Tuesday, April 24, 2012

MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA

Release No. 0132.12

 

Contact:

 

Office of Communication 202-720-4623

 


Statement by USDA Chief Veterinary Officer John Clifford Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States

 


Assures Consumers That Existing Safeguards Protected Food Supply; Reiterates Safety of Consuming Beef Products

 


WASHINGTON, April 24, 2012 – USDA Chief Veterinary Officer John Clifford today released the following statement on the detection of BSE in the United States:

 


"As part of our targeted surveillance system, the U.S. Department of Agriculture's (USDA) Animal and Plant Health Inspection Service (APHIS) has confirmed the nation's fourth case of bovine spongiform encephalopathy (BSE) in a dairy cow from central California. The carcass of the animal is being held under State authority at a rendering facility in California and will be destroyed. It was never presented for slaughter for human consumption, so at no time presented a risk to the food supply or human health. Additionally, milk does not transmit BSE.

 


"The United States has had longstanding interlocking safeguards to protect human and animal health against BSE. For public health, these measures include the USDA ban on specified risk materials, or SRMs, from the food supply. SRMs are parts of the animal that are most likely to contain the BSE agent if it is present in an animal. USDA also bans all nonambulatory (sometimes called "downer") cattle from entering the human food chain. For animal health, the Food and Drug Administration (FDA) ban on ruminant material in cattle feed prevents the spread of the disease in the cattle herd.

 


"Evidence shows that our systems and safeguards to prevent BSE are working, as are similar actions taken by countries around the world. In 2011, there were only 29 worldwide cases of BSE, a dramatic decline and 99% reduction since the peak in 1992 of 37,311 cases. This is directly attributable to the impact and effectiveness of feed bans as a primary control measure for the disease.

 


"Samples from the animal in question were tested at USDA's National Veterinary Services Laboratories in Ames, Iowa. Confirmatory results using immunohistochemistry and western blot tests confirmed the animal was positive for atypical BSE, a very rare form of the disease not generally associated with an animal consuming infected feed.

 

"We are sharing our laboratory results with international animal health reference laboratories in Canada and England, which have official World Animal Health (OIE) reference labs. These labs have extensive experience diagnosing atypical BSE and will review our confirmation of this form of the disease. In addition, we will be conducting a comprehensive epidemiological investigation in conjunction with California animal and public health officials and the FDA.

 


"BSE is a progressive neurological disease among cattle that is always fatal. It belongs to a family of diseases known as transmissible spongiform encephalopathies. Affected animals may display nervousness or aggression, abnormal posture, difficulty in coordination and rising, decreased milk production, or loss of body weight despite continued appetite.

 

"This detection in no way affects the United States' BSE status as determined by the OIE. The United States has in place all of the elements of a system that OIE has determined ensures that beef and beef products are safe for human consumption: a mammalian feed ban, removal of specified risk materials, and vigorous surveillance. Consequently, this detection should not affect U.S. trade.

 

"USDA remains confident in the health of the national herd and the safety of beef and dairy products. As the epidemiological investigation progresses, USDA will continue to communicate findings in a timely and transparent manner."

 


#

 

USDA is an equal opportunity provider and employer. To file a complaint of discrimination, write: USDA, Office of the Assistant Secretary for Civil Rights, Office of Adjudication, 1400 Independence Ave., SW, Washington, DC 20250-9410 or call (866) 632-9992 (Toll-free Customer Service), (800) 877-8339 (Local or Federal relay), (866) 377-8642 (Relay voice users).

 

 


http://www.usda.gov/wps/portal/usda/usdahome?contentid=2012/04/0132.xml&contentidonly=true





 

 

BSE found in central California, USDA confirms

Greg Henderson, Editor, Associate Publisher, Drovers CattleNetwork | Updated: April 24, 2012


America’s fourth case of bovine spongiform encephalopathy (BSE) was confirmed today in a press briefing by the USDA. John Clifford, USDA’s chief veterinarian, said a dairy cow expressing an "atypical" case of BSE was found at a rendering facility in central California and the carcass is being held under State authority and will be destroyed.

Clifford said the animal was never presented for slaughter for human consumption and was never a risk to enter the food supply for human consumption. Additionally, it was noted, milk does not transmit BSE. This is the first case of BSE found in the United States since December 2003.

Cattle futures markets locked limit down shortly before trading ended Tuesday as rumors of the BSE case circulated through the trading floor.

Clifford emphasized the safeguards in place to protect America’s food supply from BSE. "The United States has had longstanding interlocking safeguards to protect human and animal health against BSE. For public health, these measures include the USDA ban on specified risk materials, or SRMs, from the food supply. SRMs are parts of the animal that are most likely to contain the BSE agent if it is present in an animal. USDA also bans all nonambulatory (sometimes called "downer") cattle from entering the human food chain. For animal health, the Food and Drug Administration (FDA) ban on ruminant material in cattle feed prevents the spread of the disease in the cattle herd.

Clifford said the U.S. will share laboratory results with international animal health reference laboratories in Canada and England, which have official World Animal Health (OIE) reference labs. “These labs have extensive experience diagnosing atypical BSE and will review our confirmation of this form of the disease. In addition, we will be conducting a comprehensive epidemiological investigation in conjunction with California animal and public health officials and the FDA.”

Clifford also emphasized this new BSE case “in no way affects the United States' BSE status as determined by the OIE. The United States has in place all of the elements of a system that OIE has determined ensures that beef and beef products are safe for human consumption: a mammalian feed ban, removal of specified risk materials, and vigorous surveillance. Consequently, this detection should not affect U.S. trade.





http://www.cattlenetwork.com/BSE-found-in-central-California-148737145.html



Mad Cow Disease Found In California: What Are The Risks To Humans?



Posted: 04/24/2012 5:35 pm


The United States Department of Agriculture has just confirmed the country's fourth case of mad cow disease, according to news reports.
The case was a dairy cow in central California, Reuters reported.
However, HuffPost Food reported that the cow had not entered the food chain so humans are safe in terms of consuming dairy products or beef.
According to the USDA statement:
It was never presented for slaughter for human consumption, so at no time presented a risk to the food supply or human health. Additionally, milk does not transmit BSE.
While the prospect of mad cow disease in America is scary, Cornell expert Martin Wiedmann said that the discovery of the cow is actually a testament to how good the testing for mad cow is in the U.S.
"The natural reaction is that it's a problem [they found this cow], but really they did a lot of testing and we were able to prevent this animal [from entering the food system] through testing," Wiedmann told HuffPost. Wiedmann is a professor of food science and a doctor of veterinary medicine, and is also the director of the Cornell Milk Quality Improvement Program.
Mad cow disease is also known as bovine spongiform encephalopathy, or BSE. It is a neurological disease that occurs when a prion protein damages the brains of cattle, according to the Centers for Disease Control and Prevention.

The CDC reported that there have been 22 cases of mad cow disease in North America up until February 2011, with three cases in the U.S. and 19 cases in Canada.
Mad cow disease is potentially dangerous for humans because it is linked with a human form of the disease called variant Creutzfeldt-Jakob disease (vCJD); evidence is strong that humans may develop the disease by eating meat from cows that had mad cow disease, according to the World Health Organization. There have also been four cases linked with blood transfusion, though the symptoms didn't manifest until years after the transfusion, according to the WHO.
There is a "relatively good link" between mad cow disease and variant Creutzfeldt-Jakob disease, Wiedmann said, though it's not 100 percent guaranteed that if a person eats the meat he or she will develop vCJD. And especially with this newly discovered single case of mad cow disease in the U.S., "the risk is excessively low, close to nil."
Variant Creutzfeldt-Jakob disease causes a degeneration of the brain, and a person may first notice signs of it by experiencing depression, anxiety and painful senses. As the disease progresses, it causes symptoms like problems with walking and causing involuntary movements, according to the WHO, and when a person is about to die from the disease, it causes muteness and immobility.
Variant Creutzfeldt-Jakob disease is not the same disease as classic CJD; classic Creutzfeldt-Jakob disease, which is also a prion disease, is not at all linked to mad cow disease, the CDC reported.
Classic CJD often occurs just on its own, with about one case occurring for every million people each year in the U.S., according to the CDC. The risk of this form of the disease increases as people get older. (For more on classic CJD, click here.)
For example, the CDC reported that the median death age for variant CJD is 28, while it's 68 for people with classic CJD.

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

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


SEE Terry S. Singeltary Sr. Attachment WORD FILE ;
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



Wednesday, April 4, 2012

 


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





PLEASE NOTE ***



Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.




snip...




The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...




http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf


Atypical BSE in Cattle




BSE has been linked to the human disease variant Creutzfeldt Jakob Disease (vCJD). The known exposure pathways for humans contracting vCJD are through the consumption of beef and beef products contaminated by the BSE agent and through blood transfusions. However, recent scientific evidence suggests that the BSE agent may play a role in the development of other forms of human prion diseases as well. These studies suggest that classical type of BSE may cause type 2 sporadic CJD and that H-type atypical BSE is connected with a familial form of CJD.

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

snip...see full text ;

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary

Bacliff, TX, USA


Background:


An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods:

12 years independent research of available data

Results:

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.


page 114 ;






*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS




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


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)


BANNED MAD COW FEED IN COMMERCE IN ALABAMA

Date: September 6, 2006 at 7:58 am PST PRODUCT

a) EVSRC Custom dairy feed, Recall # V-130-6;

b) Performance Chick Starter, Recall # V-131-6;

c) Performance Quail Grower, Recall # V-132-6;

d) Performance Pheasant Finisher, Recall # V-133-6.

CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.

REASON

Dairy and poultry feeds were possibly contaminated with ruminant based protein.

VOLUME OF PRODUCT IN COMMERCE 477.72 tons

DISTRIBUTION AL

______________________________

http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html


PRODUCT Bulk custom dairy pre-mixes,

Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE 350 tons

DISTRIBUTION AL and MS

______________________________

PRODUCT

a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;

b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;

c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;

d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;

e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;

f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;

g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6

CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.

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

VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags

DISTRIBUTION AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###

http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html

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 PRODUCT

a) CO-OP 32% Sinking Catfish, Recall # V-100-6;

b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;

c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;

d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;

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

f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;

g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;

h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;

i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;

j) CO-OP LAYING CRUMBLES, Recall # V-109-6;

k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;

l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;

m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE

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

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

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

VOLUME OF PRODUCT IN COMMERCE 125 tons

DISTRIBUTION AL and FL

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

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


MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II

______________________________

PRODUCT

a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;

b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;

c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;

d) Feather Meal, Recall # V-082-6 CODE

a) Bulk

b) None

c) Bulk

d) Bulk

RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.

REASON

Possible contamination of animal feeds with ruminent derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons

DISTRIBUTION Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html



please see full text ;




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



Tuesday, September 14, 2010


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

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


P.9.21

Molecular characterization of BSE in Canada

Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.

Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

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




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.


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



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.

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



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 Bradleyâs 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



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.
L-BSE, TME, AND SPORADIC CJD aka mad cow disease in North America
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.




snip...

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
snip...
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Sophie Freire,1 Jürgen Richt,2 Justin Greenlee,3 Juan-Maria Torres,4 Paul Brown,1 Bob Hills5 and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Kansas State University; Manhattan, KS USA; 3USDA; Ames, IA USA; 4INIA; Madrid, Spain; 5Health Canada; Ottawa, ON Canada†Presenting author; Email: emmanuel.comoy@cea.fr

The epidemiology of Transmissible mink encephalopathy (TME) indicates an alimentary origin. Several inter-species transmission experiments have not succeeded in establishing with certainty any natural reservoir of this prion strain, although both ovine and bovine sources have been suspected. Cattle exposed to TME develop a spongiform encephalopathy that is distinct from classical Bovine Spongiform Encephalopathy (c-BSE).
Inoculation of c-BSE to cynomolgus macaque provided early evidence of a possible risk to humans, and remains an important model to define the risk of both primary (oral transmission from cattle to primate) and secondary (intravenous intra-species transmission) exposures. We have also evaluated the transmissibility of other cattle prion strains to macaques, including L- and H- atypical forms of BSE, namely BSE-L and BSE-H, and cattle-adapted TME.
BSE-L induced a neurological disease distinct from c-BSE. Peripheral exposures demonstrate the transmissibility of BSE-L by oral, intravenous, and intra-cerebral routes, with incubation periods similar to c-BSE. Cattle-adapted TME also induced a rapid disease in cynomolgus macaque. The clinical features, lesion profile, and biochemical signature of the induced disease was similar to the features observed in animals exposed to BSE-L, suggesting a link between the two prion strains. Secondary transmissions to a common host (transgenic mouse overexpressing bovine PrP) of cattle-TME and BSE-L before or after passage in primates induced diseases with similar incubation periods: like the c-BSE strain, these cattle strains maintained their distinctive features regardless of the donor species and passages.
If the link between TME and BSE-L is confirmed, our results would suggest that BSE-L in North America may have existed for decades, and highlight a possible preferential transmission of animal prion strains to primates after passage in cattle.


=====================end...tss====================
link url not available, please see PRION 2011 ;








Volume 13, Number 12–December 2007
Research


Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model


Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* andRichard A. Bessen†*Agence Française de Sécurité Sanitaire des Aliments–Lyon, Lyon, France; and†Montana State University, Bozeman, Montana, USA
Abstract


Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profiles, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME.The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE.
snip...


Conclusion


These studies provide experimental evidence that the Stetsonville TME agent is distinct from typical BSE but has phenotypic similarities to L-type BSE in TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely candidate for a bovine source of TME infection than typical BSE. In the scenario that a ruminant TSE is the source for TME infection in mink, this would be a second example of transmission of a TSE from ruminants to non-ruminants under natural conditions or farming practices in addition to transmission of typical BSE to humans, domestic cats, and exotic zoo animals(37). The potential importance of this finding is relevant to L-type BSE, which based on experimental transmission into humanized PrP transgenic mice and macaques, suggests that L-type BSE is more pathogenic for humans than typical BSE (24,38).




PLEASE NOTE *




Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...


The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...


PLoS One. 2012; 7(2): e31449.
Published online 2012 February 21. doi: 10.1371/journal.pone.0031449
PMCID: PMC3283643

Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy
The present data offer novel information on the tropism of the BASE agent and highlight relevant public health issues. While the transmission barrier for classical BSE is high in most species, BASE prions are readily transmissible to a variety of mammals including non-human primates [11]–[13], [35]. Accordingly, the possibility of spreading of BASE prions through skeletal muscle to other species should be taken into account and evaluated in risk analysis studies.






Saturday, November 6, 2010



TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU



Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation









Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>



Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)











Saturday, June 25, 2011



Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque



"BSE-L in North America may have existed for decades"









Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.


snip...


The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...









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.








P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS


Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA


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). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.


III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)








I ask Professor Kong ;



Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment


''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''


Professor Kong reply ;



.....snip



''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''


Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA


END...TSS




Thursday, December 04, 2008 2:37 PM


"we have found that H-BSE can infect humans."


personal communication with Professor Kong. ...TSS


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.











Tuesday, July 14, 2009 U.S.


Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book


Date: February 14, 2000 at 8:56 am PST


WHERE did we go wrong $$$








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.










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)







her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).



This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009








P.9.21 Molecular characterization of BSE in Canada



Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada



Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.



Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.



Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis. Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.



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.








Saturday, July 23, 2011


CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE






Saturday, November 6, 2010


TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU


Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation






Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>


Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)






October 2009 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.









Sunday, February 5, 2012


February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE







IMPORT EXPORT BEEF, LIVE, PRODUCTS, CANADA AND USA









> > > 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










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 ;







Saturday, March 5, 2011


MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA






Sunday, February 12, 2012


National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas








pink slime and a ship of fools, with Governor Rick Perry at the helm.



john gummer of England, force fed his daughter mad cow beef. a few years later, a young friend of theirs (23) died from mad cow disease. NOW, Governor Rick Perry, shows he is as big a fool as John Gummer.












see more on this sad sad saga here ;




Wednesday, March 14, 2012



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








Sunday, August 28, 2011



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








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





MOM DOD 12-14-97 Heidenhain Variant Creutzfeldt Jakob Disease ‘confirmed’ TEXAS, YEARS OF RICK PERRY BEING TEXAS AGRICULTURE COMMISSIONER, THEN ON TO GOVERNOR OF TEXAS, WHERE TWO MAD COWS WERE COVERED UP under Perry’s watch, ONE SUCCESSFULLY, AND ONE THAT TOOK AN ACT OF CONGRESS and 7 MONTHS TO FINALLY CONFIRM via WEYBRIDGE ENGLAND.






Wednesday, April 4, 2012



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





Wednesday, April 25, 2012






USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 – 2012


http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/usa-mad-cow-disease-and-cjd-there-from.html






 http://www.commondreams.org/view/2012/04/26-1





TSS
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Monday, April 23, 2012

BOVINE SPONGIFORM ENCEPHALOPATHY BSE CJD TSE PRION DISEASE UPDATE CANADA 2012

BOVINE SPONGIFORM ENCEPHALOPATHY BSE CJD TSE PRION DISEASE UPDATE CANADA 2012



Sample Status and Testing Results



Updated monthly. Last updated 2012-03-31



No validated live animal test for BSE currently exists. Accordingly, testing for BSE can only be done on the brains of dead animals. Brain samples are screened using rapid tests that accurately and quickly detect a BSE positive sample nearly 100% of the time. Rapid tests can, in rare cases, react when a sample is not infected with BSE. These are known as "inconclusive" results. All samples that yield inconclusive results using a rapid test are sent to the CFIA laboratory in Lethbridge, Alberta for confirmatory testing.



2012




Month Samples Collected Samples Pending Negative Positive
March 2593 0 2593 0
February 2696 0 2696 0
January 2429 0 2429 0



2011





Month Samples Collected Samples Pending Negative Positive
December 1656 0 1656 0
November 2354 0 2354 0
October 2019 0 2019 0
September 1984 0 1984 0
August 2319 0 2319 0
July 1984 0 1984 0
June 2904 0 2904 0
May 3300 0 3300 0
April 4069 0 4069 0
March 4199 0 4199 0
February 3390 0 3389 1
January 3280 0 3280 0
Year to date 33458 0 33457 1







Previously published reports are available in archives maintained by Library and Archives Canada.



Reports for results from 2008 to 2010










Samples collected





"Samples collected" indicates the number of samples submitted or being submitted to provincial or federal laboratories. Each sample represents one animal. Monthly values represent only the number of samples obtained in that month. "Year to date" values represent cumulative samples.



In January 2004, the Government of Canada announced that it would enhance its BSE surveillance testing to at least 8,000 cattle during the first year and to 30,000 per year in subsequent years to calculate the prevalence of BSE in Canadian adult cattle. The level and design of this enhanced program continues to be in full accordance with the guidelines recommended by the OIE.



BSE surveillance samples come from a variety of sources, including the farm, federal, provincial and territorial abattoirs, rendering and deadstock operations, veterinary practitioners, and university and provincial veterinary diagnostic laboratories.



Samples Pending



Pending samples are those for which final results are unavailable. This may be because they have yet to be tested, or testing is ongoing. Monthly values represent only the number of samples pending in that month. "Year to date" values represent cumulative pending samples.



Negative



Negative samples have been determined negative based on screening results or confirmatory testing. Monthly values represent only the number of samples testing negative in that month. "Year to date" values represent cumulative negative samples.



Positive



Positive samples are those that have been confirmed as positive by immunohistochemistry (IHC), or in the case of poor quality samples and IHC negative suspect tests, the SAP immunoblot, both internationally recognized confirmatory tests for BSE. Monthly values represent only the number of samples testing positive in that month. "Year to date" values represent cumulative positive samples.





http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/bse/enhanced-surveillance/eng/1323992647051/1323992718670





BSE surveillance












About this time next month, nine years will have passed since the May 2003 detection of BSE in Canada. Although the numbers continue to decline in terms of detected cases, both in Canada and globally, it will be a few more years before Canada can fully demonstrate the full effectiveness of the control measures in place to eradicate the disease from the national herd.

Dr. Brian Evans, Chief Veterinary officer for Canada, said the BSE surveillance program is the most critical means for Canada to demonstrate just how effective the control measures in place, particularly the feed ban, have been. He is reminding producers that the surveillance program helps Canada to meet the commitments it made to its trading partners as part of the recovery of markets post-BSE.

"While the economic prospects for the sector are looking reasonably good at this point in time, we did make collective commitments on behalf of the industry and government to trading partners in the negotiations that have got us the level of market recovery that we currently have," said Dr. Evans. "We recognize the past nine years have not been easy for producers but if we are to stay the course for a period longer we can achieve what we collectively set out to do."

The stewardship and strong support of producers to date has been an important element in sustaining consumer trust in Canada and noted repeatedly by regulatory officials in other countries in their decision making to restore market access, he said.

During the month of March, a total of 2,593 surveillance samples were tested for BSE, compared with 4,199 samples a year earlier. During the three months between January 1 and March 31, 2012, a total of 7,718 surveillance samples were tested, compared with 10,869 samples last year. About 30,000 samples are required per year, in accordance with World Organization for Animal Health (OIE) guidelines. The surveillance targets have been adjusted to take into account the reduced size of the national herd and changes in the overall age of the herd.

Dr. Evans said Canada is in its fifth year of the enhanced feed ban, and is just at the mean average incubation period. The real proof will come in the next two to three years, he said, and that's what the CFIA is focussing on.

"If we can sustain this effort through to 2015 we should be in a very good position at the international level to adjust our surveillance activities accordingly on the recognition that we've done our due diligence and that the measures we've demonstrated scientifically are effective measures, and then we can then make further programming adjustments as part of the BSE roadmap forward," he said.

Last year, there were a total of 29 BSE cases globally in countries that test for it, and a 50 per cent decrease in cases every year over the last four or five years.

While producers may see that as a signal to finally put BSE behind them, Dr. Evans said continued vigilance at home is still required, given the fact that we have restored markets for beef products and live animals.






Friday, March 4, 2011


Alberta dairy cow found with mad cow disease







Wednesday, August 11, 2010


REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA







Thursday, August 19, 2010


REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA







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







BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS







BSE Cases Identified in Canadian-born Cattle


As of March 2011, 19 BSE cases in Canadian-born cattle have been identified, 18 in Canada and 1 in the U.S. Of these 19 cases, 13 were known to have been born after the implementation of the 1997 Canadian feed ban ; 12 of these 13 were born after March 1, 1999. (See Figure above: BSE Cases in North America, by Year and Country of Death, 1993-03/2011). This latter date is particularly relevant to the U.S. because since a USDA rule went into effect on November 19, 2007, Canadian cattle born on or after March 1, 1999 have been legally imported into this country for any use. One of the 19 Canadian-born BSE cases was reported in an animal that was most likely born before or possibly very shortly after implementation of the 1997 feed ban. Based on the known or most likely year of birth, an average of 1.4 cases of BSE occurred among the group of animals born each year in Canada from 1991 through 2004. The highest reported number of cases by birth year in a single year, 3 BSE cases, occurred in 2000, 2001 and 2002. The most recently reported case extends the period of BSE transmission in Canada through at least the latter half of 2004.


Strains of BSE


There is increasing evidence that there are different strains of BSE: the typical BSE strain responsible for the outbreak in the United Kingdom and two atypical strains (H and L strains).


Typical BSE strain -- The BSE strain responsible for most of the BSE cases in Canada is the same classic or typical strain linked to the outbreak in the United Kingdom. It is known to be preventable through elimination of BSE contaminated feed and has been causally linked to vCJD in humans. This typical strain has not yet been identified in any U.S.-born cattle.


Atypical BSE strain -- In July 2007, the UK Spongiform Encephalopathy Advisory Committee (SEAC) suggested that atypical BSE may be a distinct strain of prion disease. Unlike typical BSE, cases of atypical BSE, according to SEAC, may have risen spontaneously (although transmission through feed or the environment cannot be ruled out). Recently reported French surveillance data support this theory that unlike typical BSE, atypical BSE appears to represent sporadic disease


Both of the U.S.-born BSE cases and two of the 19 Canadian-born BSE cases were 10 years of age or older. Of these older North American cases, 3 were linked to an atypical BSE strain known as the H-type. The strain type for the fourth older North American case, a 13 year-old BSE-infected Canadian cow, has been identified as the L-type.








Molecular, Biochemical and Genetic Characteristics of BSE in Canada



Sandor Dudas1, Jianmin Yang1,2,3, Catherine Graham1, Markus Czub4, Tim A. McAllister2, Michael B. Coulthart5, Stefanie Czub1* 1 Canadian and OIE Reference Laboratories for BSE, Canadian Food Inspection Agency Lethbridge Laboratory, Lethbridge, Alberta, Canada, 2 Agriculture and Agri-Food Canada Research Centre, Lethbridge, Alberta, Canada, 3 College of Veterinary Medicine, China Agricultural University, Beijing, China, 4 Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada, 5 Canadian Creutzfeldt-Jakob Disease Surveillance System, Public Health Agency of Canada, Winnipeg, Manitoba, Canada


Abstract


The epidemiology and possibly the etiology of bovine spongiform encephalopathy (BSE) have recently been recognized to be heterogeneous. In particular, three types [classical (C) and two atypical (H, L)] have been identified, largely on the basis of characteristics of the proteinase K (PK)-resistant core of the misfolded prion protein associated with the disease (PrPres). The present study was conducted to characterize the 17 Canadian BSE cases which occurred prior to November 2009 based on the molecular and biochemical properties of their PrPres, including immunoreactivity, molecular weight, glycoform profile and relative PK sensitivity. Two cases exhibited molecular weight and glycoform profiles similar to those of previously reported atypical cases, one corresponding to H-type BSE (case 6) and the other to L-type BSE (case 11). All other cases were classified as C-type. PK digestion under mild and stringent conditions revealed a reduced protease resistance in both of these cases compared to the C-type cases. With Western immunoblotting, N-terminal-specific antibodies bound to PrPres from case 6 but not to that from case 11 or C-type cases. C-terminal-specific antibodies revealed a shift in the glycoform profile and detected a fourth protein fragment in case 6, indicative of two PrPres subpopulations in H-type BSE. No mutations suggesting a genetic etiology were found in any of the 17 animals by sequencing the full PrP-coding sequence in exon 3 of the PRNP gene. Thus, each of the three known BSE types have been confirmed in Canadian cattle and show molecular characteristics highly similar to those of classical and atypical BSE cases described from Europe, Japan and the USA. The occurrence of atypical cases of BSE in countries such as Canada with low BSE prevalence and transmission risk argues for the occurrence of sporadic forms of BSE worldwide. Citation: Dudas S, Yang J, Graham C, Czub M, McAllister TA, et al. (2010) Molecular, Biochemical and Genetic Characteristics of BSE in Canada. PLoS ONE 5(5): e10638. doi:10.1371/journal.pone.0010638 Editor: Carles Lalueza-Fox, Institute of Evolutionary Biology (CSIC-UPF), Spain Received February 9, 2010; Accepted April 21, 2010; Published May 14, 2010 Copyright: 2010 Dudas et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: Funding for this project was provided by the Canadian Food Inspection Agency. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. * E-mail: stefanie.czub@inspection.gc.ca




SNIP...




The origin of atypical BSE is unknown, but sporadic, infectious and genetic mechanisms have all been suggested. Several groups have argued that these cases may represent the existence of a sporadic prion disease in bovines, perhaps similar in etiology to sporadic Creutzfeldt-Jakob disease in humans [2], [6], [12], [19]. Experimental infection of cattle with an isolate of naturally occurring British sheep scrapie resulted in differences in the PrPres electrophoretic profiles compared to classical C-type BSE which led to the suggestion that atypical BSE may be a result of transmission of a prion disease from a different natural host into cattle [14]. In addition, an American H-type BSE case with a mutation (E211K) in the PRNP gene has been reported [19]. This represents the first case of BSE with a potentially pathogenic mutation within the bovine PRNP gene, and experiments are underway to determine the potential importance of this mutation in the development of prion disease in cattle [19]. We did not observe such mutations in the Canadian BSE cases analyzed as of November 2009, and negative results of a large population survey in US cattle strongly suggest that the E211K allele is not common in North American cattle [31]. However, the intrinsically recurrent nature of genetic mutation, as shown particularly for the homologous E200K mutation known to cause genetic Creutzfeldt-Jakob disease in humans [32], means that the possibility that a small subpopulation of cattle that carry such mutations exist cannot be eliminated.


Our results indicate that the range of molecular characteristics of misfolded PrP in Canadian BSE cases is very similar to that observed in other countries and suggests a number of criteria to use when typing BSE cases (Table 6). It is also interesting that the Canadian atypical BSE cases match so well with cases from other countries in terms of their epidemiological profiles, including detection in older animals and no definitive cause of disease. Ongoing inoculation studies with Canadian BSE types in cattle and transgenic mice will provide clarification on how similar these isolates are after transmission using defined and controlled experimental inoculations. These studies should help to answer some of the many outstanding questions about atypical BSE and aid in policy development to reduce the risk of atypical BSE transmission to animals and humans.








PLEASE NOTE, spontaneous TSE prion disease has never, ever, been proven in natural field cases of BSE TSE prion disease. ...TSS




bbbut, what about FEED AND ATYPICAL BSE ???





Thursday, June 23, 2011



Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits








Saturday, June 25, 2011



Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque



"BSE-L in North America may have existed for decades"









Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.


snip...


The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...









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.








P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS


Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA


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). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.


III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)








I ask Professor Kong ;



Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment


''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''


Professor Kong reply ;



.....snip



''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''


Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA


END...TSS




Thursday, December 04, 2008 2:37 PM


"we have found that H-BSE can infect humans."


personal communication with Professor Kong. ...TSS


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.











Tuesday, July 14, 2009 U.S.


Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book


Date: February 14, 2000 at 8:56 am PST


WHERE did we go wrong $$$








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.










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)







her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).



This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009








P.9.21 Molecular characterization of BSE in Canada



Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada



Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.



Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.



Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis. Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.



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.








Saturday, July 23, 2011


CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE






Saturday, November 6, 2010


TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU


Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation






Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>


Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)






October 2009 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.









Sunday, February 5, 2012


February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE







IMPORT EXPORT BEEF, LIVE, PRODUCTS, CANADA AND USA









Tuesday, January 17, 2012



Canadian Inspectors criticize plan to cut inspections at meat plants Meat inspectors' union warns of cuts to government's food-safety program








Tuesday, November 02, 2010



BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992







Monday, October 10, 2011

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

snip...

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.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1



http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf




see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html





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

snip...

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






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.







Thursday, February 23, 2012


Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012








Wednesday, April 4, 2012


20120402 - Breach of quarantine/Violation de la mise en quarantaine of an ongoing Scrapie investigation







Monday, November 30, 2009


USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE






Wednesday, February 16, 2011



IN CONFIDENCE



SCRAPIE TRANSMISSION TO CHIMPANZEES



IN CONFIDENCE


http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html






Sunday, April 18, 2010




SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010



http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html





Monday, April 25, 2011



Experimental Oral Transmission of Atypical Scrapie to Sheep



Volume 17, Number 5-May 2011



http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html








WHICH CAME FIRST, THE CART OR THE HORSE ???





Minnesota



CAPTIVE CWD CONFIRMED 2002



FREE RANGING CWD CONFIRMED 2011


http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm





Colorado



Captive CWD discovered 1967



Free ranging CWD discovered 1981



PLEASE STUDY THIS MAP !



SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. ...TSS


http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm






*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***



Saturday, February 18, 2012



Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease



CDC Volume 18, Number 3—March 2012



SNIP...



Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).



SNIP...



Reasons for Caution There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD. Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation. Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified, ...



see full text ;




*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***





Saturday, February 18, 2012



Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease



CDC Volume 18, Number 3—March 2012









see much more here ;



http://chronic-wasting-disease.blogspot.com/2012/02/occurrence-transmission-and-zoonotic.html





Sunday, January 22, 2012



Chronic Wasting Disease CWD cervids interspecies transmission


 
http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html






Thursday, January 26, 2012



The Risk of Prion Zoonoses



Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167


http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html





Thursday, January 26, 2012


Facilitated Cross-Species Transmission of Prions in Extraneural Tissue



Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659


http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html




Monday, April 23, 2012




CREUTZFELDT JAKOB DISEASE CJD HUMAN TSE CANADA UPDATE 2012










Sunday, February 12, 2012 





National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas




http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html






Monday, April 16, 2012




Continuing Enhanced National Surveillance for Prion Diseases in the United States


http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/continuing-enhanced-national.html
 
 
 
 
 
TSS
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