BSE CASE CONFIRMED IN ALBERTA OTTAWA August 15, 2008

[flounder]

BSE CASE CONFIRMED IN ALBERTA OTTAWA, August 15, 2008 - The Canadian Food Inspection Agency (CFIA) has confirmed bovine spongiform encephalopathy (BSE) in a six-year-old beef cow from Alberta. No part of the animal’s carcass entered the human food or animal feed systems.

The animal’s birth farm has been identified, and an investigation is underway. The CFIA is tracing the animal's herdmates at the time of birth and examining possible sources of infection. The age and location of the infected animal are consistent with previous cases detected in Canada.

This case was detected through the national BSE surveillance program, which has been highly successful in demonstrating the low level of BSE in Canada. The program continues to play an important role in Canada’s strategy to manage BSE.

Canada remains a Controlled Risk country for BSE, as recognized by the World Organisation for Animal Health (OIE). Accordingly, this case should not affect exports of Canadian cattle or beef.

- 30 -

For information:

Canadian Food Inspection Agency Media relations: 613-228-6682

http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/ab2008/14notavie.shtml

Amazing what you will find when you look. The Canadians are doing a far better job than the US in confirming BSE/TSE cases. ...TSS




Friday, August 15, 2008
BSE CASE CONFIRMED IN ALBERTA OTTAWA, August 15, 2008

http://madcowtesting.blogspot.com/2008/08/bse-case-confirmed-in-alberta-ottawa.html

http://organicconsumers.org/forum/index.php?showtopic=1933



TSS

[Kathy]

If anybody knows the location where these animals are being found, and/or the owners (who are willing to talk about the situation) please call me at 403 854-2433

The CFIA and our governments are hiding these exact locals from us, so that we cannot do our own investigations into the environment in the areas. Wouldn't you like to know what is causing this disease?

Don't forget to read Mark Purdey's book "Animal Pharm" - check out your library systems in Alberta. Or order it from Amazon.com

I'm sure after we are all signed up for our Premise ID numbers, they might actually bring in testing of all cattle over 30 months. Things could get quite interesting then.

[grassfarmer]

"The CFIA and our governments are hiding these exact locals from us, so that we cannot do our own investigations into the environment in the areas."
Er, no - I believe individual farm locations are not being released to protect the identity of the poor guy who happens to get a case. Remember the disgraceful media circus around the first case in particular? The Government made a sensible decision on this one.

[wilagro]

I wonder what we will do when they announce that the animal is TWO years of age or less?

Seems to me that the age of these "discovered" animals is getting younger. Something is not ringing true about the BSE situation.

Rumours also abound around some communities every time that ANOTHER animal is found...as to who's farm possibly harboured the critter, especially when they announce the general area where it was discovered.

The CFIA always sounds so positive and upbeat everytime they make an announcement as if they are winning the battle against BSE. I am seriously starting to doubt their analysis of the situation.

[Kathy]

grassfarmer, I have had this argument on the rancher.net site several times. I am not asking for the ranchers name and address to be made public. I am asking, just as with the CWD deer in Alberta, that the hunting zones are noted.

I am asking (here and now, also) for the (all) ranchers directly affected to call me personally. I can keep their identity quiet. At the same time, we can look at their location and see what kinds of factors have influence on their catte.

This can include feed. If the feed you are buying is GM, if it is sprayed with chemicals (especially the dessicants).

I do not believe that the CFIA is helping these ranchers to look at any of these other probable sources of rogue metal/protein contamination.

As an Albertan, let alone a cattle producer, I have a right to know where the animals are being located (especially now that clusters are evident). Hiding the zone from us, is not protecting that rancher - it is prolonging the agony of every rancher in this province... because we are kept from communicating with each other and learning the truth for ourselves.

[per]

Yes but Kathy "your" truth might not fit the paradigm. How could they save face if "the" truth is anything other than the official line?

[grassfarmer]

Kathy, I agree it is a travesty that the truth behind BSE has never been brought to light and I commend you for seeking the truth. That said I've a lot more experience of the negative financial effects of BSE that most people in Canada. As such the comments from yourself and Wilagro make it sound like we are all facing a melt down of our industry due to BSE. Nothing could be further from the truth.
Although there are reasonable yearling prices at the moment the returns for cow/calf operators could take a turn for the worse very quickly. With grain costing 25% more than a year ago the demand for lighter calves might still be very poor. On top of that many are facing a drought situation - hay has already doubled in price in many areas and some producers are already sending their cow calf pairs to town with the cows getting a trip to the packers. We have lots of problems so lets not add to them by trying to fan the flames of a BSE crisis that has fallen into obscurity.

[flounder]

Copper deficiency in the young bovine results in dramatic decreases in brain copper concentration but does not alter brain prion protein biology

L. R. Legleiter, J. W. Spears and H. C. Liu Department of Animal Science and Interdepartmental Nutrition Program, North Carolina State University, Raleigh, NC

Jerry_Spears@ncsu.edu

Abstract

A manganese (Mn) for copper (Cu) substitution on cellular prion proteins (PrPc) in the brain that results in biochemical changes to PrPc has been implicated in the pathogenesis of transmissible spongiform encephalopathies. Recent research in the mature bovine does _NOT_ support this theory. The present study tested this hypothesis using progeny from gestating cows receiving Cu-deficient diets or Cu-deficient diets coupled with high dietary Mn. Copper-adequate cows (n = 39) were assigned randomly 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. The -Cu Mn treatment also received 500 mg supplemental Mn/kg dietary DM. Calves were weaned at 180 d and maintained on the same treatments as their respective dams for 260 d. Copper-deficient calves (-Cu and -Cu Mn) had decreased (P = 0.001) brain (obex) Cu and tended to have increased (P = 0.09) obex Mn relative to controls. Obex Mn/Cu ratios were substantially increased (P < 0.001) in calves receiving -Cu and -Cu Mn treatments compared to controls and were higher (P < 0.001) in -Cu Mn calves than in -Cu calves. Obex prion protein characteristics, including proteinase K degradability, superoxide dismutase (SOD)-like activity, and glycoform distributions, were largely unaffected. Obex tissue antioxidant capacity was not compromised by perturbations in brain metals, but Cu-deficient calves tended to have decreased (P = 0.06) Cu/Zn SOD activity and increased (P = 0.06) Mn SOD activity. Although obex copper was decreased due to Cu deficiency and Mn increased due to exposure to high dietary Mn, the obex metal imbalance had minimal effects on PrPc functional characteristics in the calves.

http://jas.fass.org/cgi/content/abstract/jas.2007-0403v1

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

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 int****ritoneal.

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

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: fdadockets@oc.fda.gov

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 ehoover@lamar.colostate.edu

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/

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

Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST

snip... see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ;

see full text ;

Friday, April 25, 2008

Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46

http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html

SPECIFIED RISK MATERIALS

http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.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

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_v2_en1,0.pdf

TSS

[Kathy]

Once the ALMS is in place, the government will introduce mandatory testing of animals over 30 months (if not all animals)... This will likely lead to many more diagnosed cases of BSE. Then those who in the past, and present, have been more closely affected by this animal disease will have lots of company.

BSE may well turn out to be linked to polioencephalomalacia (PEM). This is a predisposing factor which is common in western Canada (sulfur in the environment, feed - as well as a soil deficiency of copper, zinc and selenium).

The addition of industrial and military practices that release these toxic metals into the environment, exaccerbate the PEM and turn the brain into toxic mush with a twist.

I`d like to see some experiments where a diagnosed PEM brain, was used for transmission experiments, to see if there was a corresponding outcome - more PEM.

The transmissible portion of TSEs has to do with the metal nucleating centers (as described by Vitaly Vodyanoy (proteons and prions), and by prion dudes John Collinge and Charles Weismann in their patent where-in they state that the prion dissintegrates in 24 hours unless it becomes attached to certain metals - like gold, silver, stainless steel or alloys there-of)....

Excessive sulfur, whether via ingestion or inhalation, upsets the balance of the stomach and thiamine production - as well as Vitamin B12 production. If the smart researchers out their took these affected animals and also exposed them to the ingestion and-or inhalation of the toxic metals that replace or occupy the regions of the prion protein that normally are taken by copper.... they would be able to determine if the prion is a prodege of this multifactoral environmental disease.

Only the truth will set us free!

[flounder]

Friday, August 22, 2008

MEXICO blocks Alberta cattle following the discovery of Canada's 14th case of mad cow disease

http://madcowtesting.blogspot.com/2008/08/mexico-blocks-alberta-cattle-following.html



BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA

http://madcowtesting.blogspot.com/



TSS