Saturday, February 11, 2012

PrPSc Detection and Infectivity in Semen from Scrapie-Infected Sheep

PrPSc Detection and Infectivity in Semen from Scrapie-Infected Sheep


Richard Rubenstein1,5,
Marie S Bulgin2,
Binggong Chang1,
Sharon Sorensen-Melson2,
Robert B Petersen3 and
Giuseppe LaFauci4

+ Author Affiliations





1 SUNY Downstate Medical Center, Brooklyn, NY, USA;
2 University of Idaho, Caldwell, ID, USA;
3 Case Western Reserve University, Cleveland, OH, USA;
4 NYS Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA

↵5 E-mail: richard.rubenstein@downstate.edu

Received 13 October 2011.
Accepted 3 February 2012.


Abstract



A scrapie-positive ewe was found in a flock that had been scrapie free for 13 years, but housed adjacent to scrapie-positive animals, separated by a wire fence. Live animal testing of the entire flock of 24 animals revealed 7 more subclinical scrapie-positive ewes. We hypothesized that they may have contracted the disease from scrapie-positive rams used for breeding four months prior, possibly through the semen. The genotypes of the ewe flock were highly scrapie-susceptible and the rams were infected with the "Caine" Scrapie Strain having a short incubation time of 4.3-14.6 mo. in sheep with 136/171 VQ/VQ and AQ/VQ genotypes. PrPSc accumulates in a variety of tissues in addition to the central nervous system. Although transmission of prion diseases, or transmissible spongiform encephalopathies, has been achieved via peripheral organ or tissue homogenates as well as by blood transfusion, neither infectivity nor PrPSc have been found in semen from scrapie-infected animals. Using serial protein misfolding cyclic amplification followed by a surround optical fiber immunoassay, we demonstrate that semen from rams infected with a short incubation time scrapie strain contains prion disease-associated seeding activity that generated PrPSc in sPMCA. Injection of the ovinized transgenic mouse line TgSShpPrP with semen from scrapie-infected sheep resulted in PrPSc seeding activity in clinical and, probably as a result of the low titer, nonclinical mouse brain. These results suggest that the transmissible agent, or at least the seeding activity, for sheep scrapie is present in semen. This may be a strain specific phenomenon.







http://vir.sgmjournals.org/content/early/2012/02/02/vir.0.038802-0.abstract







price of poker goes up for those Boone-Crocket type straw bred bucks...tss





Thursday, February 09, 2012

50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html







Saturday, February 11, 2012


Prion cross-species transmission efficacy is tissue dependent



http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html




2012





PIG IN A POKE !







Sunday, January 29, 2012


Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety
Dr. Detwiler


Dr. Detwiler published Prion Disease Risks in the 21st Century 2011 PDA
European Virus-TSE Safety Forum\Presentations TSE\ Page 33 and 34 of 44 ;




http://www.pda.org/





http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/prion-disease-risks-in-21st-century.html









Wednesday, February 1, 2012




CJD and PLASMA / URINE PRODUCTS EMA Position Statements Alberto Ganan
Jimenez, European Medicines Agency PDA TSE Safety Forum, 30 June 2011




http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/cjd-and-plasma-urine-products-ema.html









Dr. Michael Coulthart, et al, Public Health Agency of Canada




- although not occurring to date, he estimates that report of just one
probable case of human CWD could trigger a public health crisis in North
America.


- epidemiological studies so far indicate the probability is very slight,
however, prion agents and their transmission properties are highly mutable
and adaptable and the possibility can not be ruled out.


- suggests those involved in human prion disease surveillance should
consider the possibility of human CWD and develop a readiness to deal with
it.



snip...



http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html







Saturday, February 04, 2012

Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html









Envt.18: Mother to Offspring Transmission of Chronic Wasting Disease






Candace K. Mathiason,† Amy Nalls, Kelly Anderson, Jeanette Hayes-Klug, Jenny G. Powers, Nicholas J. Haley and Edward A. Hoover






Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu






We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by four months post infection. Ten fawns were born to these CWD-infected doe— four of the fawns were viable, five were non-viable and one was a first trimester fetus harvested from a CWD-infected doe euthanized at end-stage disease. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn by IHC as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yielded positive results on another fawn at ten days of age. In addition, sPMCA assays have demonstrated amplifiable prions in fetal placental or spleen tissue of three non-viable fawns and mammary tissue of the dams.






Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.











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







PPo3-18: A Possible Case of Maternal Transmission of the BSE Agent within Captive Cheetah Affected with Feline Spongiform Encephalopathy





Anna Bencsik, Sabine Debeer, Thierry Petit and Thierry Baron





Afssa; Unité ATNC; Lyon, France; Zoo de la Palmyre; Les Mathes, France





Key words: BSE, FSE, vertical transmission





Introduction. Feline spongiform encephalopathy (FSE) is considered to be related to bovine spongiform encephalopathy (BSE). It has been reported in domestic cats as well as in captive wild cats including cheetahs, first in the United Kingdom (UK) and then in other European countries. In France, several cases were described in cheetahs either imported from UK or born in France. Here we report details of two other FSE cases in captive cheetah. These cases are of particular interest since the 2nd case of FSE in a cheetah born in France, appears most likely due to maternal transmission.1





Results. Complete PrPd study showed the close likeness between the two cheetah cases. The TgOvPrP4 mouse brains infected with cattle BSE and cheetah FSE revealed similar vacuolar lesion profiles, PrPd brain mapping with occurrence of typical florid plaques.





Materials and Methods. Using immunohistochemistry (IHC), pathological form of PrP(PrPd) was analyzed in the brains and peripheral organs of these two cheetahs. Transmission studies to the TgOvPrP4 mouse line were also performed, for comparison with the transmission of cattle BSE. Lesion profiles of the infected transgenic mice were analyzed as well as type and brain distribution of PrPd.





Conclusion. Collectively, these data indicate that both FSE cases harbor the same strain of agent as the cattle BSE agent. Because this is most probably a case of maternal transmission of the disease, this new observation may have some impact on our knowledge of vertical transmission of BSE agent-linked TSEs such as in human variant Creutzfeldt Jakob disease.





References





1. Bencsik et al. PLoS One 2009; 4:6929.









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









PPo3-40: Mother to Offspring Transmission of Chronic Wasting Disease







Candace K. Mathiason, Amy V. Nalls, Kelly Anderson, Jeanette Hayes-Klug, Nicholas Haley and Edward A. Hoover





Colorado State University, Department of Microbiology, Immunology and Pathology, Fort Collins, CO USA





Key words: Chronic wasting disease, vertical transmission, muntjac deer





We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by 4 months post infection. Six fawns were born to these CWD-infected doe. Six fawns were born to 6 CWD-infected doe; 4 of the fawns were non-viable. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age. In addition, sPMCA assays have also demonstrated amplifiable prions in maternal placental (caruncule) and mammary tissue of the dam.





Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.







PRION 2011





landesbioscience.com









International Prion Congress: From agent to diseaseSeptember 8–11, 2010Salzburg, Austria









Friday, December 23, 2011


Detection of PrPres in Genetically Susceptible Fetuses from Sheep with Natural Scrapie




http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/detection-of-prpres-in-genetically.html









Studies into the maternal transmission of BSE

The early epidemiological studies did not find evidence of cattle to cattle transmission. Additional research was undertaken to investigate further whether BSE could be transmitted from cow to calf (otherwise known as vertical transmission).



Maternal transmission

A long-term cohort study was initiated in 1989 to examine maternally-associated risk factors for BSE. Interim findings were presented to SEAC in July 1996 and SEAC advised that maternal transmission would not sustain the BSE epidemic.



Since 2002, the probability of maternal transmission has been estimated to be approximately 1% in the last six months of the maternal incubation period (3). In 2003, SEAC were advised of the potential future change from culling all offspring born after July 1996, to a cull of offspring born within two years of the clinical onset of disease in the dam. SEAC advised that they saw no scientific grounds for maintaining the policy for culling offspring in the UK in place at that time.



Research has shown that embryos from BSE-infected cows inseminated with semen from BSE-infected bulls are unlikely to carry BSE infectivity even if they have been collected at the end-stage of the disease, when the risk of maternal transmission is believed to be highest (4). This finding contributed to the lifting of the EU ban on the export of embryos from the UK in 2002.



Action taken

Data from the epidemiological studies has been used by Defra to implement BSE and disease control and eradication strategies. As a result, the number of BSE cases in the UK - has declined dramatically.



References

1. Wilesmith JW, Wells GA, Cranwell MP & Ryan JB (1988) Vet. Rec. 123: 638-644.



2. Wilesmith JW, Ryan JB & Hueston WD (1992) Res. Vet. Sci. 52(3): 325-331.



3. Donnelly CA, Ferguson NM, Ghani AC & Anderson RM (2002) Proceedings of the Royal Society of London, Series B 269: 2179-2190. Full text available.



4. Wrathall AE et al. (2002) Vet. Rec. 150(12): 365-378.



Links to other information

Table of all currently active and recently completed projects

Veterinary Risk Assessment on BSE Cohort Controls (May 2007, PDF 98 KB)





http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/science-research/cattle/epidem-modelling.htm











Wednesday, December 30, 2009





Is there evidence of vertical transmission of variant CJD ?





J Neurol Neurosurg Psychiatry doi:10.1136/jnnp.2009.172148







http://creutzfeldt-jakob-disease.blogspot.com/2009/12/is-there-evidence-of-vertical.html










Friday, February 10, 2012



Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous Tonsil Archive



http://creutzfeldt-jakob-disease.blogspot.com/2012/02/creutzfeldt-jakob-disease-cjd-biannual.html








24 Jul 00 Trade Statistics: UK to US




Compiled by Terry S.Singeltary Sr of Bacliff, Texas




[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep.





This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human
medicines. What has become of these?


Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.







Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]




10 January 1990 COMMERCIAL IN CONFIDENCE

NOT FOR PUBLICATION

COMMITTEE ON SAFETY OF MEDICINES
WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY

SURGICAL CATGUT SUTURES


2.1 At the first meeting of the Working Party on Bovine
Spongiform Encephalopathy on 6 September 1989, detailed
consideration was given to XXXXX Surgical Catgut. This
arose from the Company's response to the Letter to Licence
Holders, indicating that the bovine small intestine source
material was derived from UK cattle, unlike 8 other
licenced catgut sutures. In contrast XXXXX Surgical
Catgut was stated to hold over 90% share of the market for
catgut sutures, and to constitute approximately 83% of all
sutures used in U.K.


IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY;


3006.10.0000: STERILE SURGICAL CATGUT, SIMILAR STERILE SUTURE MATERIALS
AND STERILETISSUE ADHESIVES FOR SURGICAL WOUND CLOSURE; AND SIMILAR
STERILE MATERIAL
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 ---> <--- 1998 YTD --->
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 10,801 3,116 143,058 40,068

Belgium . . . . . . . . . --- --- 107 14
France . . . . . . . . . 81 49 2,727 1,132
Switzerland . . . . . . . --- --- 1,357 1,693
United Kingdom . . . . . 1,188 242 35,001 5,564

U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
Subheading 300210: ANTISERA AND OTHER BLOOD FRACTIONS, AND MODIFIED
IMMUNOLOGICAL PRODUCTS

3002.10.0010: HUMAN BLOOD PLASMA
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 25,740 1,827 270,357 20,476
Belgium . . . . . . . . . 14 8 145 60
France . . . . . . . . . --- --- 134 60
Netherlands . . . . . . . --- --- 11 5
Switzerland . . . . . . . 10,462 597 86,101 5,894
United Kingdom . . . . . --- --- 335 62

3002.10.0020: NORMAL HUMAN BLOOD SERA, WHETHER OR NOT FREEZE-DRIED
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 1,039 817 19,056 22,678
Austria . . . . . . . . . --- --- 9,194 18,707
Belgium . . . . . . . . . --- --- 22 15
Netherlands . . . . . . . 353 2 6,733 41
Switzerland . . . . . . . 374 218 1,084 440
United Kingdom . . . . . --- --- 1 4

3002.10.0030: HUMAN IMMUNE BLOOD SERA
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars)
(Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 1,926 461 14,484 3,563
...
United Kingdom . . . . . 2 8 464 192

3002.10.0040: FETAL BOVINE SERUM (FBS)
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 2,727 233 131,486 8,502
...
Belgium . . . . . . . . . --- --- 17 32
United Kingdom . . . . . 329 82 743 756


3002.10.0090: OTHER BLOOD FRACTIONS NOT ELSEWHERE SPECIFIED OR INCLUDED
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars)
(Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 88,467 27,343 944,412 309,947
...
United Kingdom . . . . . 1,887 2,300 26,823 23,585

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


http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-December/
Imports/30/300290.html

U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date

Subheading 300290: HUMAN BLOOD; ANIMAL BLOOD PREPARED FOR THERAPEUTIC,
ETC. USES; TOXINS, CULTURES OF MICRO-ORGANISMS (EXCLUDING YEASTS) AND
SIMILAR PRODUCTS NESOI

<--- Dec 1998 --- <--- 1998 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 36,178 643 250,982 11,604
...
United Kingdom . . . . . 584 39 11,292 588


http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-Month/Imports/
05/051199.html

U.S. Imports for Consumption: March 1999 and 1999 Year-to-Date

Subheading 051199: ANIMAL PRODUCTS, NESOI; DEAD HORSES AND OTHER EQUINE
ANIMALS, BOVINE ANIMALS, SHEEP, GOATS AND POULTRY, UNFIT FOR HUMAN
CONSUMPTION, NESOI

0511.99.2000: PARINGS AND SIMILAR WASTE OF RAW HIDES OR SKINS; GLUE
STOCK, NOT ELSEWHERE SPECIFIED OR INCLUDED
U.S. Imports for Consumption: March 1999 and 1999 Year-to-Date
(Customs Value, in Thousands of Dollars)
(Units of Quantity: Kilograms)


0511.99.4024: DAIRY CATTLE EMBRYOS
U.S. Imports for Consumption: March 1999 and 1999 Year-to-Date
(Customs Value, in Thousands of Dollars)
(Units of Quantity: Number)

<--- Mar 1999 --- <--- 1999 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . --- --- 53 16
Canada . . . . . . . . . --- --- 9 3
France . . . . . . . . . --- --- 44 13

0511.99.4050: ANIMAL PRODUCTS NOT ELSEWHERE SPECIFIED OR INCLUDED;
DEAD ANIMALS OF CHAPTER 1, UNFIT FOR HUMAN CONSUMPTION
U.S. Imports for Consumption: March 1999 and 1999 Year-to-Date
(Customs Value, in Thousands of Dollars)
(Units of Quantity: Kilograms)

<--- Mar 1999 --- <--- 1999 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 718,476 2,313 2,206,867 4,739
Belgium . . . . . . . . . --- --- 13 18
France . . . . . . . . . 1,088 14 1,489 20
United Kingdom . . . . . 11 3 38 9

http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-December/
Imports/30/300220.html


U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date

Subheading 300220: VACCINES FOR HUMAN MEDICINE

3002.20.0000: VACCINES FOR HUMAN MEDICINE
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars)
(Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 25,702 26,150 550,258 378,735
Belgium . . . . . . . . . 14,311 12,029 248,041 199,036
France . . . . . . . . . 3,902 4,859 87,879 92,845
Switzerland . . . . . . . 716 353 9,303 4,271
United Kingdom . . . . . 4,075 1,172 162,960 47,148

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


http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-December/
Imports/30/300230.html

U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date

Subheading 300230: VACCINES FOR VETRINARY MEDICINE

List of (6-digit) Subheadings in this (2-digit) Chapter
Next (6-Digit) Subheading ... Descending ... Ascending

Latest Monthly Data

Switch from U.S. Imports to U.S. Exports

About These Trade Data Tables

3002.30.0000: VACCINES FOR VETRINARY MEDICINE
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars)
(Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD ---
Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 6,528 237 87,149 2,715
Canada . . . . . . . . . --- --- 2,637 305
Federal Rep. of Germany --- --- 104 5
Netherlands . . . . . . . 138 64 472 192
New Zealand . . . . . . . 6,390 173 83,882 1,895
United Kingdom . . . . . --- --- 54 318

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


http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-December/
Imports/30/300610.html

U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date

Subheading 300610: STERILE SURGICAL CATGUT, SIMILAR STERILE SUTURE
MATERIALS AND STERILE TISSUE ADHESIVES FOR SURGICAL WOUND CLOSURE;
STERILE HAEMOSTATICS, ETC.

3006.10.0000: STERILE SURGICAL CATGUT, SIMILAR STERILE SUTURE MATERIALS
AND STERILETISSUE ADHESIVES FOR SURGICAL WOUND CLOSURE; AND SIMILAR
STERILE MATERIAL
U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date
(Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

Belgium . . . . . . . . . --- --- 107 14
Federal Rep. of Germany 1,795 356 16,878 3,741
France . . . . . . . . . 81 49 2,727 1,132

Subject: Re: exports from the U.K. of it's MBM to U.S.???
Date: Tue, 8 Feb 2000 14:03:16 +0000
From: S.J.Pearsall@esg.maff.gsi.gov.uk
To: flounder@wt.net (Receipt Notification Requested) (Non Receipt
Notification Requested)

Terry
meat and bonemeal is not specifically classified for overseas trade
purposes. The nearest equivalent is listed as "flours and meals of meat
or offals (including tankage), unfit for human consumption; greaves". UK
exports of this to the US are listed below:

Country Tonnes
1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990

Subject: Re: Imports of MBM or Ruminants to the U.S. from foreign
Countries with the potential risk of BSE...
Date: Tue, 28 Dec 1999 17:19:15 -0500
From: Linda Detwiler
To: flounder@wt.net (Receipt Notification Requested)

I have attached the file ibov96.txt containing all of the bovine imports for 1996.

Subject: [Fwd: IMPORTED UK AND NETHERLANDS BEEF?] -Reply
Date: Thu, 3 Sep 1998 6:54:00 -0400
From: Linda Detwiler
To: flounder@wt.net (Receipt Notification Requested)

I will check on this as I had not heard about the UK. The Netherlands
would not have suprised me as they did not have a case until March
1997.
...
now my question would be, how many of these animals that fed on MBM's
from these countries, were imported to the United States,
via 3rd country routes??? i will give you that answer below...TSS

Marva Thompson
Foreign Trade Reference Room
202/482-2185

"The U.S. is apparently still importing beef, pork, sheep, and lamb
from countries in which BSE is found [this is probably
completely legal under regulations applicable at time of import--
webmaster]:

Bovine anmls bnlss ex prcssd frozen/U.S. Imports for Consumption 1997
year to date (custom value, in thousands of dollars)
(units of quantity: kilograms)

United Kingdom 37,122 kilograms, 43 thousand dollars
Netherlands 56,260 kilograms, 413 thousand dollars
Canada 18,141,481 kilograms, 23,914 million dollars

Livers of bovine animals, edible, frozen. U.S. Imports for consumption

Netherlands 19,230 kilograms, 25 thousand dollars
Canada 160,632 kilograms, 147 thousand dollars

Tongues of bovine animals, edible, frozen U.S. Imports for consumption

Netherlands 1,047 kilograms, 4 thousand dollars
Canada 767,859 kilograms, 2,028 million

Hi-qulty beef cuts w/bone in prcssd f/c u.S. Imports for consumption

Canada 25,332 kilograms, 37 thousand dollars

Beef cuts w/bone in excpt prcdssd fr/ch u.S. Imports for consumption

Netherlands 5,276 kilograms, 30 thousand dollars
Canada 117,142 kilograms, 353 thousand dollars

Meat bovine anmls cuts w/bone ex prrocssd fr us imports for consumption

Netherlands 51,836 kilograms, 444 thousand dollars
Canada 120,955,010 kilograms, 253,199 million

Cattle hides, whole, fresh or wet-salt u.S. Imports for consumption

Belgium 1,270 pieces, 112 thousand dollars
United kingdom 36 pieces, 3 thousand dollars
Ireland 12,797 pieces, 839 thousand dollars
Italy 50 pieces, 10 thousand dollars
Fr germany 2,500 pieces, 36 thousand dollars
Canada 1,405,430 pieces, 67,320 million dollars

Hides/skins
bovine anmls nesoi whole frh/wet-saltd u.S. Imports for consumption

United kingdom 13 pieces, 1 thousand dollars
Italy 4 pieces, 4 thousand dollars
Germany 9,455 pieces, 139 thousand dollars
Canada 567,816 pieces, 17,196 million dollars

Cattle hides, whole, fresh or wet-salted u.S. Imports for consumption

1998 year to date
Italy 7 pieces, 2 thousand dollars
Ireland 1,408 pieces, 85 thousand dollars
France 25 pieces 2 thousand dollars
Canada 965,355 pieces, 37,244 million dollars

Hides and skins of bovine animals, whole, nesoi, fresh or wet-salted
U.S. Imports for consumption

United kingdom 18 pieces, 3 thousand dollars
Sweden 1 pieces, 1 thousand dollars
Italy 2 pieces, 2 thousand dollars
Germany 5,565 pieces, 72 thousand dollars
Canada 84,327 pieces, 2,257 million dollars

Sheep, lamb skins, no wool, nesoi, pickled not split, u.S. Imports for
Consumption

United kingdom 9,504 pieces, 88 thousand dollars
Sheep, lamb skins, no wool, nesoi, pickled, split u.S. Imports for
Consumption

United Kingdom 149,580 pieces, 1,212 million dollars
Netherlands 50,400 pieces, 267 thousand dollars
Italy 4,175 pieces, 64 thousand dollars
France 13,644 pieces, 57 thousand dollars
Canada 131,642 pieces, 241 thousand dollars


Flawed inspection of food is a danger, senate panel told
9-11-98 Knight Rider Tribune News

The government's current system to check food imports for possible
health dangers is dangerously flawed, experts in the food
business told a Senate subcommittee Thursday. U.S. inspectors
check only 2 percent of all foreign shipments and consistently
issue low penalties to importers who break the rules, experts
said. Unscrupulous importers typically import large amounts of
products that will not pass (Food and Drug Administration)
inspection, said a former West Coast customs broker.

He said importers easily bypass inspections by docking at
high-volume ports, such as Los Angeles-Long Beach and New
York, where the inspection force is stretched thin.
Inspections are so low there they virtually pass right through.

Subject: MBM/U.K. imports of MBM to the U.S./BSE Inquiry
http://www.bse.org.uk/dfa/dfa25.htm
Date:Mon, 10 Apr 2000 15:14:21 -0700
From: "Terry S. Singeltary Sr."
To: flounder@wt.net

69. On 14 February 1990, Mr Meldrum wrote a letter to the
Chief Veterinary Officers of a number of countries. [76] On 15
February 1990, Mrs Attridge and other officials were sent a
copy of the letter of 14 February 1990 and a list of the
countries to which it had been sent. They were stated to be
the countries which had imported ruminant based meat
and bone meal from the United Kingdom. The countries listed
were Norway; Sweden, Switzerland, Czechoslovakia,
Hungary, Nigeria, Thailand, South Africa, Malaysia, Taiwan,
Hong Kong, South Korea, Japan, Canada, USA,
Turkey, Kenya, Malta, Libera, Lebanon, Saudi Arabia, Sri
Lanka, Puerto Rico, Curacao, Finland.[77] The letter from
Mr Meldrum included the following:
Although we have kept the Office Internationale des Epizooties (OIE)
fully informed about this new disease, and they will
shortly be disseminating information and recommendations to member
countries, I am writing to you on a personal basis to
ensure that you are aware of all the developments in relation to BSE,
including its likely cause. The majority of our findings
have now been published in the Veterinary Record.�[78]
70. On 20 February 1990, Dr Pickles wrote to Ms Verity
(APS/CMO). Dr Pickles� minute included the following:
1. Mr Meldrum is arguing that MAFF have already taken all the
necessary and responsible steps to warn importing countries
of the BSE dangers in UK meat and bone meal. Yet the action taken
so far overseas suggest the message has not got
through, or where it has this has been late. The first nation
that woke up to the danger did so a year after our own feed
ban. It seems even now several EC countries neither ban our
imports or the general feeding of ruminant protein. It also
seems the OIE and CVO have yet to inform the rest of the world.
2. I do not see how this can be claimed to be responsible�. We
do not need an expert group of the Scientific Veterinary
Committee to tell us British meat and bone meal is unsafe for
ruminants. I fail to understand why this cannot be tackled
from the British end which seems to be the only sure way of doing
it, preferably by banning exports. As CMO says in his
letter of 3 January surely it is short sighted for us to risk
being seen in future as having been responsible for the
introduction of BSE to the food chain in other countries.��[79]


http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh







Sunday, February 5, 2012


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


http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/february-2012-update-on-feed.html








http://scrapie-usa.blogspot.com/




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





http://chronic-wasting-disease.blogspot.com/





http://bse-atypical.blogspot.com/





http://bseusa.blogspot.com/





http://madcowusda.blogspot.com/





http://transmissible-mink-encephalopathy.blogspot.com/






TSS
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Prion cross-species transmission efficacy is tissue dependent

Prion cross-species transmission efficacy is tissue dependent
Claire Williams, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 0SP

Prions are proteinaceous infectious agents which result in fatal neurodegenerative disorders in a range of animals, including humans. Prions are misfolded forms of the ubiquitously expressed host protein PrPc. When PrPc becomes misfolded it is known as PrPsc and forms macromolecular complexes which are deposited in the brain, and sometimes in lymphoid tissue. When PrPsc is introduced into a healthy animal it induces the transformation of the normal PrPc into the misfolded PrPsc form. Such transmission does occur between different species, for example the transmission of bovine spongiform encephalopathy (BSE) into humans. However such transmission is much less efficient than transmission within a species. It is hypothesised that the cross-species transmission of prions is restricted due to steric incompatibility between the infecting PrPsc and the host PrPc. A paper published in Science this week suggests that the efficiency of cross-species prion transmission may actually vary between tissues and be higher than previously thought (1).

Béringue et al. looked at the transmission of prions from elk, hamsters and cattle into mice which had been genetically engineered to express either the sheep or human version of PrPc. The mice were infected by intra-cerebral injection and euthanised at regular intervals post exposure. The presence of PrPsc in the brain and the spleen of these animals was assessed by immunoblotting. Unsurprisingly given the cross-species barriers involved, none of the mice developed neurological disease during the study and only small numbers of animals had detectable PrPsc in their brains. However, many more animals had PrPsc detected in their spleens. Using the experiment looking at the transmission of BSE into mice with human PrPc as an example, 7% of animals had detectable PrPsc in brain tissue, compared with detection of the abnormal protein in the spleens of 63% of the animals.

These results suggest that the spleen is much more permissive than the brain to foreign prions. This could have significant implications for human medicine. To date around 200 individuals have developed variant Creutzfeldt-Jakob disease as a result of infection with BSE, however there has been much discussion about people potentially being silent carriers of the infection. This study, along with others looking at the prevalence of PrPsc in archived appendix tissue, raises the possibility that BSE exposure led to lymphoid tissue colonisation in more individuals than developed, or will develop, neuroinvasive disease. This has important public health implications with regards potential human to human spread of prions through organ transplantation, surgical instruments etc. As the prion is now adapted to humans, it is possible that the risk of lethal infection is higher than seen with cattle to human transmission.

References:

1. Béringue V, Herzog L, Jaumain E, Reine F, Sibille P, Le Dur A, Vilotte J-L, Laude H. Facilitated Cross-Species Transmission of Prions in Extraneural Tissue. Science 2012 Jan;335(6067):472 -475. doi:10.1126/science.1215659

Story image from Wikimedia Commons.

http://www.cambridgemedicine.org/news/1328879145




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





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







> > > Can the disease be transfered to cattle?


YES, and with an attack rate of 86%. this was done in the lab, and not under natural conditions, but with a second strain of CWD emerging i.e. the ‘WISCONSIN STRAIN’, there is much concern for the _potential_ for an atypical CWD strain that would naturally transmit to cattle. please see ;





CWD to cattle figures CORRECTION



Greetings,



I believe the statement and quote below is incorrect ;



"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."

Please see ;

Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.



http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089




" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "




shouldn't this be corrected, 86% is NOT a low rate. ...




kindest regards,

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518





Thank you!

Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.

http://cshperspectives.cshlp.org/letters/submit



re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu

http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html




Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.




snip...




http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html




please see CWD potential to humans here ;

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html






MARCH 1, 2011



UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;



----- Original Message -----

From: David Colby

To: flounder9@verizon.net

Cc: stanley@XXXXXXXX

Sent: Tuesday, March 01, 2011 8:25 AM

Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

Dear Terry Singeltary,

Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.

Warm Regards, David Colby

--

David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware



====================END...TSS==============



http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html





UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html





Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011

Prions

David W. Colby1,* and Stanley B. Prusiner1,2

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html





PLEASE NOTE ON SECOND PASSAGE, ALL CATTLE 100% HAD CONTRACTED CWD ;



When brainstems of CWD-infected cattle were analysed by WB for the presence of PrPres, only three of six samples were found to be positive (Table 1). In contrast, all samples from the midbrain area were positive by this technique (Table 1; Fig. 5). It was noteworthy, however, that both brainstem and midbrain sections of all animals infected with CWD gave positive IHC results (Table 1) and a positive WB was associated with strong IHC labelling. This may indicate that the IHC procedure is more sensitive than the WB method for cattle-passaged CWD.



http://ddr.nal.usda.gov/bitstream/10113/34009/1/IND43787291.pdf







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

This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;

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



Wednesday, March 31, 2010

Atypical BSE in Cattle

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.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2





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



Rural and Regional Affairs and Transport References Committee

The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010

2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50

http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf





And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

full text 18 pages ;

http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf





please see full text ;

http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html





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

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

http://whqlibdoc.who.int/publications/2003/9241545887.pdf





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

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

The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"

http://www.promedmail.org/direct.php?id=20100405.1091







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.




This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.



http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2







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"



http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html







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





Thursday, February 09, 2012

50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE

snip...



Dr. Michael Coulthart, et al, Public Health Agency of Canada



- although not occurring to date, he estimates that report of just one probable case of human CWD could trigger a public health crisis in North America.


- epidemiological studies so far indicate the probability is very slight, however, prion agents and their transmission properties are highly mutable and adaptable and the possibility can not be ruled out.



- suggests those involved in human prion disease surveillance should consider the possibility of human CWD and develop a readiness to deal with it.





snip...




http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html









Saturday, March 5, 2011

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



http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html





Friday, February 10, 2012



Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous Tonsil Archive



http://creutzfeldt-jakob-disease.blogspot.com/2012/02/creutzfeldt-jakob-disease-cjd-biannual.html





layperson



TSS
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Sunday, February 5, 2012

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

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






February 2, 2012






To help prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) through feed in the United States, the Food and Drug Administration (FDA) implemented a final rule that prohibits the use of most mammalian protein in feeds for ruminant animals. This rule, Title 21 Part 589.2000 of the Code of Federal Regulations, here called the Ruminant Feed Ban, became effective on August 4, 1997.






A second rule, Title 21 Part 589.2001 of the Code of Federal Regulations, here called the Enhanced Feed Ban, became effective on April 27, 2009. This rule prohibits the use of certain cattle-derived materials in all animal feed. The BSE inspection report form has been revised and is being used for determining compliance with both the ruminant feed ban and the enhanced feed ban. The inspection results summarized below reflect the compliance status for both rules.






The following is an update on FDA enforcement activities regarding the ruminant feed ban. FDA's Center for Veterinary Medicine (CVM) has summarized results of those inspections that have been entered into FDA's inspection database as of January 28, 2012. As of January 28, 2012, FDA had received over 93,000 inspection reports since 1997. Approximately 73% of these inspections have been conducted by State feed control officials, with the remainder conducted by FDA officials.






Inspections conducted by FDA or State investigators are classified to reflect the compliance status at the time of the inspection based upon the objectionable conditions documented. These inspection conclusions are reported as Official Action Indicated (OAI), Voluntary Action Indicated (VAI), or No Action Indicated (NAI).






An OAI inspection classification occurs when significant objectionable conditions or practices were found and regulatory sanctions are warranted in order to address the establishment's lack of compliance with the regulation. An example of an OAI inspection classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspections classified with OAI violations will be promptly re-inspected following the regulatory sanctions to determine whether adequate corrective actions have been implemented.






A VAI inspection classification occurs when objectionable conditions or practices were found that do not meet the threshold of regulatory significance, but do warrant advisory actions to inform the establishment of findings that should be voluntarily corrected. Inspections classified with VAI violations are more technical violations of the Ruminant Feed Ban. These include provisions such as minor recordkeeping lapses and conditions involving non-ruminant feeds.






An NAI inspection classification occurs when no objectionable conditions or practices were found during the inspection or the significance of the documented objectionable conditions found does not justify further actions. A firm’s compliance status and whether the firm handles prohibited material is based on its most recent inspection.






The results to date are reported here both by “segment of industry” and “in total”. NOTE – A single firm can operate as more than one firm type. As a result, the categories of the different industry segments are not mutually exclusive.






RENDERERS


These firms are the first to handle and process (i.e., render) animal proteins and to send these processed materials to feed mills and/or protein blenders for use as a feed ingredient.






Number of active firms inspected – 279


Number of active firms handling materials prohibited from use in ruminant feed – 152 (54% of those active firms inspected)


Of the 152 active firms handling prohibited materials, their most recent inspection revealed that:


2 firms (1.3%) were classified as OAI


9 firms (5.9%) were classified as VAI




LICENSED FEED MILLS




FDA licenses these feed mills to produce medicated feed products. The license is required to manufacture and distribute feed using certain potent drug products, usually those requiring some pre-slaughter withdrawal time. This licensing has nothing to do with handling prohibited materials under the feed ban regulation. A medicated feed license from FDA is not required to handle materials prohibited under the Ruminant Feed Ban.






Number of active firms inspected – 1,046


Number of active firms handling materials prohibited from use in ruminant feed – 459 (44% of those active firms inspected)


Of the 459 active firms handling prohibited materials, their most recent inspection revealed that:


0 firms (0%) were classified as OAI


10 firms (2.2%) were classified as VAI




FEED MILLS NOT LICENSED BY FDA




These feed mills are not licensed by the FDA to produce medicated feeds.






Number of active firms inspected – 5,304


Number of active firms handling materials prohibited from use in ruminant feed – 2,751 (52% of those active firms inspected)


Of the 2,751 active firms handling prohibited materials, their most recent inspection revealed that:


0 firms (0%) were classified as OAI


30 firms (1.1%) were classified as VAI




PROTEIN BLENDERS




These firms blend rendered animal protein for the purpose of producing quality feed ingredients that will be used by feed mills.






Number of active firms inspected – 284


Number of active firms handling materials prohibited from use in ruminant feed – 129 (45% of those active firms inspected)


Of the 129 active firms handling prohibited materials, their most recent inspection revealed that:


0 firms (0%) were classified as OAI


2 firm (1.6%) was classified as VAI




RENDERERS, FEED MILLS, AND PROTEIN BLENDERS MANUFACTURING WITH PROHIBITED MATERIAL




This category includes only those firms that actually use prohibited material to manufacture, process, or blend animal feed or feed ingredients.






Total number of active renderers, feed mills, and protein blenders inspected – 6,696


Number of active renderers, feed mills, and protein blenders processing with prohibited materials – 471 (7.0%)


Of the 471 active renderers, feed mills, and protein blenders processing with prohibited materials, their most recent inspection revealed that:


2 firms (0.4%) were classified as OAI


18 firms (3.8%) were classified as VAI




OTHER FIRMS INSPECTED




Examples of such firms include ruminant feeders, on-farm mixers, pet food manufacturers, animal feed salvagers, distributors, retailers, and animal feed transporters.






Number of active firms inspected – 28,217


Number of active firms handling materials prohibited from use in ruminant feed – 9,293 (33% of those active firms inspected)


Of the 9,293 active firms handling prohibited materials, their most recent inspection revealed that:


0 firms (0%) were classified as OAI


123 firms (1.3%) were classified as VAI




TOTAL FIRMS




Note that a single firm can be reported under more than one firm category; therefore, the summation of the individual OAI/VAI firm categories will be more than the actual total number of OAI/VAI firms, as presented below.






Number of active firms whose initial inspection has been reported to FDA – 30,124


Number of active firms handling materials prohibited from use in ruminant feed – 9,819 (33% of those active firms inspected)


Of the 9,819 active firms handling prohibited materials, their most recent inspection revealed that:


2 firms (0.02%) were classified as OAI


130 firms (1.3%) were classified as VAI








WITH the looks of things, the BSE GBR risk assessment for the USA in 2012 should be held stead fast at BSE GBR III. but as I said long ago, the BSE GBR risk assessment should be BSE GBR IV due to the terribly failed, if not fraudulent USDA FDA BSE TESTING, AND SURVEILLANCE FOR BSE, since the inception of the programs. all failed terribly. ...TSS


AN appalling amount of violations, that most likely led to a great deal of banned suspect mad cow protein in commerce. however sadly, the way the violations are now wrote up, the common layperson cannot know exact what the violations were, or how much banned suspect mad cow protein actually went out into commerce. as was the infamous decade post partial and voluntary feed ban violations, where the one in 2007 let loose 10,000,000 LBS of banned blood laced MBM into commerce ;






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










see much more tonnage of recalled prohibited banned suspect BSE contaminated feed here ;






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, July 23, 2011




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










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.








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...






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...






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 ;










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, 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...








14th ICID International Scientific Exchange Brochure -


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.










Sunday, January 29, 2012


Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Dr. Detwiler


Dr. Detwiler published Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Forum\Presentations TSE\ Page 33 and 34 of 44 ;








Wednesday, February 1, 2012


CJD and PLASMA / URINE PRODUCTS EMA Position Statements Alberto Ganan Jimenez, European Medicines Agency PDA TSE Safety Forum, 30 June 2011






Wednesday, February 1, 2012


Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Update on CJD and VCJD Transmission RG Will






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







Tuesday, May 27, 2008


FDA BSE/Ruminant Feed Inspections Firms Inventory Report Texas Legend Ranch OAI 05/10/2008












Friday, September 4, 2009


FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009






Saturday, August 29, 2009


FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009







C O N F I R M E D




----- Original Message -----


From: "Terry S. Singeltary Sr."


To:


Sent: Thursday, November 05, 2009 9:25 PM


Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009








PLEASE UNDERSTAND, with a Transmissible Spongiform Encephalopathy, once clinical, the disease is 100% fatal. There should be NO debate of the 'unacceptable risk factor', with any TSE. ...TSS




Sunday, June 26, 2011


Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque






Saturday, June 13, 2009


BSE FEED VIOLATIONS USA UPDATE From 01/01/2009 To 06/10/2009








Monday, April 5, 2010


Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010








Monday, January 17, 2011


MAD COW Update on Feed Enforcement Activities to Limit the Spread of BSE January 13, 2011







Friday, January 6, 2012



OIE 2012 Training Manual on Wildlife Diseases and Surveillance and TSE Prion disease








TSS
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