Kathy said:
You can come to my home anytime and discuss this situation.
Until the truth is known, and we all know that the CFIA is just following the UK mantra, the more people looking at this problem the better.
You are free to trust the "authorities" to tell you what's best; but, for now, I am free to ask my questions and make my statements.
Thought police are not needed here.
Unless you are the most recent rancher "directly affected" by the new BSE case, you have no right to speak for the affected individual.
Certainly, it is devastating for them, especially when they take onto themselves ALL the blame for feeding that darn contaminated MBM/feed. They might be pleasantly surprised to learn that there are other hypotheses out there (the prion/MBM theory is just a hypothesis, not proven science). They might have legal venues which they could pursue, should they wish, to discover if some "industrial/military practice" contributed to their positive animal.
By the way, we are all directly affected by this. Our keeping quiet is exactly what the CFIA and other government officials want. Divide and conquer!
I'm from East Central Alberta too. My ranch may be affected next.
If a case is ever found on our premises, I will not be quiet. The wind can carry contaminates for hundreds, if not thousands of miles, depending on the source of contamination, eg. mine tailings
The very least that officials should release is the "hunting zone" number.
the only contaminant i see flying in the wind here is the BS you are spreading kathy, hope it's not contagious :lol: :lol2: :tiphat:
Transmissible Spongiform Encephalopathy (TSE) risk assessment of the use
of bovine spray dried red cells in feeds for fish, in consideration of a report
produced by the European Animal Protein Association1
Scientific Opinion of the Panel on Biological Hazards
(Question No EFSA-Q-2007-105)
Adopted on 6 December 2007
PANEL MEMBERS
Olivier Andreoletti, Herbert Budka, Sava Buncic, Pierre Colin, John D Collins,
Aline De Koeijer, John Griffin, Arie Havelaar, James Hope, Günter Klein, Hilde Kruse,
Simone Magnino, Antonio Martínez López, James McLauchlin, Christophe Nguyen-The,
Karsten Noeckler, Birgit Noerrung, Miguel Prieto Maradona, Terence Roberts, Ivar Vågsholm,
Emmanuel Vanopdenbosch.
SUMMARY
In its Opinion of 21 October 2004 on BSE risk from dissemination of brain particles in blood
and carcass following stunning, the EFSA concluded that the brain damage caused by both
penetrating and non-penetrating captive bolt stunning in cattle, as well as that caused by
penetrating captive bolt in sheep can result in occurrence of central nervous system tissue in
venous blood draining the head. The risk could however not be quantified.
In its Opinion of 28 April 2005 on the assessment of the health risks of feeding of ruminants
with fishmeal in relation to the risk of TSE the EFSA concluded that if there is any risk of TSE
in fishmeal, this could arise from the mammalian feed being fed to fish which are then included
in fishmeal or through fishmeal contaminated by Meat and Bone Meal (MBM). The risk of TSE
in fish, either being fed directly or by amplification of infectivity is remote.
Against this background, the European Commission has requested to the Scientific Panel on
Biological Hazards to deliver a scientific opinion on a TSE risk assessment of the use of bovine
blood in feeds for fish, in consideration of a report produced by the European Animal Protein
Association (EAPA).
The EFSA opinion considers that the EAPA report is well written and comprehensive. However,
its qualitative approach does not fully take into account the uncertainties surrounding several of
its risk parameters. Consequently, its conclusions may be overly optimistic.
1 For citation purposes: Opinion of the Scientific Panel on Biological Hazards on the request from the European
Commission on a Transmissible Spongiform Encephalopathy risk assessment of the use of bovine spray dried red
cells in feeds for fish, in consideration of a report produced by the European Animal Protein Association. The
EFSA Journal (2007), 596, 1-45.
Opinion on a TSE risk assessment of the use of bovine spray dried red cells in feeds for fish,
in consideration of a report produced by the European Animal Protein Association
The EFSA Journal (2007) 596, 2-45
A human or animal health risk may arise if recycling of BSE-contaminated bovine SDRC occurs
directly (bovine SDRC fed to cattle) or indirectly (fishmeal made from fish recently fed with
BSE contaminated bovine SDRC given to cattle) because this would be equivalent to feeding
cattle by-products to cattle (intra-species recycling).
The assessment of the BSE related-risk of bovine SDRC from slaughtered bovine animals
considered fit for human consumption to be included in aqua feed is theoretically feasible both
semi-quantitatively and quantitatively by developing a probabilistic risk assessment model.
However, key parameter limits of this model (i.e. endogenous bovine blood BSE infectivity and
degree of contamination with CNS by current stunning and slaughter methods) can only be
developed from expert opinion and judgement, as there is currently not experimental data
available. Both the degree of uncertainty of this type of data (which would reduce the robustness
of any risk estimates) and the extensive work that would be needed to produce such model
makes its development unrealistic in the frame of this opinion.
On the other hand and considering the current implementation of the EU feed-ban, the inclusion
of bovine blood products in the authorized list of ingredients in fish feed would potentially limit
the suitability of current available tools, to detect the presence of prohibited bovine by-products
(i.e. SRM)
Following this, the BIOHAZ panel recommends to develop and assess the outcome of a semiquantitative
or quantitative risk model of the BSE risk of bovine SDRC employed in aqua feed.
In order to enhance the robustness of that risk assessment with experimental data which is
currently not available, it is further recommended to quantitatively evaluate different risk
parameters. These would include the evaluation of the endogenous blood infectivity levels in
incubating and terminally BSE affected cattle, the evaluation of the current allowed methods for
cattle stunning for the potential to produce embolism and the quantitative assessment of the CNS
contamination risk posed by different blood collection methods.
Finally, a combination of tests capable of detecting, with a high level of sensitivity, the species
and tissue origin of the animal proteins included in fish feed should be developed and validated.
snip...
CONCLUSIONS AND RECOMMENDATIONS
CONCLUSIONS
• The EAPA report is well written and comprehensive. However, its qualitative approach
does not fully take into account the uncertainties surrounding several of its risk
parameters. Consequently, its conclusions may be overly optimistic.
• A human or animal health risk may arise if recycling of BSE-contaminated bovine SDRC
occurs directly (bovine SDRC fed to cattle) or indirectly (fishmeal made from fish
recently fed with BSE contaminated bovine SDRC given to cattle) because this would be
equivalent to feeding cattle by-products to cattle (intra-species recycling).
• The production technology employed for the manufacturing of SDRC as described in the
EAPA report would be unlikely to reduce BSE infectivity if present.
• The assessment of the BSE related-risk of bovine SDRC from slaughtered bovine
animals considered fit for human consumption to be included in aqua feed is theoretically
feasible both semi-quantitatively and quantitatively by developing of a probabilistic risk
assessment model. However, key parameter limits of this model (i.e. endogenous bovine
blood BSE infectivity and degree of contamination with CNS by current stunning and
slaughter methods) can only be developed from expert opinion and judgement, as there is
Opinion on a TSE risk assessment of the use of bovine spray dried red cells in feeds for fish,
in consideration of a report produced by the European Animal Protein Association
The EFSA Journal (2007) 596, 16-45
currently not experimental data available. Both the degree of uncertainty of this type of
data (which would reduce the robustness of any risk estimates) and the extensive work
that would be needed to produce such model makes its development unrealistic in the
frame of this opinion.
• Inclusion of bovine blood products in the authorized list of ingredients in fish feed would
potentially limit the suitability of current available tools, to detect for the presence of
prohibited bovine by-products (i.e. SRM). The results of PCR and other DNA based
methods would be particularly prone to misinterpretation if bovine SDRC, which
includes DNA containing leucocytes, was included in feed.
RECOMMENDATIONS
• To develop and assess the outcome of a semi-quantitative or quantitative risk model of
the BSE risk of bovine SDRC employed in aqua feed.
• To evaluate the endogenous blood infectivity levels in incubating and terminally BSE
affected cattle, in order to provide a quantitative estimate of this source of blood
infectivity as a parameter for the quantitative risk model.
• To evaluate the potential of currently allowed methods for cattle stunning to produce
embolism, in order to provide a quantitative estimate of this source of blood infectivity as
a parameter for the quantitative risk model.
• To assess in a quantitative way the risk of CNS contamination posed by different blood
collection methods.
• To develop and validate a combination of tests capable of detecting with a high level of
sensitivity, the species and tissue origin of the animal proteins included in fish feed.
http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej596_blood_feeds_fish_en.pdf
EFSA opinion on the BSE related public health risks of certain animal proteins in animal feed
15/11/2007
It is widely accepted that BSE[1] was most likely spread in cattle because they were given feed that contained BSE-contaminated animal proteins. With limited exceptions, the practice of feeding animal protein to cattle or any other farmed livestock used for food has been banned since 2001 [2]. At the request of the European Parliament, EFSA has issued an opinion on the BSE related public health risks of certain animal proteins in animal feed, which will help inform any future consideration of amendments to the existing feed ban.
EFSA's BIOHAZ[3] Panel's opinion particularly addressed feed containing pig protein being fed to poultry and feed containing poultry protein being fed to pigs. The concern relates to the risk of transmission of the BSE agent through animal feed and hence the risk of causing BSE related exposure in humans. The Panel has concluded, with certain qualifications, that the risks to public health would be negligible: up to now, BSE has not been identified in pigs or poultry under natural conditions, therefore the risk of transmitting BSE to pigs through feeding poultry processed proteins and vice-versa is considered negligible. Hence the Panel conclusion in relation to public health.
Certain important qualifications are attached to this opinion. The Panel's conclusions take into account the decline in the BSE epidemic and the current control measures in place. The Panel stressed that their opinion only remains valid in the context of the continued effective implementation of the other current BSE control measures. Whilst BSE has so far not been found to occur under natural conditions in either pigs or poultry, if a TSE were ever found to occur naturally there would be a need to reassess the risk. It is also noted that it is not yet possible, with the currently approved method, to distinguish the species origin of proteins in a feed product.
The Panel also considered a further request from the Parliament on the public health risks in relation to introducing possible tolerance levels for small quantities of any animal protein in animal feed. The Panel concluded that it is not currently possible to define the parameters that would enable risk managers to establish such tolerance levels, due to the lack of internationally agreed scientific methodology.
The Panel also noted that introducing any tolerance level would lead to an increase in the risk of transmission of BSE compared to the current EU situation. Given that it is not currently possible to quantify amounts of animal proteins in feed, it is not possible to determine whether the amounts would be above or below what may be considered as the tolerance level. The Panel recommended further studies on detection limits and techniques to quantify animal proteins in feed.
Under the current protective measures, if a tolerance level for animal protein in feed was to be introduced, the risk of transmitting BSE to cattle or other ruminants cannot be excluded. The few infected animals that could arise would probably not be able to maintain the presence of BSE in the cattle population but would increase the potential risk of human exposure to BSE. However, the risk of transmitting BSE to non-ruminants, if a tolerance level was to be introduced, is lower than to ruminants, as long as intra-species recycling is avoided and so in this scenario the Panel concluded that any increase in the exposure risk of BSE for humans would be negligible.
--------------------------------------------------------------------------------
[1] Bovine Spongiform Encephalopathy (BSE), which affects cattle, is the most well known Transmissible Spongiform Encephalopathy (TSE). TSE's are a family of transmissible progressive diseases that mainly affect the central nervous system. Other examples of TSEs include Creutzfeldt-Jakob disease (CJD) in humans and scrapie in sheep
[2] Regulation EC No 999/2001 of the European Parliament and of the Council lays down rules for the prevention., control and eradication of certain TSEs
[3] EFSA's Scientific Panel on Biological Hazards (BIOHAZ)
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178659674461.htm
Parma, 11 May 2007
PRESS RELEASE
EFSA opinion on the likelihood of BSE infectivity in specified risk material
from cattle at different age groups
EFSA has today published an opinion on the likelihood of BSE infectivity in specified risk materials
(SRM)1 from cattle at different age groups. SRMs are the tissues in cattle containing the highest
risk of BSE infectivity. These are removed as a key element of the EU BSE controls2. EFSA was
asked by the European Commission to follow-up on one of its recommendations from its previous
opinion (EFSA, 20053) on SRM removal by further estimating the likelihood of the infectivity in
SRMs derived from BSE-infected cattle. Following evaluation of new experimental data, the EFSA
Panel on biological hazards (BIOHAZ) confirmed that its earlier opinion of 2005 is still valid, which
said that BSE infectivity in the central nervous system of cattle occurs during the last quarter of the
incubation period in the animal before the disease becomes clinically detectable.
Experimental data confirmed that the "marker" for BSE (the disease-associated prion protein) in the
central nervous system of cattle becomes detectable during the last quarter of the BSE incubation period
in the animal, before the disease becomes clinically manifest. In applying this prediction model on the
likely natural exposure of cattle (rather than artificial laboratory experiments), the BSE "marker" would
either not be detectable or would still be absent in the vertebral column in cattle up to and including the
age of 33 months. However, the interpretation of such experimental data needs to take into account the
exceptional detection of BSE infection in animals younger than 33 months in EU cohorts born after 2000,
and the fact that failure to detect the BSE "marker" does not guarantee absence of infectivity in a tissue4.
1 Specified Risk Materials are animal tissues in cattle, such as the spinal cord, brain, vertebral column (that includes nervous
ganglia), and tonsils which are most likely to carry the infective BSE agent.
2 Various SRM materials are removed either at all ages (eg tonsils); over 12 months (eg the skull and spinal cord); or at 24
months (eg vertebral column) in cattle in the EU.
Full details: http://europa.eu.int/eur-lex/lex/LexUriServ/site/en/oj/2006/l_116/l_11620060429en00090013.pdf
The 24 month vertebral column risk management decision was made by the European Commission informed by the 2005
EFSA opinion on SRMs:
http://eurlex.
europa.eu/Notice.do?val=418201:cs&lang=en&list=438337:cs,429650:cs,426000:cs,425765:cs,424532:cs,422602:cs,4220
90:cs,418201:cs,406122:cs,402452:cs,&pos=8&page=1&nbl=29&pgs=10&hwords=999/2001~
3 http://www.efsa.europa.eu/en/science/biohaz/biohaz_opinions/938.html
4 In updating its previous opinion, the BIOHAZ Panel became aware that scientific consensus on the preferred approach to
calculating BSE infectivity recommended by experts in 2005, could not be achieved. This approach, drawing on surveillance
data from Member States, would have developed a predictive model of the number of BSE cases in different age groups. The
possibility that this approach might not be viable had been anticipated in 2005 as a potential limitation. Hence, the Panel based
its opinion on new experimental studies and additional experimental data on BSE detection in cattle together with actual
epidemiological data from surveillance rather than any predictive modelling.
The Panel also noted that the BSE epidemic is in decline5, and is likely to continue to decrease further, in
the different EU Member States. However, the Panel also recommended that there is good reason to
consider the risk level of each Member State separately or consider groups with similar characteristics
because of differences at the start of various control measures and surveillance between EU member
states, as well as differences in the country specific level of exposure.
It is for the European Commission and risk managers in Member States to decide whether any
modifications to current controls are warranted, informed by EFSA's opinion.
The opinion is available on the EFSA website at:
http://www.efsa.europa.eu/en/science/biohaz/biohaz_opinions/biohaz_op_ej476_srm.html
For media enquiries, please contact:
E-mail:
[email protected]
Alun Jones, Press Officer
Tel: +39 0521 036 487
or
Anne-Laure Gassin, EFSA Communications Director
Tel: +39 0521 036 248
Mobile: +39 348 640 3434
5 Since the implementation of the TSE Regulation in 2001, more than 50 million of adult bovine animals have been tested
across the EU and around 7.000 cases have been detected. A constant decline (about 35 % per year) in the number of cases has
been recorded: from 2.167 cases in 2001 to around 520 cases in 2005. Only 22 cases concerned animals born after introduction
of the total feed ban.
European Food Safety Authority - Largo N. Palli 5/a, I - 43100 Parma
0521 036 111 • Fax: (+39) 0521 036 110 •
[email protected] • www.efsa.europa.eu
http://www.efsa.europa.eu/EFSA/News_PR/pr_biohaz_srm_en,0.pdf
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3;
Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1
1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto
Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden;
5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans
to contract BSE through contaminated food. For this purpose, BSE brain was
titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50)
for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for
humans. Secondly, we aimed at examining the course of the disease to identify
possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of
BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study,
animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the onset of the
clinical phase. However, there are differences in the clinical course between orally and
intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral
route using less than 5 g BSE brain homogenate. The difference in the incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However,
there are rapid progressors among orally dosed monkeys that develop simian vCJD as
fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study "BSE in primates"
supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.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
2
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100
grams) was probably given with the benefit of hindsight; particularly if one
considers that later in the same answer Mr Bradley expresses his surprise that it
could take as little of 1 gram of brain to cause BSE by the oral route within the
same species. This information did not become available until the "attack rate"
experiment had been completed in 1995/96. This was a titration experiment
designed to ascertain the infective dose. A range of dosages was used to ensure
that the actual result was within both a lower and an upper limit within the study
and the designing scientists would not have expected all the dose levels to trigger
infection. The dose ranges chosen by the most informed scientists at that time
ranged from 1 gram to three times one hundred grams. It is clear that the designing
scientists must have also 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/s147f.pdf
2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 7
Terry S. Singeltary Sr.
Vol #: 1
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]
snip...
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
BODE'S GAME FEED SUPPLEMENT #400
A RATION FOR DEER
NET WEIGHT 50 POUNDS
22.6 KG.
snip...
_animal protein_
http://www.bodefeed.com/prod7.htm
J Infect Dis. 2004 Aug 1;190(3):653-60.
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.
http://www.ncbi.nlm.nih.gov/sites/entrez?...
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. 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
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the United States of America (USA)
Question number: EFSA-Q-2003-083
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_v2_en1,0.pdf
Subject: FATEPriDE Environmental Factors that Affect the Development of
Prion Diseases
Date: February 18, 2006 at 9:24 am PST
FATEPriDE
Environmental Factors that Affect the Development of Prion Diseases.
Project funded by the European Commission under the Quality of Life
Programme.
Contract No: QLK4-CT-2002-02723
Project No: QLRT-2001-02723
Start Date
1st January 2003
Duration
36 months plus 6 month extension
Partners
1. The University of Bristol, UK (Co-ordinator)
2. National Environment Research Council-The British Geological Society, UK
3. University of Bath, UK
4. Free University of Berlin, Germany
5. University of Iceland, Iceland
6. Universita degli studi di Perugia, Italy
7. Universite Joseph Fourier Grenoble, France
8. Alpine Institute of Environmental Dynamics, France
Introduction
The work proposed here brings together top EU geo and biochemists focusing
on determining the environmental factors that affect the development of
prion diseases such as scrapie, bovine spongiform enchpalitis (BSE), chronic
wasting disease (CWD) and Creutzfeld-Jacobs disease (CJD). First the
geographical distribution of manganese and copper in soils will be
investigated as risk factors. This will be undertaken due to the fact that
prion diseases often are found in clusters. It now has been established that
the normal metal for prion protein is copper but if that metal is replaced
with manganese, the structure of the prion protein is altered. The role of
organophosphate pesticides will also be investigated because it has been
suggested that copper is complexed with organophosphate, preventing copper
absorption.
Objectives
There is clear evidence that the occurrence of prion diseases often has a
non-random distribution, suggesting a link to some environmental factors.
The work proposed here will investigate risk factors, including the role of
trace elements and organophosphates. Analysis of regional variation in local
manganese/copper levels will be determined and compared to the incidence of
the diseases. The ability of manganese and/or organophosphates in
influencing conversion of the prion protein to an abnormal and/or infectious
protein will be determined. In combination with geographical occurrence and
geo-chemical considerations this program will identify whether these
environmental considerations should be acted upon to bring about effective
prevention or at least risk minimalisation of prion diseases in the EU and
further afield.
Description of the Work
Recently it has been suggested that disbalance in dietary trace-elements
and/or exposure to organophosphates might either cause or be a risk factor
for prion disease development. In particular, high incidence of scrapie
(e.g. in Iceland), chronic wasting disease, and in Slovakia and Italy CJD
are associated with regions where soil and foliage are reported to be low in
copper and high in manganese. This proposal will address whether exposure to
a diet that has a high manganese/copper ratio can influence prion disease
will also be addressed. In particular, we shall investigate this theory at
the level of protein, cells, animals as well as geographical and
geo-chemical associations with prion diseases. Animal models of prion
disease and sheep from farms in regions of high scrapie will be investigated
for a possible influence of level of manganese and copper on incidence or
onset of these diseases. Bio-chemical and biophysical techniques will be
used to investigate interaction of the prion protein with copper and
manganese to determine the mechanism by which Mn substitution for Cu
influences conversion to the abnormal isoform of the protein and whether
such conversion results in protein that is infectious in mouse bioassay for
infectivity. Additionally, a cell culture model will be used to generate
abnormal prion protein by exposure to manganese. Cell culture model of
infection will be used to assay whether prion disease alters manganese
metabolism and transport of manganese into cells. The level of expression of
the prion protein is in itself a risk factor for prion disease as it
shortens the incubation time for the disease. This research will result in
understanding of the role of disbalance in the trace elements Cu and Mn on
the onset and mechanisms behind the occurrence of prion diseases and will
for the first time define whether there are environmental risk factors for
prion diseases.
Milestones and Expected Results
The study proposed here will produce a geo-chemical map of Europe for
manganese and copper. These maps will be used to target field areas where
prion diseases have occurred as clusters. The bio-chemical studies will
establish whether the replacement of manganese for copper in prion protein
is a risk factor for the disease _development_. Organophosphate will also be
investigated as a risk factor. The study aims at minimising the risk of
prion diseases for humans and animals in the EU.
http://www.arp-manchester.org.uk/FatePride.htm
SINCE THEN ;
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
TSS
???: :roll: :lol: ) attitudes as that...