Tuesday, May 21, 2013

Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$

Bad feed, mad cows: Why we know three BSE cases had a common origin

May 20, 2013. 2:27 pm • Section: Alberta, Business

In late 2003, days after a Canadian cow was found with bovine spongiform encephalopathy south of the border, a Canadian Food Inspection Agency investigator revealed to me he’d found a tentative link between that animal and the one that, 10 years ago today, was confirmed as Canada’s first homegrown case of BSE.

My paper at the time, the Edmonton Journal, put this on their front page on Dec. 31. This bombshell finding was mentioned internationally, from Toronto to Fox News to the New York Times. And the CFIA clammed up pretty quickly, insisting this was merely a theory that hadn’t been proven.

By Jan. 23, 2006, nearly all of Canadian journalism had moved on from the mad cow story. There was a much bigger story that day: the federal election that would punt the Liberals and launch the Stephen Harper prime ministership.

That same day, the CFIA quietly published online an epidemiological report on the roots of BSE. It confirmed that not only did Cow 1 and Cow 2 share a link at the feed level, but so did a third mad cow.

Here’s my Edmonton Journal story on that 2006 report:

One day, one plant, three mad cows: On the third anniversary of Canada’s BSE crisis, The Journal reveals how investigators traced the source of the outbreak to a single day’s shipment of cattle protein from an Edmonton rendering plant

Sat May 20 2006

EDMONTON – On Feb. 28, 1997, three loads of cattle protein left an Edmonton rendering plant, destined for livestock feed mills in St. Paul, Edmonton and Westlock.

The shipments were a perfectly normal event. Nobody would know it for several years, but on that day the seed was planted for Canada’s mad cow crisis.

The protein all three mills received contained the boiled-down remains of an animal with mad cow disease that days or weeks earlier slipped, undetected, past the inspection system, government investigators now believe.

Each of the three mills unwittingly turned those contaminated morsels into cattle feed and each sold that feed to a farmer, who by giving it to his calves infected one with the fatal, brain-wasting disease called bovine spongiform encephalopathy, BSE. The practice of feeding cattle remains to cattle would be banned months later to halt BSE, but was perfectly legal in early 1997.

Three cows, three farmers, three feed mills, one renderer, one day.

The shipments are now suspected as the origin of North America’s first three cases of BSE found in homegrown cattle — including the initial case announced in Alberta three years ago today. The discovery of that first mad cow eventually choked off Canada’s global cattle trade and cost ranchers $7 billion in lost sales.

The other two cases were an Alberta-born Holstein discovered in December 2003 in Washington state and a cow found near Barrhead in January 2005. All were born between October 1996 and April 1997 in north-central Alberta or western Saskatchewan, and probably ate feed made of material that came from the Edmonton renderer that ultimately fateful day in February 1997.

This common link between the three mad cows is revealed in a report by the Canadian Food Inspection Agency. Its detailed analysis raises some difficult, controversial questions.

How many more mad cows or similar “clusters” are still out there? How many other diseased cattle were never found, contaminating other cattle back in the mid-1990s, when Canada tested a minute fraction of the number of cows it tests for BSE today? Are Canada’s anti-BSE safeguards strict enough to protect Canadians and the cattle supply? What does all this do to reassure consumers that eating beef is still safe and mad cow is not widespread in Canada?

The report tries to clarify things by answering other nagging queries.

“One of the questions that we’re always challenged to try to explain is, ‘Why Alberta? Why now? How did we get it?’ ” said Gary Little, a leading veterinarian on the CFIA’s expansive mad cow file.


And what does this one-day link mean?

Think of a single shotgun shell, whose pellets spread to hit several targets at once. The cluster points to one shotgun shell doing in all three cows. According to this hypothesis, one mad cow, not two or three, infected these cattle. And fewer shells fired could mean fewer potential hits elsewhere.

The “geographic cluster” explains why BSE has been found mostly in Alberta and not in Manitoba, Ontario or Quebec — although authorities will not rule out finding future mad cows outside our province.

This cluster theory does not mean all cattle who ate feed originating from that renderer’s shipments likely have BSE. The vast majority were either slaughtered too young to get BSE or didn’t eat the diseased molecules. Among the mad cows’ herdmates tested, none had BSE.

But the reported link only covers the first three Canadian BSE cases. There have been three more since, and nothing the CFIA has found connects them to the cluster traced to that day in February 1997.

One diseased animal, born in 1998 and discovered in January 2005, may have been infected by feed-meal processed by a renderer in Calgary or Saskatoon, the CFIA report says.

Two more cases that emerged earlier this year, both animals born in 2000, were not covered in the report. One came from north-central Alberta, the other was found last month in B.C.’s Fraser Valley, far from Canada’s existing BSE loop.

The report on the B.C. mad cow hunt, expected out next week, will point to tainted feed from several possible sources, including Alberta, Little said.

“There’s a theory that would say, ‘Yeah, it’s likely the meat and bone meal would have come from an Alberta plant, consistent with the other cases, gone to B.C. and could have resulted in cross-contamination’ (with cattle feed),” he said.

Gerald Ollis, Alberta’s chief veterinarian, hopes some link to this province exists. Otherwise, “We have a new cluster” in Canada, he said, raising the possibility of further cases in B.C.

“All I can do is hope they can trace it back to meat and bone meal from this area,” Ollis said.

Ted Jacob/Herald


The three cases outside the original cluster expose loopholes in the 1997 ban on cattle-to-cattle feeding, designed as the leading firewall against mad cow. Authorities admit the ban will not eradicate BSE, since cattle remains can still be used in feed for poultry, swine or other livestock that do not chew cud. Traces of other feed can cross-contaminate cattle feed. The CFIA has concluded at least one post-ban cow likely got sick because of improper practices at one feed mill.

Only a miniscule amount of contaminated protein is enough to infect another animal, European research has shown. Other countries, including the U.K., have found BSE-infected animals born after a feed ban, although the number of cases had dropped significantly.

To stop this cross-contamination, the CFIA proposed in December 2004 to expand the feed ban to exclude BSE-prone cattle parts — brains, spine and other “high-risk” tissues — from all animal feed. The rule remains unimposed 11/2 years later, while cattle-industry groups worry about the disposal costs and environmental effects of tonnes of waste.

While conceding that BSE cases may still emerge, disease experts insist consumers are still safe. In 2003, Canada began removing high-risk cattle parts from the human food chain. This is internationally accepted as one of the best ways to prevent the human form of mad cow, variant Creutzfeldt-Jakob disease.

Little admits the CFIA will never know how many BSE cattle went undetected before the first discovered case in 2003. But Canadian slaughterhouse inspectors have for decades barred sickly cattle from being killed for meat, Ollis said.

By not taking more decisive early action, Canada did put its animals and citizens at risk, argues William Leiss, a University of Ottawa scientist and author of Mad Cows and Mother’s Milk.

Because Canada tested so few animals in the 1990s, unknown numbers of diseased cattle slipped through the system then — the “first generation” of homegrown mad cows — and were processed into feed that infected the “second generation”of BSE cases since 2003, Leiss said.

“We have no idea how much infectivity there was in the first generation (of Canadian BSE) because we had such lousy surveillance,” he said. “Our surveillance stank. We didn’t want to know.”

Leiss has long pushed for tighter feed controls and more testing, and still believes stronger measures, like an enhanced feed ban, are needed.

The CFIA argues the steps Canada took in the 1990s met and exceeded international targets for countries without homegrown BSE, and current regulations now surpass expectations for countries with BSE. Little also said the post-feed-ban cases underline the need for a tougher ban.

The hunt for BSE origins in Canada stretches back nearly two decades and has featured some of the most elaborate sleuthing in CFIA history, from sifting through 1980s farm-health records in Britain to checking sales receipts in Alberta farms and mills. The exhaustive search wound up connecting three mad cows to one day’s rendering plant shipments.


BSE, first discovered in British cattle in 1986, has turned up in 23 countries, including Canada, the U.S. and Japan. International scientific consensus holds that BSE is spread when cattle eat the high-risk materials of infected cattle.

In 1990, as the disease was becoming a crisis overseas, Canada banned imports of live cattle from Britain.

When one of the British cows on a farm near Red Deer tested positive for BSE in 1993, the CFIA tracked the other 167 cattle imported from the U.K. since 1982. It destroyed and tested all those still alive, and none had BSE. But 68 of the imported cattle had already been slaughtered or died naturally, nearly half of them in Alberta.

Investigators contacted Britain for farm histories of those dead British animals. Ten became classified as “high risk” because they came from farms that reported other BSE cases. One died in Quebec, two in Ontario, seven in Alberta.

The CFIA’s hypothesis contends that at least one of those 68 cattle had the disease, and died in the early 1990s, likely in Alberta. Its carcass was boiled down at a rendering plant, which sent its protein to dozens of feed mills, where it was processed for cattle feed long before the BSE feed ban was imposed.

That protein infected one or more Canadian-born animals, and since BSE is known to normally incubate for six years or more before symptoms emerge, those diseased animals died around 1996 or 1997. They were never detected, at a time when mere hundreds of cows were tested each year for BSE among the more than three million cattle slaughtered. Now, authorities test about 5,000 cattle a month, focussing on the ones most likely to have BSE: aging cattle that are diseased, “downers” or dead.

One of these animals was killed or died in north-central Alberta, and its remains would have been shipped to Northern Alberta Processing Co. in Edmonton, the only rendering plant in Alberta north of Calgary. This happened days or weeks

before Feb. 28, 1997.

Fast-forward to recent years, and the ranches where the latest BSE cases were born. CFIA investigators pored over farmers’ years-old purchasing records, queried their feeding practices, and pinpointed feed containing protein meal the mad cows had eaten as calves. Some farmers kept complete records and sales receipts, but there were gaps, which made the tracing difficult, Little said.

Investigators then went to mills where suspect feed had been bought, in most cases multiple mills per mad cow. They discovered what ingredients were in each feed, and learned which renderers the mills bought from. When the trail led to Northern Alberta Processing, shipping manifests helped lock in the final puzzle pieces, leading to the theory of consecutive shipments in February 1997.

While the one-day link is compelling, the federal veterinarian cautions that it cannot be confirmed. It is impossible to determine exactly what a cow ate several years ago, and there is none of the old feed left to be tested. The report can at best pose a hypothesis and draw links, experts insist.

Alberta might continue to find mad cows because of the disease’s history and the province’s testing program, Ollis said. Alberta ranchers get $225 for each bovine head surrendered for government testing, the richest incentive in Canada. The province performs more than half of Canada’s BSE tests.

“The enhanced level of BSE surveillance in Alberta set us up for finding a cluster,” Ollis said. “Obviously it’s here, so we want to know how much of it is here.”

The CFIA cannot pinpoint how many future mad cows will emerge, but has adopted a promising new tool — a prediction model developed by scientists in Europe and given preliminary praise by the European Food Safety Authority.

The BSurvE model processed data on surveillance statistics, the feed ban, cattle population and other factors. It predicted three more mad cows in Canada beyond the ones already discovered at the time the CFIA report was written. “The model also predicted that these infected cattle would have been born before or during the implementation of the 1997 feed ban,” the report says.

On Jan. 23, 2006, the same day the report was made public, CFIA announced the discovery of a mad cow in north-central Alberta that had been born in 2000 — three years after Canada’s feed ban and contrary to the model’s prediction. Then in April, another mad cow was found in B.C.

This does not mean that, based on the BSurvE model, inspectors will only find one more mad cow, Little said. Rather, it shows the BSurvE model is not perfect.

But since it did not predict several dozen or hundreds of diseased cattle lurking out there to be discovered, it should give comfort to Canadian consumers. And based on European history, Canada’s existing feed ban, even with its loopholes, will eventually reduce mad cow cases to close to zero.

“Probably more important than the number three is the fact it shows that based on the information we have, BSE is a very, very rare event in this country,” Little said of the BSurvE model. “Whether it’s three (cases) or it’s 10 is probably not as important.”

on the 10 year anniversary of mad cow disease in Canada, your still just kidding yourself, your readers, and at the same time, putting everyone at risk by this fallacy. ...tss

CFIA, USDA, AND OIE SHOOT, SHOVEL, AND SHUT THE HELL UP SSS BSE TSE PRION MAD COW TYPE POLICY $$$, and the media is buying it hook, line, and sinker $$$

EDMONTON - Some of former Alberta premier Ralph Klein's most colourful quotes — and the reactions they elicited:


"This all came about through the discovery of a single, isolated case of mad cow disease in one Alberta cow on May 20th.

The farmer — I think he was a Louisiana fish farmer who knew nothing about cattle ranching.

*** I guess any self-respecting rancher would have shot, shovelled and shut up, but he didn't do that." — Klein recalls how the mad cow crisis started and rancher Marwyn Peaster's role.

The premier was speaking at the Western Governors Association meeting in Big Sky, Mont. September 2004.

Wednesday, December 22, 2010.

Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease?


Canada has had a COVER-UP policy of mad cow disease since about the 17th case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored $$$.

THIS proves there is indeed an epidemic of mad cow disease in North America, and it has been covered up for years and years, if not for decades, and it’s getting worse $$$.

Thursday, February 10, 2011.

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31.

Thursday, January 17, 2013.

Canada, U.S. agree on animal-disease measures to protect trade, while reducing human and animal health protection.

Wednesday, August 11, 2010.


Thursday, August 19, 2010.


Friday, March 4, 2011.

Alberta dairy cow found with mad cow disease.

Increased Atypical Scrapie Detections.

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

please note, I do not know how much of this 125 TONS of banned mad cow protein was part of the ;

e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;

bbbut, this was about 10 years post mad cow feed ban from 1997. 10 years later, and still feeding banned mad cow protein to cervids???

considering that .005 gram is lethal to several bovines, and we know that the oral consumption of CWD tainted products is very efficient mode of transmission of CWD.

Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

Date: August 6, 2006 at 6:16 pm PST


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


Product manufactured from 02/01/2005 until 06/06/2006


Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.


Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".


125 tons


AL and FL



*** 10,000,000 lbs banned blood laced meat and bone meal mbm 2007 one decade post partial and voluntary mad cow feed ban was put in place ;

snip...see more here ;

Saturday, August 4, 2012

Final Feed Investigation Summary - California BSE Case - July 2012


Summary Report BSE 2012

Executive Summary

Saturday, August 4, 2012

Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation

Saturday, December 15, 2012

Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012

Saturday, December 15, 2012

Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012

Friday, April 19, 2013


Monday, March 25, 2013

Minnesota Firm Recalls Bone-In Ribeye That May Contain Specified Risk Materials Recall Release CLASS II RECALL FSIS-RC-024-2013

Friday, April 19, 2013.

APHIS 2013 Stakeholder Meeting (March 2013) BSE TSE PRION.

Monday, October 10, 2011.

EFSA Journal 2011 The European Response to BSE: A Success Story.


EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.


Thursday, August 12, 2010.

Seven main threats for the future linked to prions.

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

Second threat


Sunday, February 10, 2013

Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection report/CJD

Tuesday, March 5, 2013

Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)

FDA believes current regulation protects the public from BSE but reopens comment period due to new studies

Tuesday, March 05, 2013

A closer look at prion strains Characterization and important implications Prion

7:2, 99–108; March/April 2013; © 2013 Landes Bioscience

Wednesday, March 20, 2013

GAO-13-244, Mar 18, 2013 Dietary Supplements FDA May Have Opportunities to Expand Its Use of Reported Health Problems to Oversee Product

From: Terry S. Singeltary Sr.

Sent: Tuesday, March 19, 2013 2:46 PM

To: gomezj@gao.gov

Cc: siggerudk@gao.gov ; youngc1@gao.gov ; oighotline@gao.gov

Wednesday, February 20, 2013

World Organization for Animal Health Recommends United States' BSE Risk Status Be Upgraded

Statement from Agriculture Secretary Tom Vilsack:

Thursday, February 14, 2013

*** The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease

Thursday, February 21, 2013

National Prion Disease Pathology Surveillance Center Cases Examined January 16, 2013


Monday, January 14, 2013

Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe

Monday, December 31, 2012

Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012

Tuesday, December 25, 2012


Tuesday, June 26, 2012

*** Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012

type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA

Wednesday, June 13, 2012


*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.


OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles

Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA

Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.

Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.

Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.

In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.

Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.

The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

Wednesday, March 28, 2012


Sunday, March 31, 2013

Creutzfeldt Jakob Disease CJD worlds youngest documented victim, 11 years old, shall we pray

Monday, April 15, 2013

Dr. Stephen B. Thacker Director Centers for Disease Control and Prevention′s Office of Science, Epidemiology and Laboratory Services (OSELS) dies from Creutzfeldt Jakob Disease CJD


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