secured at the sampling site, and was subsequently transferred to the CFIA Laboratory in Lethbridge for incineration

How long before BSE shows up down-wind of this Lethbridge incinerator.

My God, is the CFIA really this dumb. "Incineration" is part of the problem!

Metals do not disappear with incineration, they gasefy and recondense in the cooler atmosphere forming the nanoparticle spheres (Proteon nucleating centers - PNCs) spoken of in Dr. Vitaly Vodyanoy's USA patent application 20070122799.

The Swan Hills incinerator north-west of Edmonton, must be shut down.

The flaring by the oil and gas industry must be stopped. [they brag that they have reduced flaring levels by 40% of early 1990's levels] Time to take this much farther.

There was no pasture use on the farm, and all forages (hay and silages) were grown on land fertilized with commercial fertilizer

Also, time to look at the "commercial fertilizer" for levels of metals. Uranium goes hand in hand with phosphorous.

The Frazer Valley has seen uranium mining activity again, starting in 1987, after a moritorium of many years. Time to put that moritorium back in place. "Uranium Free BC" www.uraniumfreebc.org/

USA Food and Drug Administration has a draft of Potential Hazardous Contaminants in animal feed. I note that they list strontium 90 BUT NOT Cesium 137/134. www.fda.gov/cvm/DocketHazardAnimalFeed.htm

The fallout from nuclear testing and Chernobyl deposited Cesium and Strontium all over this planet (as has other nuclear incidents we are not as familiar with). Cesium decays into Barium. Mark Purdey found elevated levels of Barium and Strontium in antler material from a CWD zone in AB/Sask. with lower levels in non-CWD zones. The Barium may be the decay product of Cesium 137. IT actually makes alot of sense. With a decay half-life of 30 years, where-ever this fallout deposited (after the 1986 Chernobyl melt down), it is steadily transforming into the next decay product. Contamination of the brain - for example - with Cs137 may not cause any problems, UNTIL that transformation occurs. Millions of electron volts destroy cells within a close proximity to the decaying particles.

CFIA admits it does not examine research linked to "cause"; its' mandate is for diagnosis, transmission etc.... Well, it is very hard to stop the disease, when you won't admit what is causing it!



i agree kathy, and problem is, you will not admit it.
no matter how hard to try to make metals, nuclear proliferation, op's, etc., the cause of any TSE, it just ain't so kathy.
nice try though. you should concentrate on the real issues, like TSE tainted feed, cross contamination, and we must worry about true environmental causes like vertical, lateral transmissions, but nuclear proliferation, op's, metals, as _cause_ of TSE, just aint so, never has been, no matter how much kathy wants it too happen. smoke and mirrors kathy, they will just continue to spread this agent, transmissions studies do not lie. ...TSS



J. Anim Sci., doi: 10.2527/jas.2007-0215
©Copyright, 2007, The American Society of Animal Science


ARTICLE

Exposure to low dietary copper or low copper coupled with high dietary
manganese for one year does not alter brain prion protein characteristics in
the mature bovine

L. R. Legleiter 1, H. C. Liu 1, K. E. Lloyd 1, S. L. Hansen 1, R. S. Fry 1,
J. W. Spears 1*
1 Department of Animal Science and Interdepartmental Nutrition Program,
North Carolina State University, Raleigh, NC



* To whom correspondence should be addressed. E-mail: [email protected].


Abstract


It is now widely accepted that abnormal prion proteins are the likely
causative agent in bovine spongiform encephalopathy (BSE). Cellular prion
proteins (PrPc) bind copper (Cu), which appears to be required to maintain
functional characteristics of the protein. The replacement of Cu on PrPc
with manganese (Mn) has resulted in loss of function and increased protease
resistance. Twelve mature cows were used to determine the effects of Cu
deficiency, alone and coupled with high dietary Mn, on brain Cu and Mn
concentrations, and PrPc functional characteristics. Copper-adequate cows
were randomly assigned to treatments: 1) control (adequate in Cu and Mn), 2)
Cu-deficient (-Cu), and 3) Cu-deficient plus high dietary Mn (-Cu+Mn). Cows
assigned to treatments -Cu and -Cu+Mn received no supplemental Cu and were
supplemented with molybdenum (Mo) to further induce Cu deficiency. After 360
d, Cu-deficient cows (-Cu and -Cu+Mn) tended to have less concentrations of
Cu (P = 0.09) in the obex region of the brainstem. Brain Mn tended (P =
0.09) to be greater in -Cu+Mn cattle vs. -Cu cattle. Western blots revealed
that PrPc relative optical densities, proteinase K degradability, elution
profiles, molecular weights, and glycoform distributions were not different
among treatments. The concentration of PrPc, as determined by ELISA, was
similar across treatment groups. Brain tissue (obex) Mn superoxide dismutase
activity was greatest (P = 0.04) in cattle receiving -Cu+Mn, while
immunopurified PrPc had similar superoxide dismutase-like activities among
treatments. Immunopurified PrPc had similar Cu concentrations across
treatments while Mn was undetectable. We conclude that Cu deficiency coupled
with excessive Mn intake in the bovine may decrease brain Cu and increase
brain Mn. Copper deficiency, alone or coupled with high dietary Mn, did not
cause detectable alterations in PrPc functional characteristics.

http://jas.fass.org/cgi/content/abstract/jas.2007-0215v1


Subject: FATEPriDE KEY FINDINGS ORGANOPHOSPHATE NO RELATIONSHIP TO CAUSE TSE
Date: May 3, 2007 at 8:41 am PST

KEY FINDINGS

Organophosphate Studies

6. Studies using phosmet (an organophosphate pesticide) were
carried out throughout the project. No relationship between this
compound and the potential to cause a TSE were identified. In
studies with oral dosing of rats, it was shown that PrP expression
levels increased in the brain but there was no association between
this and formation of proteinase K (PK) resistant PrP.


snip...


12. A model of seed protein aggregation and fibril formation was
established using PrP charged with Mn2+. PrP-Mn2+ was found to
form small circular aggregates able to catalyse further protein
aggregation and fibrilisation of PrP. This model unlike other
published models (for example those of Baskakov et al.1) does not
require the presence of denaturants and is not an autocatalytic
process (i.e. the substrate of the reaction did not aggregate). The
results suggest that Mn2+ may play a role in the formation of prion
seeds

__although further studies showed that this material was not
infectious in mouse bioassay.__

snip...

24. The project also generated information concerning the relation of
TSEs to environmental factors:
• __Potentially no role for organophosphates in TSEs.__
• Increased Mn in the diet results in higher PrP levels in the
brain.
• No conclusion is yet possible in terms of the relationship
between environmental trace element concentrations and the
geographical occurrence of TSEs (classical scrapie or BSE).
• Some confirmation was provided that in some specific farms
occurrence of classical scrapie correlates with high Mn levels.


http://www.seac.gov.uk/papers/97-4.pdf



a) As regards the involvement of organophosphates in the origin of BSE, no
new scientific
information providing evidence or supporting the hypothesis by valid data
became
available after the adoption of the last opinion of the SSC on this issue.
Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for
registration of
plant protection products and veterinary medicines – addressed in the
enquiries – provide
the basis for safe use of registered compounds and their formulations.
Regarding the
alleged intoxication cases reported and OP exposure it must be concluded
that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R.,
Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar,
H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs
Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant
Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE
and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and
transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf



OP'S MEETING WITH PURDEY

http://www.bseinquiry.gov.uk/files/yb/1994/02/09001001.pdf



transmission studies do not lie, amplification and transmission!

1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of
known infectious tissues. The asymptomatic incubation period in the one
monkey exposed to the virus of kuru was 36 months; that in the two monkeys
exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months,
respectively; and that in the two monkeys exposed to the virus of scrapie
was 25 and 32 months, respectively. Careful physical examination of the
buccal cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has remained
asymptomatic during the 39 months that it has been under observation.

snip...


The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides
further grounds for concern that scrapie-infected meat may occasionally give
rise in humans to Creutzfeldt-Jakob disease. ...end

(from full text study pdf...TSS)

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE

This is provided by the statistically significant increase in the incidence
of sheep scrape from 1985, as determined from analyses of the submissions
made to VI Centres, and from individual case and flock incident studies.
........


http://www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf



look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa


It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


SHORT COMMUNICATION

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

1 Wyoming Game and Fish Department, 2362 Highway 34, Wheatland, Wyoming 82201, USA;
2 Department of Veterinary Sciences, University of Wyoming, Laramie, Wyoming 82071, USA
3 Corresponding author (email: [email protected] )

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.
Key words: Alces alces shirasi, chronic wasting disease, enzyme-linked immunosorbent assay, immunohistochemistry, moose, oral inoculation, prion, PrPCWD.


http://www.jwildlifedis.org/cgi/content/abstract/42/3/640




http://www.usaha.org/committees/reports/2005/report-wd-2005.pdf



-------- 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: [email protected]



Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA 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;

1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant
materials being fed back to cattle is terribly flawed. without the
_total_ and _mandatory_ ban of all ruminant materials being fed
back to ruminants including cattle, sheep, goat, deer, elk and mink,
chickens, fish (all farmed animals for human/animal consumption),
this half ash measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent
findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and sub-clinical),
we must ban not only documented CWD infected deer/elk, but healthy
ones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials),
but ALL tissues. recent new and old findings support infectivity
in the rump or ash muscle. wether it be low or high, accumulation
will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified
TSE in USA cattle. all this has been proven, but the TSE in USA
cattle has been totally ignored for decades. i will document this
data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but
cattle in sufficient numbers to find (1 million rapid TSE test in
USA cattle annually for 5 years), any partial measures such as the
ones proposed while ignoring sub-clinical TSEs and not rapid TSE
testing cattle, not closing down feed mills that continue to violate the
FDA's BSE feed regulation (21 CFR 589.2000) and not making
freely available those violations, will only continue to spread these
TSE mad cow agents in the USA. I am curious what we will
call a phenotype in a species that is mixed with who knows
how many strains of scrapie, who knows what strain or how many
strains of TSE in USA cattle, and the CWD in deer and elk (no
telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the
USA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state
(especially ''sporadic'' cjd), and that a CJD Questionnaire must
be issued to every family of a victim of TSE. only checking death
certificates will not be sufficient. this has been proven as well
(see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make
the same mistakes...

REFERENCES


Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
[email protected]

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. 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...

These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757



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 Developer
For Deer and Game in the wild
Guaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm


DEPARTMENT OF HEALTH & HUMAN SERVICES
PUBLIC HEALTH SERVICE
FOOD AND DRUG ADMINISTRATION

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN 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 cattle
or 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 from
the regulations. As a manufacturer of materials intended for animal
feed use, you are responsible for assuring that your overall operation
and the products you manufacture and distribute are in compliance with
the law. We have enclosed a copy of FDA's Small Entity Compliance Guide
to assist you with complying with the regulation... blah, blah, blah...tss

http://www.fda.gov/foi/warning_letters/g1115d.pdf


SNIP...FULL TEXT ;


http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm


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

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html

snip...end...tss



NOW, please note what the FDA claims was a safe level ;



FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html



then you have to worry more from the friendly fire, there of ;




1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8


Transmission of Creutzfeldt-Jakob disease to a chimpanzee by
electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral
cortex of a middle aged woman with progressive dementia were
previously implicated in the accidental transmission of
Creutzfeldt-Jakob disease (CJD) to two younger patients. The
diagnoses of CJD have been confirmed for all three cases. More than
two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the
electrodes were implanted in the cortex of a chimpanzee. Eighteen
months later the animal became ill with CJD. This finding serves to
re-emphasise the potential danger posed by reuse of instruments
contaminated with the agents of spongiform encephalopathies, even
after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract





http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf



http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf



TSS
 
flounder, do people really read your lengthy postings?...

internalized ionizing radiation

BSE test kits - BIO-RAD duh... biological radiation!

French Atomic Energy Commission, Univ. of California, Livermore

DU - depleted uranium weapons
(Hiroshima and Nagasoki bombs had DU tamping to reflect energy back to core)

CWD - Suffield, Wainwright, Cold Lake, Namao (CFBs), Swan Hills Incinerator

CWD - Rockyflats Nuclear Facility, Nevada Missile Test Range

www.markpurdey.com or www.purdeyenvironment.com

Hide and seek..... cat and mouse.... truth and lies

Truth always prevails!
 
Kathy said:
flounder, do people really read your lengthy postings?...


I appreciate all you do Terry and respect what you are fighting for.But I try to read your posts and half way through my head hurts :???: .
Do you think you could dumb it down for some us us?You know like all the books perhaps a format like BSE for dummies :o .
 

Latest posts

Back
Top