Are USDA assurances on mad cow case 'gross oversimplification'?

Are USDA assurances on mad cow case 'gross oversimplification'?

2 May 2012 11:24am, EDT

By Robert Bazell, Chief science and medical correspondent, NBC News

The mad cow discovered in California last week was not really a mad cow. It suffered from a closely related disease. There is no cause for alarm at this point, but several top scientists say the public health implications may not be as clear the U.S. Department of Agriculture would have us believe.

The diseased dairy cow from a rendering (or carcass recycling) plant in Hanford, Calif., near Fresno, was infected with a condition variously known as BASE (bovine amyloidotic spongiform encephalopathy), atypical BSE and L-type BSE, which has so far been found in about 70 animals in the world. Lyndsay Cole, a spokeswoman for USDA, confirmed the diagnosis in an email Tuesday.

This condition, first reported in two Italian cows in 2004, causes the same rapid crippling and death as the classic bovine spongiform encephalopathy (BSE) that swept through Britain and much of Europe in the 1980s and '90s. But the brains of the animals look very different after their demise.

Some experiments have shown that this rare disease can jump from species to species, infecting lab mice and even non-human primates. The research also suggests that the infectious agent for the rare disease could be more virulent than BSE, more likely to appear in meat (classical BSE is mostly in brain and nervous tissue) and might be carried in milk. Many scientists are quick to point out that all this research consists of studies too small to be conclusive.

The U.S. government has confirmed the first case of mad cow disease in six years, but the government is stressing there is no threat to human health. NBC's Robert Bazell reports.

However, there is an urgent need for further study, they say.

What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”

The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”

“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.

In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said

The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.

The British and European outbreaks of BSE ignited because the industry turned cattle -- natural vegetarians -- into cannibals, feeding them the remains of cattle and other animals. U.S. farmers did the same, but Britain had a huge incidence of a related disease in sheep called scrapie, and many scientists believe that was the source of the massive cattle outbreak. Although experiments showed that BSE could infect monkeys and other animals, it was not until the first human infections that anyone realized the threat it poses to people. The human form of the disease, first discovered in Britain in the 1980s, has been blamed for the deaths of at least 280 people worldwide, with 175 in the UK alone.

How could the California cow have been infected with feed? Following the British outbreak, ranchers in the U.S. and most of the rest of the world stopped feeding cattle the remains of cattle, sheep and other mammals. But a farmer’s feed still could get contaminated by other means. The USDA still allows chickens to consume the remains of cattle. Chicken litter, containing urine and feces, is fed to cows. That could theoretically transmit the infection to cattle.

And if it is feed, what does that say about the potential of an outbreak in the rest of this cow’s heard? It appears the USDA and the California Department of Food and Agriculture are investigating. Dr. Jim Cullor, associate dean of the University of California, Davis, School of Veterinary Medicine and an expert on many animal illnesses, spoke to me from his office, which is close to the dairy farm that housed the sick cow. He would not identify the farm (nor will any government agency) but he did say dairy farms in the area usually have about 3,000 animals (about half of them milk producers). But some farms in the area have as many as 10,000 head, Cullor explains. Typically, the inspectors would visit the farm’s “hospital,” where sick animals are treated. They would also go over the hospital’s records as well as the farmer’s feed and records of past feed purchases.

“That farmer will feel like he’s had a visit from the IRS,” Cullor quipped.

But does such an inspection guarantee safety? Dr. Michael Hansen of the Consumers Union, along with many scientists, argues that, like Europe, the U.S. should test all animals that look sick or are over 6-years-old before they enter the food supply. The rationale behind testing healthy animals 6 years old or older is that BSE usually takes that long to develop.

"With thorough testing we would know the food supply is safe,” Hansen said. “We wouldn’t be guessing.”

We would also learn the true incidence and origin of spontaneous and atypical cases.

But the U.S. tests far fewer animals -- about 40,000 of the 35 million cattle slaughtered annually. The argument is about cost, an estimated $25 to $30 per animal. Widespread testing would add a few cents to the cost of a pound of beef. Britain, Europe, Japan and several other nations have decided it is worth it. The USDA says it is not and declares: “The surveillance program allows USDA to detect the disease if it exists at very low levels in the U.S. cattle population.”

Few scientists would argue that the one California cow which never was headed to the U.S. food supply represents a health hazard. But many maintain that the current surveillance is insufficient. Dr. Kurt Giles, an expert in neurogenerative diseases now at the University of California, San Francisco, was at Oxford during the British outbreak. He told me USDA’s assurances about safety today remind him of British statements during the 1980s.

“It is so reminiscent of that absolute certainty,” he said.

Robert Bazell is NBC's chief science and medical correspondent. Follow him on Facebook and on Twitter @RobertBazellNBC

http://vitals.msnbc.msn.com/_news/2012/05/02/11501754-are-usda-assurances-on-mad-cow-case-gross-oversimplification?lite

Friday, May 25, 2012

R-CALF USDA’s New BSE Rule Eliminates Important Protections Needed to Prevent BSE Spread

http://bseusa.blogspot.com/2012/05/r-calf-usdas-new-bse-rule-eliminates.html

Subject: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68

Comment from Terry Singeltary Document ID: APHIS-2008-0010-0008 Document Type: Public Submission This is comment on Proposed Rule: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products Docket ID: APHIS-2008-0010 RIN:0579-AC68

Topics: No Topics associated with this document View Document: More Document Subtype: Public Comment Status: Posted Received Date: March 22 2012, at 12:00 AM Eastern Daylight Time Date Posted: March 22 2012, at 12:00 AM Eastern Daylight Time Comment Start Date: March 16 2012, at 12:00 AM Eastern Daylight Time Comment Due Date: May 15 2012, at 11:59 PM Eastern Daylight Time Tracking Number: 80fdd617 First Name: Terry Middle Name: S. Last Name: Singeltary City: Bacliff Country: United States State or Province: TX Organization Name: CJD TSE PRION Submitter's Representative: CONSUMERS

Comment: comment submission Document ID APHIS-2008-0010-0001

Greetings USDA,

OIE et al, what a difference it makes with science, from one day to the next. i.e. that mad cow gold card the USA once held. up until that fateful day in December of 2003, the science of BSE was NO IMPORTS TO USA FROM BSE COUNTRY. what a difference a day makes$ now that the shoe is on the other foot, the USDA via the OIE, wants to change science again, just for trade $ I implore the OIE decision and policy makers, for the sake of the world, to refuse any status quo of the USA BSE risk assessment. if at al, the USA BSE GBR should be raise to BSE GBR IV, for the following reasons. North America is awash with many different TSE Prion strains, in many different species, and they are mutating and spreading. IF the OIE, and whatever policy makers, do anything but raise the risk factor for BSE in North America, they I would regard that to be highly suspicious. IN fact, it would be criminal in my opinion, because the OIE knows this, and to knowingly expose the rest of the world to this dangerous pathogen, would be ‘knowingly’ and ‘willfully’, just for the almighty dollar, once again. I warned the OIE about all this, including the risk factors for CWD, and the fact that the zoonosis potential was great, way back in 2002. THE OIE in collaboration with the USDA, made the legal trading of the atypical Nor-98 Scrapie a legal global commodity. yes, thanks to the OIE and the USDA et al, it’s now legal to trade the atypical Nor-98 Scrapie strain all around the globe. IF you let them, they will do the same thing with atypical BSE and CWD (both strains to date). This with science showing that indeed these TSE prion strains are transmissible. I strenuously urge the OIE et al to refuse any weakening to the USA trade protocols for the BSE TSE prion disease (all strains), and urge them to reclassify the USA with BSE GBR IV risk factor.

SEE REFERENCE SOURCES IN ATTACHMENTS

PLEASE SEE Terry S. Singeltary Sr. _Attachment_ WORD FILE ;

http://www.regulations.gov/#!documentDetail;D=APHIS-2008-0010-0008

http://www.regulations.gov/#!docketDetail;D=APHIS-2008-0010

***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

snip...

http://www.neuroprion.org/en/np-neuroprion.html

MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...

***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

http://wwwnc.cdc.gov/eid/article/18/1/pdfs/11-1092.pdf

***Infectivity in skeletal muscle of BASE-infected cattle

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf

***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.

http://www.neuroprion.org/en/np-neuroprion.html

The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.

In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.

http://www.veterinaryresearch.org/content/pdf/1297-9716-42-79.pdf

in the url that follows, I have posted

SRM breaches first, as late as 2011.

then

MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007, when they ceased posting them.

then,

MAD COW SURVEILLANCE BREACHES.

Friday, May 18, 2012

Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/05/update-from-aphis-regarding-detection.html

> > > Ackerman says downed cattle are 50 times more likely to have mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of mad cow disease in North America since 1993, at least 16 have involved downer cattle, he said. < < <

don’t forget the children...

PLEASE be aware, for 4 years, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens.

who will watch our children for CJD for the next 5+ decades ???

WAS your child exposed to mad cow disease via the NSLP ???

SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

http://downercattle.blogspot.com/2009/05/who-will-watch-children.html

http://downercattle.blogspot.com/

DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???

you can check and see here ;

http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf

http://transmissiblespongiformencephalopathy.blogspot.com/

http://nor-98.blogspot.com/

http://creutzfeldt-jakob-disease.blogspot.com/

TSS

SLIMED WITH BSE USA

re-Blogger tackles consumer questions about LFTB, BSE

Story by Amanda Radke Mitchell, S.D.

Saturday, May 26, 2012

http://www.thefencepost.com/article/20120526/NEWS/120529951/1032&ParentProfile=1001

SLIMED

EDITORIAL My beef with bloggers (pg 2)

http://www.meatingplace.com/Print/Archives/Details/4159

THE ISSUES SLIMED What the hell happened (pg 20)

http://www.meatingplace.com/Print/Archives/Details/4162

http://www.meatingplace.com/Print/Archives/Stories?publication=1&issue=201205

=====================

PINK SLIME LFTB MSM MRM BSE TSE PRION

Saturday, April 21, 2012

HISD seeks refund on burgers with 'pink slime'

http://downercattle.blogspot.com/2012/04/hisd-seeks-refund-on-burgers-with-pink.html

Wednesday, March 14, 2012

PINK SLIME, MRM’s, BSE AKA MAD COW DISEASE, AND THE USDA NSLP

http://madcowusda.blogspot.com/2012/03/pink-slime-mrms-bse-aka-mad-cow-disease.html

Sunday, August 28, 2011

Rick Perry, Texas, BSE aka mad cow disease, CJD, and 12 years of lies there from

http://sciencebushwhacked.blogspot.com/2011/08/rick-perry-texas-bse-aka-mad-cow.html

BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!

Friday, May 25, 2012

R-CALF USDA’s New BSE Rule Eliminates Important Protections Needed to Prevent BSE Spread

http://bseusa.blogspot.com/2012/05/r-calf-usdas-new-bse-rule-eliminates.html

Subject: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68

Comment from Terry Singeltary Document ID: APHIS-2008-0010-0008 Document Type: Public Submission This is comment on Proposed Rule: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products Docket ID: APHIS-2008-0010 RIN:0579-AC68

Topics: No Topics associated with this document View Document: More Document Subtype: Public Comment Status: Posted Received Date: March 22 2012, at 12:00 AM Eastern Daylight Time Date Posted: March 22 2012, at 12:00 AM Eastern Daylight Time Comment Start Date: March 16 2012, at 12:00 AM Eastern Daylight Time Comment Due Date: May 15 2012, at 11:59 PM Eastern Daylight Time Tracking Number: 80fdd617 First Name: Terry Middle Name: S. Last Name: Singeltary City: Bacliff Country: United States State or Province: TX Organization Name: CJD TSE PRION Submitter's Representative: CONSUMERS

Comment: comment submission Document ID APHIS-2008-0010-0001

Greetings USDA,

OIE et al, what a difference it makes with science, from one day to the next. i.e. that mad cow gold card the USA once held. up until that fateful day in December of 2003, the science of BSE was NO IMPORTS TO USA FROM BSE COUNTRY. what a difference a day makes$ now that the shoe is on the other foot, the USDA via the OIE, wants to change science again, just for trade $ I implore the OIE decision and policy makers, for the sake of the world, to refuse any status quo of the USA BSE risk assessment. if at al, the USA BSE GBR should be raise to BSE GBR IV, for the following reasons. North America is awash with many different TSE Prion strains, in many different species, and they are mutating and spreading. IF the OIE, and whatever policy makers, do anything but raise the risk factor for BSE in North America, they I would regard that to be highly suspicious. IN fact, it would be criminal in my opinion, because the OIE knows this, and to knowingly expose the rest of the world to this dangerous pathogen, would be ‘knowingly’ and ‘willfully’, just for the almighty dollar, once again. I warned the OIE about all this, including the risk factors for CWD, and the fact that the zoonosis potential was great, way back in 2002. THE OIE in collaboration with the USDA, made the legal trading of the atypical Nor-98 Scrapie a legal global commodity. yes, thanks to the OIE and the USDA et al, it’s now legal to trade the atypical Nor-98 Scrapie strain all around the globe. IF you let them, they will do the same thing with atypical BSE and CWD (both strains to date). This with science showing that indeed these TSE prion strains are transmissible. I strenuously urge the OIE et al to refuse any weakening to the USA trade protocols for the BSE TSE prion disease (all strains), and urge them to reclassify the USA with BSE GBR IV risk factor.

SEE REFERENCE SOURCES IN ATTACHMENTS

PLEASE SEE Terry S. Singeltary Sr. _Attachment_ WORD FILE ;

http://www.regulations.gov/#!documentDetail;D=APHIS-2008-0010-0008

http://www.regulations.gov/#!docketDetail;D=APHIS-2008-0010

***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

snip...

http://www.neuroprion.org/en/np-neuroprion.html

MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...

***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

http://wwwnc.cdc.gov/eid/article/18/1/pdfs/11-1092.pdf

***Infectivity in skeletal muscle of BASE-infected cattle

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf

***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.

http://www.neuroprion.org/en/np-neuroprion.html

The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.

In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.

http://www.veterinaryresearch.org/content/pdf/1297-9716-42-79.pdf

Friday, May 18, 2012

Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/05/update-from-aphis-regarding-detection.html

> > > Ackerman says downed cattle are 50 times more likely to have mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of mad cow disease in North America since 1993, at least 16 have involved downer cattle, he said. < < <

don’t forget the children...

PLEASE be aware, for 4 years, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens.

who will watch our children for CJD for the next 5+ decades ???

WAS your child exposed to mad cow disease via the NSLP ???

SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

http://downercattle.blogspot.com/2009/05/who-will-watch-children.html

http://downercattle.blogspot.com/

DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???

you can check and see here ;

http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf

http://transmissiblespongiformencephalopathy.blogspot.com/

http://nor-98.blogspot.com/

http://creutzfeldt-jakob-disease.blogspot.com/

TSS

R-CALF USDA’s New BSE Rule Eliminates Important Protections Needed to Prevent BSE Spread

R-CALF United Stockgrowers of America

“Fighting for the U.S. Cattle Producer”

For Immediate Release Contact: R-CALF USA CEO Bill Bullard

May 23, 2012 Phone: 406-252-2516; r-calfusa@r-calfusa.com

USDA’s New BSE Rule Eliminates Important Protections Needed to Prevent BSE Spread

Billings, Mont. – Contrary to meatpacking industry claims, the U.S. Department of Agriculture’s (USDA’s) proposed rule regarding bovine spongiform encephalopathy (BSE or mad cow disease) eliminates key protections contained in current regulations that are designed to prevent the introduction and spread of BSE into the United States from foreign countries. Current USDA regulations require that bone-in beef imported from BSE-affected Canada be derived only from cattle “that have been subject to a ruminant feed ban equivalent to the requirements established by the U.S. Food and Drug Administration. . .”

That requirement is in addition to the requirement that the beef also be derived from cattle that have had all specified risk materials (SRMs) removed at slaughter.

“Under USDA’s newly proposed BSE rule, bone-in beef from Canada will no longer be required to be derived only from cattle subject to a ruminant feed ban, meaning beef from older Canadian cattle born before the effective date of Canada’s feed ban could be freely imported into the United States,” said R-CALF USA CEO Bill Bullard.

“Not only that,” he added, “USDA intends to open our borders to countries that have had over a thousand cases of BSE, such as Ireland, France, and the United Kingdom; and to countries that have had hundreds of cases of BSE, such as Portugal, Spain, and Germany, and USDA would not require the beef from any of those countries to be derived only from cattle that have been subject to a ruminant feed ban.”

Bullard said many of the countries from where USDA wants to begin importing beef continue to detect new BSE cases and no one, including the USDA, can explain why those new cases persist even after those countries have purportedly adopted all recommended mitigation measures. “USDA’s proposed BSE rule is reckless. If it is adopted, the risk of introducing BSE into the United States from foreign countries will increase,” Bullard concluded.

# # #

R-CALF USA (Ranchers-Cattlemen Action Legal Fund, United Stockgrowers of America) is a national, nonprofit organization dedicated to ensuring the continued profitability and viability of the U.S. cattle industry. For more information, visit www.r-calfusa.com or, call 406-252-2516.

http://r-calfusa.com/news_releases/2012/120523BSE.pdf

Subject: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68

Comment from Terry Singeltary Document ID: APHIS-2008-0010-0008 Document Type: Public Submission This is comment on Proposed Rule: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products Docket ID: APHIS-2008-0010 RIN:0579-AC68

Topics: No Topics associated with this document View Document: More Document Subtype: Public Comment Status: Posted Received Date: March 22 2012, at 12:00 AM Eastern Daylight Time Date Posted: March 22 2012, at 12:00 AM Eastern Daylight Time Comment Start Date: March 16 2012, at 12:00 AM Eastern Daylight Time Comment Due Date: May 15 2012, at 11:59 PM Eastern Daylight Time Tracking Number: 80fdd617 First Name: Terry Middle Name: S. Last Name: Singeltary City: Bacliff Country: United States State or Province: TX Organization Name: CJD TSE PRION Submitter's Representative: CONSUMERS

Comment: comment submission Document ID APHIS-2008-0010-0001

Greetings USDA,

OIE et al, what a difference it makes with science, from one day to the next. i.e. that mad cow gold card the USA once held. up until that fateful day in December of 2003, the science of BSE was NO IMPORTS TO USA FROM BSE COUNTRY. what a difference a day makes$ now that the shoe is on the other foot, the USDA via the OIE, wants to change science again, just for trade $ I implore the OIE decision and policy makers, for the sake of the world, to refuse any status quo of the USA BSE risk assessment. if at al, the USA BSE GBR should be raise to BSE GBR IV, for the following reasons. North America is awash with many different TSE Prion strains, in many different species, and they are mutating and spreading. IF the OIE, and whatever policy makers, do anything but raise the risk factor for BSE in North America, they I would regard that to be highly suspicious. IN fact, it would be criminal in my opinion, because the OIE knows this, and to knowingly expose the rest of the world to this dangerous pathogen, would be ‘knowingly’ and ‘willfully’, just for the almighty dollar, once again. I warned the OIE about all this, including the risk factors for CWD, and the fact that the zoonosis potential was great, way back in 2002. THE OIE in collaboration with the USDA, made the legal trading of the atypical Nor-98 Scrapie a legal global commodity. yes, thanks to the OIE and the USDA et al, it’s now legal to trade the atypical Nor-98 Scrapie strain all around the globe. IF you let them, they will do the same thing with atypical BSE and CWD (both strains to date). This with science showing that indeed these TSE prion strains are transmissible. I strenuously urge the OIE et al to refuse any weakening to the USA trade protocols for the BSE TSE prion disease (all strains), and urge them to reclassify the USA with BSE GBR IV risk factor.

SEE REFERENCE SOURCES IN ATTACHMENTS

PLEASE SEE Terry S. Singeltary Sr. _Attachment_ WORD FILE ;

http://www.regulations.gov/#!documentDetail;D=APHIS-2008-0010-0008

http://www.regulations.gov/#!docketDetail;D=APHIS-2008-0010

***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

snip...

http://www.neuroprion.org/en/np-neuroprion.html

MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...

***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

http://wwwnc.cdc.gov/eid/article/18/1/pdfs/11-1092.pdf

***Infectivity in skeletal muscle of BASE-infected cattle

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf

***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.

http://www.neuroprion.org/en/np-neuroprion.html

The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.

In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.

http://www.veterinaryresearch.org/content/pdf/1297-9716-42-79.pdf

Friday, May 18, 2012

Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/05/update-from-aphis-regarding-detection.html

TSS

More than 50 dead cows found buried in manure piles, SSS mad cow policy alive and well USA

More than 50 dead cows found buried in manure piles at Merced County dairy 

Gustine dairy owner ordered to remove carcasses by March 30

JOSHUA EMERSON SMITH




jsmith@mercedsunstar.com

SEE PHOTO;

 

 

 

 

 

State water regulators found more than 50 decomposing cow carcasses at a Merced County dairy, and the operator could face fines and a referral to the state Attorney General's office.
The Central Valley Regional Water Quality Control Board issued a cleanup order this week to the Rego Dairy, located at 6255 Haley Road in Gustine. Owner Franklin Rego has until March 30 to dispose of the carcasses. If he can't meet that deadline, he could face fines.





State inspectors found the rotting cows partially buried in manure several weeks ago during a routine visit to the farm.





"The unhealthy and dangerous conditions at this small dairy are severe," said water board executive officer Pamela Creedon in a press release. "The vast majority of dairy operators in the Central Valley work hard to follow good management practices, and blatant disregard for the law impacts both surface and groundwater, posing dangers to public health and polluting the waters of the State of California."
Inspectors found a number of other water quality concerns, including eroded paths where wastewater had flowed off the property and into a nearby drainage ditch, excessive weeds and rodent holes, and multiple discarded veterinary medical supplies, including syringes. Inspectors also found evidence of cropland being used as a dumping area for manure wastewater from the lagoon, according to the press release.





The owner of the dairy, Franklin Rego, said cows were buried there three or four years ago after the animals got sick and died because of a bad batch of feed. When the cows died, Rego had some of them taken away by a rendering company. But concerns about mad cow disease years ago left the job undone, he said.





"Once they decomposed I was dumbfounded," he said. "I didn't know what to do. We were clueless of what do with them. We only found out yesterday of what do with them on the (water board's) website."
Once cows and other animals decompose past a certain point, rendering plants can no longer take them, said Robert Busby, regional water board spokesman. In this case, the carcasses must be taken to a specific landfill that's state certified to accept the remains.





This was the first time since 2007 the Rego dairy had been inspected, said Busby, adding this kind of violation "happens, but the board is not aware of it happening too often. There are 1,600 dairies in California. We inspect which ones we can on a regular basis."
Rego said he and his family won a lawsuit against a Land-O-Lakes subsidiary that sold them the bad cow feed. But he said the money received from the lawsuit barely covered his losses from losing the cows and from other expenses.





The family plans to put the farm up for auction in about thirty days, he said. "It's just the dairy business. The banks don't work with anybody. It's been a rough five years. We're getting out of the business."




The water board is investigating the dairy's effects on water quality, and the California Department of Fish and Game is reviewing the effects on local aquatic life, Busby said. The state is requiring Rego to conduct his own study of water quality effects.
Reporter Josh Smith can be reached at (209) 385-2486 or jsmith@mercedsunstar.com.

Read more here: http://www.sacbee.com/2012/03/16/4343482/more-than-50-dead-cows-found-buried.html#storylink=cpy

Read more here: http://www.sacbee.com/2012/03/16/4343482/more-than-50-dead-cows-found-buried.html#storylink=cpy

http://www.sacbee.com/2012/03/16/4343482/more-than-50-dead-cows-found-buried.html

no mad cows there in that pile, RIGHT!

I am sure they were all tested for BSE typical or atypical ???

 

 

 

this is what we call THE USDA SSS MAD COW POLICY, shoot, shovel, and shut the hell up$

 

 

 

course, California ought to be use to it by now after the QFC debacle.

 

 

 

BSE MAD COW SSS POLICY ALIVE AND WELL IN THE USA 2012

 

 

 

 

2012

 

 

 

Subject: Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy

 

 

UPDATE NORTH AMERICA MAD COW DISEASE

Monday, March 19, 2012

 

 

Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy

 

 

 

PLoS One. 2012; 7(2): e31449.

http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/infectivity-in-skeletal-muscle-of.html

Sunday, March 11, 2012

APHIS Proposes New Bovine Spongiform Encephalopathy Import Regulations in Line with International Animal Health Standards Proposal Aims to Ensure Health of the U.S. Beef Herd, Assist in Negotiations

http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/aphis-proposes-new-bovine-spongiform.html

Sunday, November 13, 2011

California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/california-bse-mad-cow-beef-recall-qfc.html

TSS

BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle

Published online ahead of print on 13 October 2010 as doi:10.1099/vir.0.025387-0 J Gen Virol (2010), DOI 10.1099/vir.0.025387-0 © 2010 Society for General Microbiology

BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle

Anne Balkema-Buschmann1, Martin Eiden, Christine Hoffmann, Martin Kaatz, Ute Ziegler, Markus Keller and Martin H. Groschup

Friedrich-Loeffler-Institut

1 E-mail: anne.buschmann@fli.bund.de

The pathogenesis of bovine spongiform encephalopathy (BSE) infections in cattle has been studied in recent years by using highly sensitive transgenic mouse bioassays. It has been shown that in this species, the BSE agent amplifies almost exclusively in the central and peripheral nervous system. Even in animals that were killed in the clinical end stage of the disease, the lymphoreticular system was shown to be free of the infectious agent. No other animal species investigated to date exhibit such a restricted BSE infectivity distribution pattern. However, there is growing evidence for a centrifugal spread from the central nervous system (CNS) into the periphery at the late stages of the disease. In this study, we challenged transgenic mice overexpressing the bovine prion protein with homogenates prepared from a wide variety of tissue samples collected from BSE infected cattle. As prion infections involve the conversion of the cellular prion protein into its abnormally folded isoform (PrPSc), we applied various detection methods, such as the purification of scrapie-associated fibrils (SAF), immunohistochemistry (IHC), and the protein misfolding cyclic amplification (PMCA) technique. Despite negative results using these highly sensitive biochemical methods, we were for the first time able to detect BSE infectivity in the tongue and in the nasal mucosa of terminally diseased BSE field cases as well as experimentally challenged cattle by transgenic mouse bioassay. This shows that BSE infectivity can be present in peripheral tissues of terminally diseased cattle, including tissues used for human consumption.

Received 13 July 2010; accepted 11 October 2010.

http://vir.sgmjournals.org/cgi/content/abstract/vir.0.025387-0v1



"This shows that BSE infectivity can be present in peripheral tissues of terminally diseased cattle, including tissues used for human consumption."



Wednesday, April 30, 2008

Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/consumption-of-beef-tongue-human-bse.html


Sunday, October 18, 2009

Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009

http://madcowfeed.blogspot.com/2009/10/wisconsin-firm-recalls-beef-tongues.html


Thursday, October 15, 2009

Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009

http://madcowfeed.blogspot.com/2009/10/nebraska-firm-recalls-beef-tongues-that.html


Thursday, June 26, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

http://madcowfeed.blogspot.com/2008/06/texas-firm-recalls-cattle-heads-that.html


Tuesday, July 1, 2008

Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs

http://madcowfeed.blogspot.com/2008/07/missouri-firm-recalls-cattle-heads-that.html


Friday, August 8, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed

http://madcowfeed.blogspot.com/2008/08/texas-firm-recalls-cattle-heads-that.html


Saturday, April 5, 2008

SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/srm-mad-cow-recall-406-thousand-pounds.html


Sent: Monday, April 05, 2010 10:45 PM

Subject: North Dakota Firm Recalls Whole Beef Head Products That Contain Prohibited Materials

North Dakota Firm Recalls Whole Beef Head Products That Contain Prohibited Materials

Recall Release CLASS II RECALL FSIS-RC-023-2010 HEALTH RISK: LOW

Congressional and Public Affairs (202) 720-9113 Catherine Cochran

WASHINGTON, April 5, 2010 - North American Bison Co-Op, a New Rockford, N.D., establishment is recalling approximately 25,000 pounds of whole beef heads containing tongues that may not have had the tonsils completely removed, which is not compliant with regulations that require the removal of tonsils from cattle of all ages, the U.S. Department of Agriculture's Food Safety and Inspection Service (FSIS) announced today.

Tonsils are considered a specified risk material (SRM) and must be removed from cattle of all ages in accordance with FSIS regulations. SRMs are tissues that are known to contain the infective agent in cattle infected with Bovine Spongiform Encephalopathy (BSE), as well as materials that are closely associated with these potentially infective tissues. Therefore, FSIS prohibits SRMs from use as human food to minimize potential human exposure to the BSE agent.

The product subject to recall includes: Various weight cases of "Beef Heads KEEP FROZEN." Each case bears the establishment number "EST. 18859" inside the USDA mark of inspection and a case code number "16999." "North Dakota Natural Beef" is printed in the bottom left-hand corner of each label.

The recalled products were produced between June 25, 2009, and February 19, 2010. These products were shipped to distribution centers in Md., Mich., and Minn. for further sale.

The problem was discovered during FSIS inspection activities at the establishment. FSIS routinely conducts recall effectiveness checks to verify recalling firms notify their customers of the recall and that steps are taken to make certain that the product is no longer available to consumers.

Media with questions about the recall should contact Philip Wicke, Vice President of Operations, at (701) 356-7723. Consumers with questions about the recall should contact Jeremy Anderson, Director of Customer Service, at (952) 545-2495.

Consumers with food safety questions can "Ask Karen," the FSIS virtual representative available 24 hours a day at AskKaren.gov. The toll-free USDA Meat and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through Friday. Recorded food safety messages are available 24 hours a day. #

http://www.fsis.usda.gov/News_&_Events/Recall_023_2010_Release/index.asp


Thursday, June 26, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

http://madcowfeed.blogspot.com/2008/06/texas-firm-recalls-cattle-heads-that.html


Tuesday, July 1, 2008

Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs

http://madcowfeed.blogspot.com/2008/07/missouri-firm-recalls-cattle-heads-that.html


Friday, August 8, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed

http://madcowfeed.blogspot.com/2008/08/texas-firm-recalls-cattle-heads-that.html


Saturday, April 5, 2008

SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/srm-mad-cow-recall-406-thousand-pounds.html


http://madcowfeed.blogspot.com/


http://madcowspontaneousnot.blogspot.com/


Thursday, October 07, 2010

Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice

http://bse-atypical.blogspot.com/2010/10/experimental-transmission-of-h-type.html



THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$


10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007


Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm


Tuesday, March 2, 2010

Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA

http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html


Monday, March 1, 2010

ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010

http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html


Tuesday, September 14, 2010

Feed Safety and BSE/Ruminant Feed Ban Support Project (U18)

http://madcowfeed.blogspot.com/2010/09/feed-safety-and-bseruminant-feed-ban.html


Friday, October 8, 2010

Scientific reasons for a feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food

http://madcowfeed.blogspot.com/2010/10/scientific-reasons-for-feed-ban-of-meat.html


Date: June 21, 2007 at 2:49 pm PST

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half

http://www.usda.gov/oig/webdocs/sarc070619.pdf


Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program ­ Phase II and Food Safety and Inspection Service

Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III

Report No. 50601-10-KC January 2006

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain

http://www.usda.gov/oig/webdocs/50601-10-KC.pdf


"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.

http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r



Discussion:

The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.


http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf



P03.137

Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC

Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan

Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.

P03.138

Clustering of PrPres in Central Brain Regions of BSE-infected Macaques (M. Fascicularis)

Motzkus, D1; Montag, J1; Hunsmann, G1; Schulz-Schaeffer, W2 1German Primate Center, Dept. Virology and Immunology, Germany; 2University of Göttingen, Dept. Neuropathology, Germany

According to biochemical and epidemiological findings bovine spongiform encephalopathy (BSE) was transmitted to humans causing variant Creutzfeldt Jakob disease (vCJD). Previous studies have shown intracerebral (i.c.) transmission of BSE affected brain from cattle can cause TSEs in cynomolgus macaques (M. fascicularis). The lesion profile resembles that of vCJD. Recently, oral infection of M. fascicularis with macaque-adapted BSE material was reported. In cooperation with five European partners a quantitative study for the transmission of the BSE agent to M. fascicularis was initiated to assess the risk of vCJD infection in humans through contaminated food products (EU study QLK1-CT-2002-01096). Titration was performed orally and intracerebrally to determine the minimal infectious dose for cynomolgus monkeys. Here we report the outcome of the intracerebral infection with 50 mg BSE brain homogenate in six non-human primates. All animals showed clinical symptoms of TSE after an average of 1100 days. Using immunohistological and biochemical methods prion protein (PrP) deposits were confirmed in the brains of all animals. Using Western blot analysis the glycosylation pattern was compared to the inoculum and to the pattern of different CJD subtypes. Simian PrPres was detected with the monoclonal anti prion antibody 11C6, which revealed a higher sensitivity in comparison to 12F10 and 3F4. We found that the PrP glycopattern in BSE-infected cynomolgus macaques resembles human CJD type 2. We further analysed the distribution of PrPres by microdissection of seven different brain regions of all infected macaques. High concentrations of PrPres were detected in central brain regions, as gyrus cinguli, nucleus caudatus, vermis cerebelli and basis pontis. In contrast, in the peripheral regions gyrus frontalis, gyrus parietalis and gyrus occipitalis PrPres was hardly detectable.

Thus, the incubation period related to the life expectancy, the PrPres glycosylation pattern as well as the distribution in certain brain regions resemble those in vCJD patients. The relative abundance of PrPres in macaques will be compared to that of orally infected animals.

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.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf


PRION 2009 CONGRESS BOOK OF ABSTRACTS

O.4.3

Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission

Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany

Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).

Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.

Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.

Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.

Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.

O.4.4

PrPSc distribution pattern in cattle experimentally challenged with H-type and L-type atypical BSE

Anne Buschmann1, Ute Ziegler1, Leila McIntyre2, Markus Keller1, Ron Rogers3, Bob Hills3, Martin H. Groschup1 1Friedrich-Loeffler-Institut, INEID, Germany; 2Faculty of Veterinary Medicine, University of Calgary, Canada; 3Health Canada, Ottawa, Canada

Background: After the detection of two novel BSE forms designated H-type and L-type BSE, the question of the pathogenesis and the agent distribution in cattle affected with these forms was fully open. From initial studies, it was already known that the PrPSc distribution in L-type BSE affected cattle differed from that known for classical BSE (C-type) where the obex region always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved. No information was available on the distribution pattern in H-type BSE.

Objectives: To analyse the PrPSc and infectivity distribution in cattle experimentally challenged with H-type and L-type BSE.

Methods: We analysed CNS and peripheral tissue samples collected from cattle that were intracranially challenged with Htype (five animals) and L-type (six animals) using a commercial BSE rapid test (IDEXX HerdChek), immunohistochemistry (IHC) and a highly sensitive Western blot protocol including a phosphotungstic acid precipitation of PrPSc (PTA-WB). Samples collected during the preclinical and the clinical stages of the disease were examined. For the detection of BSE infectivity, selected samples were also inoculated into highly sensitive Tgbov XV mice overexpressing bovine prion protein (PrPC).

Results: Analysis of a collection of fifty samples from the peripheral nervous, lymphoreticular, digestive, reproductive, respiratory and musculo-skeletal systems by PTA-WB, IDEXXHerdChek BSE EIA and IHC revealed a general restriction of the PrPSc accumulation to the central nervous system.

Discussion: Our results on the PrPSc distribution in peripheral tissues of cattle affected with H-type and L-type BSE are generally in accordance with what has been known for C-type BSE. Bioassays are ongoing in highly sensitive transgenic mice in order to reveal infectivity.

O.11.3

Infectivity in skeletal muscle of BASE-infected cattle

Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta” Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy

Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.

Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.

Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.

Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.

P.5.3

Differences in the expression levels of selected genes in the brain tissue of cattle naturally infected with classical and atypical BSE.

Magdalena Larska1, Miroslaw P. Polak1, Jan F. Zmudzinski1, Juan M. Torres2 1National Veterinary Institute, Poland; 2CISA/INIA

Background: Recently cases of BSE in older cattle named BSE type L and type H were distinguished on the basis of atypical glycoprofiles of PrPres. The nature of those strains is still not fully understood but it is suspected that the atypical BSE cases are sporadic. Hitherto most BSE cases were studied in respect to the features of PrPSc. Here we propose gene expression profiling as a method to characterize and distinguish BSE strains.

Objectives: The aim of the study was to compare the activities of some factors which are known to play a role in TSE’s pathogenesis in order to distinguish the differences/similarities between all BSE types.

Methods: 10 % homogenate of brain stem tissue collected from obex region of medulla oblongata from 20 naturally infected BSE cows (8 assigned as classical BSE, other 8 and 4 infected with atypical BSE L type and H type respectively) was used in the study. As negative control animals we’ve used 8 animals in the age between 2.5 and 13 years. The genes were relatively quantified using SYBR Green real time RT-PCR. Raw data of Ct values was transformed into normalized relative quantities using Qbase Plus®. Results and

Discussion: In most of the tested genes significant differences in the expression levels between the brain stem of healthy cattle and animals infected with different BSE types were observed. In c-type BSE in comparison to healthy and atypical BSE the overexpression of the gene of bcl-2, caspase 3, 14-3-3 and tylosine kinase Fyn was significant.

Simultaneously in atypical BSEs type-L and type-H the levels of prion protein, Bax and LPR gene was elevated in comparison to c-BSE. Additionally L-BSE was characterized by the overexpression of STI1 and SOD genes compared to the other of BSE types. The downregulation of the gene encoding NCAM1 was observed in all BSE types in comparison to healthy cows. Different gene expression profiles of bovine brains infected with classical and atypical BSE indicates possible different pathogenesis or source of the disease.

O.10.1

Transmission of uncommon forms of bovine prions to transgenic mice expressing human PrP: questions and progress

Vincent Béringue, Hubert Laude INRA, UR 892, Virologie Immunologie Moléculaires, France

The active, large-scale testing of livestock nervous tissues for the presence of protease-resistant prion protein (PrPres) has led to the recognition of 2 uncommon PrPres molecular signatures, termed H-type and L-type BSE. Their experimental transmission to various transgenic and inbred mouse lines unambiguously demonstrated the infectious nature of such cases and the existence of distinct prion strains in cattle. Like the classical BSE agent, H- and L-type (or BASE) prions can propagate in heterologous species. In addition L-type prions acquire molecular and neuropathologic phenotypic traits undistinguishable from BSE or BSE-related agents upon transmission to transgenic mice expressing ovine PrP (VRQ allele) or wild-type mice. An understanding of the transmission properties of these newly recognized prions when confronted with human PrP sequence was therefore needed. Toward this end, we inoculated mice expressing human PrP Met129 with several field isolates. Unlike classical BSE agent, L-type prions appeared to propagate in these mice with no obvious transmission barrier. In contrast, we repeatedly failed to infect them with Htype prions. Ongoing investigations aim to extend the knowledge on these uncommon strains: are these agents able to colonize lymphoid tissue, a potential key factor for successful transmission by peripheral route; is there any relationship between these assumedly sporadic forms of TSE in cattle and some sporadic forms of human CJD are among the issues that need to be addressed for a careful assessment of the risk for cattle-to-human transmission of H- and L-type prions.


P.4.23

Transmission of atypical BSE in humanized mouse models

Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA

Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.

Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.

Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.

Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice.

BSE-H is also transmissible in our humanized Tg mice.

The possibility of more than two atypical BSE strains will be discussed.

Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf


Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf



WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.

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://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf


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

http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf



LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.

This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$

ALABAMA MAD COW g-h-BSEalabama

In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156


http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF


Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html


2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html


Wednesday, July 28, 2010

re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010

http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html


Discussion:

The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf


REPORT OF THE WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY 1989

snip...

4.2.9 ...Also, if it resulted from a localised chance transmission of the scrapie strain from sheep to cattle giving rise to a mutant, a different pattern of disease would have been expected: its range would have increased with time. Thus the evidence from Britain is against the disease being due to a new strain of the agent, but we note that in the United States from 1984 to 1988 outbreaks of scrapie in sheep flocks are reported to have Increased markedly, now being nearly 3 times as high as during any previous period (18).


http://collections.europarchive.org/tna/20080102132706/http://www.bseinquiry.gov.uk/files/ib/ibd1/tab02.pdf


http://collections.europarchive.org/tna/20080102193106/http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf


CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER

" Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle."

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas. She left 6 Kids and a Husband. The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.-

Physician Discharge Summary, Parkland Hospital, Dallas Texas

Admit Date: 12/29/2009

Discharge Date: 1/20/2010

Attending Provider: Greenberg, Benjamin Morris;

General Neurology Team: General Neurology Team

Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence. She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers. The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically.

Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.

http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8


Terry S. Singeltary Sr. has added the following comment:

"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed .

The key word here is diverse. What does diverse mean?

If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"

SEE FULL TEXT ;

http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101


.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.

32 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606-12

33 YB88/10.00/1.1

http://web.archive.org/web/20040823105233/www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf



Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)

(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)

SEE where sporadic cjd in the USA went from 59 cases in 1997, to 216 cases in 2009. a steady increase since 1997. ...TSS


http://www.cjdsurveillance.com/pdf/case-table.pdf


see full text ;


http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html



TSS