tag:blogger.com,1999:blog-300088382024-02-08T11:33:04.186-08:00MADCOW DISEASE USA SPONTANEOUS OR FEED ?spontaneous TSE of any species has never been proven.
THERE is NO evidence of a 'spontaneous' TSE anywhere that is infectious and shows the pathology of any natural TSE. what prusiner and soto produced looked like no nature TSE. are we expected to believe that the tooth fairy and or santa claus brought this disease to us? i think not. we have mad cows in Alabama, we have mad cow feed in Alabama, we have mad cows in Texas, we have mad cow feed in Texas.
http://www.prwatch.org/node/4883Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.comBlogger13125tag:blogger.com,1999:blog-30008838.post-27619125810255259362017-07-20T12:04:00.002-07:002017-07-20T12:08:16.991-07:00Alabama atypical L-type BASE BSE TSE Prion Mad Cow Disease<div style="font-family: arial; font-size: 13.3333px;">
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USDA Detects a Case of Atypical Bovine Spongiform Encephalopathy in Alabama </div>
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USDA Animal and Plant Health Inspection Service sent this bulletin at 07/18/2017 07:05 PM EDT </div>
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USDA Detects a Case of Atypical Bovine Spongiform Encephalopathy in Alabama</div>
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Washington, D.C., July 18, 2017 – The U.S. Department of Agriculture (USDA) announced an atypical case of Bovine Spongiform Encephalopathy (BSE), a neurologic disease of cattle, in an eleven-year old cow in Alabama. This animal never entered slaughter channels and at no time presented a risk to the food supply, or to human health in the United States. </div>
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USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Laboratories (NVSL) have determined that this cow was positive for atypical (L-type) BSE. The animal was showing clinical signs and was found through routine surveillance at an Alabama livestock market. APHIS and Alabama veterinary officials are gathering more information on the case.</div>
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BSE is not contagious and exists in two types - classical and atypical. Classical BSE is the form that occurred primarily in the United Kingdom, beginning in the late 1980’s, and it has been linked to variant Creutzfeldt-Jakob disease (vCJD) in people. The primary source of infection for classical BSE is feed contaminated with the infectious prion agent, such as meat-and-bone meal containing protein derived from rendered infected cattle. Regulations from the Food and Drug Administration (FDA) have prohibited the inclusion of mammalian protein in feed for cattle and other ruminants since 1997 and have also prohibited high risk tissue materials in all animal feed since 2009. Atypical BSE is different, and it generally occurs in older cattle, usually 8 years of age or greater. It seems to arise rarely and spontaneously in all cattle populations. </div>
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This is the nation’s 5th detection of BSE. Of the four previous U.S. cases, the first was a case of classical BSE that was imported from Canada; the rest have been atypical (H- or L-type) BSE.</div>
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The World Organization for Animal Health (OIE) has recognized the United States as negligible risk for BSE. As noted in the OIE guidelines for determining this status, atypical BSE cases do not impact official BSE risk status recognition as this form of the disease is believed to occur spontaneously in all cattle populations at a very low rate. Therefore, this finding of an atypical case will not change the negligible risk status of the United States, and should not lead to any trade issues. </div>
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The United States has a longstanding system of interlocking safeguards against BSE that protects public and animal health in the United States, the most important of which is the removal of specified risk materials - or the parts of an animal that would contain BSE should an animal have the disease - from all animals presented for slaughter. The second safeguard is a strong feed ban that protects cattle from the disease. Another important component of our system - which led to this detection - is our ongoing BSE surveillance program that allows USDA to detect the disease if it exists at very low levels in the U.S. cattle population.</div>
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<a href="https://content.govdelivery.com/accounts/USDAAPHIS/bulletins/1aadf32" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://content.govdelivery.com/accounts/USDAAPHIS/bulletins/1aadf32</a></div>
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THURSDAY, JULY 20, 2017 </div>
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USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200</div>
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<a href="http://bovineprp.blogspot.com/2017/07/usda-oie-alabama-atypical-l-type-base.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/07/usda-oie-alabama-atypical-l-type-base.html</a></div>
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THURSDAY, JULY 20, 2017</div>
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Alabama Atypical BSE CJD CWD TSE Prion Update</div>
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<a href="http://bseusa.blogspot.com/2017/07/alabama-atypical-bse-cjd-cwd-tse-prion.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://bseusa.blogspot.com/2017/07/alabama-atypical-bse-cjd-cwd-tse-prion.html</a></div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-19689451734751012082012-05-18T18:52:00.002-07:002012-05-18T18:52:23.144-07:00Re: USA ruminant-to-ruminant feed ban warning letters ??? December 23, 2002 at 12:12 pm PSTSubject: Re: USA ruminant-to-ruminant feed ban warning letters ???<br />Date:
Mon, 23 Dec 2002 12:56:07 -0600<br />From: "Terry S. Singeltary Sr." <flounder @wt.net=""><br />Reply-To: <a class="kLink" href="wlmailhtml:{DF7DDD7C-C70A-41E4-A8B1-D5D27F4F623C}mid://00000774/!x-usc:http://www.vegsource.com/talk/madcow/messages/#" id="KonaLink0" jquery1337227130872="6" style="position: static; text-decoration: underline !important;"><span style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: static;"><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Bovine </span><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Spongiform </span><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Encephalopathy</span></span></a> <bse-l @uni-karlsruhe.de=""><br />To:
BSE-L@uni-karlsruhe.de<br />References: <ddc34c4e6d23d311a1100008c756b642057cc919 @cvs003.cvm.fda.gov="">
</ddc34c4e6d23d311a1100008c756b642057cc919></bse-l></flounder><br />
######## Bovine Spongiform Encephalopathy <bse-l @uni-karlsruhe.de="">#########
</bse-l><br />
Greetings and Happy Holidays,
<br />
hi Linda,
<br />
many thanks for this reply, was just checking in to see<br />if anything new
had happened since our last correspondence.<br />i thought i had missed something?
<br />
> Unfortunately, the new database is much more complicated than
<br />
> the old one, and it does not lend itself to presenting data in
<br />
> a simple spreadsheet as we did in the past.
<br />
how convenient;-) i had no problems with the old one...
<br />
> Please be assured that CVM is working to solve this problem,
<br />
> and we do plan to post this data in the future.
<br />
thank you, if USDA/APHIS are lucky, i will hold my breath until<br />that
time;-)
<br />
nothing personal Linda, take care, and may the New Year bring
<br />
PEACE...
<br />
TSS
<br />
CVM HomePage wrote:
<br />
> Dear Mr. Singeltary:<br />><br />> As mentioned in my e-mail of
December 4, FDA's Center for Veterinary<br />> Medicine never posted the
Warning Letters for ruminant feed violations on<br />> our "BSE" page --
http://www.fda.gov/cvm/index/bse/bsetoc.html. However,<br />> these Warning
Letters have been included on the FDA "Warning Letters" page<br />> --
http://www.fda.gov/foi/warning.htm that is located on the FDA's<br />>
"Electronic Freedom of Information Reading Room" page. But, not as a<br />>
separate category of Warning Letters for violations of the ruminant feed<br />>
rules.<br />><br />> I checked the Warning Letter page, and found that quite a
few Warning<br />> Letters have been posted since May; however, I did not find
any more recent<br />> than May 7, 2002, regarding "Animal Proteins Prohibited
in Ruminant<br />> Feed/Misbranded" (ruminant feed rule violations.) You may
wish to file a<br />> Freedom of Information Act (FOIA) request to determine if
more recent<br />> Warning Letters have been issued, but not posted on the FDA
Home Page.<br />> Information about filing a FOIA request may be found
at:<br />>
http://www.fda.gov/opacom/backgrounders/foiahand.html<br />><br />> As
mentioned on the "CVM and Ruminant Feed (BSE) Inspections" site
--<br />><br />> "After March 11, 2002, FDA discontinued the database that was
used to<br />> compile these listings. The Agency started a new database on
April 15, 2002,<br />> and future updates on BSE enforcement and inspectional
findings will draw<br />> from it. The format of the information presented here
may change, due to<br />> design changes of the new database. This site will be
updated after a period<br />> of time that allows for transition into the new
database system."<br />><br />> Unfortunately, the new database is much more
complicated than the old one,<br />> and it does not lend itself to presenting
data in a simple spreadsheet as we<br />> did in the past. Please be assured
that CVM is working to solve this<br />> problem, and we do plan to post this
data in the future.<br />><br />> We have nothing new to report at this
time.<br />><br />> I hope that this information is helpful.<br />><br />>
Sincerely yours,<br />><br />> Linda A. Grassie for the FDA Home
Page<br />><br />><br />> -----Original Message-----<br />> From: Terry S.
Singeltary Sr. [mailto:flounder@wt.net]<br />> Sent: Saturday, December 21,
2002 4:03 PM<br />> To: CVMHomeP@cvm.fda.gov<br />> Subject: USA
ruminant-to-ruminant feed ban warning letters ???<br />><br />><br />>
Greetings,<br />><br />> i have noticed the inspections and warning
letters<br />> from firms not complying with the ruminant-to-ruminant<br />>
feed ban violations has not been updated since (March 11, 2002)?<br />><br />>
2) Firms Currently Considered as Not in Compliance with the BSE Feed
Rule<br />><br />> The following spreadsheet is a subset of Spreadsheet 1 and
contains the<br />> name, address, and firm identifier of all firms that were
considered as<br />> not being in compliance with the BSE feed regulation at
their most<br />> recent inspection, according to the BSE inspection database.
Compliance<br />> status was determined by examination of the BSE Inspection
Checklist.<br />> The dates of the inspections and the specific BSE provision
violations<br />> for each inspection are also included. The listing is
organized<br />> alphabetically first by the FDA District and then by the state
in which<br />> the inspected facility is located.<br />><br />> Most Recent
BSE Inspections, Firms Not in Compliance<br />><br />>
http://www.fda.gov/cvm/efoi/InpectionListDescriptionforHP.htm<br />><br />> i
would be interested to know if all firms are now complying and that no<br />>
warning letters have been issued since may of 2002, or have they just
not<br />> been posted?<br />><br />> if so, how can i locate
them?<br />><br />> thank you,<br />> kind regards,<br />>
terry<br />><br />>
<br />
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
<br />
Subject: Re: re-USA BSE/TSE RUMINANT-TO-RUMINANT FEED BAN VIOLATIONS
''cover-up''<br />Date: Thu, 5 Dec 2002 11:28:24 -0600<br />From: "Terry S.
Singeltary Sr." <flounder @wt.net=""><br />Reply-To: Bovine Spongiform Encephalopathy
<bse-l @uni-karlsruhe.de=""><br />To: BSE-L@uni-karlsruhe.de<br />References:
<3dee84d2.705.1804289383@wt.net>
</bse-l></flounder><br />
######## Bovine Spongiform Encephalopathy <bse-l @uni-karlsruhe.de="">#########
</bse-l><br />
Greetings List Members,
<br />
for those that were interested, it seems they have taken<br />the 'animal
protein' search title and only listed<br />4 with that search title. this is the
same search title<br />i have used since searching ruminant-to-ruminant
feed<br />ban warning letters for the last 5 years. it seems they<br />have archived
all of them and they are now not listed<br />in search, unless you go back to
archive, except for these<br />four. i knew they had to be somewhere, but still
is<br />odd we now have to file FOIA to see what we were able<br />to see for the
last five years every Tues.? i had read<br />a while back Senator Kennedy was very
worried due to the<br />fact that the new administration had decided to
cease<br />posted many of these warning letters, or just to stop issuing<br />them
all together? at any rate, it does seem that they have<br />ceased to document
them since may 2002, if they are continuing<br />to even issue them at all? or
maybe we could be lucky enough<br />as to have not had any violations since may;-)
i guess if i<br />want to find out, i must file FOIA, and by the time they<br />send
me that data, they will probably post on WWW???<br />round and round we go, when
we stop, nobody knows;
<br />
> Again, I am not involved in posting warning letters<br />> on that
page, so I cannot answer your question on where<br />> newer letters on
ruminant feed violations are being posted.<br />> In fact, I do not know if FDA
has issued any Warning Letters<br />> on this subject since last May. You will
need to file a FOIA<br />> request for that information.
<br />
for anyone interested, here are the urls for archive,<br />i did not look under
'M' medicated feeds, i remember<br />some time ago some BSE warning letters were
for medicated<br />feeds as well.
<br />
http://www.accessdata.fda.gov/scripts/wlcfm/subject.cfm?FL=A
<br />
http://www.accessdata.fda.gov/scripts/wlcfm/subject_archive.cfm?FL=A
<br />
TSS
<br />
flounder wrote:<br />> ######## Bovine Spongiform Encephalopathy <bse-l @uni-karlsruhe.de="">#########<br />><br />> -------- Original Message
--------<br />> Subject: Re: ruminant-to-ruminant feed ban violations
???<br />> Date: Wed, 4 Dec 2002 15:49:19 -0500<br />> From: "Grassie, Linda
A" <lgrassie @cvm.fda.gov=""><br />> To: "'flounder@wt.net'" <flounder @wt.net=""><br />> CC: "Bataller, Neal" <nbatalle @cvm.fda.gov=""><br />><br />>
Dear Mr. Singeltary:<br />><br />> Your request for information on violations
of FDA's ruminant<br />> feed rule<br />> has been forwarded to me for
reply.<br />><br />> We (FDA's <a class="kLink" href="wlmailhtml:{DF7DDD7C-C70A-41E4-A8B1-D5D27F4F623C}mid://00000774/!x-usc:http://www.vegsource.com/talk/madcow/messages/#" id="KonaLink1" jquery1337227130872="5" style="position: static; text-decoration: underline !important;"><span style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: static;"><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Center </span><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">for </span><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Veterinary </span><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Medicine</span></span></a>) never posted the<br />> Warning<br />>
Letters for ruminant feed violations on our "BSE" page --<br />> <br />>
http://www.fda.gov/cvm/index/bse/bsetoc.html. However,<br />> these
Warning<br />> Letters have been included on the FDA "Warning Letters"
page<br />> --<br />> <br />> http://www.fda.gov/foi/warning.htm<br />> that
is located on the FDA's "Electronic Freedom of<br />> Information
Reading<br />> Room" page. But, not as a separate category of Warning<br />>
Letters for<br />> violations of the ruminant feed rules.<br />><br />> I
checked the Warning Letter page, and found that quite a<br />> few
Warning<br />> Letters have been posted since May; however, I did not
find<br />> any more<br />> recent than May 7, 2002, regarding "Animal
Proteins<br />> Prohibited in<br />> Ruminant Feed/Misbranded" (ruminant feed
rule violations.)<br />> You may<br />> wish to file a Freedom of Information
Act (FOIA) request to<br />> determine if<br />> more recent Warning Letters
have been issued, but not posted<br />> on the FDA<br />> Home Page.
Information about filing a FOIA request may be<br />> found at:<br />>
http://www.fda.gov/opacom/backgrounders/foiahand.html<br />> <br />><br />>
As mentioned on the "CVM and Ruminant Feed (BSE)<br />> Inspections" site
--<br />><br />> "After March 11, 2002, FDA discontinued the database
that<br />> was used to<br />> compile these listings. The Agency started a
new database on<br />> April 15,<br />> 2002, and future updates on BSE
enforcement and inspectional<br />> findings<br />> will draw from it. The
format of the information presented<br />> here may<br />> change, due to
design changes of the new database. This site<br />> will be<br />> updated
after a period of time that allows for transition<br />> into the new<br />>
database system."<br />><br />> Unfortunately, the new database is much more
complicated<br />> than the old<br />> one, and it does not lend itself to
presenting data in a<br />> simple<br />> spreadsheet as we did in the past.
Please be assured that<br />> CVM is<br />> working to solve this problem, and
we do plan to post this<br />> data in the<br />> future.<br />><br />> I
hope that this information is helpful.<br />><br />> Sincerely
yours,<br />><br />> Linda A. Grassie<br />> Public Information
Specialist<br />> FDA/Center for <a class="kLink" href="wlmailhtml:{DF7DDD7C-C70A-41E4-A8B1-D5D27F4F623C}mid://00000774/!x-usc:http://www.vegsource.com/talk/madcow/messages/#" id="KonaLink2" jquery1337227130872="4" style="position: static; text-decoration: underline !important;"><span style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: static;"><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Veterinary </span><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Medicine</span></span></a><br />><br />> -----Original
Message-----<br />> From: Terry S. Singeltary Sr. [
mailto:flounder@wt.net<br />> ]<br />> Sent: Tuesday, December 03, 2002 12:00
PM<br />> To: Nbatalle@cvm.fda.gov<br />> Subject: ruminant-to-ruminant feed
ban violations ???<br />><br />> greetings,<br />><br />> i have noticed
that no ruminant-to-ruminant feed ban<br />> violations have been posted for
some time. i have also<br />> noticed that since about april or may of 2002,
the warning<br />> letters have ceased to be posted publicly, and at the
site<br />> CVM and Ruminant feed inspections site url, they have not<br />>
been updated either.<br />><br />> is this correct or not ?<br />><br />> if
not correct, then where are they now being posted ?<br />><br />> outdated
data here;<br />><br />>
http://www.fda.gov/cvm/efoi/InpectionListDescriptionforHP.ht<br />> m<br />>
<br efoi="" />> tm><br />><br />> thank you,<br />> kind
regards,<br />><br />> Terry S. Singeltary Sr.<br />>
==========================<br />><br />> Greetings BSE-L
members,<br />><br />> as you can see above, i got a reply about the<br />>
ruminant-to-ruminant<br />> ban warning letters that have ceased to be posted
publically<br />> since May. i find a few comments interesting to say
the<br />> least;<br />><br />><br />>>I checked the Warning Letter page,
and found that quite<br />>>a few Warning Letters have been posted since
May; however,<br />>>I did not find any more recent than May 7, 2002,
regarding<br />>>"Animal Proteins Prohibited in Ruminant
Feed/Misbranded"<br />>>(ruminant feed rule
violations.)<br />><br />><br />> so did i, this is where i have always
searched for them.<br />> what did i find today;<br />><br />> Darling
International, Inc.<br />> 5/07/02<br />> Seattle District Office Animal
Proteins Prohibited in<br />> Ruminant Feed/Misbranded [PDF]<br />>
[HTML]<br />> All American Feed & Tractor<br />> 4/01/02<br />> Seattle
District Office Animal Proteins Prohibited in<br />> Ruminant Feed/Adulterated
[PDF]<br />> [HTML]<br />> Tyson Foods<br />> 2/12/02<br />> Seattle
District Office Animal Proteins Prohibited in<br />> Ruminant Feed/Misbranded
[PDF]<br />> [HTML]<br />> The Feed Bucket<br />> 12/11/01<br />> Atlanta
District Office Animal Proteins Prohibited in<br />> Ruminant
Feed/Adulterated/Misbranded [PDF]<br />> [HTML]<br />><br />> well well, i do
not see the "quite a few Warning Letters<br />> have<br />> been posted since
May" that FDA spoke of. only 4 ???<br />><br />><br />>>You may wish to
file a Freedom of Information Act (FOIA)<br />>>request to determine if more
recent Warning Letters have<br />>>been issued, but not posted on the FDA
Home Page.<br />><br />><br />> this is absolutely as i thought. they are
_not_ listing<br />> them for public viewing anymore. i never had to file
a<br />> FOIA for this information before. so, what would you call<br />>
this??? more politics and more BSeee, or just another<br />> USA cover-up on
human/animal TSEs in the USA.<br />><br />> GBR RISK ASSESSMENT SHOULD BE
CHANGED TO ALL TSEs...<br />><br />> USA GBR SHOULD BE CHANGED TO GBR
III...<br />><br />> TSS<br />><br />><br />>>######## Bovine Spongiform
Encephalopathy<br />>><bse-l @uni-karlsruhe.de="">
#########<br />>>Greetings Dr. Gomez and other List members and
Lurkers,<br />>><br />>>Gomez, Thomas M.
wrote:<br />>><br />>>Subject: Re: Speaking Note on BSE Agriculture
Council,<br />>>Brussels, 2 8<br />>> November 2002 (compare TSE
testing)<br />>>Date: Tue, 3 Dec 2002 10:21:41 -0500<br />>>From:
"Gomez, Thomas M." <tmg1 @cdc.gov=""><br />>>Reply-To: Bovine Spongiform
Encephalopathy BSE-L<br />>><br />>> > 1. I'm not able to comment on
feed ban violations.<br />>> > Regulatory authority for Substances
Prohibited From Use<br />>>in<br />>> > Animal Food or Feed; Animal
Proteins Prohibited in<br />>>Ruminant<br />>> > Feed is the FDA, not
the USDA.<br />>><br />>>snip...<br />>><br />>>thank you again
Dr. Gomez, i did not realize you<br />>>could not speak about the
ruminant-to-ruminant<br />>>feed ban. odd some FDA lurkers have not
replied?<br />>>maybe Dr. Freas will know, but i don't think
the<br />>>big guns lurk here. like Dr. <a class="kLink" href="wlmailhtml:{DF7DDD7C-C70A-41E4-A8B1-D5D27F4F623C}mid://00000774/!x-usc:http://www.vegsource.com/talk/madcow/messages/#" id="KonaLink3" jquery1337227130872="3" style="position: static; text-decoration: underline !important;"><span style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: static;"><span class="kLink" style="color: green !important; font-family: comic sans ms; font-size: 10pt; font-weight: 400; position: relative;">Detwiler</span></span></a>, she has her<br />>>other people do
the dirty work here, replies through<br />>>them. odd, you replied about 50
State BSE Conference<br />>>call on Jan. 9, 2001, and that's pretty much all
that<br />>>was about was all the BSE feed ban violations in the
USA.<br />>>no matter, i will ask FDA
officials.<br />>><br />>>Subject: USDA/APHIS response to BSE-L--U.S. 50
STATE<br />>>CONFERENCE CALL Jan. 9, 2001<br />>>Date: Wed, 10 Jan 2001
14:04:21 -0500<br />>>From: "Gomez, Thomas M." <tmg1 @cdc.gov=""><br />>>Reply-To: Bovine Spongiform
Encephalopathy<br />>><br />>>USDA/APHIS would like to provide
clarification on the<br />>>following point from Mr. Singeltary's 9 Jan
posting<br />>>regarding the 50 state conference call.<br />>>[Linda
Detwiler asking everyone (me) not to use emergency<br />>>BSE number, unless
last resort. (i thought of calling them<br />>>today, and reporting the
whole damn U.S. cattle herd ;-)<br />>> 'not']<br />>>Dr. Detwiler was
responding to an announcement made during<br />>>the call to use the FDA
emergency number if anyone wanted<br />>>to report a cow with signs suspect
for BSE. Mr.<br />>>Singeltary is correct that Dr. Detwiler asked
participants<br />>>to use the FDA emergency number as a last resort to
report<br />>>cattle suspect for BSE. What Mr. Singeltary failed to
do<br />>>was provide the List with Dr. Detwiler's entire
statement.<br />>> Surveillance for BSE in the United States is
a<br />>>cooperative effort between states, producers,
private<br />>>veterinarians, veterinary hospitals and the USDA.
The<br />>>system has been in place for over 10 years. Each
state<br />>>has a system in place wherein cases are reported to
either<br />>>the State Veterinarian, the federal Veterinarian in
Charge<br />>>or through the veterinary diagnostic laboratory
system.<br />>>The states also have provisions with emergency
numbers.<br />>>Dr. Detwiler asked participants to use the
systems<br />>>currently in place to avoid the possibility of
a<br />>>BSE-suspect report falling through the cracks. Use of
the<br />>>FDA emergency number has not been established as a
means<br />>>to report diseased cattle of any
nature...<br />>>snip...<br />>><br />>>FYI see full text with my
reply
here;<br />>><br />>>http://www.vegsource.com/talk/madcow/messages/8219.html<br />>><br />>>and
a better reply than mine would be here;<br />>><br />>> >would you
and the USDA/APHIS be so kind as to supply<br />>> >this list with a full
text version of the conference<br />>> >call and or post on<br />>>
>your web-site?<br />>><br />>> >if not, why not?<br />>>
><br />>> >> The system has been in place for over 10
years.<br />>> ><br />>> > only test 10,700 cattle from some 1.5
BILLION head<br />>>(including<br />>> >calf crop). Especially since
French >are testing some<br />>>20,000 weekly and<br />>> >the
E.U. as a whole,<br />>><br />>>==-=-=<br />>><br />>>Right. The
US has 101 million cows where as France has 5.7<br />>>million. This being
17.7 as many cows, the US would need<br />>>to test 17.7 x 20,000 = 354,386
cows a week to be testing<br />>>proportionately. This compares to about 50
cows a week<br />>>tested now. In other words, the US needs to test
7,000<br />>>cows where it is now testing 1 to keep up
with<br />>>international norms.<br />>>Once a country starts serious
testing, they get religion.<br />>>After stomaching some bad results, then
they want their<br />>>trading partners to test just like they
did.<br />>><br />>>No one can predict what, if anything, would turn up
in the<br />>>US from a European scale of testing. Right now the US
has<br />>>not been using the international gold standard of
the<br />>>Prionics test.<br />>>Just as Austria and Belgium have been
forced into<br />>>unwilling testing, the US is going to have to test at
an<br />>>adequate level or forget about foreign trade in
bovine<br />>>byproducts, cosmetics, nutriceuticals,
veterinary<br />>>products, and pharmaceuticals. You can see this just
from<br />>>announcements in Japan.<br />>><br />>>Nobody is going
to buy into theoretical reasons why there<br />>>shouldn't be BSE in the US
or Canada when the choice is<br />>>real-world testing that proved so
informative in other<br />>>theoretical countries such as
Germany.<br />>>In my opinion, the US should have been preparing long
ago<br />>>for a soft landing with the consumer instead of going
with<br />>>the heavy-handed germanic denial
system.<br />>><br />>>http://www.vegsource.com/talk/madcow/messages/8222.html<br />>><br />>>i
have also sent many letters to FDA with no reply.<br />>>i have ask all
parties that represent this industry<br />>>to respond to my question, with
no luck. so again,<br />>>i ask all USA Gov. lurkers on this list,
including<br />>>all FDA officials, please answer my
question;<br />>><br />>>where are the ruminant-to-ruminant feed ban
violations<br />>>now being documented for public viewing
???<br />>><br />>>for some humorist
reading;<br />>><br />>>http://www.fda.gov/ohrms/dockets/dailys/01/Nov01/112901/01<br />>>N-0423-EC-18.html<br />>>http://www.fda.gov/ohrms/dockets/dailys/01/Nov01/112901/01<br />>>N-0423-EC-20.html<br />>>http://www.fda.gov/ohrms/dockets/dailys/01/Nov01/112901/01<br />>>N-0423-EC-11.html<br />>>http://www.fda.gov/ohrms/dockets/dailys/01/Nov01/112901/01<br />>>N-0423-EC-19.html<br />>>http://www.fda.gov/OHRMS/DOCKETS/98fr/100501b.htm<br />>><br />>>http://www.access.gpo.gov/nara/cfr/waisidx_01/21cfr589_01.<br />>>html<br />>>snip...<br />>><br />>>As
of March 11, CVM had received inspection reports<br />>>covering inspections
(both initial inspections and<br />>>re-inspections) of 10,458 different
firms. The majority of<br />>>these inspections (around 80%) were conducted
by State<br />>>officials under contract to FDA and the remainder by
FDA<br />>>officials.<br />>>Various segments of the feed industry had
different levels<br />>>of compliance with this feed ban regulation. The
results<br />>>to date are reported here both by "segment of
industry"<br />>>and "in
total".<br />>>RENDERERS<br />>><br />>>(These firms are the first
to handle rendered protein and<br />>>send materials to feed mills and
ruminant feeders.)<br />>><br />>> *<br />>><br />>> NUMBER OF
FIRMS WHOSE INITIAL INSPECTION HAS BEEN<br />>>REPORTED TO CVM -
239<br />>> *<br />>><br />>> NUMBER OF FIRMS HANDLING MATERIALS
PROHIBITED FOR<br />>>USE IN RUMINANT FEED - 171 (72% of those
firms<br />>>inspected/reported).<br />>> * Of the 171 renderers
handling prohibited<br />>>materials, at their most recent inspection (could
have<br />>>been an initial or a follow-up inspection):<br />>> - 4 (2%)
had products that were not labeled as<br />>>required<br />>> - 3 (2%)
did not have adequate systems to prevent<br />>>co-mingling<br />>> - 1
(1%) did not adequately follow record keeping<br />>>regulations<br />>>
- 4 (2%) firms were found to be out of compliance<br />>>(some firms were
out of compliance with more than one<br />>>aspect of the
rule)<br />>>FDA LICENSED FEED MILLS<br />>><br />>>(FDA licenses
these mills to produce medicated feed<br />>>products. This licensing has
nothing to do with handling<br />>>prohibited materials under the feed ban
rule: 21 CFR<br />>>589.2000. A license from FDA is not required to
handle<br />>>materials prohibited under 21 CFR 589.2000.)<br />>>
*<br />>><br />>> NUMBER OF FIRMS WHOSE INITIAL INSPECTION HAS
BEEN<br />>>REPORTED TO CVM - 1,203<br />>> *<br />>><br />>>
NUMBER OF FIRMS HANDLING MATERIALS PROHIBITED FOR<br />>>USE IN RUMINANT
FEED - 370 (31% of those firms<br />>>inspected/reported)<br />>> * Of
the 370 licensed feed mills handling prohibited<br />>>materials, at their
most recent inspection (could have<br />>>been an initial or a follow-up
inspection):<br />>> - 8 (2%) had products that were not labeled
as<br />>>required<br />>> - 2 (1%) did not have adequate systems to
prevent<br />>>co-mingling<br />>> - 3 (1%) did not adequately follow
record keeping<br />>>regulations<br />>> - 10 (3%) firms were found to
be out of compliance<br />>>(some firms were out of compliance with more
than one<br />>>aspect of the rule)<br />>>FEED MILLS NOT LICENSED BY
FDA<br />>><br />>> *<br />>><br />>> NUMBER OF FIRMS WHOSE
INITIAL INSPECTION HAS BEEN<br />>>REPORTED TO CVM - 4,867<br />>>
*<br />>><br />>> NUMBER OF FIRMS HANDLING MATERIALS PROHIBITED
FOR<br />>>USE IN RUMINANT FEED - 1,224 (25% of those
firms<br />>>inspected/reported)<br />>> * Of the 1,224 feed mills not
licensed by FDA<br />>>handling prohibited materials, at their most
recent<br />>>inspection (could have been an initial or a
follow-up<br />>>inspection):<br />>> - 55 (4%) had products that were
not labeled as<br />>>required<br />>> - 28 (2%) did not have adequate
systems to prevent<br />>>co-mingling<br />>> - 28 (2%) did not
adequately follow record keeping<br />>>regulations<br />>> - 86 (7%)
firms were found to be out of compliance<br />>>(some firms were out of
compliance with more than one<br />>>aspect of the rule)<br />>>OTHER
FIRMS INSPECTED<br />>><br />>>(Examples of such firms include: ruminant
feeders, on-farm<br />>>mixers, protein blenders, and
distributors.)<br />>><br />>> *<br />>><br />>> NUMBER OF FIRMS
WHOSE INITIAL INSPECTION HAS BEEN<br />>>REPORTED TO CVM - 4,710<br />>>
*<br />>><br />>> NUMBER OF FIRMS HANDLING MATERIALS PROHIBITED
FOR<br />>>USE IN RUMINANT FEED - 565 (12% of those
firms<br />>>inspected/reported)<br />>> * Of the 565 such firms
handling prohibited<br />>>materials, at their most recent inspection (could
have<br />>>been an initial or a follow-up inspection):<br />>> - 17
(3%) had products that were not labeled as<br />>>required<br />>> - 2
(less than 1%) did not have adequate systems<br />>>to prevent
co-mingling<br />>> - 7 (1%) did not adequately follow record
keeping<br />>>regulations<br />>> - 25 (4%) firms were found to be out
of compliance<br />>>(some firms were out of compliance with more than
one<br />>>aspect of the rule)<br />>>TOTALS (as of March 11,
2002)<br />>><br />>> *<br />>><br />>> NUMBER OF FIRMS WHOSE
INITIAL INSPECTION HAS BEEN<br />>>REPORTED TO CVM - 10,458<br />>>
*<br />>><br />>> NUMBER OF FIRMS HANDLING MATERIALS PROHIBITED
FOR<br />>>USE IN RUMINANT FEED - 2,153 (21% of those
firms<br />>>inspected/reported)<br />>> * Of the 2,153 firms handling
prohibited materials,<br />>>at their most recent inspection (could have
been an<br />>>initial or a follow-up inspection):<br />>> - 77 (4%) had
products that were not labeled as<br />>>required<br />>> - 34 (2%) did
not have adequate systems to prevent<br />>>co-mingling<br />>> - 35
(2%) did not adequately follow record keeping<br />>>regulations<br />>>
- 113 (5%) firms were found to be out
of<br />>>compliance<br />>>RE-INSPECTIONS<br />>><br />>>When
firms are found to be out of compliance with the feed<br />>>ban rule, FDA
lists them for a re-inspection. As of March<br />>>11, 2002, reports of
2,185 re-inspections have been<br />>>submitted to CVM. On re-inspection of
these 2,185 firms,<br />>>32 (1%) were found still to be out of compliance
with this<br />>>rule. Firms previously found to be not in compliance
have<br />>>corrected problems through a variety of ways,
including<br />>>further training of employees about the rule,
developing<br />>>systems to prevent co-mingling, re-labeling their
products<br />>>properly, and adhering to record keeping
regulations.<br />>>Other firms have achieved compliance by
eliminating<br />>>prohibited materials from their
operations.<br />>>DATABASE CHANGE<br />>><br />>>After March 11,
2002, FDA discontinued the database that<br />>>was used to compile these
numbers. The Agency is starting<br />>>a new database on April 15, 2002, and
future updates on<br />>>BSE enforcement will draw from
it.<br />>>snip...<br />>><br />>>http://www.fda.gov/cvm/index/fdavet/2002/May_June.htm#Rumi<br />>>nant<br />>>no
where did it state that they would cease to publish
the<br />>>ruminant-to-rumiant feed ban violations after the
above<br />>>publication. so, again, where are these now being
posted<br />>>on the web, what URL???<br />>><br />>>let us look at
a review of past ruminant BSE feed ban<br />>>warning letters. these are
just the ones i found. most of<br />>>you have seen them in the past, but it
does not hurt to<br />>>remind us of why they no longer post them to the
public.<br />>>if that is the case?<br />>><br />>>USA 8/4/97
RUMINANT-TO-RUMINANT FEED BAN that never was...<br />>><br />>>'ANIMAL
PROTEIN' SEARCH
9/9/02<br />>>==============================<br />>><br />>>Darling
International, Inc.<br />>>5/07/02<br />>>Seattle District Office Animal
Proteins Prohibited in<br />>>Ruminant Feed/Misbranded
[PDF]<br />>>[HTML] All American Feed &
Tractor<br />>>4/01/02<br />>>Seattle District Office Animal Proteins
Prohibited in<br />>>Ruminant Feed/Adulterated [PDF]<br />>>[HTML] Tyson
Foods<br />>>2/12/02<br />>>Seattle District Office Animal Proteins
Prohibited in<br />>>Ruminant Feed/Misbranded [PDF]<br />>>[HTML] The
Feed Bucket<br />>>12/11/01<br />>>Atlanta District Office Animal
Proteins Prohibited in<br />>>Ruminant Feed/Adulterated/Misbranded
[PDF]<br />>>[HTML] Finlayson Ag
Center<br />>>11/08/01<br />>>Minneapolis District Office Animal
Proteins Prohibited in<br />>>Ruminant Feed/Adulterated
[PDF]<br />>>[HTML] Dixon Feeds, Inc.<br />>>10/24/01<br />>>Seattle
District Office Animal Proteins Prohibited in<br />>>Ruminant
Feed/Adulterated [PDF]<br />>>[HTML] Buckeye Feed Mills,
Inc.<br />>>9/20/01<br />>>Cincinnati District Office Animal Proteins
Prohibited in<br />>>Ruminant Feed/Adulterated/Misbranded
[PDF]<br />>>[HTML] Wilcox Farms, Inc.<br />>>9/14/01<br />>>Seattle
District Office Animal Proteins Prohibited in<br />>>Ruminant Feed [PDF]
[HTML]<br />>><br />>>http://www.accessdata.fda.gov/scripts/wlcfm/full_text.cfm?<br />>>full_text=animal+protein&Search=Search<br />>>now,
compare search on
8/8/01...tss<br />>>===================================<br />>><br />>>'ANIMAL
PROTEIN' SEARCH
8/8/01<br />>>==============================<br />>><br />>>Date:
Tue, 28 Aug 2001 11:13:43 -0700<br />>>Reply-To: BSE-L<br />>>Sender:
Bovine Spongiform Encephalopathy BSE-L<br />>>From: "Terry S. Singeltary
Sr."<br />>>Subject: MAD COW FEED BAN WARNING LETTERS U.S.A. AUGUST
8,<br />>>2001<br />>>DEPARTMENT OF HEALTH AND HUMAN
SERVICES<br />>><br />>>Food and Drug
Administration<br />>><br />>>Seattle District Pacific Region 22201 23rd
Drive SE<br />>>Bothell, WA 98021-4421<br />>>Telephone: 426-486-8788
FAX: 426-483-4996<br />>><br />>>August 8,
2001<br />>><br />>>VIA CERTIFIED MAIL RETURN RECEIPT
REQUESTED<br />>><br />>>In reply refer to Warning Letter SEA
01-75<br />>><br />>>William W. Himmelspach, Owner 22195 S.W. 78th
Tualatin,<br />>>Oregon 97062<br />>>WARNING
LETTER<br />>><br />>>Dear Mr. Himmelspach:<br />>><br />>>An
investigation at your animal feed manufacturing<br />>>operation located at
22195 S.W. 78th Tualatin, Oregon<br />>>97062, conducted by a Food and Drug
Administration<br />>>investigator on July 12, 2001, found
significant<br />>>deviations from the requirements set forth in Title
21,<br />>>Code of Federal Regulations, Part 589.2000 -
Animal<br />>>Proteins Prohibited in Ruminant Feed. The regulation
is<br />>>intended to prevent the establishment and amplification
of<br />>>Bovine Spongiform Encephalopathy (BSE). Such
deviations<br />>>cause products being manufactured at this facility to
be<br />>>adulterated within the meaning of Section
402(a)(2)(C),<br />>>and 402(a)(4) of the Federal Food, Drug and Cosmetic
Act<br />>>(the Act).<br />>>Our investigation found a failure to
separate the receipt,<br />>>processing, and storage of the product
containing<br />>>prohibited material from non-prohibited material;
failure<br />>>to establish a written system, including clean-out
and<br />>>flushing procedures, to avoid commingling
and<br />>>cross-contamination of common equipment; and failure
to<br />>>maintain records sufficient to track the
materials<br />>>throughout the receipt, processing, and distribution
of<br />>>your products.<br />>>In addition, our investigation found a
failure to label<br />>>your products with the required cautionary,
statement "Do<br />>>Not Feed to Cattle or Other Ruminants," Your pig
feeds,<br />>>containing prohibited materials, were not labeled with
the<br />>>cautionary statement, and you reuse poly-tote bags
for<br />>>ruminant feed and pig feed, where the bags could
become<br />>>contaminated with prohibited material. The FDA
suggests<br />>>the statement be distinguished by different type size
or<br />>>color or other means of highlighting the statement so
that<br />>>it is easily noticed by a purchaser.<br />>>The above is not
intended to be an all-inclusive list of<br />>>deviations from the
regulations. As a manufacturer of<br />>>materials intended for animal feed
use, you are<br />>>responsible for assuring that your overall operation
and<br />>>the products you manufacture and distribute are
in<br />>>compliance with<br />>>William W. Himmelspach Tualatin, Oregon
Re: Warning Letter<br />>>SEA 01-75 Page 2<br />>>your overall operation
and the products you manufacture<br />>>and distribute are in compliance
with the law. We have<br />>>enclosed a copy of the FDA's Small Entity
Compliance Guide<br />>>to assist you with complying with the
regulation.<br />>><br />>>You should take prompt action to correct
these violations,<br />>>and you should establish a system whereby such
violations<br />>>do not recur. Failure to promptly correct these
violations<br />>>may result in regulatory action without further
notice,<br />>>such as seizure and/or injunction.<br />>>You should
notify this office in writing within 15 working<br />>>days of receipt of
this letter, of the steps you have<br />>>taken to bring your firm into
compliance with the law.<br />>>Your response should include an explanation
of each step<br />>>being taken to correct the violations, and prevent
their<br />>>recurrence. If corrective action cannot be completed in
15<br />>>working days, state the reason for the delay and the
date<br />>>by which the corrections will be completed. Include
copies<br />>>of any available documentation demonstrating
that<br />>>corrections have been made.<br />>>Your reply should be
directed to the Food and Drug<br />>>Administration, Attention: Bruce
Williamson, Compliance<br />>>Officer. If you have any questions please
contact Mr.<br />>>Williamson at (425)
483-4976.<br />>>Sincerely,<br />>><br />>>Charles M. Breen District
Director<br />>><br />>>Enclosure; Form FDA 483 Small Entity Compliance
Guide<br />>><br />>>http://www.fda.gov/foi/warning_letters/g1619d.pdf<br />>><br />>>Warning
Letters Index - Search Form Results Company Name<br />>>Date Issued Issuing
Office<br />>><br />>>Subject<br />>><br />>>File Adrian
Elevator, Inc. 5/03/01 Minneapolis District<br />>>Office Animal Proteins
Prohibited in Ruminant Feed<br />>><br />>>View File Alaska Garden and
Pet Supply, Inc. 4/27/01<br />>>Seattle District Office Animal Proteins
Prohibited in<br />>>Ruminant Feed<br />>>View File Bryan Enterprises
2/20/01 Cincinnati District<br />>>Office Feed Mill/Animal Proteins
Prohibited in Ruminant<br />>>Feed/Adulterated<br />>>View File
Carrollton Farmers Exchange 7/12/01 Cincinnati<br />>>District Office Animal
Proteins Prohibited in Ruminant<br />>>Feed<br />>>View File Centerburg
Mill and General Store, Inc 3/23/01<br />>>Cincinnati District Office Animal
Proteins Prohibited in<br />>>Ruminant Feed<br />>>View File Centerburg
Mill and General Store, Inc. 5/23/01<br />>>Cincinnati District Office
Animal Proteins Prohibited in<br />>>Ruminant Feed<br />>>View File
Central Ohio Farmers Cooperative, Inc. 5/24/01<br />>>Cincinnati District
Office Animal Protein Prohibited in<br />>>Ruminant Feed<br />>>View
File Champaign Landmark, Inc. 3/05/01 Cincinnati<br />>>District Office
Animal Proteins Prohibited in
Ruminant<br />>>Feed/Misbranded<br />>>View File Countryline Co-Op, Inc.
5/14/01 Cincinnati<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Dorset Milling 4/16/01 Cincinnati
District<br />>>Office Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View File Earl B. Olson Feed Mill 4/23/01
Minneapolis<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Faler Feed Store, Inc. 3/21/01
Cincinnati<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Farmers Mill & Elevator
Company 3/30/01 Atlanta<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Farnam Companies, Inc. 7/20/01
Kansas City<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed/Adulterated<br />>>View File Greeley Elevator
Company 4/04/01 Denver District<br />>>Office Animal Proteins Prohibited in
Ruminant Feed<br />>><br />>>View File Hartville Elevator Company, Inc.
2/22/01<br />>>Cincinnati District Office Feed Mill/Animal
Proteins<br />>>Prohibited in Ruminant Feed/Adulterated<br />>>View File
Himmelspach, William W. 8/08/01 Seattle District<br />>>Office Animal
Proteins Prohibited in Ruminant Feed<br />>><br />>>View File Integral
Fish Foods, Inc. 6/12/01 Denver<br />>>District Office Animal Proteins
Prohibited in Ruminant<br />>>Feed<br />>>View File Jefferson Milling
Company 4/16/01 Cincinnati<br />>>District Office Animal Proteins Prohibited
in Ruminant<br />>>Feed<br />>>View File Lime Creek Ag Services, Inc.
4/25/01 Minneapolis<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Material Resources LLC 5/04/01
Chicago District<br />>>Office Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View File Material Resources, LLC 5/04/01 Chicago
District<br />>>Office Animal Protein Prohibited in Ruminant
Feed<br />>><br />>>View File Medina Landmark, Inc. 3/23/01
Cincinnati<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Minister Farmers Cooperative
Exchange, Inc.<br />>>4/10/01 Cincinnati District Office Animal
Proteins<br />>>Prohibited in Ruminant Feed/Feed Mill<br />>>View File
Peco Foods, Inc. 2/23/01 New Orleans District<br />>>Office CGMP
Requirements for Medicated Feeds/Animal<br />>>Proteins Prohibited in
Ruminant Feed<br />>>View File Perry Coal and Feed Company 4/16/01
Cincinnati<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Rietdyk's Milling Company 3/05/01
Seattle<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File River Valley Co-Op 3/22/01
Cincinnati District<br />>>Office Animal Proteins Prohibeted in Ruminant
Feed<br />>><br />>>View File River Valley Co-Op 5/22/01 Cincinnati
District<br />>>Office Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View File Round Lake Farmers Coop. 5/30/01
Minneapolis<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Rudy, Inc. 3/22/01 Cincinnati
District Office<br />>>Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View File Rudy, Inc. 5/22/01 Cincinnati District
Office<br />>>Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View File Sandy Lake Mills 4/09/01 Philadelphia
District<br />>>Office Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View File Shields Feed and Supply Company 3/07/01
New<br />>>Orleans District Office Animal Proteins Prohibited
in<br />>>Ruminant Feed<br />>>View File Stewart's Farm Supply 3/21/01
Cincinnati<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Superior Feeds 6/06/01 Seattle
District Office<br />>>Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View File The Scoular Company 5/30/01 Minneapolis
District<br />>>Office Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View File University of Minnesota 5/10/01
Minneapolis<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Valley Feed Mill, Inc. 5/22/01
Cincinnati<br />>>District Office Animal Proteins Prohibited in
Ruminant<br />>>Feed<br />>>View File Wallowa County Grain Growers, Inc.
5/17/01<br />>>Seattle District Office Animal Proteins Prohibited
in<br />>>Ruminant Feed<br />>>View File Wallowa County Grain Growers,
Inc. 5/17/01<br />>>Seattle District Office Animal Proteins Prohibited
in<br />>>Ruminant Feed<br />>>View File Western Reserve Farm
Cooperative 3/21/01<br />>>Cincinnati District Office Animal Protein
Prohibited in<br />>>Ruminant Feed<br />>>View File Yachere Feed, Inc.
4/09/01 Philadelphia District<br />>>Office Animal Proteins Prohibited in
Ruminant Feed<br />>><br />>>View File Z & W Mill, Inc. 3/27/01
Denver District Office<br />>>Animal Proteins Prohibited in Ruminant
Feed<br />>><br />>>View
File<br />>><br />>>http://63.75.126.221/scripts/wlcfm/resultswl.cfm<br />>><br />>>(TYPE
IN 'ANIMAL PROTEIN')<br />>><br />>>we must not forget the ANIMAL
PROTEIN FED TO DEER/ELK.<br />>>those warning letters were stopped long
ago;<br />>><br />>>Subject: MAD DEER/ELK DISEASE AND POTENTIAL
SOURCES<br />>>Date: Sat, 25 May 2002 18:41:46 -0700<br />>>From: "Terry
S. Singeltary Sr." <flounder @wt.net=""><br />>>Reply-To: BSE-L<br />>>To:
BSE-L<br />>><br />>>8420-20.5% Antler Developer<br />>>For Deer and
Game in the wild<br />>>Guaranteed Analysis Ingredients / Products
Feeding<br />>>Directions<br />>>snip...<br />>><br />>>_animal
protein_<br />>><br />>>http://www.surefed.com/deer.htm<br />>><br />>>BODE'S
GAME FEED SUPPLEMENT #400<br />>>A RATION FOR DEER<br />>>NET WEIGHT 50
POUNDS<br />>>22.6
KG.<br />>><br />>>snip...<br />>><br />>>_animal
protein_<br />>><br />>>http://www.bodefeed.com/prod7.htm<br />>><br />>>Ingredients<br />>><br />>>Grain
Products, Plant Protein Products, Processed Grain<br />>>By-Products, Forage
Products, Roughage Products 15%,<br />>>Molasses Products, __Animal Protein
Products__,<br />>>snip...<br />>><br />>>http://www.bodefeed.com/prod6.htm<br />>>===================================<br />>><br />>>MORE
ANIMAL PROTEIN PRODUCTS FOR DEER<br />>><br />>>Bode's #1 Game
Pellets<br />>>A RATION FOR
DEER<br />>>F3153<br />>><br />>>GUARANTEED
ANALYSIS<br />>>Crude Protein (Min) 16%<br />>>Crude Fat (Min)
2.0%<br />>>snip...<br />>><br />>>Ingredients<br />>><br />>>Grain
Products, Plant Protein Products, Processed Grain<br />>>By-Products, Forage
Products, Roughage Products, 15%<br />>>Molasses Products, __Animal Protein
Products__,<br />>>Monocalcium Phosphate, Dicalcium Phosphate,
Salt,<br />>>snip...<br />>><br />>>FEEDING
DIRECTIONS<br />>>Feed as Creep Feed with Normal
Diet<br />>><br />>>http://www.bodefeed.com/prod8.htm<br />>><br />>>INGREDIENTS<br />>><br />>>Grain
Products, Roughage Products (not more than 35%),<br />>>Processed Grain
By-Products, Plant Protein Products,<br />>>Forage Products, __Animal
Protein Products__,<br />>>L-Lysine, Calcium Carbonate, Salt,
Monocalcium/Dicalcium<br />>>snip...<br />>><br />>>DIRECTIONS FOR
USE<br />>><br />>>Deer Builder Pellets is designed to be fed to deer
under<br />>>range conditions or deer that require higher levels
of<br />>>protein. Feed to deer during gestation,
fawning,<br />>>lactation, antler growth and pre-rut, all phases
which<br />>>require a higher level of nutrition. Provide
adequate<br />>>amounts of good quality roughage and fresh water at
all<br />>>times.<br />>>http://www.profilenutrition.com/Pro...er_pellets.html<br />>><br />>>DEPARTMENT
OF HEALTH & HUMAN SERVICES<br />>>PUBLIC HEALTH SERVICE<br />>>FOOD
AND DRUG ADMINISTRATION<br />>><br />>>April 9, 2001 WARNING
LETTER<br />>><br />>>01-PHI-12<br />>>CERTIFIED
MAIL<br />>>RETURN RECEIPT REQUESTED<br />>><br />>>Brian J.
Raymond, Owner<br />>>Sandy Lake Mills<br />>>26 Mill
Street<br />>>P.O. Box 117<br />>>Sandy Lake, PA
16145<br />>>PHILADELPHIA DISTRICT<br />>><br />>>Tel:
215-597-4390<br />>><br />>>Dear Mr.
Raymond:<br />>><br />>>Food and Drug Administration Investigator
Gregory E.<br />>>Beichner conducted an inspection of your animal
feed<br />>>manufacturing operation, located in Sandy
Lake,<br />>>Pennsylvania, on March 23, 2001, and determined that
your<br />>>firm manufactures animal feeds including feeds
containing<br />>>prohibited materials. The inspection found
significant<br />>>deviations from the requirements set forth in Title
21,<br />>>code of Federal Regulations, part 589.2000 -
Animal<br />>>Proteins Prohibited in Ruminant Feed. The regulation
is<br />>>intended to prevent the establishment and amplification
of<br />>>Bovine Spongiform Encephalopathy (BSE) . Such
deviations<br />>>cause products being manufactured at this facility to
be<br />>>misbranded within the meaning of Section 403(f), of
the<br />>>Federal Food, Drug, and Cosmetic Act (the Act).<br />>>Our
investigation found failure to label your swine feed<br />>>with the
required cautionary statement "Do Not Feed to<br />>>cattle or other
Ruminants" The FDA suggests that the<br />>>statement be distinguished by
different type-size or color<br />>>or other means of highlighting the
statement so that it is<br />>>easily noticed by a purchaser.<br />>>In
addition, we note that you are using approximately 140<br />>>pounds of
cracked corn to flush your mixer used in the<br />>>manufacture of animal
feeds containing prohibited<br />>>material. This flushed material is fed to
wild game<br />>>including deer, a ruminant animal. Feed material which
may<br />>>potentially contain prohibited material should not be
fed<br />>>to ruminant animals which may become part of the
food<br />>>chain.<br />>>The above is not intended to be an
all-inclusive list of<br />>>deviations from the regulations. As a
manufacturer of<br />>>materials intended for animal feed use, you
are<br />>>responsible for assuring that your overall operation
and<br />>>the products you manufacture and distribute are
in<br />>>compliance with the law. We have enclosed a copy of
FDA's<br />>>Small Entity Compliance Guide to assist you with
complying<br />>>with the regulation... blah, blah,
blah...<br />>>http://www.fda.gov/foi/warning_letters/g1115d.pdf<br />>>===================================================<br />><br />><br />>
SNIP...<br />><br />> TSS<br />><br />> ###########
http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############</flounder></tmg1></tmg1></bse-l></nbatalle></flounder></lgrassie></bse-l>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-43061406861170103762010-07-27T12:21:00.000-07:002010-07-27T12:43:50.164-07:00Spontaneous generation of mammalian prionsSpontaneous generation of mammalian prions<br /><br /><br />Julie A. Edgeworth, Nathalie Gros, Jack Alden, Susan Joiner, Jonathan D. F. Wadsworth, Jackie Linehan, Sebastian Brandner, Graham S. Jackson, Charles Weissmann1,2, and John Collinge1 + Author Affiliations<br /><br />Medical Research Council Prion Unit, Department of Neurodegenerative Disease, University College London Institute of Neurology, London WC1N 3BG, United Kingdom ? 2Present address: Department of Infectology, Scripps Florida, Jupiter, FL 33458.<br /><br />Edited by David S. Eisenberg, University of California, Los Angeles, CA, and approved June 29, 2010 (received for review March 28, 2010)<br /><br />Abstract Prions are transmissible agents that cause lethal neurodegeneration in humans and other mammals. Prions bind avidly to metal surfaces such as steel wires and, when surface-bound, can initiate infection of brain or cultured cells with remarkable efficiency. While investigating the properties of metal-bound prions by using the scrapie cell assay to measure infectivity, we observed, at low frequency, positive assay results in control groups in which metal wires had been coated with uninfected mouse brain homogenate. This phenomenon proved to be reproducible in rigorous and exhaustive control experiments designed to exclude prion contamination. The infectivity generated in cell culture could be readily transferred to mice and had strain characteristics distinct from the mouse-adapted prion strains used in the laboratory. The apparent ”spontaneous generation” of prions from normal brain tissue could result if the metal surface, possibly with bound cofactors, catalyzed de novo formation of prions from normal cellular prion protein. Alternatively, if prions were naturally present in the brain at levels not detectable by conventional methods, metal surfaces might concentrate them to the extent that they become quantifiable by the scrapie cell assay.<br /><br />snip...<br /><br />Discussion Human prion diseases may be acquired, inherited (with pathogenic germline mutation in PRNP) or sporadic, probably as a consequence of rare, stochastic de novo formation of prions (25).<br /><br />Deleault et al. (8) reported de novo generation of prions by the protein misfolding cyclic amplification (PMCA) procedure, using PrPC purified from normal brain as substrate. However, the resulting strain could not be distinguished from RML. Generation of novel prion strains by PMCA was also reported by Barria et al. (26) and by Wang et al. in a novel PMCA system based on purified recombinant PrP, a synthetic anionic lipid and liver RNA (10).<br /><br />Prion strains, even those subjected to biological cloning, may be heterogeneous at a molecular level and consist of an ensemble or quasispecies which may be selected by, and adapt in, different hosts (23, 24). According to such a model, this novel strain may have been selected from an ensemble of spontaneous prions as the preferred molecular species for stable propagation in PK1 cells, essentially adapting to PK1 cells in a similar way in which RML prions appear to have done.<br /><br />PrPSc could occur at very low levels in healthy brains, almost never reaching levels that lead to disease (27). If so, “uninfected” brain homogenates might contain undetected PrPSc seeds that are concentrated on steel wires (16) and infect PK1 cells in our experiments. However, if normal brain is devoid of prions, our results mean that infectivity is generated de novo, perhaps by a mechanism in which seed formation is catalyzed by the steel surface (Fig. S1). It is also possible that brain lipids and/or RNA, known to be able to act as cofactors in some experimental systems (8, 10), could have bound to wires and played a role in triggering de novo prion formation in PK1 cells.<br /><br />This raises the question as to whether “spontaneous prions” are indeed generated de novo or whether brains from uninfected animals contain a low level of prions that are concentrated by adsorption to the wire surface and thereby rendered detectable by the SCA. Differentiating between these possibilities is a challenging one but could be achieved by kinetic experiments: propagation of preexistent seed should be proportional to brain homogenate concentration; de novo seed formation would be a higher-order function of concentration (28, 29).<br /><br /><a href="http://www.pnas.org/content/early/2010/07/16/1004036107.abstract?etoc">http://www.pnas.org/content/early/2010/07/16/1004036107.abstract?etoc</a><br /><br /><br /><br />This article contains supporting information online at<br /><br /><a href="http://www.pnas.org/content/suppl/2010/07/18/1004036107.DCSupplemental">http://www.pnas.org/content/suppl/2010/07/18/1004036107.DCSupplemental</a><br /><br /><br /><br />FULL TEXT PDF ;<br /><br /><a href="http://www.pnas.org/content/early/2010/07/16/1004036107.full.pdf+html">http://www.pnas.org/content/early/2010/07/16/1004036107.full.pdf+html</a><br /><br /><br /><br />Greetings,<br /><br />SO, problem solved ? Are we all suppose to believe that the atypical BSE strains and sporadic CJD strains, are just another happenstance of spontaneous mutation in all cases, just an old cow disease such as sporadic CJD in humans i.e. old people disease, another spontaneous mutation in all cases of sporadic CJD. SO, we are suppose to believe that out of all these atypical BSE cases popping up around the globe, NONE were caused by feed ? I don't believe that for a New York minute. I don't believe all cases of sporadic CJD are all spontaneous either. Either the UKBSEnvCJD theory was totally wrong, or this BSe that all other TSE are of a spontaneous mutation is wrong. You cannot have your cake, and eat it too.<br /><br />With headlines like, Contact with steel 'linked to CJD' , or Infectious prions can suddenly erupt from normal brain tissue , or infectious prions can arise spontaneously in normal brain tissue , I decided to wait and look at the study. glad I did. nothing about this study shows that 85% to 90% of all human TSE i.e. the sporadic CJD's show they are a spontaneous generation from nothing. It does however cause confusion, of which, in my opinion, could have been resolved. I will ask the same question here, I ask Professor Stanley Prusiner, of which I never did receive an answer, I ask this same question. OF this supposedly Spontaneous generation of mammalian prions in this study, does this mean all sporadic CJD is spontaneous? does it mean half ? does in mean one third, one tenth, one hundredth, one thousandth, one millionth, just exactly what ? what does this really show ? Does this study show what many officials and industry is hoping, that it is all spontaneous mutation from nothing ? IF so, why did the authors of this study not explain this ? THERE is something terribly wrong with this prion and the UKBSEnvCJD only theory. It just does not compute, and I believe that this study raises more questions than answers. I believe that the authors of this study should have explained better whether or not this study shows that indeed all cases of sporadic CJD are of a spontaneous mutation cause, or not. They could have done a much better job of explaining what this study shows, or what it _does not_ show, and in my opinion, it damn sure does not show that all cases of sporadic CJD strains, and or atypical BSE strains arise spontaneously, a natural mutation, without any route and source of agent. But, this is what this study insinuates, and that is how it will be interpreted by industry groups and officials. I think the Authors of this study could have better interpreted that to the public, either way, either sporadic CJD is all spontaneous, or not, if not, how much is spontaneous. After 2+ decades of debating this, they owe the public this in my opinion. Stand Tall and tell us how much of this spontaneous mutation from nothing, how much of the 85% to 90% of all human TSE (well, maybe more than that IF you include the infamous sporadic FFI?) i.e. sporadic CJD, how much of this spontaneous mutation from nothing does this consist of ? 1 in a 100 cases, 1 in a thousand, 1 in a million, 1 in a billion, of sporadic CJD and sFFI cases etc. ? please tell me, or at least tell the public that this study does NOT insinuate what it does.<br /><br />My reply and question to Professor Stanley Prusiner (of which he never would answer), the same question I now address to Julie A. Edgeworth, Nathalie Gros, Jack Alden, Susan Joiner, Jonathan D. F. Wadsworth, Jackie Linehan, Sebastian Brandner, Graham S. Jackson, Charles Weissmann1,2, and John Collinge1 + Author Affiliations. ...<br /><br />REPORT ON MEASURES RELATING TO BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN THE UNITED STATES Terry S. Singeltary Sr. February 11, 2004<br /><br />Greetings,<br /><br />as a lay person;-) i am thankful for Dr. Prusiners report below. I only wish that he would elaborate on the spontaneous aspect of sporadic CJD and how many of the 85%+ of all CJDs does he think happens spontaneously without route and source of the agent? I am concerned that people who read this, will come to the conclusion that all sporadic CJDs are a spontaneous mutation, when in reality all sporadic CJD is, is CJD from unknown route and source and they could be many. in fact, there could be many phenotypes of CJD that are now called sporadic CJD...<br /><br />snip...full text ;<br /><br /><a href="http://www.agobservatory.org/library.cfm?refID=30406">http://www.agobservatory.org/library.cfm?refID=30406</a><br /><br /><br /><br />Stanley Prusiner comments January 27, 2004 ;<br /><br />Statement from Stanley B. Prusiner, M.D., about ‘Mad Cow’ disease in the United States - January 27, 2004<br /><br />Thank you, I am pleased to be here to address the Food Safety Caucus of the House of Representatives of the United States Congress about Mad Cow disease. I appear here as a concerned citizen, a loving parent, a dedicated physician specializing in Neurology, an educator who is a Professor of Neurology at the University of California, and scientist-businessman who is the Founder of InPro Biotechnology. I am also an expert on prion diseases, one of which is Mad Cow disease or bovine spongiform encephalopathy, often-abbreviated BSE. Both Federal and State Governments now find themselves embroiled over concerns over Mad Cow disease after Secretary of Agriculture, Ann Veneman, announced on December 23, 2003, that a 6.5-year-old cow from Mabton, Washington, had been diagnosed with Mad Cow disease. I would like to discuss five points concerning Mad Cow disease and what I believe should be done in our country to combat this malady.<br /><br />1. Prions cause Mad Cow disease: First, Mad Cow disease is caused by an infectious agent that is so small that it cannot even be seen with the most powerful microscopes. These small infectious agents are called prions. Although large aggregates of prions can be studied with electron microscopes, we still cannot see the individual prions. For more than a century, viruses that can be seen in the electron microscope were the smallest known microbes. But, prions are much smaller than viruses and this extremely small size makes prions extremely difficult to kill.<br /><br />2. Prion disease is always fatal: Second, prions cause severe destruction of the brain. The prion diseases of humans and animals are 100% fatal. Indeed, everyone with prion disease eventually dies. A single prion is sufficient to initiate the multiplication process that results in hundreds of prions being made followed by thousands, then millions and finally billions. It is well documented that billions of prions destroy the brain and spinal cord. From a wide variety of biomedical investigations, we know that prions from cattle can infect humans and destroy their brains. More than 150 teenagers and young adults in Europe have died of prion disease that they contracted after eating prion tainted beef or beef products.<br /><br />3. Spontaneously induced prions: Third, prions arise spontaneously. This is an extremely important concept; furthermore, the ability to arise spontaneously is a feature that distinguishes prions from viruses. Any mammal is capable of producing prions spontaneously.<br /><br />2<br /><br />In humans, the most common form of prion disease results from the spontaneous formation of prions. Despite decades of looking for prions in the environment, there is no evidence for exposure to prions in spontaneous cases of prion disease.<br /><br />The initial event in an epidemic of human prion disease referred to as kuru must have been a spontaneous case of prion disease. Once kuru prions arose spontaneously, they were propagated by ritualistic cannibalism that was practiced among New Guinea natives. While halting cannibalism of dead relatives resulted in the disappearance of kuru in a small population of natives, it did not eliminate the spontaneous formation of human prions. Similarly, stopping industrial cannibalism where cattle are fed the rendered offal of other cattle has diminished the number of cattle with BSE in Britain but will not prevent spontaneous prions from being formed. Thus, while changing feeding practices for cattle will stop the amplification of prions, it will not prevent the spontaneous formation of bovine prions.<br /><br />As I said, prions can develop spontaneously within any mammal. We don’t know what triggers this process but there are several reasonable hypotheses, one or more of which may eventually explain the spontaneous formation of prions.<br /><br />4. The Japanese solution: Fourth, I cannot understand as the father of two daughters and the uncle of a niece and nephew why our country remains unwilling to adopt the Japanese policy of testing every cow and bull destined for consumption by humans. I have difficulty explaining to these young people that the beef in Japan is safer than that in the U.S.<br /><br />The United States has the same problem that the Japan has, but the Japanese test all of the cattle that they slaughter. This issue particularly troubles children when they learn that the time from exposure to prions until the onset of neurological disease can exceed 50 years. Some New Guinea natives developed kuru more than 50 years after ingesting prions during cannibalistic feasts.<br /><br />5. Prion science is new: Fifth, the science of prions is still very young. Only 25 years ago, I discovered prions and named these unprecedented infectious agents. Thus, the naysayers, who continue to deny the existence of prions, should not surprise you. A chorus of naysayers has always accompanied big changes in scientific thinking. When Galileo wrote about the planets orbiting the sun, he was imprisoned. How dare he think that the earth was not the center of universe? From the time that Einstein proposed his special theory of relatively in 1905 until his death 50 years later, the naysayers scorned him almost daily. Each week, at least two or three letters arrived at his Princeton office that declared him insane and his theories impossible. Only his death terminated this non-sense! Philip Semelweiss, a Viennese obstetrician, was eventually admitted to an insane asylum. Semelweiss was ridiculed mercilessly for proposing that his<br /><br />3<br /><br />colleagues could prevent deadly bacterial infections in mothers after childbirth if they would only wash their hands between the deliveries of newborn infants. And few believed Alfred Wagener when he proposed continental drift as a mechanism to explain the shapes and positions of the landmasses on our planet.<br /><br />I recited a few instances of “scientific heresy” to place the discovery of prions in some perspective for you. For much of my career, I faced a legion of scientists who vehemently argued that prions couldn’t exist! They yelled, “prions are nonsense. They are impossible!” Twenty-five years after my discovery of prions, there remain some people who are still unable or unwilling to comprehend the novel concepts of prion biology. The famous German physicist Max Planck encountered many naysayers when he and others set forth the principles of quantum mechanics. In frustration, Planck once remarked, “a new scientific truth does not win out by convincing its opponents, rather they eventually die off and a whole generation familiar with it grows up.”<br /><br />In non-scientific terms, prions must be considered new, strange and scary microbes by any measure. Twenty-five years ago, there were no prions – now the biology of prions is taught in every medical school throughout the world. Prion biology is also taught in many high schools and most colleges. Moreover, the word “prion” appears in every dictionary.<br /><br />Because the discovery of prions ushered in major changes in our thinking, your duties as Congresswomen and Congressmen have and will continue to be subject to much misinformation with respect to Mad Cow disease. But I hasten to add that this is inevitable when an entirely new field of science emerges. Despite the fact that prions were once branded scientific heresy and are now considered orthodoxy by most scholars, the naysayers still exist. This means that you and your staff will hear some opinions that are not based on the body of scientific knowledge that has been accumulated over the past quarter century. Instead, you will hear views that ignore a constantly enlarging body of scientific information that has been verified by experimental studies.<br /><br />Concluding remarks: In conclusion, from studies over the past half-century, we know that people should not eat prions, particularly prions of human or bovine origin. I want to reiterate that the problem of prion contamination in the food supply will not disappear. If we do nothing, confidence in the safety of food supply will only continue to erode. The sooner we face the problem of prion contamination, the more easily we shall be able to contain it. Only the Japanese solution of testing every slaughtered cow or bull will eliminate prions from the food supply and restore consumer confidence. Certainly, the citizens of the most prosperous and accomplished nation on our planet deserve to eat meat that is devoid of prions.<br /><br /><a href="http://www.agobservatory.org/library.cfm?refID=30405">http://www.agobservatory.org/library.cfm?refID=30405</a><br /><br /><br /><br />2010 atypical BSE<br /><br />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.<br /><br /><a href="http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2">http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2</a><br /><br /><br /><br />Saturday, June 12, 2010<br /><br />PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse<br /><br /><a href="http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html">http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html</a><br /><br /><br /><br />14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)<br /><br />18.173 page 189<br /><br />Experimental Challenge of Cattle with H-type and L-type Atypical BSE<br /><br />A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada<br /><br />Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.<br /><br />Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.<br /><br />Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.<br /><br /><br /><a href="http://www.isid.org/14th_icid/">http://www.isid.org/14th_icid/</a><br /><br /><br /><a href="http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf">http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf</a><br /><br /><br /><a href="http://www.isid.org/publications/ICID_Archive.shtml">http://www.isid.org/publications/ICID_Archive.shtml</a><br /><br /><br /><br />14th ICID International Scientific Exchange Brochure -<br /><br />Final Abstract Number: ISE.114<br /><br />Session: International Scientific Exchange<br /><br />Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America<br /><br />update October 2009<br /><br />T. Singeltary<br /><br />Bacliff, TX, USA<br /><br />Background:<br /><br />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.<br /><br />Methods:<br /><br />12 years independent research of available data<br /><br />Results:<br /><br />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.<br /><br />Conclusion:<br /><br />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.<br /><br />see page 114 ;<br /><br /><br /><a href="http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf">http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf</a><br /><br /><br /><br />Sent: Friday, April 16, 2010 11:38 AM Subject: PRO-MED ATYPICAL SCRAPIE<br /><br />Background -----------<br /><br />"Retrospective studies have identified cases predating the initial identification of this form of scrapie, and epidemiological studies have indicated that it does not conform to the behaviour of an infectious disease, giving rise to the hypothesis that it represents spontaneous disease. However, atypical scrapie isolates have been shown to be infectious experimentally, through intracerebral inoculation in transgenic mice and sheep. [Many of the neurological diseases can be transmitted by intracerebral inoculation, which causes this moderator to approach intracerebral studies as a tool for study, but not necessarily as a direct indication of transmissibility of natural diseases. - Mod.TG]<br /><br />"The 1st successful challenge of a sheep with 'field' atypical scrapie from an homologous donor sheep was reported in 2007.<br /><br />"Results --------<br /><br />"This study demonstrates that atypical scrapie has distinct clinical, pathological, and biochemical characteristics which are maintained on transmission and sub-passage, and which are distinct from other strains of transmissible spongiform encephalopathies in the same host genotype.<br /><br />"Conclusions ------------<br /><br />Atypical scrapie is consistently transmissible within AHQ homozygous sheep, and the disease phenotype is preserved on sub-passage."<br /><br />Lastly, this moderator wishes to thank Terry Singletary for some of his behind the scenes work of providing citations and references for this posting. - Mod.TG]<br /><br />The HealthMap/ProMED-mail interactive map of Australia is available at <http:>. - Sr.Tech.Ed.MJ]<br /><br /><br /><a href="http://www.promedmail.org/pls/otn/f?p=2400:1001:962575216785367::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,81729">http://www.promedmail.org/pls/otn/f?p=2400:1001:962575216785367::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,81729</a><br /><br /><br /><br />Archive Number 20100405.1091 Published Date 05-APR-2010<br /><br />Subject PRO/AH/EDR> Prion disease update 1010 (04)<br /><br />snip...<br /><br />[Terry S. Singeltary Sr. has added the following comment:<br /><br />"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.<br /><br /><br />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?"<br /><br /><br /><a href="http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101">http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101</a><br /><br /><br /><br />Monday, March 29, 2010<br /><br />CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER<br /><br /><br />>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<<br /><br /><br /><a href="http://recordandoalinda.com/index.php?option=com_content&view=article&id=19&Itemid=8">http://recordandoalinda.com/index.php?option=com_content&view=article&id=19&Itemid=8</a><br /><br /><br /><a href="http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=2:frontpage&catid=1:frontpage">http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=2:frontpage&catid=1:frontpage</a><br /><br /><br /><br />WHY IS IT THE 'GOLD STANDARD' TO IGNORE THIS SCIENCE $$$<br /><br /><br />2008 Emerg Infect Dis. 2008 December; 14(12): 1898-1901. doi: 10.3201/eid1412.080941. PMCID: PMC2634647 Copyright notice<br /><br /><br />Transmission of Atypical Bovine Prions to Mice Transgenic for Human Prion Protein<br /><br /><br />Vincent Béringue, Laëtitia Herzog, Fabienne Reine, Annick Le Dur, Cristina Casalone, Jean-Luc Vilotte, and Hubert Laude Institut National de la Recherche Agronomique, Jouy-en-Josas, France (V. Béringue, L. Herzog, F. Reine, A. Le Dur, J.-L. Vilotte, H. Laude) Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Turin, Italy (C. Casalone) Corresponding author. Address for correspondence: Vincent Béringue, Institut National de la Recherche Agronomique, UR892, Virologie Immunologie Moléculaires, F-78350 Jouy-en-Josas, France; email: <a href="mailto:vincent.beringue@jouy.inra.fr">vincent.beringue@jouy.inra.fr</a><br /><br /><br />This article has been cited by other articles in PMC.<br /><br /><br />Abstract<br /><br /><br />To assess risk for cattle-to-human transmission of prions that cause uncommon forms of bovine spongiform encephalopathy (BSE), we inoculated mice expressing human PrP Met129 with field isolates. Unlike classical BSE agent, L-type prions appeared to propagate in these mice with no obvious transmission barrier. H-type prions failed to infect the mice.<br /><br /><br />Keywords: prions, BSE, PrP, strains, transgenic mice, dispatch<br /><br /><br />Abstract<br /><br /><br />The epizootic of bovine spongiform encephalopathy (BSE) is under control in European countries >20 years after the first cases were diagnosed in the United Kingdom. Thus far, BSE is the only animal prion disease known to have been transmitted to humans, leading to a variant form of Creutzfeldt-Jakob disease (vCJD) (1). The large-scale testing of livestock nervous tissues for the presence of protease-resistant prion protein (PrPres) has enabled assessment of BSE prevalence and exclusion of BSE-infected animals from human food (2). This active surveillance has led to the recognition of 2 variant PrPres molecular signatures, termed H-type and L-type BSE. They differ from that of classical BSE by having protease-resistant fragments of a higher (H) or a slightly lower (L) molecular mass, respectively, and different patterns of glycosylation (3-5). Both types have been detected worldwide as rare cases in older animals, at a low prevalence consistent with the possibility of sporadic forms of prion diseases in cattle (6). Their experimental transmission to mice transgenic for bovine PrP demonstrated the infectious nature of such cases and the existence of distinct prion strains in cattle (5,7-9). Like the classical BSE agent, H- and L-type prions can propagate in heterologous species (7-11). Thus, both agents are transmissible to transgenic mice expressing ovine PrP (VRQ allele). Although H-type molecular properties are conserved on these mice (9), L-type prions acquire molecular and neuropathologic phenotypic traits undistinguishable from BSE or BSE-related agents that have followed the same transmission history (7). Similar findings have been reported in wild-type mice (8). An understanding of the transmission properties of these newly recognized prions when confronted with the human PrP sequence is needed. In a previous study, we measured kinetics of PrPres deposition in the brain to show that L-type prions replicate faster than BSE prions in experimentally inoculated mice that express human PrP (7). In a similar mouse model, the L-type agent (alternatively named BASE) was also shown to produce overt disease with an attack rate of ~30% (12). However, no strict comparison with BSE agent has been attempted. As regards the H-type agent, its potential virulence for mice that express human PrP Met129 remains to be assessed. We now report comparative transmission data for these atypical and classical BSE prions.<br /><br />snip...<br /><br />Conclusions<br /><br />We found that atypical L-type bovine prions can propagate in human PrP transgenic mice with no significant transmission barrier. Lack of a barrier is supported by the 100% attack rate, the absence of reduction of incubation time on secondary passage, and the conservation of PrPres electrophoretic profile. In comparison, transmission of classical BSE agent to the same mice showed a substantial barrier. Indeed, 3 passages were necessary to reach a degree of virulence comparable to that of vCJD agent in these mice (13), which likely reflects progressive adaptation of the agent to its new host. At variance with the successful transmission of classical BSE and L-type agents, H-type agent failed to infect tg650 mice. These mice overexpress human PrP and were inoculated intracranially with a low dilution inoculum (10% homogenate). Therefore, this result supports the view that the transmission barrier of BSE-H from cattle to humans might be quite robust. It also illustrates the primacy of the strain over PrP sequence matching for cross-species transmission of prions (15). Extrapolation of our data raises the theoretical possibility that the zoonotic risk associated with BSE-L prions might be higher than that associated with classical BSE, at least for humans carrying the Met129 PrP allele. This information underlines the need for more intensive investigations, in particular regarding the tissue tropism of this agent. Its ability to colonize lymphoid tissues is a potential, key factor for a successful transmission by peripheral route. This issue is currently being explored in the tg650 mice. Although recent data in humanized mice suggested that BSE-L agent is likely to be lymphotropic (12), preliminary observations in our model suggested that its ability to colonize such tissues is comparatively much lower than that of classical BSE agent.<br /><br /><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2634647/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2634647/</a><br /><br /><br /><br />2002<br /><br />BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein<br /><br />Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002. This article has been cited by other articles in PMC. Other Sections?<br /><br />Abstract<br /><br />Variant Creutzfeldt-Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.<br /><br />Keywords: BSE/Creutzfeldt-Jakob disease/prion/transgenic<br /><br /><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed</a><br /><br /><br /><br />2004<br /><br />Originally published in Science Express on 11 November 2004 Science 3 December 2004: Vol. 306. no. 5702, pp. 1793 - 1796 DOI: 10.1126/science.1103932<br /><br />Reports Human Prion Protein with Valine 129 Prevents Expression of Variant CJD Phenotype Jonathan D. F. Wadsworth, Emmanuel A. Asante, Melanie Desbruslais, Jacqueline M. Linehan, Susan Joiner, Ian Gowland, Julie Welch, Lisa Stone, Sarah E. Lloyd, Andrew F. Hill,* Sebastian Brandner, John Collinge<br /><br />Variant Creutzfeldt-Jakob disease (vCJD) is a unique and highly distinctive clinicopathological and molecular phenotype of human prion disease associated with infection with bovine spongiform encephalopathy (BSE)-like prions. Here, we found that generation of this phenotype in transgenic mice required expression of human prion protein (PrP) with methionine 129. Expression of human PrP with valine 129 resulted in a distinct phenotype and, remarkably, persistence of a barrier to transmission of BSE-derived prions on subpassage. Polymorphic residue 129 of human PrP dictated propagation of distinct prion strains after BSE prion infection. Thus, primary and secondary human infection with BSE-derived prions may result in sporadic CJD-like or novel phenotypes in addition to vCJD, depending on the genotype of the prion source and the recipient.<br /><br />Medical Research Council (MRC) Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK.<br /><br />* Present address: Department of Biochemistry and Molecular Biology and Department of Pathology, University of Melbourne, Parkville, Victoria 3010, Australia.<br /><br />To whom correspondence should be addressed. E-mail: j.collinge@prion.ucl.ac.uk<br /><br /><a href="http://www.sciencemag.org/cgi/content/abstract/306/5702/1793">http://www.sciencemag.org/cgi/content/abstract/306/5702/1793</a><br /><br /><br /><br />2008<br /><br />Prominent and Persistent Extraneural Infection in Human PrP Transgenic Mice Infected with Variant CJD<br /><br />The evolution of the variant Creutzfeldt-Jakob disease (vCJD) epidemic is hazardous to predict due to uncertainty in ascertaining the prevalence of infection and because the disease might remain asymptomatic or produce an alternate, sporadic-like phenotype.<br /><br />Transgenic mice were produced that overexpress human prion protein with methionine at codon 129, the only allele found so far in vCJD-affected patients. These mice were infected with prions derived from variant and sporadic CJD (sCJD) cases by intracerebral or intraperitoneal route, and transmission efficiency and strain phenotype were analyzed in brain and spleen. We showed that i) the main features of vCJD infection in humans, including a prominent involvement of the lymphoid tissues compared to that in sCJD infection were faithfully reproduced in such mice; ii) transmission of vCJD agent by intracerebral route could lead to the propagation of either vCJD or sCJD-like prion in the brain, whereas vCJD prion was invariably propagated in the spleen, iii) after peripheral exposure, inefficient neuroinvasion was observed, resulting in an asymptomatic infection with life-long persistence of vCJD prion in the spleen at stable and elevated levels.<br /><br />Our findings emphasize the possibility that human-to-human transmission of vCJD might produce alternative neuropathogical phenotypes and that lymphoid tissue examination of CJD cases classified as sporadic might reveal an infection by vCJD-type prions. They also provide evidence for the strong propensity of this agent to establish long-lasting, subclinical vCJD infection of lymphoreticular tissues, thus amplifying the risk for iatrogenic transmission.<br /><br />snip...<br /><br />Discussion Top In this study we used tg650 mice, a newly developed transgenic line expressing human PrPC, to investigate some aspects of the pathogenesis of vCJD infection. As main findings, we demonstrate that prion strain divergence can occur upon transmission of human, primary vCJD to such mice, and that peripheral challenge leads to an asymptomatic, life-long infection of the lymphoid compartment. A feature of tg650 mice is that following primary intracerebral vCJD challenge they developed a neurological disease with typically 100% attack rate, unlike for previously established PrP129Met, including overexpressing lines [16], [19]. The mean survival time - typically around 500 days in homozygous mice - did not change notably on subpassaging, implying that vCJD agent might clinically infect the tg650 mice with little or no transmission barrier. This discrepant result may reflect the use of different constructs and genetic backgrounds (Text S1), and the transgene expression levels, although the latter does not seem to greatly differ as far as the tg650+/- and tg45 mice [16] are concerned.<br /><br />A surprising result of these studies is the alternate pattern of disease that was induced by one of the inoculated vCJD cases, a WHO reference case here designated vCJD no. 4. Indeed, while vCJD strain features were faithfully propagated in the majority of tg650 mice, almost half of the vCJD 4-inoculated mice were found to propagate a prion replicating faster than vCJD agent, and exhibiting sCJD-like PrPres and neuropathological features. Although strain divergence upon transmission of BSE/vCJD agent to mice was reported to occur in earlier studies [16], [24], it was unprecedented within a context of homotypic transmission, i.e. full matching between the donor and receiver PrP sequences. To address the issue of a possible contamination, we performed independent transmission experiments, involving separate inoculum batches of the incriminated case, which all produced consistent results. Therefore, we consider the data inconsistent with contamination of the VCJD no. 4 material by a sCJD infectious source within our laboratory. An alternate possibility, i.e. a cross-contamination of the source material, was judged highly improbable owing to the procedures applied during the collect of the specimen and the preparation of the homogenates ([25] and P. Minor, personal communication). On the other hand, our observation intriguingly parallels the phenotypic disjunction observed upon transmission of BSE agent to human PrP129Met mice (tg35 line [16]). Together, these findings lend support to the hypothesis that a minor strain component might be created upon cattle-to-human transmission of BSE agent and could emerge upon subsequent human-to-human transmission. It is also worth mentioning that, while the probability to detect such a variant through mouse bioassay would be expected to depend on the amount - and possibly the regions - of brain tissue taken to establish the source material, the vCJD-4 homogenate was prepared using a larger amount of tissue from the same brain than for the other homogenates analyzed in this study (i.e. 100 mg instead of 1 mg of frontal cortex [25]).<br /><br />The above finding has obvious implications in terms of public health as it raises the concern that some humans iatrogenically infected by vCJD agent may develop a clinical disease that would not be recognized as of vCJD origin [17], [26]. Strikingly however, all vCJD-4-inoculated mice, notwithstanding the strain phenotype divergence propagated bona fide vCJD agent in their spleen, based on the PrPres pattern and the disease phenotype produced by secondary transmission to tg650 mice. This result is of direct relevance to the diagnosis of variant and sporadic CJD. Indeed, looking for peripheral lymphoreticular deposition of abnormal PrP on cases diagnosed as sporadic CJD might reveal a vCJD infection resulting from human-to-human, or cattle-to-human transmission. In this respect, it would be of interest to examine whether BSE-inoculated tg35 mice showing discordant PrPres signatures [16], or vCJD-challenged PrP129Val transgenic mice producing 'type 5' prion in their brain [17] do accumulate PrPvCJD in their spleens. In any case, our findings provide clear evidence that, as a consequence of strain-related tropism disparities, the same mouse can propagate different prions in different tissues following a single infection event.<br /><br />Another salient finding emerging from this study was the remarkable ability of vCJD agent to establish asymptomatic infection despite sustained, life-long propagation in extraneural tissues. When challenged peripherally, tg650 mice remained asymptomatic over the whole observation period, and did not accumulate PrPres at detectable levels in their brain before 750 days pi, near the life end-stage. In the spleen of these mice however, PrPres accumulation reached its maximum at an early stage of infection, and remained at stable and substantial levels until death. Plateauing of prion infection in the spleen is consistent with earlier observations, and has been suggested to reflect an exhaustion of target cells (for review [22]) Importantly, the spleen tissue was highly infectious as it killed 100% of intracerebrally challenged mice within the minimal mean incubation time (~500 days). Altogether these data support the view that the sustained multiplication of the vCJD prion in lymphoid tissues was not accompanied by an efficient neuroinvasion in tg650 mice. Such an extremely delayed neuroinvasion appears to be rare in TSE rodent models, and to our knowledge was only reported for the mouse-adapted strain 87V on IM mice infected intraperitoneally with diluted inoculum [27]. Clearly, while early accumulation of prions in lymphoid tissues may be essential for efficient neuroinvasion [22], efficient lymphoinvasion does not inevitably lead to rapid neuroinvasion. This finding strengthens the notion that humans infected by vCJD from a human source - including individuals of the MM genotype - might remain clinically asymptomatic for a very prolonged period of time while harboring relatively high levels of prion infectivity in their lymphoid tissues from an early stage of infection on, thereby amplifying the risk of iatrogenic transmission. It also supports the view that the large-scale survey of lymphoreticular tissues [28] may lead to a reliable assessment of the actual prevalence of vCJD infection in the UK population.<br /><br />Finally, the human PrP transgenic model described in this study may help to further our understanding of peripheral vCJD pathogenesis, for instance in trying to identify factors that might enhance neuroinvasion efficiency, or modulate the shedding of prion infectivity from the lymphoreticular to the blood compartment. Moreover, preliminary results indicate that the search for abnormal PrP in the spleen of such mice culled at time intervals post infection [29], [30] could allow the detection of low levels of vCJD infectivity within a reasonably short time scale.<br /><br />Citation: Béringue V, Le Dur A, Tixador P, Reine F, Lepourry L, et al. (2008) Prominent and Persistent Extraneural Infection in Human PrP Transgenic Mice Infected with Variant CJD. PLoS ONE 3(1): e1419. doi:10.1371/journal.pone.0001419<br /><br />Academic Editor: Adam Ratner, Columbia University, United States of America<br /><br />Received: September 20, 2007; Accepted: December 17, 2007; Published: January 9, 2008<br /><br />Copyright: © 2008 Beringue 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.<br /><br />Funding: This work was supported by INRA, Institut de Veille Sanitaire (InVS) and the Ministry of Research, France. The sponsors of this study had no role in study conduct, collection analysis, interpretation of the data, writing of the report or approval of the manuscript.<br /><br />Competing interests: The authors have declared that no competing interests exist.<br /><br />* To whom correspondence should be addressed. E-mail: hubert.laude@jouy.inra.fr (HL); vincent.beringue@jouy.inra.fr (VB)<br /><br /><a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0001419">http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0001419</a><br /><br /><br /><br /><br />THESE ELECTRODES, and infection there from during neurosurgery, were not of a spontaneous nature ;<br /><br /><br />1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8<br /><br />Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.<br /><br />Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.<br /><br />Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.<br /><br />Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.<br /><br /><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract</a><br /><br /><br /><br /><br />SPONTANEOUS TSE<br /><br /><br />Perspectives BIOMEDICINE: A Fresh Look at BSE Bruce Chesebro*<br /><br />Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle form of a family of progressive brain diseases. These diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease (CWD) in deer and elk. They are also known as either "prion diseases" because of the association of a misfolded cellular prion protein in pathogenesis or "transmissible spongiform encephalopathies" (TSEs) because of the spongelike nature of the damaged brain tissue (1).<br /><br />The recent discovery of two BSE-infected cows, one in Canada and one in the United States, has dramatically increased concern in North America among meat producers and consumers alike over the extent to which BSE poses a threat to humans as well as to domestic and wild animals. The European BSE epidemic of the late-1980s seems to have been initiated a decade earlier in the United Kingdom by changes in the production of meat and bone meal (MBM) from rendered livestock, which led to contamination of MBM with the BSE infectious agent. Furthermore, the fact that UK farmers fed this rendered MBM to younger animals and that this MBM was distributed to many countries may have contributed to the ensuing BSE epidemic in the United Kingdom and internationally (2).<br /><br />Despite extensive knowledge about the spread of BSE through contaminated MBM, the source of BSE in Europe remains an unsolved mystery (2). It has been proposed that BSE could be derived from a cross-species infection, perhaps through contamination of MBM by scrapie-infected sheep tissues (see the figure). Alternatively, BSE may have been an endemic disease in cattle that went unnoticed because of its low level of horizontal transmission. Lastly, BSE might have originated by "spontaneous" misfolding of the normal cellular prion protein into the disease-associated abnormal isoform (3), which is postulated to be the infectious agent or "prion."<br /><br />Five possible sources of BSE in North American cattle. Sheep, deer, and elk could spread prion diseases (TSEs) to cattle through direct animal contact or contamination of pastures. Endemic BSE has not been proven to exist anywhere in the world, but it is difficult to exclude this possibility because of the inefficient spread of BSE infectivity between individual animals (2). BSE caused by spontaneous misfolding of the prion protein has not been proven. CREDIT: KATHARINE SUTLIFF/SCIENCE<br /><br />snip...<br /><br />Nevertheless, the idea that BSE might originate due to the spontaneous misfolding of prion proteins has received renewed interest in the wake of reports suggesting the occurrence of atypical BSE (9-11). These results imply that new strains of cattle BSE might have originated separately from the main UK outbreak. Where and how might such strains have originated? Although such rare events cannot be studied directly, any number of sources of the original BSE strain could also explain the discovery of additional BSE strains in cattle (see the figure). However, it would be worrisome if spontaneous BSE were really a valid etiology because such a mechanism would be impossible to prevent--unlike other possible scenarios that could be controlled by large-scale eradication of TSE-positive animals.<br /><br />Another way to look at this problem is to examine evidence for possible spontaneous TSE disease in other animals besides cattle. Spontaneous BSE would be extremely difficult to detect in cattle, where horizontal spread is minimal. However, in the case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at birth as well as between adults, spontaneous disease should be detectable as new foci of clinical infection. In the early 1950s scrapie was eradicated in both Australia and New Zealand, and the mainland of both these countries has remained scrapie-free ever since. This scrapie-free status is not the result of selection of sheep resistant to scrapie because sheep from New Zealand are as susceptible as their UK counterparts to experimental scrapie infection (12). These experiments of man and nature appear to indicate that spontaneous clinical scrapie does not occur in sheep. Similarly, because CWD is known to spread horizontally, the lack of CWD in the deer or elk of eastern North America but its presence in western regions would also argue against a spontaneous disease mechanism. This is particularly noteworthy in New Zealand, where there are large numbers of deer and elk farms and yet no evidence of spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer, this would suggest that spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are unlikely to be found in cattle or humans. The main caveat to this notion is that spontaneous disease may arise in some animal species but not others. In humans, sCJD--which is considered by some researchers to begin by spontaneous misfolding of the prion protein--usually takes more than 50 years to appear. Thus, in animals with a shorter life-span, such as sheep, deer, and cattle, an analogous disease mechanism might not have time to develop.<br /><br />What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? "Sporadic" pertains to the rarity of disease occurrence. "Spontaneous" pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE of unknown etiology--might be a better term to describe the origin of this malady. ...<br /><br />snip...full text ;<br /><br /><a href="http://www.sciencemag.org/cgi/content/full/sci;305/5692/1918">http://www.sciencemag.org/cgi/content/full/sci;305/5692/1918</a><br /><br /><br /><br />Release No. 0106.04<br /><br />Contact: Office of Communications (202) 720-4623<br /><br />Transcript of Remarks From Technical Briefing on BSE and Related Issues With Agriculture Secretary Ann M. Veneman and USDA Chief Veterinary Officer Dr. Ron DeHaven Washington D.C. - March 15, 2004<br /><br />snip...<br /><br />OPERATOR : “Yes. Our next one is coming from Elizabeth Weiss. Please state your company.”<br /><br />ELIZABETH WEISS: “This is Elizabeth Weiss with USA Today.”<br /><br />“I actually had two questions. First off, when you say you're looking for 1 in 10,000 cases, is USDA doing any work to find out the possibility of whether or not BSE exists in a spontaneous form in the way that it does in humans and elk populations?<br /><br />“And secondly, how will any of this fit into some of the consternation that's been raised in California and with the Midwest packer that wanted to test all of its cattle?<br /><br />“Thanks.”<br /><br />DR. DEHAVEN: “All right. I think we've got three different questions in there, and I'll try to touch on each one of them.<br /><br />“First of all, let me correct just a technical issue, and that is you mentioned 1 in 10,000. And actually our surveillance system currently is designed, the one that we have in place now is designed to detect 1 positive in 1 million cattle, and I gave some numbers between 200,000 and 268,000 that would allow us to detect 1 in 10 million as opposed to 1 in 10,000.<br /><br />“So we would, if we were able to collect in the ballpark of those numbers of samples then we with increasing numbers of samples have an increasingly statistically valid sample from which to determine, one, whether or not the disease exists and, if so, at what prevalence level.<br /><br />“So our real emphasis is to test as many of those animals as we can, ensure that we get an appropriate geographical distribution, but not setting a specific number as far as a target. Again, consistent with the recommendation from the International Review Team, their recommendation was to test all of them.<br /><br />“So that's consistent with where we're going is to test as many as we possibly can.<br /><br />“As far as spontaneous cases, that is a very difficult issue. There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative. We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million. We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.<br /><br />“Again, it's a very difficult situation to prove a negative.<br /><br />“So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.<br /><br />snip...<br /><br /><a href="http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2004/03/0106.html">http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2004/03/0106.html</a><br /><br /><br /><br />P2-110<br /><br />TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY TO MICROCEBUS MURINUS, A NON-HUMAN PRIMATE. DEVELOPMENT OF CLINICAL SYMPTOMS AND TISSUE DISTRIBUTION OF PRPRES<br /><br />Nadine Mestre-Frances1, Anne-Gaelle Biacabe2, Sylvie Rouland1, Thierry Baron2, Jean-Michel Verdier1, 1INSERM U710, Montpellier, France; 2AFSSA, Lyon, France. Contact e-mail: nfrances@univmontp2. fr<br /><br />Background: Atypical BSE cases have been observed in Europe, Japan and North America. They differ in their PrPres profiles from those found in classical BSE. These atypical cases fall into 2 types, depending on the molecular mass of the unglycosylated PrPres band observed by Western blot: the L-type (lower molecular mass than the typical BSE cases) and H-type (higher molecular mass than the typical BSE cases).<br /><br />Methods: Height animals (4 males and 4 females) were intracerebrally inoculated with 50 l of a 10% brain homogenates of atypical (L and H-type) French BSE cases.<br /><br />Results: Only one of the four lemurs challenge with H-type BSE died without clinical signs after 19 months post inoculation (mpi), the 4 animals inoculated with L-type BSE died at 19 mpi (2 males) and 22 mpi (2 females). Three months before their sacrifice, they developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms get worse according to the disease progression, until severe ataxia. The brain tissue were biochemically and immunocytochemically investigated for PrPres. For the H-types, spongiform changes without PrPres accumulation were observed in the brainstem. Western blot analysis confirmed that no PrPres was detected into the brain. For the L-types, severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem, whereas into the cortex the spongiosis was evidenced, but the vacuolisation was weaker. Strong deposits of PrPres was detected by western blot, PET-blot and immunocytochemistry in the CNS: dense accumulation was observed into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques. Western blot analysis confirmed the presence of protease-resistant prion protein.<br /><br />Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain.<br /><br /><a href="http://download.journals.elsevierhealth.com/pdfs/journals/1552-5260/PIIS1552526008013447.pdf">http://download.journals.elsevierhealth.com/pdfs/journals/1552-5260/PIIS1552526008013447.pdf</a><br /><br /><br /><br /><br />>>> Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain. >>><br /><br /><br />seems the survival time was the same for the h-type BSE and the l-type BSE i.e. 19 months post inoculation (mpi), interesting. ...TSS<br /><br /><br />Wednesday, March 31, 2010<br /><br />Atypical BSE in Cattle / position: Post Doctoral Fellow<br /><br /><br /><a href="http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html">http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html</a><br /><br /><br /><br />Wednesday, February 24, 2010<br /><br />Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th<br /><br />ICID International Scientific Exchange Brochure -<br /><br /><br /><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html">http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html</a><br /><br /><br /><br />Saturday, June 12, 2010<br /><br />PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse<br /><br /><br /><a href="http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html">http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html</a><br /><br /><br /><br />Saturday, July 17, 2010<br /><br />Variant Creutzfeldt-Jakob disease Ironside JW., Haemophilia. 2010 Jul;16 Suppl 5:175-80<br /><br />REVIEW ARTICLE<br /><br /><a href="http://vcjdtransfusion.blogspot.com/2010/07/variant-creutzfeldtjakob-disease.html">http://vcjdtransfusion.blogspot.com/2010/07/variant-creutzfeldtjakob-disease.html</a><br /><br /><br /><br /><br />Saturday, June 19, 2010<br /><br />U.S. DENIED UPGRADED BSE STATUS FROM OIE<br /><br />see full text and reasons why here ;<br /><br /><a href="http://usdameatexport.blogspot.com/2010/06/us-denied-upgraded-bse-status-from-oie.html">http://usdameatexport.blogspot.com/2010/06/us-denied-upgraded-bse-status-from-oie.html</a><br /><br /><br /><br /><br /><br /><br />TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-28611139191141008482009-11-20T10:25:00.000-08:002009-11-20T10:31:44.354-08:00Bovine spongiform encephalopathy, DenmarkBovine spongiform encephalopathy, Denmark<br /><br />Information received on 20/11/2009 from Dr Jan Mousing, Chief Veterinary Officer, Danish Veterinary and Food Administration, Ministry of Food, Agriculture and Fisheries, Soborg, Denmark<br /><br />Summary<br /><br />Report type Immediate notification<br />Start date 17/11/2009<br />Date of first confirmation of the event 19/11/2009<br />Report date 19/11/2009<br />Date submitted to OIE 20/11/2009<br />Reason for notification Reoccurrence of a listed disease<br />Date of previous occurrence 09/2005<br />Manifestation of disease Sub-clinical infection<br />Causal agent Bovine spongiform encephalopathy agent<br />Nature of diagnosis Laboratory (advanced)<br />This event pertains to the whole country<br /><br />New outbreaks Summary of outbreaks Total outbreaks: 1<br />Location(s) South (Ærøskøbing, Ærø kommune)<br /><br />Total animals affected Species Susceptible Cases Deaths Destroyed Slaughtered<br />Cattle 116 1 0 1 0<br /><br />Outbreak statistics Species Apparent morbidity rate Apparent mortality rate Apparent case fatality rate Proportion susceptible animals lost*<br />Cattle 0.86% 0.00% 0.00% 0.86%<br /><br />* Removed from the susceptible population through death, destruction and/or slaughter<br /><br /><br />Epidemiology Source of the outbreak(s) or origin of infection Unknown or inconclusive<br /><br />Epidemiological comments The affected animal was born before the tightening of the feed ban in 1997 and 2001. In 1990, feeding ruminant MBM to ruminants was prohibited. In 1997, feeding mammalian MBM to ruminants was prohibited. On 1 January 2001, the Danish Veterinary and Food Administration introduced a total ban on feeding processed animal protein (including meat and bone meal (MBM), fish meal, etc.) to animals that are kept, fattened or bred for the production of food.<br />Control measures will be conducted in accordance with European Union regulation no. 999/2001.<br /><br /><br />Control measures Measures applied Quarantine<br />No vaccination<br />No treatment of affected animals<br /><br />Measures to be applied Modified stamping out<br /><br /><br /><br />Diagnostic test results Laboratory name and type National Veterinary Institute (National laboratory)<br />Tests and results Species Test Test date Result<br />Cattle western blotting 19/11/2009 Positive<br /><br /><br /><br />Future Reporting The event is continuing. Weekly follow-up reports will be submitted.<br /><br /><br /><br /><br /><br />Encefalopatía espongiforme bovina, Dinamarca<br /><br />Información recibida el 20/11/2009 desde Dr Jan Mousing, Chief Veterinary Officer, Danish Veterinary and Food Administration, Ministry of Food, Agriculture and Fisheries, Soborg, Dinamarca<br /><br />Resumen<br /><br />Tipo de informe Notificación inmediata<br />Fecha de inicio 17/11/2009<br />Fecha de la primera confirmación del evento 19/11/2009<br />Fecha del informe 19/11/2009<br />Fecha de envio del informe a la OIE 20/11/2009<br />Motivo de la notificación Reaparición de una enfermedad de la Lista de la OIE<br />Fecha de la anterior aparición de la enfermedad 09/2005<br />Manifestación de la enfermedad Infección sub-clínica<br />Agente causal Agente de la encefalopatía espongiforme bovina<br />Naturaleza del diagnóstico Pruebas de diagnóstico de laboratorio avanzadas (ej. virología, microscopía electrónica, biología molecular e inmunología)<br />Este evento concierne todo el país<br /><br />Nuevos focos Resumen de los focos Número total de focos: 1<br />Localización South (Ærøskøbing, Ærø kommune)<br /><br />Número total de animales afectados Especies Susceptibles Casos Muertos Destruidos Sacrificados<br />Bovinos 116 1 0 1 0<br /><br />Estadística del foco Especies Tasa de morbilidad aparente Tasa de mortalidad aparente Tasa de fatalidad aparente Proporción de animales susceptibles perdidos*<br />Bovinos 0.86% 0.00% 0.00% 0.86%<br /><br />* Descontados de la población susceptible a raíz de su muerte, destrucción o sacrificio<br /><br /><br />Epidemiología Fuente del o de los focos u origen de la infección Desconocida o no concluyente<br /><br />Otros detalles epidemiológicos / comentarios El animal afectado nació antes de que se endureciera en 1997 y 2001 la prohibición relativa a la alimentación animal. En 1990, se prohibió alimentar a los rumiantes con harinas de carne y hueso de rumiante. En 1997, se prohibió alimentar a los rumiantes con harinas de carne y hueso de mamífero. El 1 de enero de 2001, la Administración danesa de veterinaria y de alimentos introdujo una prohibición total de alimentar los animales criados o engordados para la producción de alimentos con proteínas animales transformadas (incluyendo harinas de carne y hueso, harinas de pescado, etc.).<br />Las medidas de control se aplicarán de acuerdo con el reglamento n° 999/2001 de la Unión Europea.<br /><br /><br />Medidas de Control Medidas implementadas Cuarentena<br />Vacunación: no<br />Ningún tratamiento de los animales afectados<br /><br />Medidas para implementar Sacrificio sanitario parcial<br /><br /><br /><br />Resultados de las pruebas diagnósticas Nombre y tipo de laboratorio Instituto veterinario nacional (Laboratorio nacional)<br />Pruebas y resultados Especies Prueba Fecha de la prueba Resultados<br />Bovinos prueba de inmunodetección 19/11/2009 Positivo<br /><br /><br /><br />Informes futuros El episodio continúa. Informes de seguimiento semanales serán enviados<br /><br /><br /><br /><br /><br />Encéphalopathie spongiforme bovine, Danemark<br /><br />Information reçue le 20/11/2009 de Dr Jan Mousing, Chief Veterinary Officer, Danish Veterinary and Food Administration, Ministry of Food, Agriculture and Fisheries, Soborg, Danemark<br /><br />Résumé<br /><br />Type de rapport Notification immédiate<br />Date de début 17/11/2009<br />Date de première confirmation de l´événement 19/11/2009<br />Date du rapport 19/11/2009<br />Date d'envoi à l'OIE 20/11/2009<br />Raison de notification Réapparition d’une maladie appartenant à la liste de l'OIE<br />Date de la précédente apparition de la maladie 09/2005<br />Manifestation de la maladie Infection sub-clinique<br />Agent causal Agent de l'encéphalopathie spongiforme bovine<br />Nature du diagnostic Tests approfondis en laboratoire (i.e. virologie, microscopie électronique, biologie moléculaire, immunologie)<br />Cet événement se rapporte à tout le pays<br /><br />Nouveaux foyers Récapitulatif des foyers Nombre total de foyers : 1<br />Localisation(s) South (Ærøskøbing, Ærø kommune)<br /><br />Nombre total d'animaux atteints Espèce(s) Sensibles Cas Morts Détruits Abattus<br />Bovins 116 1 0 1 0<br /><br />Statistiques sur le foyer Espèce(s) Taux de morbidité apparent Taux de mortalité apparent Taux de fatalité apparent Proportion d'animaux sensibles perdus*<br />Bovins 0.86% 0.00% 0.00% 0.86%<br /><br />* Soustraits de la population sensible suite à la mort, à l´abattage et/ou à la destruction<br /><br /><br />Epidémiologie Source du/des foyer(s) ou origine de l´infection Inconnue ou incertaine<br /><br />Autres renseignements épidémiologiques / Commentaires L'animal atteint est né avant le durcissement ayant eu lieu en 1997 et 2001 de l'interdiction relative aux aliments pour animaux. En 1990, les farines de viande et d'os provenant de ruminants ont été interdites dans l’alimentation pour ruminants. En 1997, les farines de viande et d'os provenant de mammifères ont été interdites dans l’alimentation pour ruminants. Le 1er janvier 2001, l’Administration vétérinaire et alimentaire danoise a introduit une interdiction totale d'alimenter les animaux engraissés ou élevés pour la production de denrées alimentaires avec des protéines animales transformées (y compris les farines de viande et d'os, la farine de poisson, etc.).<br />Les mesures de lutte seront appliquées conformément au règlement de l'Union européenne n° 999/2001.<br /><br /><br />Mesures de lutte Mesure de lutte appliquées Quarantaine<br />Pas de vaccination<br />Aucun traitement des animaux atteints<br /><br />Mesures à appliquer Abattage sanitaire partiel<br /><br /><br /><br />Résultats des tests de diagnostics Nom du laboratoire et type Institut vétérinaire national (Laboratoire national)<br />Tests et résultats Espèce(s) Test Date du test Résultat<br />Bovins western blot 19/11/2009 Positif<br /><br /><br /><br />Rapports futurs Cet événement se poursuit. Des rapports de suivi hebdomadaires devront être envoyés.<br /><br /><br /><br /><br /><br /><a href="https://www.oie.int/wahis/reports/en_imm_0000008664_20091120_135911.pdf">https://www.oie.int/wahis/reports/en_imm_0000008664_20091120_135911.pdf</a><br /><br /><br /><br /><br />Tuesday, November 17, 2009<br /><br />SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1<br /><br /><br /><a href="http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html">http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html</a><br /><br /><br /><br /><br /><br /><br />TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-23663927961684979122009-11-16T19:09:00.000-08:002009-11-17T13:11:50.907-08:00CANADA, USA, specified risk materials (SRMs), Environment, Fertilizer, AND Politics, just more BSeCANADA, USA, specified risk materials (SRMs), Environment, Fertilizer, AND Politics, just more BSe<br /><br /><br />October 27, 2009<br /><br />Honourable Minister Gerry Ritz<br /><br />Minister of Agriculture and Agri-Food Canada 930 Carling Ave Ottawa, ON K1A 0C5<br /><br />Dear Minister Ritz,<br /><br />We, as representatives of beef and dairy cattle and beef processing industry organizations, have appreciated the opportunity to speak with you several times with respect to the cost disadvantage of slaughtering cattle in Canada. The primary cause of this disadvantage is the cost of removing and disposing of specified risk materials (SRMs). A survey of Canadian slaughter facilities conducted this summer indicates that the average cost of complying with the 2007 federal SRM removal and disposal regulation is $31.70 per animal over 30 months old (OTM).<br /><br />The Beef Value Chain Roundtable reviewed this matter at its September 15 meeting and made the following recommendation: “The Beef Value Chain Roundtable supports the findings of the Canadian Meat Council with regard to the costs associated in complying with the enhanced feed ban. The Roundtable asks Governments to promptly implement a plan to offset the costs associated with meeting the requirements of the enhanced feed ban. This recommendation would serve to be a transition measure only until a remedy is found to restore competitiveness.”<br /><br />The undersigned organizations request that the Government of Canada immediately create an OTM Cattle SRM Disposal Compensation Program. Specifically, we request a payment of $31.70/head be made to abattoirs for every OTM animal slaughtered in Canada. Both federally and provincially inspected facilities should be eligible for this payment. With an estimated annual OTM slaughter of 750,000 head, the program would cost approximately $24 million per year.<br /><br />The primary objective of any assistance must be to maintain OTM slaughter capacity in Canada. If we fail to achieve this objective, we will lose thousands of jobs throughout the nation, and Canadian beef and dairy cattle producers will be at the mercy of any disruptive US trade rules that may be introduced in the future. All the excellent work you are doing to re-establish market access for Canadian beef will be wasted if we lose the capacity to slaughter our own cattle in Canada. We are already seeing that with reduced OTM slaughter in Canada, beef imports have increased dramatically in 2009. Neither beef nor dairy cattle producers want to return to the pre-BSE practice where large numbers of Canadian OTM cattle went to the US for processing while large quantities of non-NAFTA beef were imported to satisfy Canada’s beef demand.<br /><br />We request that this OTM Cattle SRM Disposal Compensation Program remain in effect until the SRM removal and disposal policies of Canada and the United States can be harmonized. As an industry, we are committed to work closely with your officials to reduce the volumes and costs of SRM removal. There are several critical actions, that when achieved, can have a significant impact on improving our competitive position with our American counterparts. But it is also widely recognized that any of these beneficial measures will take time to implement, and that immediate need for cash remains in the short term. We recommend that a review process be formalized to ensure these improvements are implemented and the OTM Cattle SRM Disposal Compensation Program can be adjusted when necessary.<br /><br />In closing, we thank you for your recognition of this serious matter and we urge you to respond quickly. As we are now entering the peak OTM slaughter season, our request requires urgent attention to ensure that Canadian facilities can compete for their fair share of this business.<br /><br />Sincerely,<br /><br />Brad Wildeman, President Canadian Cattlemen’s Association Jacques Laforge, President Dairy Farmers of Canada Laurent Pellerin, President Canadian Federation of Agriculture Brian Read, Chair - Beef Committee Canadian Meat Council Kevin Golding, President Canadian Renderers Association Michel Dessureault, President La Fédération des producteurs de bovins du Québec Serge Michel, Chairman of the board Levinoff-Colbex SEC Brian Nilsson, President XL Foods Shane Murphy, President Atlantic Beef Producers Dennis Laycraft, Industry Co-Chair Beef Value Chain Roundtable Scott Entz, Vice President and General Manager Cargill Beef<br /><br /><a href="http://www.cattle.ca/pdf/srm-letter.pdf">http://www.cattle.ca/pdf/srm-letter.pdf</a><br /><br /><br />Other Priority Issues and Required Actions Competitiveness The top challenge facing the Canadian cattle industry today is that several factors are contributing to a lack of competitiveness in the cattle feeding and beef processing sectors. Left unchecked, greater numbers of cattle will be fed and slaughtered in the US and increasing quantities of beef will be imported into Canada. A high Canadian dollar exacerbates these problems necessitating swift action.<br /><br />Required Actions<br /><br />Promptly implement a plan to offset the cost of disposal of Specified Risk Materials (SRMs) as required by the enhanced feed ban. This would be a transitional measure until remedies are implemented to restore industry competitiveness. See coalition letter requesting a creation of an OTM Compensation Program .<br /><br />Remove the prohibition on using SRM meat and bone meal as fertilizer as a way to restore value for the SRMs Traceability should not impede commerce. Pilot projects currently underway testing scanning equipment in auction marts need to be completed prior to proceeding. Regulating additional costs to producers will put industry at greater disadvantage. Implement 2008 Federal Election commitment to cut diesel excise tax from 4 cents to 2 cents per litre, Ensure Canada’s approval process for products (veterinary/pharmaceutical, pesticides, biologics, new forage and grain varieties, etc) are as or more efficient than our international competitors such as the United States and Australia. Ensure enforcement by regulators is commensurate with consequences of non-compliance (eg: fines for lost CCIA tags; high value meat removal around spinal cord). ...SNIP...END<br /><br />FULL TEXT ;<br /><br /><a href="http://www.cattle.ca/other-priority-issues-and-required-actions/">http://www.cattle.ca/other-priority-issues-and-required-actions/</a><br /><br /><br />CANADA<br /><br /><br />> Remove the prohibition on using SRM meat and bone meal as fertilizer as a way to restore value for the SRMs<<br /><br /><br />USA<br /><br /><br />13. Q: Can CMPAF be rendered for use as fertilizer?<br /><br /><br />A: This rule does not place any restrictions on the use of CMPAF as fertilizer.<br /><br /><br /><br /><a href="http://www.fda.gov/AnimalVeterinary/GuidanceComplianceEnforcement/ComplianceEnforcement/BovineSpongiformEncephalopathy/ucm114453.htm">http://www.fda.gov/AnimalVeterinary/GuidanceComplianceEnforcement/ComplianceEnforcement/BovineSpongiformEncephalopathy/ucm114453.htm</a><br /><br /><br /><br /><br /><br /><br />SEAC 103/3<br /><br />MAMMALIAN MEAT AND BONE-MEAL AS FERTILISER ON AGRICULTURAL LAND<br /><br />ISSUE<br /><br />1. The Department for Environment, Food and Rural Affairs (Defra) has asked SEAC to consider a risk assessment (Annex A) entitled “Risk assessment of TSE related risks associated with the use of rendered Category 3 animal by-products (ABP) as fertiliser on non-pasture land” produced by the Veterinary Laboratories Agency.<br /><br />BACKGROUND<br /><br />2. In 2005, at its 87th meeting, SEAC considered (Annex B) a ‘release assessment’ which evaluated the amount of potential infectivity available in the soil of non-pasture land following the application of Category 3-derived1 fertiliser. In summary, the committee concluded:<br /><br />• It was content with the approach used and assumptions made in the risk assessment.<br /><br />• The assessment predicted that TSE infectivity levels on land as a result of the application of fertiliser would be extremely low. However, because of the likely heterogeneous nature of infectivity in fertiliser and the uneven spread of fertiliser, TSE infectivity levels might be higher in some geographical locations than predicted.<br /><br />• Controls to ensure that Category 3 ABP are processed separately from Category 1 and Category 2 ABP2 be audited.<br /><br />1 Category 3 is low risk material, most of which is fit for human consumption, but not intended for human consumption.<br /><br />2 Categories 1 & 2 are the highest risk materials, animals with a suspected or confirmed TSE, Specified Risk Material, condemned meat, diseased animals etc. • A watching brief be kept on CWD and BARB cases to assess the possible persistence of the agent in the environment.<br /><br />3. Domestic TSE legislation was then amended in 2006 to lift the ban on the application of Category 3-derived mammalian meat and bone meal (MMBM) as organic fertiliser and soil improvers (OFSI) on agricultural land. Also in 2006 EU Animal By-Products legislation was amended3 to permit application of OFSI to land in accordance with certain conditions. This change in EU legislation was underpinned by an EFSA Opinion of 3 March 2004 (Annex C).<br /><br />4. The EU Animal By-Products Regulation (1774/2002) requires that the category 3-derived MMBM must have been submitted to “Method 1” rendering. Method 1 is the most stringent of the seven rendering methods permitted by the Regulation. The animal by-products must be reduced to a particle size of no greater than 50mm, heated to a core temperature of more than 133°C at 3 bar pressure (absolute) for at least 20 minutes without interruption. The EU ABP Regulation is now being renegotiated and Defra are considering whether it is appropriate to seek a relaxation of the requirement for Method 1 rendering. To this end Defra need an understanding of the difference in the risk of transmitting a TSE, as between the use of Method 1 and Method 7, which is potentially the least stringent method. This is because Method 7 does not prescribe any particle size, time, temperature or pressure standards on the processing of animal by-products but requires the processed product to comply with a microbiological standard set out in the Regulation. It can only be used for Category 3 animal by-products.<br /><br />5. If there is a difference in risk in this context Defra would then consider whether it would be feasible to manage any increased risk resulting from the use of Method 7, for example the better labelling of the fertiliser or by reducing its palatability to animals.<br /><br />6. In order to inform this consideration, Defra commissioned a full risk assessment to evaluate the danger to cattle and sheep of becoming infected with BSE and/or scrapie as a result of the change to the domestic TSE legislation in the use of rendered Category 3 ABP with regard to MMBM being converted into fertiliser and applied to nonpasture land. This new risk assessment, which SEAC is now invited to consider, represents a significant overhaul of the original assessment and includes additional analyses.<br /><br />3 Regulation (EC) 181/2006 amended the ABP Regulation 1774/2002 as regards the use of organic fertilisers and soil improvers (except manure).<br /><br />7. The main changes compared to the previous release assessment<br /><br />are:<br /><br />• the values assigned to parameters within the release assessment have been amended to take account of an increase in scientific knowledge, legislative changes and the decline in disease incidence over time.<br /><br />• account is taken of a case study investigating the palatability to ruminants of fertilisers applied to land.<br /><br />• a new exposure assessment and a new dose response model are included.<br /><br />NEW RESULTS<br /><br />8. The effects of each of the seven processing methods on TSE infectivity are not known, with the exception of limited experimental data regarding Method 1 as set out in the risk assessment. Due to the absence of such information, the risk assessment makes a number of assumptions in order to compare two scenarios based on the use of the processing methods at opposite ends of the range permitted in legislation: Method 1 and Method 7.<br /><br />9. The main conclusions from the risk assessment are that the number of animals infected with a TSE disease annually, due to exposure to fertilizer produced from Category 3 ABP according to Method 1 is low (i.e. below one). Indeed, there is 90% certainty that the maximum number would be one new infection. The assessment concludes that when considering fertiliser produced by Method 7 the estimated mean number of new BSE new infections in cattle is 1.1, the number of new infections of scrapie is 47 and the number of new infections of sheep BSE is 0.04.<br /><br />FUTURE RESEARCH<br /><br />10. The risk assessment also considers what further investigations might help to reduce the uncertainty in the risk assessment and concludes that the following information would be helpful:<br /><br />• The proportion of processed materials destined for fertiliser production.<br /><br />• The average yearly livestock stocking density on grassland.<br /><br />• The average depth of penetration of the fertiliser within the top soil upon application.<br /><br />• The reduction rate in TSE infectivity due to processing into fertiliser.<br /><br />• The proportion of scrapie that is masking sheep BSE disease.<br /><br />• The probability that a scrapie infected sheep is slaughtered for human consumption in GB.<br /><br />ADVICE SOUGHT<br /><br />11. SEAC is asked to:<br /><br />• consider the scientific validity of the methodology used, and the assumptions made, in the new risk assessment and to comment on its findings; and<br /><br />• whether any other information, other than that suggested above, would be likely to improve the uncertainties associated with the assumptions made in the risk assessment.<br /><br />SEAC SECRETARIAT<br /><br />NOVEMBER 2009<br /><br />ANNEX A<br /><br />A copy of “Risk assessment of TSE related risks associated with the use of rendered Category 3 animal by-products as fertiliser on non-pasture land”.<br /><br />ANNEX B<br /><br />Paper from SEAC<br /><br /><a href="http://www.seac.gov.uk/papers/103-3.pdf">http://www.seac.gov.uk/papers/103-3.pdf</a><br /><br /><br /><br /><br />Prions Adhere to Soil Minerals and Remain Infectious<br /><br />Christopher J. Johnson1,2, Kristen E. Phillips3, Peter T. Schramm3, Debbie McKenzie2, Judd M. Aiken1,2, Joel A. Pedersen3,4*<br /><br />1 Program in Cellular and Molecular Biology, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 2 Department of Animal Health and Biomedical Sciences, School of Veterinary Medicine, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 3 Molecular and Environmental Toxicology Center, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 4 Department of Soil Science, University of Wisconsin Madison, Madison, Wisconsin, United States of America<br /><br />Abstract Top An unidentified environmental reservoir of infectivity contributes to the natural transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter soil environments via shedding from diseased animals and decomposition of infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of disposal has resulted in unintentional introduction of prions into subsurface environments. We examined the potential for soil to serve as a TSE reservoir by studying the interaction of the disease-associated prion protein (PrPSc) with common soil minerals. In this study, we demonstrated substantial PrPSc adsorption to two clay minerals, quartz, and four whole soil samples. We quantified the PrPSc-binding capacities of each mineral. Furthermore, we observed that PrPSc desorbed from montmorillonite clay was cleaved at an N-terminal site and the interaction between PrPSc and Mte was strong, making desorption of the protein difficult. Despite cleavage and avid binding, PrPSc bound to Mte remained infectious. Results from our study suggest that PrPSc released into soil environments may be preserved in a bioavailable form, perpetuating prion disease epizootics and exposing other species to the infectious agent.<br /><br /><a href="http://www.plospathogens.org/article/info:doi%2F10.1371%2Fjournal.ppat.0020032">http://www.plospathogens.org/article/info:doi%2F10.1371%2Fjournal.ppat.0020032</a><br /><br /><br />Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles<br /><br />Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie McKenzie2, Judd M. Aiken1,2*<br /><br />1 Program in Cellular and Molecular Biology, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 2 Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 3 Department of Soil Science and Molecular and Environmental Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 4 Biostatistics and Medical Informatics, University of Wisconsin Medical School, Madison, Wisconsin, United States of America<br /><br />Soil may serve as an environmental reservoir for prion infectivity and contribute to the horizontal transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. Here, we assess the oral infectivity of Mte- and soil-bound prions. We establish that prions bound to Mte are orally bioavailable, and that, unexpectedly, binding to Mte significantly enhances disease penetrance and reduces the incubation period relative to unbound agent. Cox proportional hazards modeling revealed that across the doses of TSE agent tested, Mte increased the effective infectious titer by a factor of 680 relative to unbound agent. Oral exposure to Mte-associated prions led to TSE development in experimental animals even at doses too low to produce clinical symptoms in the absence of the mineral. We tested the oral infectivity of prions bound to three whole soils differing in texture, mineralogy, and organic carbon content and found soil- bound prions to be orally infectious. Two of the three soils increased oral transmission of disease, and the infectivity of agent bound to the third organic carbon-rich soil was equivalent to that of unbound agent. Enhanced transmissibility of soil-bound prions may explain the environmental spread of some TSEs despite the presumably low levels shed into the environment. Association of prions with inorganic microparticles represents a novel means by which their oral transmission is enhanced relative to unbound agent.<br /><br />snip...<br /><br />Discussion These experiments address the critical question of whether soil particle­bound prions are infectious by an environmentally relevant exposure route, namely, oral ingestion. Oral infectivity of soil particle­bound prions is a conditio sine qua non for soil to serve as an environmental reservoir for TSE agent. The maintenance of infectivity and enhanced transmissibility when TSE agent is bound to the common soil mineral Mte is remarkable given the avidity of the PrPTSE­Mte interaction [22]. One might expect the avid interaction of PrPTSE with Mte to result in the mineral serving as a sink, rather than a reservoir, for TSE infectivity. Our results demonstrate this may not be the case. Furthermore, sorption of prions to complex whole soils did not diminish bioavailability, and in two of three cases promoted disease transmission by the oral route of exposure. While extrapolation of these results to environmental conditions must be made with care, prion sorption to soil particles clearly has the potential to increase disease transmission via the oral route and contribute to the maintenance of TSE epizootics.<br /><br />Two of three tested soils potentiated oral prion disease transmission. The reason for increased oral transmissibility associated with some, but not all, of the soils remains to be elucidated. One possibility is that components responsible for enhancing oral transmissibility were present at higher levels in the Elliot and Bluestem soils than in the Dodge soil. The major difference between the Dodge soil and the other two soils was the extremely high natural organic matter content of the former (34%, [22]). The Dodge and Elliot soils contained similar levels of mixed-layer illite/smectite, although the contribution of smectite layers was higher in the Dodge soil (14%­16%, [22]). The organic matter present in the Dodge soil may have obstructed access of PrPTSE to sorption sites on smectite (or other mineral) surfaces.<br /><br />The mechanism by which Mte or other soil components enhances the oral transmissibility of particle-bound prions remains to be clarified. Aluminosilicate minerals such as Mte do not provoke inflammation of the intestinal lining [39]. Although such an effect is conceivable for whole soils, soil ingestion is common in ruminants and other mammals [25]. Prion binding to Mte or other soil components may partially protect PrPTSE from denaturation or proteolysis in the digestive tract [22,40] allowing more disease agent to be taken up from the gut than would otherwise be the case. Adsorption of PrPTSE to soil or soil minerals may alter the aggregation state of the protein, shifting the size distribution toward more infectious prion protein particles, thereby increasing the specific titer (i.e., infectious units per mass of protein) [41]. In the intestine, PrPTSE complexed with soil particles may be more readily sampled, endocytosed (e.g., at Peyer's patches), or persorbed than unbound prions. Aluminosilicate (as well as titanium dioxide, starch, and silica) microparticles, similar in size to the Mte used in our experiments, readily undergo endocytotic and persorptive uptake in the small intestine [42­44]. Enhanced translocation of the infectious agent from the gut lumen into the body may be responsible for the observed increase in transmission efficiency.<br /><br />Survival analysis indicated that when bound to Mte, prions from both BH and purified PrPTSE preparations were more orally infectious than unbound agent. Mte addition influenced the effective titer of infected BH to a lesser extent than purified PrPTSE. Several nonmutually exclusive factors may explain this result: (1) other macromolecules present in BH (e.g., lipids, nucleic acids, other proteins) compete with PrPTSE for Mte binding sites; (2) prion protein is more aggregated in the purified PrPTSE preparation than in BH [45], and sorption to Mte reduces PrPTSE aggregate size, increasing specific titer [41]; and (3) sorption of macromolecules present in BH to Mte influences mineral particle uptake in the gut by altering surface charge or size, whereas the approximately 1,000-fold lower total protein concentration in purified PrPTSE preparations did not produce this effect.<br /><br />We previously showed that other inorganic microparticles (kaolinite and silicon dioxide) also bind PrPTSE [22]. All three types of microparticles are widely used food additives and are typically listed as bentonite (Mte), kaolin (kaolinite), and silica (silicon dioxide). Microparticles are increasingly included in Western diets. Dietary microparticles are typically inert and considered safe for consumption by themselves, do not cause inflammatory responses or other pathologies, even with chronic consumption, and are often sampled in the gut and transferred from the intestinal lumen to lymphoid tissue [39,46,47]. Our data suggest that the binding of PrPTSE to dietary microparticles has the potential to enhance oral prion disease transmission and warrants further investigation.<br /><br />In conclusion, our results provide compelling support for the hypothesis that soil serves as a biologically relevant reservoir of TSE infectivity. Our data are intriguing in light of reports that naïve animals can contract TSEs following exposure to presumably low doses of agent in the environment [5,7­9]. We find that Mte enhances the likelihood of TSE manifestation in cases that would otherwise remain subclinical (Figure 3B and 3C), and that prions bound to soil are orally infectious (Figure 5). Our results demonstrate that adsorption of TSE agent to inorganic microparticles and certain soils alter transmission efficiency via the oral route of exposure.<br /><br />snip...full text is here:<br /><br /><a href="http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030093">http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030093</a><br /><br /><br /><a href="http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-L.pdf">http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-L.pdf</a><br /><br /><br /><a href="http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-S.pdf">http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-S.pdf</a><br /><br /><br />PLoS ONE. 2008; 3(8): e2969. Published online 2008 August 13. doi: 10.1371/journal.pone.0002969. PMCID: PMC2493038<br /><br />Copyright This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.<br /><br /><br />Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production<br /><br /><br />Cathrin E. Bruederle,1* Robert M. Hnasko,1 Thomas Kraemer,2 Rafael A. Garcia,3 Michael J. Haas,3 William N. Marmer,3 and John Mark Carter1 1USDA-ARS WRRC, Foodborne Contaminants Research Unit, Albany, California, United States of America 2Forensic Toxicology, Institute of Legal Medicine, Saarland University, Homburg/Saar, Germany 3USDA-ARS ERRC, Fats, Oils and Animal Coproducts Research Unit, Wyndmoor, Pennsylvania, United States of America Neil Mabbott, EditorUniversity of Edinburgh, United Kingdom * E-mail: cathrin.bruederle@gmail.comConceived and designed the experiments: CEB RMH WNM JMC. Performed the experiments: CEB RMH TK. Analyzed the data: CEB TK JMC. Contributed reagents/materials/analysis tools: CEB RMH TK RAG MJH JMC. Wrote the paper: CEB. Received April 21, 2008; Accepted July 24, 2008. Other Sections? AbstractIntroductionResultsDiscussionMaterials and MethodsSupporting InformationReferencesAbstract The epidemic of bovine spongiform encephalopathy (BSE) has led to a world-wide drop in the market for beef by-products, such as Meat-and-Bone Meal (MBM), a fat-containing but mainly proteinaceaous product traditionally used as an animal feed supplement. While normal rendering is insufficient, the production of biodiesel from MBM has been suggested to destroy infectivity from transmissible spongiform encephalopathies (TSEs). In addition to producing fuel, this method simultaneously generates a nutritious solid residue. In our study we produced biodiesel from MBM under defined conditions using a modified form of alkaline methanolysis. We evaluated the presence of prion in the three resulting phases of the biodiesel reaction (Biodiesel, Glycerol and Solid Residue) in vitro and in vivo. Analysis of the reaction products from 263K scrapie infected MBM led to no detectable immunoreactivity by Western Blot. Importantly, and in contrast to the biochemical results the solid MBM residue from the reaction retained infectivity when tested in an animal bioassay. Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.<br /><br /><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/</a><br /><br /><br /><br />Sunday, April 12, 2009<br /><br />CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains<br /><br /><a href="http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html">http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html</a><br /><br /><br />DEPENDS ALSO what were calling srm's now?<br /><br />WITH the atypical BSE's, ARS said they were going to update and possibly enhance SRM regulations as the transmission studies were due out in 2009 i.e. (h-BSE, and l-BSE) ??<br /><br />Animal fats/oils certified with maximum insoluble impurities of less than 0.15% in weight (bovine origin animal fats imported for animal consumption must also come from animals that passed FSIS inspection, and must not be derived from the head, distal ileum, spinal cord, or vertebral column of cattle of any age);<br /><br /><a href="http://www.aphis.usda.gov/newsroom/hot_issues/bse/background/bse_trade_ban_status.shtml">http://www.aphis.usda.gov/newsroom/hot_issues/bse/background/bse_trade_ban_status.shtml</a>...<br /><br /><br /><a href="http://www.aphis.usda.gov/newsroom/hot_issues/bse/background/bse_trade_ban_status.shtml">http://www.aphis.usda.gov/newsroom/hot_issues/bse/background/bse_trade_ban_status.shtml</a>...<br /><br /><br /><br />2. Annex XI, Part A is amended as follows:<br /><br />(a) point 1(a)(i) is replaced by the following:<br /><br />"(i) the skull excluding the mandible and including the brain and eyes, and the spinal cord of bovine animals aged over 12 months, the vertebral column excluding the vertebrae of the tail, the spinous and transverse processes of the cervical, thoracic and lumbar vertebrae and the median sacral crest and wings of the sacrum, but including the dorsal root ganglia of bovine animals aged over 24 months, and the tonsils, the intestines from the duodenum to the rectum and the mesentery of bovine animals of all ages;"<br /><br /><a href="http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2005:317:0004:01:EN:HTML">http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2005:317:0004:01:EN:HTML</a><br /><br /><br /><br />HOWEVER, as with other non-effective BSE regulations put forth by the O.I.E., SRM regulations are being watered down now by AGE. ...<br /><br />The sensitivity of PrPTSE detection is still lower than certain bioassays: failure to detect PrPTSE does not guarantee absence of infectivity in a tissue. Opinion on the likelihood of the infectivity in SRM derived from cattle at different age groups estimated by back calculation modelling...<br /><br /><a href="http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej476_srm_en.pdf?ssbinary=true">http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej476_srm_en.pdf?ssbinary=true</a><br /><br /><br /><br />Tuesday, November 10, 2009<br /><br />Surveillance On the Bovine Spongiform Encephalopathy and rabies in Taiwan and USA<br /><br /><a href="http://usdavskorea.blogspot.com/2009/11/surveillance-on-bovine-spongiform.html">http://usdavskorea.blogspot.com/2009/11/surveillance-on-bovine-spongiform.html</a><br /><br /><br /><br />Monday, October 19, 2009<br /><br />Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009<br /><br /><a href="http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html">http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html</a><br /><br /><br /><br />2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006<br /><br /><a href="http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html">http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html</a><br /><br /><br /><br />Monday, October 26, 2009<br /><br />MAD COW DISEASE, AND U.S. BEEF TRADE<br /><br />MAD COW DISEASE, CJD, TSE, SOUND SCIENCE, COMMERCE, AND SELLING YOUR SOUL TO THE DEVIL<br /><br /><a href="http://usdameatexport.blogspot.com/2009/10/mad-cow-disease-and-us-beef-trade.html">http://usdameatexport.blogspot.com/2009/10/mad-cow-disease-and-us-beef-trade.html</a><br /><br /><br /><br />IN A NUT SHELL ;<br /><br />(Adopted by the International Committee of the OIE on 23 May 2006)<br /><br />11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,<br /><br /><a href="http://www.oie.int/eng/Session2007/RF2006.pdf">http://www.oie.int/eng/Session2007/RF2006.pdf</a><br /><br /><br /><br />Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary<br /><br /><a href="http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1">http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1</a><br /><br /><br /><br />Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028 Public Submission Title Comment from Terry S Singletary<br /><br />Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY<br /><br />THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.<br /><br />MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???<br /><br />go figure. ...<br /><br /><a href="http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8151">http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8151</a><br /><br /><br /><br />Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028.1 Public Submission Title Attachment to Singletary comment<br /><br />January 28, 2007<br /><br />Greetings APHIS,<br /><br />I would kindly like to submit the following to ;<br /><br />BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01<br /><br /><a href="http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8">http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8</a><br /><br /><br /><br />Thursday, November 12, 2009<br /><br />BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009<br /><br /><a href="http://madcowfeed.blogspot.com/2009/11/bse-feed-recall-misbranding-of-product.html">http://madcowfeed.blogspot.com/2009/11/bse-feed-recall-misbranding-of-product.html</a><br /><br /><br /><br /><a href="http://madcowtesting.blogspot.com/">http://madcowtesting.blogspot.com/</a><br /><br /><br /><br />HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory<br /><br /><a href="http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648027c28e&disposition=attachment&contentType=pdf">http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648027c28e&disposition=attachment&contentType=pdf</a><br /><br /><br /><br />TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-51697476518887951982009-07-09T13:49:00.000-07:002009-07-09T13:52:10.713-07:00Transcriptional changes in the brain of cattle orally infected with BSE precede detection of infectivityJ. Virol. doi:10.1128/JVI.00352-09 Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.<br /><br />Transcriptional changes in the brain of cattle orally infected with BSE precede detection of infectivity<br /><br />Yue Tang, Wei Xiang, Steve A.C. Hawkins, Hans A. Kretzschmar, and Otto Windl* Department of Molecular Pathogenesis and Genetics and Department of Pathology, Veterinary Laboratories Agency, Woodham Lane, New Haw, Surrey KT15 3NB, UK; Institute of Neuropathology, Ludwig-Maximilians-University Munich, Munich, Germany<br /><br />* To whom correspondence should be addressed. Email: <a href="mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000173/!x-usc:mailto:o.windl@vla.defra.gsi.gov.uk">mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000173/!x-usc:mailto:o.windl@vla.defra.gsi.gov.uk</a>.<br /><br />Abstract<br /><br />Bovine spongiform encephalopathy (BSE) is a fatal, transmissible, neurodegenerative disease of cattle. BSE can be transmitted experimentally between cattle through the oral route and in this study brain tissue samples from animals at different time points post inoculation were analysed for changes in gene expression. The aims of this study were to identify differentially regulated genes during the progression of BSE using microarray based gene expression profiling and to understand the effect of prion pathogenesis on gene expression. A total of 114 genes were found to be differentially regulated over the time course of the infection and many of these 114 genes encode proteins involved in immune response, apoptosis, cell adhesion, stress response and transcription. This study also revealed a broad correlation between gene expression profiles and the progression of BSE in cattle. At 21 months post inoculation, the largest number of differentially regulated genes was detected, suggesting that there are many pathogenic processes in the animal brain even prior to the detection of infectivity in the CNS of these orally dosed cattle. Moreover, evidence is presented to suggest that it is possible to predict the infectious status of animals using the expression profiles from this study.<br /><br /><br /><br /><a href="http://jvi.asm.org/cgi/content/abstract/JVI.00352-09v1?etoc">http://jvi.asm.org/cgi/content/abstract/JVI.00352-09v1?etoc</a><br /><br /><br /><br />Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]<br /><br /><br /><br /><a href="http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html">http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html</a><br /><br /><br /><br />Monday, June 01, 2009<br /><br />Biochemical typing of pathological prion protein in aging cattle with BSE<br /><br /><br /><br /><a href="http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html">http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html</a><br /><br /><br /><br />Sunday, June 07, 2009<br /><br />L-TYPE-BSE, H-TYPE-BSE, C-TYPE-BSE, IBNC-TYPE-BSE, TME, CWD, SCRAPIE, CJD, NORTH AMERICA<br /><br /><br /><br /><a href="http://bse-atypical.blogspot.com/2009/06/l-type-bse-h-type-bse-c-type-bse-ibnc.html">http://bse-atypical.blogspot.com/2009/06/l-type-bse-h-type-bse-c-type-bse-ibnc.html</a><br /><br /><br /><br />Sunday, May 10, 2009<br /><br />Identification and characterization of bovine spongiform encephalopathy cases diagnosed and NOT diagnosed in the United States<br /><br /><br /><br /><a href="http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html">http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html</a><br /><br /><br /><br />Sunday, December 28, 2008<br /><br />MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy<br /><br /><br /><br /><a href="http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html">http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html</a><br /><br /><br /><br />Saturday, February 28, 2009<br /><br />NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009 SEAC 102/2<br /><br /><br /><br /><a href="http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html">http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html</a><br /><br /><br /><br />Saturday, June 13, 2009<br /><br />BSE FEED VIOLATIONS USA UPDATE From 01/01/2009 To 06/10/2009<br /><br /><br /><br /><a href="http://madcowfeed.blogspot.com/2009/06/bse-feed-violations-usa-update-from.html">http://madcowfeed.blogspot.com/2009/06/bse-feed-violations-usa-update-from.html</a><br /><br /><br /><br />Thursday, March 19, 2009<br /><br />MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA<br /><br /><br /><br /><a href="http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html">http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html</a><br /><br /><br /><br />WHO WILL FOLLOW THE CHILDREN FOR CJD SYMPTOMS ???<br /><br />Saturday, May 2, 2009<br /><br />U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM<br /><br /><br /><br /><a href="http://downercattle.blogspot.com/2009/05/us-government-sues-westlandhallmark.html">http://downercattle.blogspot.com/2009/05/us-government-sues-westlandhallmark.html</a><br /><br /><br /><br />Sunday, April 12, 2009 BSE MAD COW TESTING USA 2009 FIGURES Month Number of Tests<br /><br />Feb 2009 -- 1,891<br /><br />Jan 2009 -- 4,620<br /><br /><br /><br /><a href="http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml">http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml</a><br /><br /><br /><br />SEE FULL TEXT ;<br /><br /><br /><br /><a href="http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html">http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html</a><br /><br /><br /><br />Monday, May 4, 2009<br /><br />Back to the Past With New TSE Testing Agricultural Research/May-June 2009<br /><br /><br /><br /><a href="http://madcowtesting.blogspot.com/2009/05/back-to-past-with-new-tse-testing.html">http://madcowtesting.blogspot.com/2009/05/back-to-past-with-new-tse-testing.html</a><br /><br /><br /><br />Saturday, June 13, 2009<br /><br />Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009<br /><br />snip...<br /><br /><br /><br /><a href="http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html">http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html</a><br /><br /><br /><br /><br />Terry S. Singeltary Sr.<br /><br />P.O. Box 42<br /><br />Bacliff, Texas USA 77518Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-11480792391930294162009-01-28T07:51:00.000-08:002009-04-09T09:15:53.521-07:00TAFS1 Position Paper on Specified Risk Materials (January, 2009)TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation<br /><br />(January 2009)<br /><br />TAFS1 Position Paper on Specified Risk Materials<br /><br />Specified Risk Materials, or SRM, are tissues that have been designated for removal from the carcases of cattle, and excluded from human food. They have been shown, or assumed, to contain significant amounts of BSE infectivity in infected animals. By prohibiting their consumption it is considered to provide a substantial reduction in risk to consumers in countries where BSE has been shown to exist and in countries having a likely BSE-risk. SRM are also designated in sheep and goats. This was stipulated as a precautionary measure assuming that sheep and goats may have become infected with BSE. The finding of BSE in one goat has confirmed this assumption. SRM are also usually removed from animal feed as well, and this strengthens more general feed bans that are intended to prevent infection of cattle and small ruminants with BSE and lead to the elimination of BSE in each country. This document essentially concentrates on SRM in the context of human health, except in explaining the evolution of definitions and protective measures. Considerable confusion surrounds the term “specified risk materials” or SRM. This confusion ranges from the reasons for designation of such tissues or organs for destruction rather than consumption, and the extent to which it is necessary to ensure full compliance with regulations that require their removal from the food chain. This note briefly summarises the reasons for the designation of SRM, and concludes by listing current rules in the Europe. This table will be modified as rules change. Although the table includes a list of sheep and goat tissues that are defined as SRM, the note primarily addresses the background to bovine SRM.<br /><br />Why are tissues designated as SRM?<br /><br />? This note does not propose to describe the full chronology of SRM definition, but will give an explanation for the designation of each current SRM below.<br /><br />? In 1989, in the early stages of the BSE eradication programme in the United Kingdom, it was recognised that for every cow that was identified with clinical<br /><br />1 TAFS is an international platform created by a group of scientists, food industry experts, animal health regulators, epidemiologists, diagnosticians, food producers, and consumers. Its purpose is to establish and maintain lines of communication for the dissemination of reliable information to the public that can maintain confidence in the safety of food with regard to Transmissible Animal Diseases (TAD).<br /><br />TAFS<br /><br />2<br /><br />BSE there must have been others that were infected, but apparently healthy, that were being slaughtered for human consumption. These could not be detected while alive and prevented from being slaughtered for consumption. It was therefore felt that reliance on the slaughter and destruction of clinically affected cattle was insufficient to protect public health, and that additional measures were required.<br /><br />? As a result, consideration was given to whether the entire carcase represented a risk to consumer, or whether it was possible to identify specific tissues that could be removed and excluded from the food chain. In other words, in the absence of evidence that BSE did actually represent a risk to humans, what acceptable and proportionate additional safety measures could be put in place? Was it a ban on the consumption of any bovine tissues, or was it possible to avoid taking any action at all?<br /><br />? By 1989 research had not progressed to the point of being able to identify which bovine tissues were infectious, other than brain(3,16). The authorities therefore resorted to an analysis of known data from the similar disease of sheep, scrapie(20). Some limited research had been done that indicated the range of tissues that might be infectious, and the extent to which they might be infectious. In other words it was clear that some tissues contained higher levels of infectivity than others, and logically could be considered to represent a greater risk to consumers. This conservative approach aimed to minimise risk of human exposure through food.<br /><br />? The outcome was a list of tissues that could be removed without destroying the economic basis of the industry, and could still be defended as proportionate should the measures be challenged in court. It was recognized that other tissues, which are not on the list, might be infectious, but at such low levels that detection was difficult.<br /><br />? The initial listing in the UK excluded these tissues, then called Specified Bovine Offals (SBO), from the human food chain(20). In September 1990 they were also excluded from all animal food, and this reinforced the feed ban that was the major measure introduced to eradicate BSE. The term SBO was later changed to SRM and also adopted in EU and other legislation.<br /><br />? The development in recent years of rapid (post mortem) diagnostic tests has not eliminated the need to remove SRM. Although extremely effective, the tests are still only effective in the later stages of incubation, so they cannot detect all infected animals(27).<br /><br />Has BSE infectivity been detected in all SRM listed later in this position paper?<br /><br />? Yes. Research on bovine tissues, from naturally and experimentally infected cattle, has now progressed to the point where there is a clearer picture of which tissues are infectious, and those where no infectivity has been found(1, 2, 5, 13, 17, 18, 19, 21, 23, 26, 28-35) .<br /><br />? In naturally infected cattle the brain, spinal cord and retina (eye) have been shown to be infectious(5,16, 35). In addition, positivity or infectivity was detected in some peripheral nerves that would not normally be removed as SRM(5,17,18,19). The amount of infectivity present is low, and considered be up to 1000-fold lower than the brain.<br /><br />? In experimentally infected cattle, brain and spinal cord were again been confirmed to be infectious, but in addition the distal ileum (lower small intestine) also contained significant amounts of infectivity(31, 32). Two key ganglia, which are key intermediate points linking the central and peripheral nervous systems, namely<br /><br />TAFS<br /><br />3<br /><br />the trigeminal and dorsal root ganglia (DRG), were also clearly infectious(32, 33). This is not surprising given their close association with central nervous tissue. Peripheral nerves have also been demonstrated to become positive after the brain and spinal cord(1, 19). Completion of bioassay studies has also enabled a better understanding of the sequence of events, and rate of accumulation of infectivity, especially in relation to ileum, brain and spinal cord(1,2), and have confirmed the basic assumptions upon risk management policy were based.<br /><br />? In addition, in experimentally infected cattle, a single positive result has indicated the possible presence of infectivity in bone marrow at about the time of clinical onset(33). Further attempts to resolve this anomaly, by inoculation of cattle with bone marrow collected at different time points, were unsuccessful(21), and concluded that the presence of infectivity was either a rare event, or was more consistently present at levels below the limits of detection. As discussed by EFSA in the context of risk from lingual tonsil(11), this was considered to represent a negligible consumer risk when considered alongside the low prevalence of BSE in the EU at that time.<br /><br />? In addition, a low amount of infectivity was detected in tonsil early in the incubation and maintained during the time course(13,32, 34).<br /><br />? A single calf inoculated with pooled third eyelid tissue from naturally infected cows has succumbed to BSE, indicating the presence of infectivity in the pooled tissue. None of the remaining four inoculated cattle became infected, so this result remains uninterpretable(35).<br /><br />Why are other tissues/organs not expected to be infectious included in the list for exclusion from consumption?<br /><br />? Some SRM have not been inherently shown to be infected, but with experience it is clear that their close association with other SRM, especially the central nervous system, represents a real risk of cross contamination(26). Again, a precautionary approach has been adopted.<br /><br />? For example, the skull has not been demonstrated to be inherently infectious, but it is impossible to remove the brain from the skull without leaving traces of brain tissue behind(26). Similarly the eye is also infected. Therefore, the definition of skull as SRM acknowledges the remaining risk due to the retained brain tissue, or contamination with brain as a result of the slaughtering process. The designation of skull means that the practicalities of compliance and enforcement are easier to handle, and there is less exposure of abattoir operators to brain tissue while it remains encased within the skull. ? The vertebral column is also designated because of its close association with dorsal root ganglia (DRG) and due to contamination with spinal cord tissue. DRG sit just on the outside of the spine where the spinal nerves pass through from the spinal cord(26). If the vertebral column (spine) was left attached to meat, for example in a T-bone steak, there is therefore a danger that the DRG would be consumed. The spinal cord contamination arises as a result of the splitting process as the saw that cuts the carcase in half passes through the cord and contaminates the cut surface of the spine. ? In both situations described above the use of vertebral column for the production of mechanically recovered meat, or mechanically separated meat, would strip off the DRG and contamination, transferring infectivity into the MRM/MSM which is used in manufactured meat products. Indeed, European legislation has gone further<br /><br />TAFS<br /><br />4<br /><br />than just designating vertebral column as an SRM. The use of ruminant bones for production of mechanically recovered meat (MRM) is prohibited. Have all tissues been tested for the presence of infectivity?<br /><br />? No. There are limits to the number of tissues that can be tested. Decisions on which tissues to test have historically been driven by several factors such as:-<br /><br />? which represent a risk to consumers because they are eaten,<br /><br />? which are key tissues in understanding the biology of BSE in cattle, and<br /><br />? which represent a risk to humans through the manufacture of other products such as pharmaceuticals and medical devices.<br /><br />? Nevertheless, based upon evidence from other species (sheep scrapie) and the results of assays of bovine tissues, and audits of the use of bovine tissues, it is considered that all key tissues have been assayed. Will the list be dynamic?<br /><br />? Yes(14). Research is still ongoing, and it is still possible that infectivity will be detected in tissues that have been negative so far. The use of cattle for infectivity assays, or technological breakthroughs to produce alternative assay systems (see above) mean that the analytical sensitivity of current assays is greater than those used in earlier studies. It is therefore not possible to exclude the possibility that new positive results will arise. Their significance, in terms of quantifying the amount of infectivity present, will be critical to risk assessments that will determine whether authorities define them as SRM.<br /><br />? Nevertheless, current evidence suggests that this is a theoretical rather than real scenario. Authorities and expert committees cannot however remain oblivious to new findings, and may need to take into account consumer confidence as well as risk assessments in determining whether or not to add new tissues to the SRM list.<br /><br />? Also it has to be taken into account that new findings of positive tissues may come at a time when the prevalence of BSE is very low and decreasing and the vast majority of cattle consumed have to be considered uninfected. In this situation authorities may conclude that the addition of further tissues to the list may be disproportionate to the risk. This has indeed been the case in relation to peripheral nerves, which have not been designated at SRM.<br /><br />? In the TSE roadmap of the EU, published in July 2005(6), next steps in the BSE policy on different points are evaluated. Concerning SRM it is accepted that the list of SRM could be modified in the medium term, based on new and evolving scientific knowledge and the results of the surveillance programs, and subject to appropriate evaluation and consultation.<br /><br />Designated bovine SRM in Europe<br /><br />? Brain – expected to be infectious by extrapolation from sheep scrapie, and subsequently confirmed for BSE. Experimental evidence suggests that the brain becomes infectious in the later stages of incubation.<br /><br />? Spinal cord – expected to be infectious by extrapolation from sheep scrapie, and subsequently confirmed for BSE. Experimental evidence suggests that the spinal cord becomes infectious in the later stages of incubation(1).<br /><br />? Tonsil – expected to be infectious by extrapolation from sheep scrapie, but not subsequently confirmed for BSE from naturally infected cattle, even by bioassay<br /><br />TAFS<br /><br />5<br /><br />in cattle. Result from experimentally infected cattle, suggests that the palatine tonsil becomes infectious in the early stage of the incubation and the very low infectivity is maintained during the time course(7,13,34). Tongue itself is not considered as SRM. However, according to EU-legislation, “tongue should be harvested by a transverse cut rostral to the lingual process of the basihyoid bone”, due to possible contamination of tonsil tissue. Further consideration of the residual risk associated with lymphoid tissue that remains within the tongue after adopting this removal procedure did not result in recommendations for more extensive trimming of the tongue(11). In part this was due to the low prevalence of BSE in the EU by that time.<br /><br />? Intestine – the distal ileum was expected to be infectious by extrapolation from sheep scrapie, and this was subsequently confirmed for BSE in experimentally infected cattle especially in the early stages of incubation. Logic suggests that it must also be infectious in naturally infected cattle in the early stages of incubation. This infectivity was particularly associated with Peyer’s patches(29), collections of lymphoid tissue that form a first line of defence against infection through the intestinal wall. This result has not been replicated in naturally infected cattle, although immunostaining methods have shown the presence of abnormal prion protein in the nervous plexuses of the intestine. This discrepancy is considered to be most probably due to the fact that the Peyer’s patches regress as cattle reach maturity, and consequently reduce the likelihood of finding any infectivity that may remain. The majority of infected cows die of clinical BSE at five to seven years of age, after the Peyer’s patches have regressed. Nevertheless, the positive immunostaining of the nervous plexuses, which extend throughout the intestine, does justify continued listing of intestine as SRM while there is a danger that cattle will have been exposed to BSE(10,25).<br /><br />? Skull – designated because of association with brain and eye, with resultant contamination through the slaughtering process or because of residual brain tissue following removal of the brain.<br /><br />? Vertebral column – designated because of a combination of close association with DRG, and the superficial contamination of the cut surface of the spine with spinal cord during the carcase splitting process.<br /><br />? Age restrictions(8, 26) – all of the above tissues will not necessarily be designated for all ages of cattle consumed. This is because experimental evidence has suggested that they only represent a risk at particular stages of the incubation. If a tissue is infectious early in the incubation then it is normal to designate the tissue for all ages. If infectivity is detected late in the incubation then it is possible to designate the tissue in older animals only, especially where the designation is a result of contamination (eg. vertebral column).<br /><br />Designated ovine SRM<br /><br />? SRM designated in sheep are based primarily on evidence from the study of sheep scrapie, but the outcome is consistent with our understanding of the behaviour of BSE in sheep that are susceptible to infection with BSE(4,9,15). ? The designation adopts a cautious balance between significantly reducing the risk to consumers should BSE be present in the sheep and goat population and the introduction of extensive SRM removal which would significantly damage sheep and meat industries in affected countries(9,22,24).<br /><br />TAFS<br /><br />6<br /><br />? There is no doubt that the confirmation that BSE is present in the sheep population will result in an immediate revision of this list, or possibly even a prohibition of the consumption of certain categories of sheep meat. The confirmation of BSE in a goat(12) did not however have this effect on the definition of SRM. The list of SRMs in small ruminants was not modified as a result of this finding (see position paper on BSE in small ruminants).<br /><br />TAFS<br /><br />7<br /><br />A summary of designated SRM in Europe as at January 2009 European Union and Switzerland Cattle Skull (including brain and eyes) 12 months Tonsils All ages Spinal cord 12 months Vertebral column (including dorsal root ganglia - DRG – but excluding vertebrae of the tail and the transverse processes of lumbar and thoracic vertebrae) 30 months Intestines and mesentery All ages Sheep and goats Skull (including brain and eyes) 12 month Spinal cord 12 months Tonsils 12 months Ileum All ages Spleen All ages<br /><br />TAFS<br /><br />8<br /><br />References<br /><br />1. Arnold, M, A., Ryan, J.B.M., Konold, T., Simmons, M.M., Spencer, Y.I., Wear, A., Chaplin, M., Stack, M., Czub, S., Mueller, R., Webb, P.R., Davis, A., Spiropoulos, J., Holdaway, J., Hawkins, S.A.C., Austin, A.R. & Wells, G.A.H. (2007). Estimating the temporal relationship between PrPSc detection and incubation period in experimental bovine spongiform encelphalopathy of cattle. J. Gen. Virol. 88:3198-3208.<br /><br />2. Arnold, M.A., Hawkins, S.A.C., Green, R., Dexter, I. & Wells, G.A.H. (2009). Pathogenesis of experimental bovine spongiform encephalopathy (BSE): estimation of tissue infectivity according to incubation period. Vet. Res. 40:08<br /><br />3. Barlow R.M., & Middleton D J (1990). Dietary transmission of bovine spongiform encephalopathy to mice. Vet. Rec, 126:111-112.<br /><br />4. Bellworthy, S.J., Hawkins, S.A.C., Green, R.B., Blamire, I., Dexter, G., Dexter, I., Lockey, R., Jeffrey, M., Ryder, S., Berthelin-Baker, C. & Simmons, M.M. (2005) Tissue distribution of bovine spongiform encephalopathy infectivity in sheep following oral challenge – preliminary results. Vet. Rec. 156:197-202.<br /><br />5. Buschmann A., Groschup MH. (2005). Highly BSE-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis. 192:934-42.<br /><br />6. EC (2005) – European Commission – The TSE Roadmap. Com(2005) 322 Final.<br /><br /><br /><a href="http://ec.europa.eu/food/food/biosafety/bse/roadmap_en.pdf">http://ec.europa.eu/food/food/biosafety/bse/roadmap_en.pdf</a><br /><br /><br /><br />7. EFSA (2004). - Opinion of the Scientific Panel on Biological Hazards of the European Food Safety Authority on BSE risk from bovine tonsil and consumption of bovine tongue. The EFSA Journal 41: 1-4.<br /><br /><br /><a href="http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/opinion_biohaz_06_en1.pdf?ssbinary=true">http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/opinion_biohaz_06_en1.pdf?ssbinary=true</a><br /><br /><br /><br /><br />8. EFSA (2005). - Opinion of the Scientific Panel on Biological Hazards on the assessment of the age limit in cattle for the removal of certain specified risk materials (SRM). The EFSA Journal. 220: 1-7.<br /><br /><br /><a href="http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_opinion_ej220_srmremove_en1.pdf?ssbinary=true">http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_opinion_ej220_srmremove_en1.pdf?ssbinary=true</a><br /><br /><br /><br /><br />9. EFSA (2005). - Opinion of the Scientific Panel on Biological Hazards on a quantitative assessment of risk posed to humans by tissues of small ruminants in case BSE is present in these animal populations” The EFSA Journal. 227: 1-11.<br /><br /><br /><a href="http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_opinion_ej227_bse_goat_v2_en1.pdf?ssbinary=true">http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_opinion_ej227_bse_goat_v2_en1.pdf?ssbinary=true</a><br /><br /><br /><br /><br />10. EFSA (2007). - Opinion of the Scientific Panel on Biological Hazards on a request from the European Commission on quantitative histological studies and the re-<br /><br />TAFS<br /><br />9<br /><br />assessment of the BSE related risk of bovine intestines after processing into natural sausage casings. The EFSA Journal. 464: 1-14.<br /><br /><br /><a href="http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej464_bovine_casings_en,4.pdf?ssbinary=true">http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej464_bovine_casings_en,4.pdf?ssbinary=true</a><br /><br /><br /><br /><br />11. EFSA (2008). Scientific Opinion of the Scientific Panel on Biological Hazards on a request from the European Commission on consumption of beef tongue: human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings. EFSA Journal. 700: 1-24.<br /><br /><br /><a href="http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej700_bovine_tongue_rev2_en,1.pdf?ssbinary=true">http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej700_bovine_tongue_rev2_en,1.pdf?ssbinary=true</a><br /><br /><br /><br /><br />12. Eloit M, Adjou K, Coulpier M, Fontaine JJ, Hamel R, Lilin T, Messiaen S, Andreoletti O, Baron T, Bencsik A, Biacabe AG, Beringue V, Laude H, Le Dur A, Vilotte JL, Comoy E, Deslys JP, Grassi J, Simon S, Lantier F, Sarradin P.(2005). BSE agent signatures in a goat. Vet Rec. 156:523-4.<br /><br />13. Espinosa, J-C., Morales, ,M., Castilla, J., Rogers, M. and Torres, J.M. (2007). Progression of prion infectivity in asymptomatic cattle after oral bovine spongiform encephalopathy challenge. J. Gen. Virol. 88. 1379-1383<br /><br />14. European Commission (2007). BSE legislation - Chronological list;<br /><br /><br /><a href="http://ec.europa.eu/food/food/biosafety/bse/chronology_en.htm">http://ec.europa.eu/food/food/biosafety/bse/chronology_en.htm</a><br /><br /><br /><br /><br />15. Foster, J. D., Hope, J. & Fraser, H. (1993). Transmission of bovine spongiform encephalopathy to sheep and goats. The Veterinary Record. 133: 339-341.<br /><br />16. Fraser H, McConnell I, Wells G A H & Dawson M (1988) – Transmission of bovine spongifrom encephalopathy to mice. Vet Rec. 123:472.<br /><br />17. Hoffmann, C., Ziegler, U., Buschmann, A., Weber, A., Kupfer, L., Oelschlegel, A., Hammerschmidt, B. and Groschup, M.J. (2007). Prions spread via the autonomic nervous system in cattle incubating bovine spongiform encephalopathy. J. Gen. Virol. 88: 1048-1055.<br /><br />18. Iwata, N., Sato, Y. Higuchi, Y. Nohtomi, K. Nagata, N. Hasegawa, H. Tobiume, M. Nakamura, Y., Hagiwara, K., Furuoka, H, Horiuchi, M. Yamakawa, Y & Sata.T (2006). Distribution of PrP(Sc) in Cattle with Bovine Spongiform Encephalopathy Slaughtered at Abattoirs in Japan. Jpn J Infect Dis. 59:100-7.<br /><br />19. Masujin, K., Matthews, D., Wells, G.A.H., Mohri, S. & Yokoyama, T. (2007) Prions in the peripheral nerves of bovine spongiform encephalopathy-affected cattle. J. Gen. Virol. 88:1850-1858.<br /><br />20. Prince M. J., Bailey J. A., Barrowman, P. R., Bishop, K. J., Campbell, G. R., Wood J. M. (2003). Bovine spongiform encephalopathy, In: Rev.Sci.et Tech. Office international des Epizooties. 22 (1):37-60.<br /><br />21. Sohn, H.J., Lee, Y.H., Green, R.B., Spencer, Y.I., Hawkins, S.A.C., Stack, M.J., Konold, T., Wells, G.A.H., Matthews, D., Cho.I.S. & Joo.Y.S. (2009). Bone marrow<br /><br />TAFS<br /><br />10<br /><br />infectivity in cattle exposed to the bovine spongiform encephalopathy agent. Vet. Rec. (in press).<br /><br />22. SSC – Scientific Steering Committee (2001). Opinon on the safety of small ruminant products should BSE in small ruminants become probable / confirmed, 18-19 October 2001.<br /><br /><br /><a href="http://europa.eu.int/comm/food/fs/sc/ssc/out234_en.pdf">http://europa.eu.int/comm/food/fs/sc/ssc/out234_en.pdf</a><br /><br /><br /><br />23. SSC - Scientific Steering Committee (2001)- Opinion on TSE infectivity distribution in ruminant tissues (state of knowledge, December 2001) (adopted on 10-11 January 2002).<br /><br /><br /><a href="http://europa.eu.int/comm/food/fs/sc/ssc/out241_en.pdf">http://europa.eu.int/comm/food/fs/sc/ssc/out241_en.pdf</a><br /><br /><br /><br /><br />24. SSC - Scientific Steering Committee (2002) Opinion on safe sourcing of small ruminant materials.<br /><br /><br /><a href="http://europa.eu.int/comm/food/fs/sc/ssc/out257_en.pdf">http://europa.eu.int/comm/food/fs/sc/ssc/out257_en.pdf</a><br /><br /><br /><br /><br />25. SSC - Scientific Steering Committee (2002) SSC opinion of 4-5 April 2002 on safe sourcing of small ruminant materials (with special reference to the safety with regard to BSE risks of sheep intestines and casings).<br /><br /><br /><a href="http://europa.eu.int/comm/food/fs/sc/ssc/out281_en.pdf">http://europa.eu.int/comm/food/fs/sc/ssc/out281_en.pdf</a><br /><br /><br /><br /><br />26. SSC - Scientific Steering Committee (2002) Update of the Opinion on TSE Infectivity distribution in ruminant tissues.<br /><br /><br /><a href="http://ec.europa.eu/food/fs/sc/ssc/out296_en.pdf">http://ec.europa.eu/food/fs/sc/ssc/out296_en.pdf</a><br /><br /><br /><br /><br />27. TAFS (2009). Position paper on the testing of cattle for BSE – purpose and effectiveness.<br /><br /><br /><a href="http://tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_TESTING_OF_CATTLE_FOR_BSE_070516.pdf">http://tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_TESTING_OF_CATTLE_FOR_BSE_070516.pdf</a><br /><br /><br /><br />28. TAFS (2009) – Position paper on BSE in small ruminants.<br /><br /><br /><a href="http://www.tafsforum.org/position_papers/TAFS%20POSITION%20STATEMENT%20ON%20BSE%20IN%20SMALL%20RUMINANTS_2009.pdf">http://www.tafsforum.org/position_papers/TAFS%20POSITION%20STATEMENT%20ON%20BSE%20IN%20SMALL%20RUMINANTS_2009.pdf</a><br /><br /><br /><br /><br />29. Terry, L.A., Marsh, S., Ryder, S.J., Hawkins, S.A.C., Wells, G.A.H., Spencer, Y.I. (2003). Detection of disease specific PrP in Peyer’s patches of the distal ileum of cattle orally exposed to the BSE agent. Vet. Rec. 152: 387-392.<br /><br />30. Wells G.A.H., Dawson M ,Hawkins S.A.C., Austin A.R Green R.B., Dexter I., Horigan M.W., &. Simmons M.M. (1996). - Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy. In: Bovine spongiform encephalopathy: The BSE Dilemma, Ed. C.J. Gibbs, Serono Symposia, Norwell, USA Springer-Verlag, New York, Inc. Pp. 28-44.<br /><br />31. Wells G.A.H., Dawson M ,Hawkins S.A.C., Green R.B., Dexter I., Francis M.E., Simmons M.M., Austin A.R. & Horigan M.W (1994). Infectivity in the ileum of cattle challenged orally with bovine spongiform encephalopathy. Vet. Rec., 135:<br /><br />40-41.<br /><br />TAFS<br /><br />11<br /><br />32. Wells GA, Hawkins SA, Green RB, Austin AR, Dexter I, Spencer YI, Chaplin MJ, Stack MJ, Dawson M. (1998). Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet Rec 142:103-6.<br /><br />33. Wells GA, Hawkins SA, Green RB, Spencer YI, Dexter I, Dawson M., (1999). Limited detection of sternal bone marrow infectivity in the clinical phase of experimental bovine spongiform encephalopathy (BSE). Vet Rec. 144:292-4<br /><br />34. Wells GA, Spiropoulos J, Hawkins SA, Ryder SJ. (2005). Pathogenesis of experimental bovine spongiform encephalopathy: preclinical infectivity in tonsil and observations on the distribution of lingual tonsil in slaughtered cattle. Vet Rec. 156:401-7.<br /><br />35. World Health Organization (2006). WHO Guidelines on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies.<br /><br /><br /><a href="http://www.who.int/bloodproducts/tse/WHO%20TSE%20Guidelines%20FINAL-22%20JuneupdatedNL.pdf">http://www.who.int/bloodproducts/tse/WHO%20TSE%20Guidelines%20FINAL-22%20JuneupdatedNL.pdf</a><br /><br /><br /><br /><br /><br /><br /><br /><a href="http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_SPECIFIED%20RISK%20MATERIALS_2009.pdf">http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_SPECIFIED%20RISK%20MATERIALS_2009.pdf</a><br /><br /><br /><br /><br /><br /><br />UPDATED:TAFS POSITION PAPER ON SPECIFIED RISK MATERIALS (January, 2009)<br /><br /><br /><br /><a onclick="javascript :urchinTracker ('/downloads/PP/SRM'); " href="mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000145/!x-usc:http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_SPECIFIED%20RISK%20MATERIALS_2009.pdf" target="_blank">TAFS Position Paper - Specified Risk Materials (148 kB)</a><a onclick="javascript :urchinTracker ('/downloads/PP/SRM_JP'); " href="mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000145/!x-usc:http://www.tafsforum.org/position_papers/Japanese/TAFS_Position_Paper_on_SRM_JP.pdf" target="_blank">特定危険部位に関するTAFSポジションペーパー</a><br /><br /><br />(Japanese version not updated; status May 2007)<br /><br />Saturday, January 24, 2009<br /><br />Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report<br />Research Project: Study of Atypical BseLocation: Virus and Prion Diseases of Livestock2008 Annual Report<br /><br /><br /><br /><br /><a href="http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html">http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html</a><br /><br /><br /><br /><br /><br />Research Project: Detection of Prp**d in Tissue Samples and Bodily Fluids of Cattle from the German Bse Pathogenesis Study Location: Virus and Prion Diseases of Livestock<br /><br />2008 Annual Report<br /><br />1a.Objectives (from AD-416) The overall objective of this cooperative project is to evaluate PrP**D tissue distribution and migration in cattle orally infected with BSE of British origin. To achieve this objective, the following specific approaches will be conducted: (1) the protein misfolding cyclic amplification (PMCA) assay will be used on blinded replicate aliquots of tissue from animals in the BSE study to independently confirm whether PrP**D can be detected in the tissue samples. The Cooperator will function as lead investigator and ARS will confirm test results for the presence or absence of PrP**D in any given sample. (2) The Cooperator will analyze the proteome in tissue samples by two dimensional SDS PAGE. (3) NADC will evaluate microscopic pathology and visual function of the retina of available animals and tissues to assess PrP**D accumulation and visual function effects.<br /><br />1b.Approach (from AD-416) The German BSE oral pathogenesis study involves 56 beef cattle orally dosed with BSE containing brain tissue obtained from British cattle. The animal study is managed by the cooperator and various tissues are collected at prescribed times and at necropsy. These tissues will enable the cooperating parties to perform independent confirmation on the presence or absence of PrP**D for verification of PrP**D distribution in tissues. In addition, retinal samples will be analyzed to assess the extent of retinal pathology in infected cattle and visual system function in available remaining live cattle will be tested using electroretinography.<br /><br />3.Progress Report The overall objective of this cooperative project is to evaluate PrP**d tissue distribution and migration in cattle orally infected with Bovine spongiform encephalopathy (BSE) of British origin. The live-animal phase of this work was completed this year. Samples from this experiment will be brought to the USDA, ARS, National Animal Disease Center for further characterization in the upcoming year. Methods used for monitoring included phone contact, e-mail, and site visits. This project addresses NP 103, component 8.<br /><br /><br /><br /><br /><a href="http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=411017&fy=2008">http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=411017&fy=2008</a><br /><br /><br /><br /><br />Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock<br /><br />Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement<br /><br />Start Date: Sep 15, 2004 End Date: Sep 14, 2009<br /><br />Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.<br /><br />Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.<br /><br /><br /><br /><br /><a href="http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490">http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490</a><br /><br /><br /><br /><br /><br />CHAPTER 3 Animal Disease Eradication Programs and Control and Certification Programs<br /><br />snip...<br /><br />In FY 2007, two field cases, one validation study case, and two RSSS cases were consistent with a variant of the disease known as Nor98 scrapie.1 These five cases originated from flocks in California, Minnesota, Colorado, Wyoming, and Indiana, respectively.<br /><br />snip...<br /><br /><br /><br /><br /><a href="http://www.aphis.usda.gov/publications/animal_health/content/printable_version/AHR_Web_PDF_07/D_Chapter_3.pdf">http://www.aphis.usda.gov/publications/animal_health/content/printable_version/AHR_Web_PDF_07/D_Chapter_3.pdf</a><br /><br /><br /><br /><br /><br />NOR-98 Scrapie FY 2008 to date 1<br /><br /><br /><br /><br /><a href="http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps">http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps</a><br /><br /><br /><br /><br /><br />ATYPICAL TSEs in USA CATTLE AND SHEEP ?<br /><br /><br /><br /><br /><a href="http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf" target="_blank">http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf</a><br /><br /><br /><br /><br /><br />Monday, December 1, 2008<br /><br />When Atypical Scrapie cross species barriers<br /><br /><br /><br /><br /><a href="http://nor-98.blogspot.com/2008/12/when-atypical-scrapie-cross-species.html">http://nor-98.blogspot.com/2008/12/when-atypical-scrapie-cross-species.html</a><br /><br /><br /><br /><br /><br /><br />Tuesday, January 06, 2009<br /><br />CWD Update 93 December 29, 2008<br /><br /><br /><br /><br /><a href="http://chronic-wasting-disease.blogspot.com/2009/01/cwd-update-93-december-29-2008.html">http://chronic-wasting-disease.blogspot.com/2009/01/cwd-update-93-december-29-2008.html</a><br /><br /><br /><br /><br /><br />Sunday, December 28, 2008<br /><br />MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy<br /><br /><br /><br /><br /><a href="http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html">http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html</a><br /><br /><br /><br /><br /><br />[Docket No. FDA–2008–D–0597] Draft Guidance for Industry: Small Entities Compliance Guide for Renderers—Substances Prohibited From Use in Animal Food or Feed; Availability AGENCY: Food and Drug Administration, HHS. ACTION:<br /><br />snip...<br /><br /><br /><br /><br /><a href="http://edocket.access.gpo.gov/2008/pdf/E8-28189.pdf">http://edocket.access.gpo.gov/2008/pdf/E8-28189.pdf</a><br /><br /><br /><br /><br /><br /><br />Greetings,<br /><br />I kindly wish to submit the following to [Docket No. FDA–2008–D–0597] ;<br /><br />I would kindly like to once again comment on the failed attempts of the FDA et al to stop the spread of animal TSEs, including BSE, through the legal, and illegal feeding practices, of feeding animal protein to livestock for human and animal consumption. Since the terribly flawed, partial, and voluntary August 4, 1997 ruminant to ruminant feed ban was put into place, literally 100s of thousands of tons of banned animal protein has been fed out into commerce, even as late as 2007, when some 10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. 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. NOW, how much of that product that went out into commerce was fed out to cattle, and how much was ever recovered ? AND to think that feeding blood to livestock producing animals is still legal, when scientific study after study shows that TSEs are easily transmitted via blood. IT is absolutely unacceptable that still in 2008, the USA is still feeding highly suspect mad cow feed to USA cattle, and other livestock producing animals. Especially when the last two cases of BSE that were allowed to be tested and reported were of the atypical BSE category, of which we now know the atypical BSE is more virulent than that of the typical BSE, and when ARS research on the atypical BSE said long ago the SRM rules may need to be changed, IF the atypical BSE were to be proven to be more virulent. Why do we continue to flounder? I have submitted to these BSE feed dockets until I am blue in the face, and still to date, they still debate an issue that should have been settled long ago. IT's a fine example of how big ag, big industry, have a stranglehold on sound science and policy making thereof. How many millions of animals and humans have been needlessly exposed to this TSE agent, due to nothing more than ignorance and greed, simply because of a disease that is 100% fatal, but one that has such a long incubation period. For the government and industry as a whole, to continue to flagrantly violate said rules and regulations, in my opinion, should be regarded as criminal, and treated as such. People are dying. ...<br /><br />Please see references ;<br /><br /><br />snip...<br /><br /><br /><br /><br /><a href="http://madcowfeed.blogspot.com/2008/12/docket-no-fda2008d0597-draft-guidance.html">http://madcowfeed.blogspot.com/2008/12/docket-no-fda2008d0597-draft-guidance.html</a><br /><br /><br /><br /><br /><br />November 25, 2008<br /><br /><br />Update On Feed Enforcement Activities To Limit The Spread Of BSE<br /><br /><br /><br /><br /><br /><a href="http://madcowfeed.blogspot.com/2008/11/november-2008-update-on-feed.html">http://madcowfeed.blogspot.com/2008/11/november-2008-update-on-feed.html</a><br /><br /><br /><br /><br /><a href="http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html">http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html</a><br /><br /><br /><br /><br /><a href="http://madcowspontaneousnot.blogspot.com/">http://madcowspontaneousnot.blogspot.com/</a><br /><br /><br /><br /><br /><br />TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-57789753094365600902008-04-02T13:54:00.000-07:002009-01-28T07:26:49.094-08:00In vivo prion protein intestinal uptake in fish1: APMIS. 2008 Mar;116(3):173-80.<br /><br />In vivo prion protein intestinal uptake in fish.<br /><br />Dalla Valle AZ, Iriti M, Faoro F, Berti C, Ciappellano S.<br />Department of Food Science and Microbiology (DISTAM), Section of Human Nutrition, University of Milan, Milan, Italy.<br /><br />Intestinal uptake of abnormal prion protein (PrP(Sc)), the pathological agent involved in transmissible spongiform encephalopathies (TSEs), has been investigated in rainbow trout (Oncorhynchus mykiss). Experimental procedures were conducted in vivo by immunohistological PrP(Sc) localization in intestine and pyloric caeca after forced feeding of infected material. Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the distal intestine. It did not remain longer than 15 days in the fish intestine; furthermore, it did not cross the intestinal barrier.<br /><br />PMID: 18377582 [PubMed - in process]<br /><br /><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/18377582?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum">http://www.ncbi.nlm.nih.gov/pubmed/18377582?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum</a><br /><br /><br /><br />> Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted<br /><br />> in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the<br /><br />> distal intestine.<br /><br />> It did not remain longer than 15 days in the fish intestine;<br /><br /><br />WOULD this not be a potential risk factor for transmission of the PrPSc agent to cattle and other species via fish by-products and or fish feed ???<br /><br /><br /><br />vCJD in the USA * BSE in U.S.<br /><br />15 November 1999<br /><br />snip...<br /><br /><br />Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows.<br /><br />***I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing.<br /><br />It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.<br /><br /><br />snip...<br /><br /><br />full text ;<br /><br /><br /><a href="http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406">http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406</a><br /><br /><br /><br />Subject: CANADA BSE FACT SHEET FOR FISH BY-PRODUCT RENDERERS UPDATE<br />Date: June 5, 2007 at 1:16 pm PST<br /><br />FACT SHEET FOR FISH BY-PRODUCT RENDERERS<br />Overview<br />On July 12, 2007, a series of amendments to the Feeds Regulations, 1983, and the Health of Animals Regulations will come into effect, to further protect animal health and accelerate the eradication of bovine spongiform encephalopathy (BSE) in Canada. Since BSE was first reported in Canada in 2003, Canada’s trading partners have demanded additional assurances and certification of animal products, by-products, and feeds containing these ingredients. In addition to banning the use of certain cattle tissues in animal feed, pet food and fertilizers, the regulatory amendments will also introduce new controls on animal product renderers. It is noteworthy that many of our trading partners consider fish by-products to be an animal product.<br /><br />For the purposes of this fact sheet, fish by-product renderers are defined as those who receive inedible offal, fish or fish by-products from fish processing plants or other sources and render it to produce fish meal or fish oil products.<br /><br />New requirements for fish by-product renderers<br />As a result of the regulatory amendments described above, the following requirements will apply to all fish by-product rendering facilities as of July 12, 2007:<br /><br />All rendering facilities (including those processing fish by-products) must obtain and operate under a permit issued by the Canadian Food Inspection Agency (CFIA), and be subject to routine inspection by the CFIA;<br />Rendering facilities that import fish by-products will be required to obtain a Health of Animals import permit;<br />Rendering facilities that export fish by-products (including fish meal and fish oil) will be required to obtain a CFIA export certification; and<br />Fish by-product renderers are required to keep production and distribution records for 10 years.<br />One of the benefits of these amendments will be enhanced traceability of fish meal and fish oil from both domestic and import sources through the feed system. Fish meal and fish oil have a broad range of applications in animal feeds and fertilizers. Identifying the locations and origin of primary ingredients, such as fish meal and fish oil, allows the CFIA to more effectively direct its resources to monitoring and sampling activities related to the safety of these products. Sampling and testing these ingredients directly, rather than the finished feed products, provides a more accurate picture of the safety of the ingredients.<br /><br />CFIA fish by-product rendering survey<br />To prepare for the new regulatory requirements, the CFIA is undertaking a survey of fish by-product renderers across Canada. At some time in the next few months, if you are a fish by-product renderer, you will be contacted by someone from the CFIA, who will make arrangements to inspect your facility. The primary purpose of the survey is to collect information on how many fish rendering facilities operate separately from other renderers, and the types and quantities of products they produce. The CFIA needs this information to plan for inspections and the preparation and issuance of fish rendering permits. It is important to note that all information collected will be considered confidential.<br /><br />Conducting the survey will allow CFIA Feed Program inspectors to inform renderers about the inspection process and answer questions. Inspectors will also take the opportunity to discuss the additional requirements for importing and exporting fish meal and fish oil that will apply when the regulatory amendments come into effect.<br /><br />If you are a fish by-product renderer, you are encouraged to discuss the requirements of the rendering permit program with the CFIA inspector performing the survey, and arrange to undergo a preliminary inspection. At the time of the survey, the inspector will leave a copy of the application for a Rendering Plant permit with the facility manager and answer any questions.<br /><br />Rendering Plant Operating Permits<br />Rendering permits are issued for a period of one year, normally beginning on April 1st and ending on March 31st. There are no fees for a permit. Permit issuance is subject to an inspection of the rendering facility showing that it is in full compliance with the regulations. Once a fish by-product renderer has been identified, and a preliminary inspection completed, a temporary rendering permit will be issued to them. Any necessary modifications must be completed, and the facilities must be in full compliance with regulatory requirements, when the amended regulations enter into force on July 12, 2007.<br /><br />BY JULY 12, 2007, ALL FISH BY-PRODUCT RENDERERS MUST HAVE A CFIA RENDERING PERMIT TO CONTINUE OPERATING.<br /><br />For more information, please contact a CFIA Feed Program Specialist in your area at the appropriate telephone number:<br /><br />Atlantic Area: 902-426-1410<br />Québec Area: 514-283-3815 (ext. 377)<br />Ontario Area: 519-826-2910<br />Western Area: 204-983-7441<br /><br /><br /><a href="http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/enhren/fispoie.shtml">http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/enhren/fispoie.shtml</a><br /><br /><br />Feed Ban Enhancement<br />Questions and Answers<br /><br /><br /><a href="http://www.inspection.gc.ca/english/anima/feebet/rumin/enhqueste.shtml">http://www.inspection.gc.ca/english/anima/feebet/rumin/enhqueste.shtml</a><br /><br /><br /><br />SEE EXAMPLE OF TONNAGE OF FEED FOR FISH AT ONE MILL<br /><br /><br />Mr. Dwayne Holifield, B.S., manager of the research farm led the tour of the Delta Western Feed Mill in Indianola, MS. Delta Western Research Center has several tenth-acre ponds. The ponds are used for research projects involving nutrition and field trials of therapeutic products. The research center also has a second mill used to produce smaller lots of experimental catfish feeds. The research unit works extensively with NWAC. The main mill produces about 230,000 tons of catfish feed annually representing thirty percent of the 825,000 tons of catfish sold annually. Railroad lines bring grain products used in the feed directly to the mill. Three large warehouses store ground corn, wheat middlings and soybean meal that are pumped directly into the mill as needed. The mill has doubled its finished-feed storage capacity over the last two years to a capacity of 5,000 tons. The mill operates two 8 - 10 hour shifts depending on the time of year. The storage area is filled completely by the end of the second shift and emptied by mid-morning the next day. The feed is delivered to farms in large tanker type trucks. Each truck has a capacity of 20 tons and can be completely filled in 2 1/2 minutes.<br /><br /><br /><a href="http://www.fda.gov/cvm/Sep_Oct01.htm#2378">http://www.fda.gov/cvm/Sep_Oct01.htm#2378</a><br /><br /><br />What we know about the herd of origin What we know about the herd of origin<br /> Owner was former catfish farmer who moved Owner was former catfish farmer who moved<br />to Alberta in 2001 to Alberta in 2001<br /> Owner inexperienced in cattle production Owner inexperienced in cattle production<br /> Cow was part of 80 cow herd assembled Cow was part of 80 cow herd assembled<br />from multiple sources from multiple sources<br /> No identification saved from index case No identification saved from index case<br /> Source of index case not recorded<br /><br /><br /><br /><a href="http://www.vet.ohio-state.edu/assets/courses/vm510/EpidemiologyOfBSE.pdf">http://www.vet.ohio-state.edu/assets/courses/vm510/EpidemiologyOfBSE.pdf</a><br /><br /><br />The rancher, Marwyn Peaster, a former Mississippi catfish farmer who had married an area woman and started farming in the area, had taken off. He was upset that the TV crew had shown up his land.<br /><br /><a href="http://www.sportsshooter.com/news/950">http://www.sportsshooter.com/news/950</a><br /><br /><br />Dr. Detwiler: Canada based that question because the herd that that animal came from was in Saskatchewan, in an area with CWD. That was one of the questions they faced right off the bat: is this BSE or is this some kind of transmission from CWD-infected elk in the area? Not only the histological lesions were classic BSE lesions, but clinically it's very difficult because if you miss the other behavioral changes, which this owner did. It was someone who had been a catfish farmer. He missed the early signs. The animal presented to slaughter as a down animal, non-responsive. Clinically it looked like just a down cow, but they did send that on to the United Kingdom and they did do some comparison glycoform patterns. Those haven’t been validated, but at least on preliminary work, it looked like classical BSE.<br /><br /><a href="http://bse-atypical.blogspot.com/">http://bse-atypical.blogspot.com/</a><br /><br /><br /><br />QUESTION - was this farmer feeding catfish feed to his cattle ???<br /><br /><br />Feeding Farmed Fish<br /><br />snip...<br /><br /><br />Farming animals has suffered from the recent crises of Mad Cow Disease as well as the disastrous consequences of the accidental or fraudulent contamination of feeds with dioxins and other undesirable products. These events have accentuated the general suspicion of consumers and brought the necessary application of new and more complex laws, being more restrictive and therefore imposing more costs for the producers.<br /><br />Aquaculture does and must carry the image of food security in respect of the consumer. But it must continue constantly to battle against hearsay and unfounded criticism.<br /><br />Since aquaculture started in Europe, aquaculture feeds contain neither antibiotics (except in the case of authorized therapeutic treatment), nor hormones, nor growth enhancers or additives that could have existed in other areas of animal production. The traceability of the products used at all stages of the production process up to the consumer's purchase is, without doubt, the best answer to give confidence.<br /><br />The European Union imports products from third countries that do not always respect the same sanitary restrictions, a position which leads to food production costs that are considerably lower than in the Member States (without referring to social costs and ecological considerations). One can assert that the fish feeds produced in the EU are 10% more expensive, at an equivalent nutritive content, than elsewhere, in particular since the withdrawal of protein-rich terrestrial animal by-products (from abattoirs).<br /><br />We must therefore pay attention to this discrepancy which exists and is growing in Europe and well as with other regions of the world. The trade of seafood and aquaculture products is international and the identification [labelling] of products at the level of the consumer's purchase is another point which has not been completely resolved, in spite of the wishes of all of the professionals of the feed and aquaculture production sectors of the EU as well as the new rules for labelling and identification that have been law since the 1st January 2002.<br /><br />The new European legislation that is being elaborated for the use of animal by-products must follow the Directive 90/667/CEE that establishes «the veterinary rules for the disposal and processing of animal waste, for its placing on the market and for the prevention of pathogens in feedstuffs of animal or fish origin» . This new legislation classes animal by-products as a function of their potential risks and defines their conditions of destruction or use, where only products that are qualified as being of 'low risk' can be used for animal feeds by those establishments that have been approved for such an activity.<br /><br />Unfortunately, the fish meals and oils that are derived from the fisheries dedicated to this activity have been assimilated with the by-products of terrestrial animals and are thus considered as being waste materials at the same level as the waste products obtained from abattoirs or kitchen waste. In addition to the fact that these fisheries are managed by quotas and are wholly natural products of very high food quality, this simplified and negative classification is a source of very serious confusion.<br /><br />In particular, the rather negative image that has been given to these natural products will complicate any information and communication action of the international aquaculture community. This question merits all of our attention when we look to increase the importance of the products of fisheries and aquaculture.<br /><br /><br />snip...see full text ;<br /><br /><a href="http://www.feap.info/production/feeds/sabautcipa_en.asp">http://www.feap.info/production/feeds/sabautcipa_en.asp</a><br /><br /><br />Fish farming under threat?<br /><br />The possibility of a disease crossing the species barrier hangs like a Damocles sword over a number of farming sectors, including fish farming. ‘All farmed fish are fed feed with a 40% to 55% protein content. This can include animal protein and, hence, potentially pathogenic prion proteins,’ explains Theodoros Sklaviadis of the University of Thessaloniki (GR).<br /><br />In 1997, Carla Bolis, a researcher at the University of Milan (IT), discovered a normal prion protein, previously believed to exist only in mammals, in the brain of salmon. This means it is important to determine the risk of TSE in fish, as the programme coordinated by Sklaviadis is seeking to do. This work focuses on two areas. The first is a systematic search in the genomes of trout, sea bass and bream for the coding sequences of the prion protein in order to analyse homologies with mammal genes. The second involves feeding these fish food containing BSE and scrapie prions, to see whether it is possible to start an infection. ‘Given the incubation period of the disease, the results will not be available for several years,’ Sklaviadis warns. Patience is called for if we want to ensure that Europe’s fish farmers never experience a “mad fish” crisis.<br /><br /><br /><a href="http://ec.europa.eu/research/rtdinfo/39/01/article_302_en.html">http://ec.europa.eu/research/rtdinfo/39/01/article_302_en.html</a><br /><br /><br /><br />see where USA still feeds fish banned mad cow feed. ...tss<br /><br /><br />Archive Number 20060809.2235<br />Published Date 09-AUG-2006<br />Subject PRO/AH/EDR> BSE, bovine - USA (02): feed recall<br /><br /><br /><br />BSE, BOVINE - USA (02): FEED RECALL<br />*********************************************<br />A ProMED-mail post<br /><http:><br />ProMED-mail is a program of the<br />International Society for Infectious Diseases<br /><http:><br /><br />[1]<br />Date: Wed, 9 Aug 2006 22:26:49 +0100<br />From: "Mary Marshall" <tropical.forestry@btinternet.com><br />Source: Cattle Network 8 Aug 2006 [edited]<br /><http: contentid="58260"><br /><br /><br />Huge Feed Recall Due To Mammalian Protein<br />---------------------------------------------<br />The Food and Drug Administration announced 2 recalls, one for 27 million<br />pounds of feed produced in Michigan and the other an unknown amount of feed<br />produced in Kentucky. Both were suspected of being adulterated with ruminant<br />or mammalian protein, including ruminant meat and bone meal in the 2nd<br />recall.<br /><br />Vita Plus Corp., Gagetown, Michigan, has recalled 27 694 240 pounds of dairy<br />feed produced between February of 2005 and 16 Jun 2006, because it is<br />believed it was contaminated with mammalian protein. The feed was<br />distributed in Michigan and the recall is complete.<br /><br />Burkmann Feeds LLC, Glasgow, Kentucky, has recalled an unknown amount of custom<br />feed because it contains an ingredient called Pro-Lak, which may contain<br />ruminant-derived meat and bone meal. The Burkmann feed was distributed in<br />Kentucky.<br /><br />[By Pete Hisey on Tuesday, August 08, 2006 ]<br /><br />--<br />Mary Marshall<br /><tropical.forestry@btinternet.com><br /><br />*****<br />[2]<br />Date: 7 Aug 2006<br />From: Terry Singeltary <flounder9@verizon.net><br />Source: FDA [weekly] Enforcement Report, 2 Aug 2006 [edited]<br /><http:><br /><br /><br />(1) PRODUCT: Animal and fish feeds Recall # V-112-6<br /><br />CODE: Product manufactured from 1 Feb 2005 to 6 Jun 2006<br /><br />RECALLING FIRM/MANUFACTURER: Alabama Farmers Cooperative, Inc.,<br />Decatur, Alabama, by telephone, fax, email and visit on 9 Jun 2006.<br />FDA initiated recall is complete.<br /><br />REASON: Animal and fish feeds which were possibly contaminated with<br />ruminant-based protein not labeled as "Do not feed to ruminants."<br /><br />VOLUME OF PRODUCT IN COMMERCE: 125 tons<br /><br />DISTRIBUTION: Alabama and Florida<br /><br />(2) PRODUCT: Bulk custom dairy feeds manufactured from concentrates,<br />Recall # V-113-6<br /><br />CODE: All dairy feeds produced between 1 Feb 2005 and 16 Jun 2006 and<br />containing H. J. Baker recalled feed products.<br /><br />RECALLING FIRM/MANUFACTURER: Vita Plus Corp., Gagetown, Michigan, by<br />visit beginning on 21 Jun 2006. Firm initiated recall is complete.<br /><br />REASON: The feed was manufactured from materials that may have been<br />contaminated with mammalian protein.<br /><br />VOLUME OF PRODUCT IN COMMERCE: 27 694 240 lbs<br /><br />DISTRIBUTION: Michigan<br /><br />(3) PRODUCT: Bulk custom made dairy feed, Recall # V-114-6<br /><br />CODE: None<br /><br />RECALLING FIRM/MANUFACTURER: Burkmann Feeds LLC, Glasgow, Kentucky,<br />by letter on 14 Jul 2006. Firm initiated recall is ongoing.<br /><br />REASON: Custom made feeds contain ingredient called Pro-Lak, which<br />may contain ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE: Unknown<br /><br />DISTRIBUTION: Kentucky<br /><br />--<br />Terry Singeltary<br /><flounder9@verizon.net><br /><br />[A codified rule indicates that no mammalian material is to be<br />included in feed for ruminants. When it is found that such a<br />situation has occurred, then a recall is issued. Several years ago, a<br />similar situation happened in Gonzales, Texas, and the herd was<br />depopulated. The difference must be that the regulatory authorities<br />do not know where all the herds are that have consumed the feed. - Mod.TG]<br /><br />[see also:<br />BSE, bovine - USA: feed recall 20060621.1718]<br />..................................................tg/msp/jw<br /><br /><br />************************************************************<br /><br /><br />Subject: MAD COW FDA FEED WARNING LETTER NO. 2007-NOL-01 October 26, 2006 H.J. Baker & Bro., Inc.<br />Date: November 7, 2006 at 9:08 am PST<br /><br />Food and Drug Administration<br /><br />New Orleans District<br /><br />404 BNA Drive, Building 200, Suite 500<br /><br />Nashville, TN 37217<br /><br />Telephone: 615-366-7801<br /><br />Facsimile: 615-366-7802<br /><br />October 26, 2006<br /><br />WARNING LETTER NO. 2007-NOL-01<br /><br />FEDERAL EXPRESS<br /><br />OVERNIGHT DELIVERY<br /><br />Mr. Christopher V. B. Smith<br /><br />Corporate President, CEO<br /><br />H. J. Baker & Bro., Inc.<br /><br />228 Saugatuck Avenue<br /><br />Westport, Connecticut 06880<br /><br />Dear Mr. Smith:<br /><br />On June 6, 8, 12-15, and 23, 2006, a U.S . Food and Drug Administration (FDA) investigator inspected your animal feed protein supplement manufacturing facility, located at 603 Railroad Avenue, Albertville, Alabama. The inspection revealed significant deviations from the requirements set forth in Title 21, Code ofFederal Regulations, Part 589.2000 (21 CFR 589.2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation, resulting in products being manufactured and distributed by your facility because they are adulterated within the meaning of Section 402(a)(4) [21 USC 342(a)(4)] of the Federal Food, Drug, and Cosmetic Act (the Act) and misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Act.<br /><br />Our investigation determined adulteration resulted from the failure of your firm to establish and implement measures sufficient to prevent commingling or cross-contamination . The adulterated feed was subsequently misbranded because it was not properly labeled. Specifically, we found :<br /><br />" Your firm failed to establish and use cleanout procedures or other means to prevent carry-over of products which contain or may contain protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants, as required by 21 CFR 589.2000(e)(1)(iii)(B) .<br /><br />Specifically, you failed to establish and use such measures for a screw auger installed in February 2005 . This auger is used to convey both prohibited and non-prohibited material to bulk storage bins.<br /><br />In addition, you failed to follow the cleanout procedure your firm had developed for the receiving systems. Your feed is, therefore, adulterated under Section 402(a)(4) [21 USC 342(a)(4)] of the Act.<br /><br />" You failed to label all products which contained or may have contained prohibited materials with the BSE cautionary statement, "Do not feed to cattle or other ruminants," as required by 21 CFR 589.2000(e)(1)(i) . Such products are misbranded under Section 403(3) [21 USC 343(a)(1)] of the Act. These misbranded products include the three Pro-Pak products mentioned below, as well as Page 2 - H. J . Baker & Bro., Inc., Albertville, Alabama Warning Letter No. 2007-NOL-O 1 those bulk loads of individual feed ingredients processed through this common screw auger and distributed between the time it was installed in February 2005, and June 9, 2006 .<br /><br />This letter is not intended to serve as an all-inclusive list of violations at your facility. As a<br />manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction,<br /><br />without further notice.<br /><br />We acknowledge your June 16, 2006, voluntary recall of three products you manufactured from February 2005 to June 2006. The three products recalled were: Pro-Lak Protein Concentrate for<br /><br />Lactating Dairy Animals;<br /><br />Pro-Amino II for PreFresh and Lactating Cows;<br /><br /><br />***and, Pro-Pak Marine & Animal Protein Concentrate for Use in Animal Feed. Recall effectiveness checks and other measures<br /><br /><br />will determine the merit of this recall . We recognize you now label all products with the required BSE cautionary statement and we also acknowledge your intent, given verbally to New Orleans District management of the FDA, to discontinue the production of supplements which do not contain prohibited<br /><br />materials. In your written response to this letter, please confirm in writing you have taken these steps.<br /><br />snip...<br /><br /><br /><a href="http://www.fda.gov/foi/warning_letters/g6104d.pdf">http://www.fda.gov/foi/warning_letters/g6104d.pdf</a><br /><br /><br /><br />Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA,<br />MS, AL, GA, AND TN 11,000+ TONS<br />Date: August 16, 2006 at 9:19 am PST<br /><br />RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II<br />______________________________<br /><br />snip...<br />______________________________<br /><br />PRODUCT<br /><br />*** a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,<br />50 lb. bags, Recall # V-121-6;<br /><br /><br />b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,<br />50 lb. bags, Recall # V-122-6;<br />c) Tucker Milling, LLC #31232 Game Bird Grower,<br />50 lb. bags, Recall # V-123-6;<br />d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD<br />Medicated, 50 lb bags, Recall # V-124-6;<br />e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags,<br />Recall # V-125-6;<br />f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags,<br />Recall # V-126-6;<br />g) Tucker Milling, LLC #30116, TM Broiler Finisher,<br />50 lb bags, Recall # V-127-6<br />CODE<br />All products manufactured from 02/01/2005 until 06/20/2006<br />RECALLING FIRM/MANUFACTURER<br />Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit<br />on June 20, 2006, and by letter on June 23, 2006.<br />Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated<br />recall is ongoing.<br />REASON<br />Poultry and fish feeds which were possibly contaminated with ruminant based<br />protein were not labeled as "Do not feed to ruminants".<br />VOLUME OF PRODUCT IN COMMERCE<br />7,541-50 lb bags<br />DISTRIBUTION<br />AL, GA, MS, and TN<br /><br />END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006<br /><br />###<br /><br /><br /><a href="http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html">http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html</a><br /><br /><br />Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125<br />TONS Products manufactured from 02/01/2005 until 06/06/2006<br /><br />Date: August 6, 2006 at 6:16 pm PST<br /><br />PRODUCT<br /><br />*** a) CO-OP 32% Sinking Catfish, Recall # V-100-6;<br /><br />b) Performance Sheep Pell W/Decox/A/N, medicated,<br />net wt. 50 lbs, Recall # V-101-6;<br />c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;<br /><br />*** d) CO-OP 32% Sinking Catfish Food Medicated,<br />Recall # V-103-6;<br /><br />e) "Big Jim's" BBB Deer Ration, Big Buck Blend,<br />Recall # V-104-6;<br />f) CO-OP 40% Hog Supplement Medicated Pelleted,<br />Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;<br />g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,<br />Carbadox -- 0.0055%, Recall # V-106-6;<br />h) CO-OP STARTER-GROWER CRUMBLES, Complete<br />Feed for Chickens from Hatch to 20 Weeks, Medicated,<br />Bacitracin Methylene Disalicylate, 25 and 50 Lbs,<br />Recall # V-107-6;<br />i) CO-OP LAYING PELLETS, Complete Feed for Laying<br />Chickens, Recall # 108-6;<br />j) CO-OP LAYING CRUMBLES, Recall # V-109-6;<br />k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,<br />net wt 50 Lbs, Recall # V-110-6;<br />l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,<br />Recall # V-111-6;<br />m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,<br />Recall # V-112-6<br />CODE<br />Product manufactured from 02/01/2005 until 06/06/2006<br />RECALLING FIRM/MANUFACTURER<br />Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and<br />visit on June 9, 2006. FDA initiated recall is complete.<br />REASON<br />Animal and fish feeds which were possibly contaminated with ruminant based<br />protein not labeled as "Do not feed to ruminants".<br />VOLUME OF PRODUCT IN COMMERCE<br />125 tons<br />DISTRIBUTION<br />AL and FL<br /><br /><br />END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006<br /><br />###<br /><br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html">http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</a><br /><br /><br />MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE<br />Sun Jul 16, 2006 09:22<br />71.248.128.67<br /><br /><br />RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II<br />______________________________<br />PRODUCT<br />a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,<br />Recall # V-079-6;<br />b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),<br />Recall # V-080-6;<br /><br />*** c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL<br />FEED, Recall # V-081-6;<br /><br />d) Feather Meal, Recall # V-082-6<br />CODE<br />a) Bulk<br />b) None<br />c) Bulk<br />d) Bulk<br />RECALLING FIRM/MANUFACTURER<br />H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and<br />by press release on June 16, 2006. Firm initiated recall is ongoing.<br />REASON<br />Possible contamination of animal feeds with ruminent derived meat and bone<br />meal.<br />VOLUME OF PRODUCT IN COMMERCE<br />10,878.06 tons<br />DISTRIBUTION<br />Nationwide<br /><br />END OF ENFORCEMENT REPORT FOR July 12, 2006<br /><br />###<br /><br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html">http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html</a><br /><br /><br />Mr. Sturm was found to hold animals on his farm under conditions that are so inadequate that diseased animals and/or medicated animals bearing potentially harmful drug residues are likely to enter the food supply. In addition, he failed to use the drug, Albon, containing sulfadimethoxine, in conformance with the labeling.<br /><br />A warning letter was issued to the following firms for violations related to 21 CFR Part 589.2000—Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE).<br /><br />*** • Scott Nelson, Owner, Integra Fish Foods, Inc., Grand Junction, CO<br /><br />• Bruce A. Burgett, General Manager, The Carrollton Farmers Exchange, Carrollton, OH<br /><br />Violations included failure to label feeds that contain, or may contain, prohibited materials with the required cautionary statement "Do Not Feed to Cattle or Other Ruminants," insufficient customer records to track the distribution of products, and lack of written procedures for cleaning or flushing equipment after mixing feeds containing prohibited material.<br /><br /><br /><a href="http://www.fda.gov/cvm/Sep_Oct01.htm">http://www.fda.gov/cvm/Sep_Oct01.htm</a><br /><br /><br /><br />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;<br /><br />Risk of oral infection with bovine spongiform encephalopathy agent in primates<br /><br />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<br /><br />Summary<br /><br />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.<br /><br />snip...<br /><br />BSE bovine brain inoculum<br /><br />100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg<br /><br />Primate (oral route)* 1/2 (50%)<br /><br />Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)<br /><br />RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)<br /><br />PrPres biochemical detection<br /><br />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. icip= intracerebral and intraperitoneal.<br /><br />Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula<br /><br />Published online January 27, 2005<br /><br /><a href="http://www.thelancet.com/journal/journal.isa">http://www.thelancet.com/journal/journal.isa</a><br /><br />It is clear that the designing scientists must also have shared Mr Bradley's surprise<br /><br />at the results because all the dose levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s145d.pdf">http://www.bseinquiry.gov.uk/files/ws/s145d.pdf</a><br /><br />6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate"<br /><br />experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s147f.pdf">http://www.bseinquiry.gov.uk/files/ws/s147f.pdf</a><br /><br />PDF] Guidance for Industry 69File Format: PDF/Adobe Acrobat - View as HTML The Food and Drug Administration (FDA) has prepared this guide in accordance ... If a feed intended for ruminants contains animal protein, the protein can ... www.fda.gov/cvm/Guidance/guidance69.pdf - Similar pages - Note this<br /><br /><a href="http://www.fda.gov/cvm/Guidance/guidance69.pdf">http://www.fda.gov/cvm/Guidance/guidance69.pdf</a><br /><br />[PDF] Guidance for Industry 70File Format: PDF/Adobe Acrobat - View as HTML If a feed is intended for ruminants contains animal protein, the protein can ... with On-Farm Feed Mixing Operations,” FDA Guidance for Industry 69. ... www.fda.gov/cvm/Guidance/guidance70.pdf - Similar pages - Note this<br /><br />WHAT IS THE PURPOSE AND SCOPE OF THIS REGULATION?<br /><br />This regulation is designed to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE), sometimes referred to as “Mad Cow Disease,” through animal feed. The regulation prohibits the use of certain proteins derived from mammalian tissue in feeding ruminant animals. An example is meat and bone meal derived from cattle. However, certain products are exempt from this regulation.<br /><br /># The following protein products derived from mammals are exempt.:<br /><br />Blood and blood products P Gelatin Milk products (milk and milk proteins) Pure porcine (pork) or pure equine (horse) protein products Inspected meat products, such as plate waste, which have been cooked and offered for human food and further heat processed for animal feed<br /><br /># The following nonmammalian protein products are exempt:<br /><br />Poultry<br /><br />***Marine (fish) ***<br /><br />Vegetable<br /><br /># The following products are also exempt because they are not protein or tissue:<br /><br />Grease Fat Amino acids<br /><br />Tallow Oil<br /><br />Dicalcium phosphate<br /><br />We refer to the exempted products throughout this guide as “nonprohibited material.” We refer to all mammalian protein that is not exempted as “prohibited material.”<br /><br />Prohibited material and/or feeds containing prohibited material cannot be fed to ruminant animals. “Ruminant animals” are any animals with a four-chambered stomach including cattle, sheep, goats, buffalo, elk, and deer.<br /><br /><a href="http://www.fda.gov/cvm/Guidance/guidance70.pdf">http://www.fda.gov/cvm/Guidance/guidance70.pdf</a><br /><br />[PPT] Detection of Ruminant MBM Prohibited ProteinFile Format: Microsoft Powerpoint - View as HTML Detection of Ruminant MBM Prohibited Protein. Development of an assay to address the needs of the feed industry. Ensure consumer confidence in FDA ... aafco.org/Portals/0/public/Frank_Klein.ppt - Similar pages - Note this<br /><br /><a href="http://aafco.org/Portals/0/public/Frank_Klein.ppt">http://aafco.org/Portals/0/public/Frank_Klein.ppt</a><br /><br />[PDF] M A M M A L I A N P R O T E I N F E E D I N G B A N Feeders of ...File Format: PDF/Adobe Acrobat - View as HTML ruminant and non-ruminant feeds. If this isn't possible,. you must properly and thoroughly clean .... prohibited animal protein products:. www.fda.gov/cvm ... aafco.org/Portals/0/Public/BSE_aafco_brochure.pdf - Similar pages - Note this<br /><br />Protein products derived from non-mammalian sources are exempt:<br /><br />•Poultry; marine (fish); vegetable<br /><br />The following products are also exempt because they are not protein or tissue:<br /><br />•Fats and oils, including grease and tallow; amino acids; dicalcium phosphate Exempted animal protein products Mammalian protein products that are exempt from the feed ban are non-prohibited proteins.<br /><br />•Blood and blood products; milk products (milk and milk proteins); pure porcine (pork) or pure equine (horse) protein products; inspected meat products (such as plate waste) which have been cooked and offered for human consump - tion and further heat processed for animal feed; gelatin.<br /><br /><a href="http://aafco.org/Portals/0/Public/BSE_aafco_brochure.pdf">http://aafco.org/Portals/0/Public/BSE_aafco_brochure.pdf</a><br /><br />AND THE CIRCLE OF GREED IS COMPLETE $$$<br /><br />Using Byproducts to Feed Dairy Cattle Donna M. Amaral-Phillips and R.W. Hemken<br /><br />Various byproducts from feed processing industries are available for dairy farmers to incorporate into diets fed to dairy cows and replacement heifers. Using these feeds offers at least two benefits:<br /><br />• may decrease the feed costs depending on prices of byproducts and grains.<br /><br />• helps dispose of these byproducts in an ecologically sound manner.<br /><br />Table 1. Nutrient composition of selected byproducts and cereal grains on a dry matter basis.<br /><br />Dry Matter (%) Dry Matter Basis Crude Protein (%)<br /><br />Blood meal, ring dried 92 95.5 1.06 0.30 0.30<br /><br />snip...<br /><br />Fish meal, anchovy 92 71.2 1.01 4.06 2.69<br /><br />Fish meal, menhaden 92 68.5 1.06 5.34 3.05<br /><br />snip...<br /><br />Feather meal 93 92 0.98 0.33 0.50<br /><br />Non-ruminant Meat meal 94 57.6 1.01 8.86 4.20 Non-Ruminant Meat and Bone Meal 92 54 0.74 10.60 4.73<br /><br />snip...<br /><br />Tallow 99 ------ 2.06 ------ ------<br /><br />snip...<br /><br />Blood Meal<br /><br />1. Byproduct of the rendering industry.<br /><br />2. Made from clean, fresh animal blood exclusive of the urine, hair, stomach contents, etc.<br /><br />3. Flash drying process produces a more uniform product with a higher lysine content.<br /><br />4. Due to potential palatability problems, best used in total mixed rations (TMR). Needs to be added slowly over a two-week period. Palatability problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.<br /><br />5. Limit intake to 0.5-1.0 lbs/cow/day in total mixed rations.<br /><br />Fish Meal<br /><br />1. Made from clean, dried, ground, and undecomposed fish.<br /><br />2. Rich in essential amino acids. The amino acid profile may be similar to that required for the synthesis of milk protein.<br /><br />3. Due to potential palatability problems, best used in total mixed rations. Needs to be added slowly over a two-week period. Problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.<br /><br />Hydrolyzed Feather Meal<br /><br />1. Byproduct from the pressure treatment of clean, undecomposed feathers from slaughtered poultry.<br /><br />2. Low in lysine and methionine which are believed to control milk production. However, this product is high in cysteine which may substitute for methionine in milk production.<br /><br />3. Due to potential palatability problems, best used in total mixed rations. Needs to be added slowly over a two-week period. Problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.<br /><br />4. Limit intake to 0.3 lbs/cow/day in total mixed rations.<br /><br />Non-Ruminant Meat Meal<br /><br />1. A rendered product from the carcasses of swine or poultry excluding blood, hair, hoof, hide trimmings, feces, and stomach. Similar to meat and bone meal except no minimum phosphorus concentration required.<br /><br />2. Due to potential palatability problems, best used in total mixed rations. Needs to be added slowly over a two-week period. Problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.<br /><br />3. Limit intake to 1.5-2.5 lbs/cow/day in total mixed rations.<br /><br />4. Do not feed ruminant derived meat and bone meal back to ruminants.<br /><br />Non-Ruminant Meat and Bone Meal<br /><br />1. A rendered product from the carcass of swine or poultry excluding blood, hair, hoof, hide trimmings, feces, and stomach. It contains a minimum of 4% phosphorus with a calcium content that does not exceed 2.2 times the phosphorus concentration.<br /><br />2. Due to potential palatability problems, best used in total mixed rations. Needs to be added slowly over a two-week period. Palatability problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.<br /><br />3. Limit intake to 1.5-2.5 lbs/cow/day in total mixed rations.<br /><br />4. Do not feed ruminant derived meat and bone meal back to ruminants.<br /><br />Tallow<br /><br />1. Derived primarily from rendered beef fat but may include other animal fats.<br /><br />2. Requires special handling equipment because at room temperature it is a solid or semi-solid. To be mixed within feed, it must be heated so that it can be melted.<br /><br />3. Nine different grades of tallow are sold. Good quality (fancy bleachable) tallow should be used for the most consistent animal response.<br /><br />4. Limit to 1 lb/1200 lb cow/day.<br /><br /><a href="http://www.uky.edu/Ag/AnimalSciences/dairy/extension/nut00158.pdf">http://www.uky.edu/Ag/AnimalSciences/dairy/extension/nut00158.pdf</a><br /><br />STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995<br /><br />snip...<br /><br />To minimise the risk of farmers' claims for compensation from feed compounders.<br /><br />To minimise the potential damage to compound feed markets through adverse publicity.<br /><br />To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.<br /><br />snip...<br /><br />THE FUTURE<br /><br />4..........<br /><br />MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.<br /><br />5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.<br /><br />6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...<br /><br />SEE full text ;<br /><br /><a href="http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf">http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf</a><br /><br />like i said, and endless cycle of greed, i.e. FOR PROFIT ONLY $$$<br /><br />USDA CERTIFIED DEAD STOCK DOWNER COW SCHOOL LUNCH PROGRAM LIST OF SCHOOLS AFFECTED STATE BY STATE (dead stock downers i.e. non-ambulatory, the most high risk for mad cow disease)<br /><br /><a href="http://downercattle.blogspot.com/">http://downercattle.blogspot.com/</a><br /><br />TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-77158761301716055302008-02-16T11:31:00.000-08:002008-07-18T09:41:50.195-07:00specified risk materials (SRM)re-mad cow downers and kids<br /><br /><br />>>>But let's not forget that all specified risk materials, i.e. brain and<br />spinal tissue, are removed from the food supply on all cattle, whether they<br />can walk or not. The bottom line is that, even if my girls ate ground beef<br />from a cow that tested positive to BSE, their risk of being abused is<br />greater than their risk of acquiring BSE. And, no, I don't believe in or<br />practice child abuse.<<<<br /><br /><a href="http://www.hpj.com/archives/2008/feb08/feb18/Cowsorkids.cfm">http://www.hpj.com/archives/2008/feb08/feb18/Cowsorkids.cfm</a><br /><br /><br />i had to laugh when i read that, as sad and disgusting as it is. i wanted to post this as a comment, but the data i have is much to long to post. facts usually are. if you think that feed ban of 8/4/97 held, please think again. it was only ink on paper. also, please read the latest science on the last two mad cows in in the USA i.e. Alabama and Texas. the BASE mad cow, whether it be h or l BASE, its much more virulent to humans than the UK BSE. this is fact. i am not anti meat eater. i am anti stupid, anti corporate homicide, i,e. for profit. how could anyone feel safe by beef in the usa via USDA certified is beyond me. we must stop the big ag factory farming policy of 'don't look, dont find'. and the incubation period. these kids will not know if they will die from cjd for years and even decades to come. and if you think that is the only slaughterhouse that allow downers to still go into the human food chain, think again. i know of one right here in texas. nope, big ag has such a strangle hold on USDA, it will take much more than a democrat or republican to clean it up, there to worried about baseball and those over paid brats and steroids. ................ oh well, i have probably said too much///<br /><br /><br />Washington January 31, 2008 snip...<br /><br /><br /><a href="http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2008/02/0028.xml">http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2008/02/0028.xml</a><br /><br /><br />> TRANSCRIPT: USDA Officials Hold Technical Briefing Regarding Inhumane<br /><br />> Handling Allegations<br /><br /><br /><br />THE title is very misleading. A better title in my opinion would have read ;<br /><br /><br />HIGHLY SUSPECT BSE, H-BASE, MAD COW BEEF DISTRIBUTED NATIONALLY (35 states<br />to date), to CHILDREN AND THE ELDERLY<br /><br /><br />USDA CERTIFIED H-BASE MAD COW SCHOOL LUNCH PROGRAM<br /><br /><br /><a href="http://cjdmadcowbaseoct2007.blogspot.com/2008/02/usda-certified-h-base-mad-cow-school.html">http://cjdmadcowbaseoct2007.blogspot.com/2008/02/usda-certified-h-base-mad-cow-school.html</a><br /><br /><br /><br /><br />Terry S. Singeltary Sr.<br />P.O. Box 42<br />Bacliff, Texas USA 77518<br /><br /><br /><br /><br /><br />Certain Aspects related to the Feeding of Animal Proteins to Farm<br />Animals[1] - Scientific Opinion of the Panel on Biological Hazards<br />Question number: EFSA-Q-2007-084<br /><br /><br /><br />Adopted date: 17/10/2007 Summary<br /><br />Opinion<br /><br />Summary<br /><br />The European Food Safety Authority (EFSA) was requested by the European Parliament (EP) to assess, with respect to Bovine Spongiform Encephalopathy (BSE), the safety for human health of the utilisation of non-ruminant Meat and Bone Meal (MBM). More specifically, EFSA was requested (i) to evaluate the risk from using non-ruminant MBM in pig and poultry feed, once it is possible to distinguish protein origin up to different species and (ii) the introduction of certain tolerance levels with regard to small quantities of MBM in animal feed and the parameters which could be utilized to define these tolerance levels and quantities.<br /><br />The EFSA opinion takes account of the general control measures in place in the European Union (EU) and assumes the effectiveness of these controls in avoiding cross-contamination, both deliberate and accidental. This opinion considers all available scientific data and information related to the risk of transmission of the BSE agent through feed and, by this means, addresses the risk of causing BSE related exposure to humans, as well as risks related to some other TSE agents. In replying to the above mentioned questions, this assessment only considers the use of pig Processed Animal Proteins[2] (PAPs) in poultry feed and the use of poultry PAPs in pig feed. With respect to the introduction of certain tolerance levels with regards to small quantities of MBM in animal feed, this assessment considers such a tolerance for animal proteins of any species in animal feed.<br /><br />To date, no Transmissible Spongiform Encephalopathies (TSEs) have been identified as occurring in pigs or poultry under natural conditions. Taking account of the epidemiological situation of BSE in cattle in the EU, which indicates a decreasing trend, together with the current control measures in place to avoid exposure of pigs and poultry to BSE contaminated material, the EFSA Scientific Panel on Biological Hazards (BIOHAZ) concluded that the risk of transmitting BSE to pigs utilizing poultry PAPs and vice versa is negligible. Consequently in this scenario any increase in the exposure risk of BSE to humans would be negligible. If TSE in birds or pigs is identified in the future as occurring under natural conditions, the assessment presented here will no longer be valid.<br /><br />The BIOHAZ Panel further concluded that the risk of transmitting BSE through small quantities of animal proteins in feed to ruminants can not be excluded, but considering the current protective measures in place in the EU[3], the few infected animals that could arise from this contamination would probably not be able to sustain the BSE epidemic but would increase the human exposure risk to BSE. The risk of transmitting BSE to non-ruminants is considered to be lower than to ruminants, as long as intra-species recycling is avoided. Consequently in this scenario the increase in the exposure risk of BSE to humans is negligible.<br /><br />In the event that a tolerance level was required to be set up in order to quantify animal proteins in animal feed, the BIOHAZ Panel considered the Limit of Quantification (LOQ) of the method used to set such tolerance level as the parameter required. However the BIOHAZ Panel concluded that it is currently not possible to set a LOQ because of insufficient data on the performance of relevant detection methods for quantification. It is therefore recommended that studies be conducted to define the LOQ for different types of animal proteins in feed. In a hypothetical situation in which pigs are allowed to be fed with poultry PAPs and vice versa or, in general, inter-species recycling is allowed, currently it is not possible to quantify the level of contamination with non authorized products containing animal proteins in feed. Accordingly it is technically not possible at present to determine whether the contamination is below or above a defined tolerance level.<br /><br />The BIOHAZ Panel further concluded that compared to the current measures in place in EU, the introduction of a tolerance level, which has to be defined at a certain level above the LOQ, will lead to an increase in the risk of transmission of BSE or other TSEs, depending on the species. This increased risk can not be quantified. ___________________________ [1] For citation purposes: Opinion of the Scientific Panel on Biological Hazards on a request from the European Parliament on Certain Aspects related to the Feeding of Animal Proteins to Farm Animals, The EFSA Journal (2007) Journal number 576, 1-41 [2] In Commission Regulation (EC) No 829/2007 of 28 June 2007 is defined as: “animal protein derived entirely from Category 3 material, which have been treated in accordance with Chapter II of Annex VII so as to render them suitable for direct use as feed material or for any other use in feedingstuffs, including petfood, or for use in organic fertilisers or soil improvers; however, it does not include blood products, milk, milk-based products, colostrum, gelatine, hydrolysed proteins and dicalcium phosphate, eggs and egg-products, tricalcium phosphate and collagen”. [3] Regulation (EC) 999/2001 as amended and Regulation (EC) 1774/2002 as amended.<br /><br />Publication date: 15/11/2007<br /><br /><a href="http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej576_animal_proteins_summary_en.pdf">http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej576_animal_proteins_summary_en.pdf</a><br /><br /><a href="http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej576_animal_proteins_en.pdf">http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej576_animal_proteins_en.pdf</a><br /><br /><br />If only a proportion of infected cattle can be detected, does testing provide significant consumer protection?<br /><br />The extent to which testing increases consumer protection is still open to question, especially if other protective measures are in place (see below).<br /><br />It is conceivable that tissues not previously recognised as infected may still be found as research continues. Infectivity levels are expected to be extremely low, and undetectable with the tools used so far. If these tissues were otherwise consumed then the destruction of the carcase would afford the consumer a greater degree of protection. If the tissues are not sufficiently infectious to pose a health risk, and/or are not consumed, then the additional protection provided may be nil.<br /><br />Recent results from Japan and Germany confirm this point(2,11,12,14), with positivity or infectivity being detected in some peripheral nerves that would not normally be removed as SRM. The amount of infectivity present is low, and considered be up to 1000-fold lower than the brain. Unpublished evidence suggests that these become positive only after the brain and spinal cord. This therefore confirms that testing and removal of positive animals does provide some additional, as yet unquantifiable, protection to consumers over and above that provided by removal of SRM. Given that detection of positivity or infectivity in some peripheral nerves coincides with the onset of clinical signs, it is probable that such animals would be detected before slaughter, and therefore excluded from the food chain.<br /><br /><a href="http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_TESTING_OF_CATTLE_FOR_BSE_070516.pdf">http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_TESTING_OF_CATTLE_FOR_BSE_070516.pdf</a><br /><br /><br />10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007<br /><br />Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II ___________________________________<br /><br />PRODUCT<br /><br />Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007<br /><br />CODE<br /><br />Cattle feed delivered between 01/12/2007 and 01/26/2007<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.<br /><br />Firm initiated recall is ongoing.<br /><br />REASON<br /><br />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.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />42,090 lbs.<br /><br />DISTRIBUTION<br /><br />WI<br /><br />___________________________________<br /><br />PRODUCT<br /><br />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<br /><br />CODE<br /><br />The firm does not utilize a code - only shipping documentation with commodity and weights identified.<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.<br /><br />REASON<br /><br />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.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />9,997,976 lbs.<br /><br />DISTRIBUTION<br /><br />ID and NV<br /><br />END OF ENFORCEMENT REPORT FOR MARCH 21, 2007<br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html">http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html</a><br /><br /><br />Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV<br /><br />Date: September 6, 2006 at 7:58 am PST<br /><br />PRODUCT<br /><br />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.<br /><br />CODE None<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />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.<br /><br />REASON<br /><br />Dairy and poultry feeds were possibly contaminated with ruminant based protein.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />477.72 tons<br /><br />DISTRIBUTION<br /><br />AL ______________________________<br /><br />PRODUCT<br /><br />a) Dairy feed, custom, Recall # V-134-6; b) Custom Dairy Feed with Monensin, Recall # V-135-6. CODE None. Bulk product<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006.<br /><br />Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete.<br /><br />REASON<br /><br />Possible contamination of dairy feeds with ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />1,484 tons<br /><br />DISTRIBUTION<br /><br />TN and WV<br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html">http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html</a><br /><br /><br />Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS<br /><br />Date: August 16, 2006 at 9:19 am PST<br /><br />RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II ______________________________<br /><br />PRODUCT<br /><br />Bulk custom made dairy feed, Recall # V-115-6<br /><br />CODE None<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing.<br /><br />REASON<br /><br />Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />Approximately 2,223 tons<br /><br />DISTRIBUTION<br /><br />KY<br /><br />______________________________<br /><br />PRODUCT<br /><br />Bulk custom made dairy feed, Recall # V-116-6<br /><br />CODE None<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing.<br /><br />REASON<br /><br />Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />1,220 tons<br /><br />DISTRIBUTION<br /><br />KY<br /><br />______________________________<br /><br />PRODUCT<br /><br />Bulk custom made dairy feed, Recall # V-117-6<br /><br />CODE None<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed.<br /><br />REASON<br /><br />Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />40 tons<br /><br />DISTRIBUTION<br /><br />LA and MS<br /><br />______________________________<br /><br />PRODUCT<br /><br />Bulk Dairy Feed, Recall V-118-6<br /><br />CODE None<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete.<br /><br />REASON<br /><br />Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />7,150 tons<br /><br />DISTRIBUTION<br /><br />MS<br /><br />______________________________<br /><br />PRODUCT<br /><br />Bulk custom dairy pre-mixes, Recall # V-119-6<br /><br />CODE None<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm initiated recall is complete.<br /><br />REASON<br /><br />Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />87 tons<br /><br />DISTRIBUTION<br /><br />MS<br /><br />______________________________<br /><br />PRODUCT<br /><br />Bulk custom dairy pre-mixes, Recall # V-120-6<br /><br />CODE None<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.<br /><br />REASON<br /><br />Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />350 tons<br /><br />DISTRIBUTION<br /><br />AL and MS<br /><br />______________________________<br /><br />PRODUCT<br /><br />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<br /><br />CODE<br /><br />All products manufactured from 02/01/2005 until 06/20/2006<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />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.<br /><br />REASON<br /><br />Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />7,541-50 lb bags<br /><br />DISTRIBUTION<br /><br />AL, GA, MS, and TN<br /><br />END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006<br /><br />###<br /><br /><a href="http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html">http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html</a><br /><br /><br />Subject: MAD COW FEED RECALL MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs<br /><br />Date: August 6, 2006 at 6:14 pm PST<br /><br />PRODUCT<br /><br />Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6<br /><br />CODE<br /><br />All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.<br /><br />REASON<br /><br />The feed was manufactured from materials that may have been contaminated with mammalian protein.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />27,694,240 lbs<br /><br />DISTRIBUTION<br /><br />MI<br /><br />END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006<br /><br />###<br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html">http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</a><br /><br /><br />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<br /><br />Date: August 6, 2006 at 6:16 pm PST<br /><br />PRODUCT<br /><br />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<br /><br />CODE<br /><br />Product manufactured from 02/01/2005 until 06/06/2006<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.<br /><br />REASON<br /><br />Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />125 tons<br /><br />DISTRIBUTION<br /><br />AL and FL<br /><br />END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006<br /><br />###<br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html">http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</a><br /><br /><br />Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? Date: August 6, 2006 at 6:19 pm PST<br /><br />PRODUCT<br /><br />Bulk custom made dairy feed, Recall # V-114-6<br /><br />CODE None<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.<br /><br />REASON<br /><br />Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />?????<br /><br />DISTRIBUTION<br /><br />KY<br /><br />END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006<br /><br />###<br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html">http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</a><br /><br /><br />CJD WATCH MESSAGE BOARD TSS<br /><br />MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE<br /><br />Sun Jul 16, 2006 09:22<br /><br />71.248.128.67<br /><br />RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II<br /><br />______________________________<br /><br />PRODUCT<br /><br />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<br /><br />RECALLING FIRM/MANUFACTURER<br /><br />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.<br /><br />REASON<br /><br />Possible contamination of animal feeds with ruminent derived meat and bone meal.<br /><br />VOLUME OF PRODUCT IN COMMERCE<br /><br />10,878.06 tons<br /><br />DISTRIBUTION<br /><br />Nationwide<br /><br />END OF ENFORCEMENT REPORT FOR July 12, 2006<br /><br />###<br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html">http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html</a><br /><br /><br />Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006<br /><br />Date: June 27, 2006 at 7:42 am PST<br /><br />Public Health Service<br /><br />Food and Drug Administration<br /><br />New Orleans District 297 Plus Park Blvd. Nashville, TN 37217<br /><br />Telephone: 615-781-5380 Fax: 615-781-5391<br /><br />May 17, 2006<br /><br />WARNING LETTER NO. 2006-NOL-06<br /><br />FEDERAL EXPRESS OVERNIGHT DELIVERY<br /><br />Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204<br /><br />Dear Mr. Shirley:<br /><br />On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).<br /><br />Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:<br /><br />You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.<br /><br />You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.<br /><br />As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.<br /><br />This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.<br /><br />You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.<br /><br />Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.<br /><br />Sincerely,<br /><br />/S<br /><br />Carol S. Sanchez Acting District Director New Orleans District<br /><br /><a href="http://www.fda.gov/foi/warning_letters/g5883d.htm">http://www.fda.gov/foi/warning_letters/g5883d.htm</a><br /><br /><br />SINCE THE LAST TIME I REPORTED :<br /><br />Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through September 30, 2005<br /><br />Date: March 20, 2006 at 12:58 pm PST<br /><br />YOU can see that report at the bottom of this update.<br /><br />UPDATEs AS FOLLOWS ;<br /><br />UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT July 1, 2006 through September 30, 2006<br /><br />snip...<br /><br />Table 5. Administrative Actions: Large HACCP Plants (7/01/06 to 9/30/06)<br /><br />Administrative Actions Pending or Taken at Large HACCP Plants [includes actions initiated in prior quarters]<br /><br />CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS<br /><br />On 6/15/06, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />snip...<br /><br />EXCEL CORP 00086R M FORT MORGAN, CO<br /><br />On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.<br /><br />snip...<br /><br />TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />TYSON FRESH MEATS INC. 00245L M LEXINGTON, NE X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />snip...<br /><br />Table 6. Administrative Actions: Small HACCP Plants (7/01/06 to 9/30/06)<br /><br />Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />SSOP HACCP SPS INH INT Other LOI LOW<br /><br />BOOKER PACKING COMPANY 07162 M BOOKER, TX 6/2/06 6/5/06 X 9/19/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />SSOP HACCP SPS INH INT Other LOI LOW<br /><br />GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X 8/31/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />HI COUNTRY BEEF JERKY 01248 M01248 P LINCOLN, MT 3/24/06 4/14/06 X 8/31/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X 8/15/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />GIBSON PACKING COMPANY 05843 M05843 P SEYMOUR, MO 9/21/06 X Plant failed to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli). The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />SSOP HACCP SPS INH INT Other LOI LOW<br /><br />HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X 9/26/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06 4/14/06 6/30/06 7/5/06 X 8/11/06 On 3/16/06, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E.coli) was issued. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X 7/25/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br /><a href="http://www.fsis.usda.gov/PDF/QER_Q4_FY2006.pdf">http://www.fsis.usda.gov/PDF/QER_Q4_FY2006.pdf</a><br /><br /><br />UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT April 1, 2006 through June 30, 2006<br /><br />Table 5. Administrative Actions: Large HACCP Plants (4/01/06 to 6/30/06)<br /><br />CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X On 6/15/06, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />snip...<br /><br />EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On<br /><br />12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.<br /><br />snip...<br /><br />TYSON FRESH MEATS INC 00245L M LEXINGTON, NE X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />snip...<br /><br />SSOP HACCP SPS INH INT Other LOI LOW<br /><br />TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />BOOKER PACKING COMPANY 07162 M BOOKER, TX 4/13/06 4/19/06 X Plant failed to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli).<br /><br />6/2/06 6/5/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />???<br /><br />3/24/06 4/14/06<br /><br />X<br /><br />The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />C & C MEAT SALES, INC., 18494 M18494 P, DURHAM, NC ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.<br /><br />snip...<br /><br />FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X 4/13/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />FRONTIER FOODS & COLD STORAGE, INC 20741 M20741 P EL PASO, TX 5/31/06 X On 6/8/06, DM closed case by firm’s requested voluntary withdrawal. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X 5/19/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06 4/14/06 6/30/06 X On 3/16/06, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E.coli) was issued. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />SAVORY CONNECTION, INC., 31764 M31764 P, SELINGSGROVE, PA. ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.<br /><br />snip...<br /><br />STEAK MASTER, 21159 M21159 P, ELWOOD, NE. ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.<br /><br />snip...<br /><br />THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X 4/4/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X 5/4/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br /><a href="http://www.fsis.usda.gov/PDF/QER_Q3_FY2006.pdf">http://www.fsis.usda.gov/PDF/QER_Q3_FY2006.pdf</a><br /><br /><br />UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT January 1, 2006 through March 31, 2006<br /><br />Table 5. Administrative Actions: Large HACCP Plants (1/01/06 to 3/31/06)<br /><br />CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X 3/13/06 On 10/11/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />snip...<br /><br />EXCEL CORP. 00086R M FORT MORGAN, CO 8/11/04 2/22/05 X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.<br /><br />snip...<br /><br />TYSON FRESH MEATS INC. 00245L M 3/12/04 3/18/04 X<br /><br />LEXINGTON, NE<br /><br />X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />snip...<br /><br />TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />GULF PACKING COMPANY, 00696 M00696 P, SAN BENITO, TX, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />HI COUNTRY BEEF JERKY, 01248 M01248 P, LINCOLN, MT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />HITCHIN POST STEAK COMPANY, 20773 M20773 P, KANSAS CITY, KS, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />ROCK CREEK SLAUGHTER CO., 09150 M09150 P, FAIRBURY, NE, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />Table 7. Administrative Actions: Very Small HACCP Plants (1/01/06 to 3/31/06)<br /><br />A.J. CEKAK'S MEAT MARKET 21562 M ORD. NE, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />ALTA VISTA LOCKER 31931 M ALTA VISTA, KS, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />C&C MEAT SALES, INC. 18494 M18494 P UPPER MARLBORO, MD 2/27/06 3/16/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X 3/6/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X 1/13/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />PARAGON SPRAY DRYING, L.L.C. 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X 2/9/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />SAVORY CONNECTION, INC. 31764 M31764 P SELINGSGROVE, PA 3/14/06 3/31/06 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />STEAK MASTER, 21159 M21159 P, ELWOOD, NW, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />TEARS MARKET, 04535 M04535 P, PENN YAN, NY, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />THE MEAT SHOP, 31561 M BENSON, VT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />THEURER'S QUALITY MEATS, INC. 31647 M31647 P, LEWISTON, UT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />TOOELE VALLEY MEATS 20594 M20594 P, GRANTSVILLE, UT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL<br /><br />snip...<br /><br />WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br />WILLIAM. G. MEST PACKING CO. 04431 M STRYKERSVILLE, NY 2/2/06 2/23/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. On 3/21/06, NOIE was modified and reissued. On 6/29/06, NOIE was rescinded.<br /><br />YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X 2/23/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />snip...<br /><br /><a href="http://www.fsis.usda.gov/PDF/QER_Q1_FY2006.pdf">http://www.fsis.usda.gov/PDF/QER_Q1_FY2006.pdf</a><br /><br /><br />UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005<br /><br />SRM REMOVAL USA<br /><br />UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005<br /><br />snip....<br /><br />CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X X On 10/11/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.<br /><br />00245L M LEXINGTON, NE 3/12/04 3/18/04 X 5/4/05 X X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />9/16/05 9/29/05 X X TYSON FRESH MEATS INC. 09268 M PASCO, WA X X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />TYSON FRESH MEATS INC. X X 00245D M EMPORIA, KS On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.<br /><br />DESERET MEAT 04852 M SPANISH FORK, UT 7/20/05 8/1/05 X X 12/29/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />A.J. CEKAK'S MEAT MARKET 9/1/05 9/20/05 X X X On 9/1/05, an enforcement action 21562 M concerning failure to meet regulatory ORD, NE requirements for Escherichia coli Biotype 1 (E. coli) was taken. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />ALTA VISTA LOCKER 10/5/05 10/26/05 X X The enforcement action included, as a 31931 M basis, failure of the establishment toALTA VISTA, KS comply with Agency requirements concerning specified risk material.<br /><br />BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 8/8/05 8/16/05 X X X 11/16/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />CHAMPLAIN BEEF INC 2/28/05 3/4/05 3/8/05 X X X 08547 M WHITEHALL, NY 10/17/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />FIVE STAR PACK INC. 9/1/05 9/9/05 X X 12/29/05 On 9/1/05, an enforcement action 08725 M08725 P concerning failure to meet regulatory GOLDEN CITY, MO requirements for Escherichia coli Biotype 1 (E. coli) was taken. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. FRESH FARMS BEEF 12/16/05 12/28/05 X X X The enforcement action included, as a 18579 M basis, failure of the establishment toRUTLAND, VT comply with Agency requirements concerning specified risk material.<br /><br />GOETZ AND SONS WESTERN 11/15/05 11/23/05 12/1/05 X X MEATS INC 06245 M06245 P EVERETT, WA 12/17/05 12/28/05 X X X On 12/17/05, firm violated a regulatory control action by selling U.S.D.A retained product.<br /><br />H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 7/28/05 8/1/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 7/26/05 7/29/05 X X 11/15/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. PARAGON SPRAY DRYING, LLC 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />S & S MEAT COMPANY 01046 M01046 P KANSAS CITY, MO 8/4/05 8/19/05 X X 11/16/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />STEAK MASTER 21159 M21159 P ELWOOD, NE 11/4/05 11/17/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X X X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />THEURER'S QUALITY MEATS, INC 31647 M31647 P LEWISTON, UT 7/27/05 7/29/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />TOOELE VALLEY MEATS 20594 M20594 P GRANTSVILLE, UT 7/25/05 8/1/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />WALNUT VALLEY PACKING LLC 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.<br /><br />full text 54 pages ;<br /><br /><a href="http://www.fsis.usda.gov/PDF/QER_Q1_FY2006.pdf">http://www.fsis.usda.gov/PDF/QER_Q1_FY2006.pdf</a><br /><br /><br />Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through September 30, 2005 Date: March 20, 2006 at 12:58 pm PST<br /><br />UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT July 1, 2005 through September 30, 2005<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />DESERET MEAT 04852 M SPANISH FORK, UT 07/27/05 08/01/05 X On 7/27/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />MONTEBELLO MEAT PROCESSING, INC 19075 M19075 P MANATI, PR 08/01/05 08/18/05 X 09/26/05 On 8/1/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.<br /><br />snip...<br /><br />Table 7. Administrative Actions: Very Small HACCP Plants (7/01/05 to 9/30/05)<br /><br />snip...<br /><br />A.J. CEKAK'S MEAT MARKET 09/01/05 09/20/05 On 9/1/05, an enforcement action<br /><br />21562 M<br /><br />concerning failure to meet regulatory ORD, NE requirements for Escherichia coli X X X Biotype 1 (E. coli) and Bovine Spongiform Encephalopathy/Specified Risk Material was taken in accordance with 9 CFR Part 500.4.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 08/08/05 08/16/05 X On 8/8/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />FIVE STAR PACK INC. 08725 M08725 P GOLDEN CITY, MO 09/01/05 09/09/05 X X On 9/1/05, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli) and Bovine Spongiform Encephalopathy/Specified Risk Material was taken in accordance with 9 CFR Part 500.4.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />H AND P MEATS 21352 M SOUTH PITTSBURG, TN 07/28/05 08/08/05 08/17/05 08/19/05 X X On 8/17/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.<br /><br />snip...<br /><br />HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 07/28/05 08/01/05 X On 7/28/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 07/26/05 07/29/05 X X On 7/26/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.<br /><br />snip...<br /><br />PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 09/21/05 X On 9/21/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.<br /><br />PARAGON SPRAY DRYING, LLC 31792 M31792 P WAUKON, IA 09/06/05 09/12/05 X On 9/6/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 07/01/05 07/28/05 X On 7/1/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.<br /><br />snip...<br /><br />Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />08/04/05<br /><br />08/19/05<br /><br />On 8/4/05,<br /><br />an enforcement action 01046 M01046 P concerning Bovine SpongiformKANSAS CITY, MO X X Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.<br /><br />Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]<br /><br />snip...<br /><br />THE MEAT SHOP 08/18/05 09/06/05<br /><br />09/09/05<br /><br />On 9/6/05, a suspension action 31561 M concerning Bovine SpongiformBENSON, VT Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3. XX X X X<br /><br />THEURER'S QUALITY MEATS, 07/27/05 07/29/05<br /><br />On 7/27/05, a suspension action INC concerning Bovine Spongiform31647 M31647 P Encephalopathy and Specified Risk X X<br /><br />LEWISTON, UT Material was taken in accordance with 9 CFR Part 500.3.<br /><br />TOOELE VALLEY MEATS 07/25/05 08/01/05<br /><br />On 7/25/05, a suspension action 20594 M20594 Pconcerning Bovine Spongiform<br /><br />GRANTSVILLE, UT X X Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.<br /><br />snip...<br /><br />52 pages<br /><br /><a href="http://www.fsis.usda.gov/PDF/QER_Q4_FY2005.pdf">http://www.fsis.usda.gov/PDF/QER_Q4_FY2005.pdf</a><br /><br /><br />PREVIOUS<br /><br /><a href="http://www.fsis.usda.gov/PDF/QER_Q3_FY2005.pdf">http://www.fsis.usda.gov/PDF/QER_Q3_FY2005.pdf</a><br /><br /><br /><a href="http://www.fsis.usda.gov/PDF/QER_Q2_FY2005.pdf">http://www.fsis.usda.gov/PDF/QER_Q2_FY2005.pdf</a><br /><br /><br /><a href="http://www.fsis.usda.gov/PDF/QER_Q1_FY2005.pdf">http://www.fsis.usda.gov/PDF/QER_Q1_FY2005.pdf</a><br /><br /><br />P04.27<br /><br />Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route<br /><br />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<br /><br />Background:<br /><br />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.<br /><br />Aims:<br /><br />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.<br /><br />Methods:<br /><br />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).<br /><br />Results:<br /><br />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.<br /><br />Conclusions:<br /><br />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 v CJD as fast as intracerebrally inoculated animals.<br /><br />The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).<br /><br /><a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a><br /><br /><br />What Do We Feed to Food-Production Animals? A Review of Animal FeedIngredients and Their Potential Impacts on Human Health<br /><br />Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker11Johns Hopkins Center for a Livable Future, Bloomberg School of PublicHealth, Baltimore, Maryland, USA; 2Maryland Institute forApplied Environmental Health, College of Health and Human Performance,University of Maryland, College Park, Maryland, USA;3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA<br /><br />snip...<br /><br />Table 1. Animal feed ingredients that are legally used in U.S. animal feeds<br /><br />Animal<br /><br />Rendered animal protein from Meat meal, meat meal tankage, meat and bonemeal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals andother meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, andanimal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products<br /><br />snip...<br /><br />Conclusions<br /><br />Food-animal production in the United States has changed markedly in the past century, and these changes have paralleled major changes in animal feed formulations. While this industrialized system of food-animal production may result in increased production efficiencies, some of the changes in animal feeding practices may result in unintended adverse health consequences for consumers of animal-based food products. Currently, the use of animal feed ingredients, including rendered animal products, animal waste, antibiotics, metals, and fats, could result in higher levels of bacteria, antibiotic resistant bacteria, prions, arsenic, and dioxin like compounds in animals and resulting animal-based food products intended for human consumption. Subsequent human health effects among consumers could include increases in bacterial infections (antibiotic resistant and nonresistant) and increases in the risk of developing chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide range of potential human health impacts that could result from animal feeding practices, there are little data collected at the federal or state level concerning the amounts of specific ingredients that are intentionally included in U.S. animal feed. In addition, almost no biological or chemical testing is conducted on complete U.S. animal feeds; insufficient testing is performed on retail meat products; and human health effects data are not appropriately linked to this information. These surveillance inadequacies make it difficult to conduct rigorous epidemiologic studies and risk assessments that could identify the extent to which specific human health risks are ultimately associated with animal feeding practices. For example, as noted above, there are insufficient data to determine whether other human foodborne bacterial illnesses besides those caused by S. enterica serotype Agona are associated with animal feeding practices. Likewise, there are insufficient data to determine the percentage of antibiotic-resistant human bacterial infections that are attributed to the nontherapeutic use of antibiotics in animal feed. Moreover, little research has been conducted to determine whether the use of organoarsenicals in animal feed, which can lead to elevated levels of arsenic in meat products (Lasky et al. 2004), contributes to increases in cancer risk. In order to address these research gaps, the following principal actions are necessary within the United States: a) implementation of a nationwide reporting system of the specific amounts and types of feed ingredients of concern to public health that are incorporated into animal feed, including antibiotics, arsenicals, rendered animal products, fats, and animal waste; b) funding and development of robust surveillance systems that monitor biological, chemical, and other etiologic agents throughout the animal-based food-production chain “from farm to fork” to human health outcomes; and c) increased communication and collaboration among feed professionals, food-animal producers, and veterinary and public health officials.<br /><br />REFERENCES...snip...end<br /><br />Sapkota et al.668 VOLUME 115 NUMBER 5 May 2007 • Environmental Health Perspectives<br /><br /><a href="http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867957&blobtype=pdf">http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867957&blobtype=pdf</a><br /><br /><br />Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. ......... <a href="http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose">http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose</a><br /><br /><br />look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused7% (1 of 14) of the cows to come down with BSE;<br /><br />Risk of oral infection with bovine spongiform encephalopathy agent in primates<br /><br />Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, NathalieLescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-PhilippeDeslysSummary The uncertain extent of human exposure to bovine spongiformencephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease(vCJD)--is compounded by incomplete knowledge about the efficiency of oralinfection and the magnitude of any bovine-to-human biological barrier totransmission. We therefore investigated oral transmission of BSE tonon-human primates. We gave two macaques a 5 g oral dose of brain homogenatefrom a BSE-infected cow. One macaque developed vCJD-like neurologicaldisease 60 months after exposure, whereas the other remained free of diseaseat 76 months. On the basis of these findings and data from other studies, wemade a preliminary estimate of the food exposure risk for man, whichprovides additional assurance that existing public health measures canprevent transmission of BSE to man.<br /><br />snip...<br /><br />BSE bovine brain inoculum<br /><br />100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg<br /><br />Primate (oral route)* 1/2 (50%)<br /><br />Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)1/15 (7%)<br /><br />RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)<br /><br />PrPres biochemical detection<br /><br />The comparison is made on the basis of calibration of the bovine inoculumused in our study with primates against a bovine brain inoculum with asimilar 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. icip=intracerebral and intraperitoneal.<br /><br />Table 1: Comparison of transmission rates in primates and cattle infectedorally with similar BSE brain inocula<br /><br />Published online January 27, 2005<br /><br /><a href="http://www.thelancet.com/journal/journal.isa">http://www.thelancet.com/journal/journal.isa</a><br /><br /><br />It is clear that the designing scientists must<br /><br />also have shared Mr Bradley's surprise at the results because all the dose<br /><br />levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s145d.pdf">http://www.bseinquiry.gov.uk/files/ws/s145d.pdf</a><br /><br /><br />The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that thedesigning scientists must have also shared Mr Bradley's surprise at the resultsbecause all the dose levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s147f.pdf">http://www.bseinquiry.gov.uk/files/ws/s147f.pdf</a><br /><br /><br />2) Infectious dose:<br /><br />To cattle: 1 gram of infected brain material (by oral ingestion)<br /><br /><a href="http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml">http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml</a><br /><br /><br />IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?<br /><br />In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.<br /><br />We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.<br /><br />snip...<br /><br />PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986<br /><br /><a href="http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf">http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a><br /><br /><br />OBSERVATIONS AND RESULTS<br /><br />A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.<br /><br />Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.<br /><br />Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months.<br /><br />DISCUSSION<br /><br />These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy.<br /><br />We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster-adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed.<br /><br />ACKNOWLEDGEMENTS<br /><br />These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations.<br /><br />REFERENCES<br /><br />Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420.<br /><br />MARSH<br /><br /><a href="http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf">http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br /><br /><br />Saturday, December 01, 2007<br /><br />Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model<br /><br />Volume 13, Number 12–December 2007 Research<br /><br />Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle andL-type Bovine Spongiform Encephalopathy in a Mouse Model<br /><br />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<br /><br />Abstract<br /><br />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 TgOvPrP4mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE.<br /><br />snip...<br /><br />Conclusion<br /><br />These studies provide experimental evidence that the Stetsonville TME agentis 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).<br /><br /><a href="http://www.cdc.gov/eid/content/13/12/1887.htm?s_cid=eid1887_e">http://www.cdc.gov/eid/content/13/12/1887.htm?s_cid=eid1887_e</a><br /><br /><br />Transmissible Mink Encephalopathy TME<br /><br /><a href="http://transmissible-mink-encephalopathy.blogspot.com/">http://transmissible-mink-encephalopathy.blogspot.com/</a><br /><br /><br />USA MAD COW CASES IN ALABAMA AND TEXAS<br /><br />***PLEASE NOTE***<br /><br />USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS<br /><br /><a href="http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779">http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779</a><br /><br /><br />P02.35<br /><br />Molecular Features of the Protease-resistant Prion Protein (PrPres) in H- type BSE<br /><br />Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden<br /><br />Western blot analyses of PrPres accumulating in the brain of BSE- infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H- type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C- terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) *** reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.<br /><br />FC5.5.2<br /><br />Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease<br /><br />Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2; Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy<br /><br />The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecular basis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinct conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported two Italian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. A major limitation of transmission studies to mice is the lack of reliable information on clinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates by i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle *** and in some subtypes of inherited and sporadic Creutzfeldt-Jakob disease. Oral Abstracts 14<br /><br /><a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a><br /><br /><br />Subject: In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells<br /><br />Gerald Wells: Report of the Visit to USA, April-May 1989<br /><br />snip...<br /><br />The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised...<br /><br />snip...<br /><br />It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...<br /><br />snip...<br /><br />3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_...<br /><br />snip...please read this old full text document !<br /><br /><a href="http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf">http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a><br /><br /><br />In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.<br /><br />In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.<br /><br /><a href="http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm">http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm</a><br /><br /><br />CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006<br /><br />The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.<br /><br />The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.<br /><br />These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.<br /><br />"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."<br /><br />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.<br /><br />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.<br /><br />"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end<br /><br />http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r<br /><br />CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...<br /><br />http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm<br /><br />PAUL BROWN COMMENT TO ME ON THIS ISSUE<br /><br />Tuesday, September 12, 2006 11:10 AM<br /><br />"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."<br /><br /><a href="http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125">http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125</a><br /><br /><br />Volume 12, Number 12–December 2006<br /><br />PERSPECTIVE<br /><br />On the Question of Sporadic<br /><br />or Atypical Bovine SpongiformEncephalopathy and<br /><br />Creutzfeldt-Jakob Disease<br /><br />Paul Brown,* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§<br /><br />A link between BSE and<br /><br />sporadic CJD has been suggested on the basis of laboratory<br /><br />studies but is unsupported by epidemiologic observation.<br /><br />Such a link might yet be established by the discovery<br /><br />of a specific molecular marker or of particular combinations<br /><br />of trends over time of typical and atypical BSE and various<br /><br />subtypes of sporadic CJD, as their numbers are influenced<br /><br />by a continuation of current public health measures that<br /><br />exclude high-risk bovine tissues from the animal and<br /><br />human food chains.<br /><br />SNIP...<br /><br />Sporadic CJD<br /><br />The possibility that at least some cases of apparently sporadic CJD might be due to infection by sporadic cases of BSE cannot be dismissed outright. Screening programs needed to identify sporadic BSE have yet to be implemented, and we know from already extant testing programs that at least a proportion of infected animals have no symptoms and thus would never be identified in the absence of systematic testing. Thus, sporadic BSE (or for that matter, sporadic disease in any mammalian species) might be occurring on a regular basis at perhaps the same annual frequency as sporadic CJD in humans, that is, in the range of 1 case per million animals.<br /><br />Whether humans might be more susceptible to atypical forms of BSE cannot be answered at this time. Experimentally transmitted BASE shows shorter incubation periods than BSE in at least 1 breed of cattle, bovinized transgenic mice, and Cynomolgus monkeys (12,13). In humanized transgenic mice, BASE transmitted, whereas typical BSE did not transmit (13). Paradoxically, the other major phenotype (H) showed an unusually long incubation period in bovinized transgenic mice (12).<br /><br />The limited experimental evidence bearing on a possible relationship between BSE and sporadic CJD is difficult to interpret. The original atypical BASE strain of BSE had a molecular protein signature very similar to that of 1 subtype (type 2 M/V) of sporadic CJD in humans (5). In another study, a strain of typical BSE injected into humanized mice encoding valine at codon 129 showed a glycopattern indistinguishable from the same subtype of sporadic CJD (15). In a third study, the glycopatterns of both the H and L strains of atypical BSE evidently did not resemble any of the known sporadic CJD subtypes (12).<br /><br />To these molecular biology observations can be added the epidemiologic data accumulated during the past 30 years. The hypothesis that at least some cases of apparently sporadic CJD are due to unrecognized BSE infections cannot be formally refuted, but if correct, we might expect by now to have some epidemiologic evidence linking BSE to at least 1 cluster of apparently sporadic cases of CJD. Although only a few clusters have been found (and still fewer published), every proposed cluster that has been investigated has failed to show any common exposure to bovines. For that matter, no common exposure has been shown to any environmental vehicles of infection, including the consumption of foodstuffs from bovine, ovine, and porcine sources, the 3 livestock species known to be susceptible to transmissible spongiform encephalopathies. Additional negative evidence comes from several large case-control studies in which no statistically significant dietary differences were observed between patients with sporadic CJD and controls (16,17).<br /><br />On the other hand, the difficulty of establishing a link between BSE and CJD may be compounded by our ignorance of the infectious parameters of a sporadic form of BSE (e.g., host range, tissue distribution of infectivity, route of transmission, minimum infectious dose for humans, whether single or multiple). Presumably, these parameters would resemble those of variant CJD; that is, high infectivity central nervous system and lymphoreticular tissues of an infected cow find their way into products consumed by humans. Transmissions that might have occurred in the past would be difficult to detect because meat products are generally not distributed in a way that results in detectable geographic clusters.<br /><br />Barring the discovery of a specific molecular signature (as in variant CJD), the most convincing clue to an association will come from the observation of trends over time of the incidence of typical and atypical BSE and of sporadic and variant CJD. With 4 diseases, each of which could have increasing, unchanging, or decreasing trends, there could be 81 (34) possible different combinations. However, it is highly likely that the trends for typical BSE and variant CJD will both decrease in parallel as feed bans continue to interrupt recycled contamination. The remaining combinations are thus reduced to 9 (32), and some of them could be highly informative.<br /><br />For example, if the incidence of atypical BSE declines in parallel with that of typical BSE, its candidacy as a sporadic form of disease would be eliminated (because sporadic disease would not be influenced by current measures to prevent oral infection). If, on the other hand, atypical BSE continues to occur as typical BSE disappears, this would be a strong indication that it is indeed sporadic, and if in addition at least 1 form of what is presently considered as sporadic CJD (such as the type 2 M/V subtype shown to have a Western blot signature like BASE) were to increase, this would suggest (although not prove) a causal relationship (Figure 5).<br /><br />Recognition of the different forms of BSE and CJD depends upon continuing systematic testing for both bovines and humans, but bovine testing will be vulnerable to heavy pressure from industry to dismantle the program as the commercial impact of declining BSE cases ceases to be an issue. Industry should be aware, however, of the implications of sporadic BSE. Its occurrence would necessitate the indefinite retention of all of the public health measures that exclude high-risk bovine tissues from the animal and human food chains, whereas its nonoccurrence would permit tissues that are now destroyed to be used as before, once orally acquired BSE has disappeared.<br /><br />SNIP...<br /><br />PLEASE READ FULL TEXT ;<br /><br /><a href="http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e">http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e</a><br /><br /><br />THE SEVEN SCIENTIST REPORT ***<br /><br /><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf">http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf</a><br /><br /><br />full text ;<br /><br /><a href="http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html">http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html</a><br /><br /><br />Thursday, January 31, 2008<br /><br />Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain<br /><br />J. Virol. doi:10.1128/JVI.02561-07 Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.<br /><br />Thursday, January 31, 2008<br /><br />Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain<br /><br />J. Virol. doi:10.1128/JVI.02561-07 Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.<br /><br />Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain<br /><br />Qingzhong Kong*, Mengjie Zheng, Cristina Casalone, Liuting Qing, Shenghai Huang, Bikram Chakraborty, Ping Wang, Fusong Chen, Ignazio Cali, Cristiano Corona, Francesca Martucci, Barbara Iulini, Pierluigi Acutis, Lan Wang, Jingjing Liang, Meiling Wang, Xinyi Li, Salvatore Monaco, Gianluigi Zanusso, Wen-Quan Zou, Maria Caramelli, and Pierluigi Gambetti* Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy; Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy<br /><br />* To whom correspondence should be addressed. Email: qxk2@case.edu. pxg13@case.edu.<br /><br />Abstract<br /><br />Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to have only one strain (BSE-C). BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, BASE (or BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE-affected cattle. Sixty percent of the inoculated Tg mice became infected after 20-22 months incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE-infected Tg mice, but none of the Tg mice infected with a sporadic human prion disease, showed presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE-infected humanized Tg mouse brains are different from those of the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation time are observed in the BASE-infected Tg mice. These results suggest that, in humans, BASE is a more virulent BSE strain and likely lymphotropic.<br /><br /><a href="http://jvi.asm.org/cgi/content/abstract/JVI.02561-07v1?papetoc">http://jvi.asm.org/cgi/content/abstract/JVI.02561-07v1?papetoc</a><br /><br /><br />for those interested, further into this study, it gets very interesting ;<br /><br /><a href="http://cjdmadcowbaseoct2007.blogspot.com/2008/02/evaluation-of-human-transmission-risk.html">http://cjdmadcowbaseoct2007.blogspot.com/2008/02/evaluation-of-human-transmission-risk.html</a><br /><br /><br />Subject: Aspects of the Cerebellar Neuropathology in Nor98<br /><br />Date: September 26, 2007 at 4:06 pm PST<br /><br />P03.141<br /><br />Aspects of the Cerebellar Neuropathology in Nor98<br /><br />Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway<br /><br />Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. *** The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.<br /><br /><a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a><br /><br /><br />1: J Infect Dis 1980 Aug;142(2):205-8<br /><br />Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.<br /><br />Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.<br /><br />Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.<br /><br />PMID: 6997404<br /><br /><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br /><br /><br />12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY<br /><br />snip...<br /><br />A The Present Position with respect to Scrapie A] The Problem<br /><br />Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries.<br /><br />The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep.<br /><br />It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible.<br /><br />Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"<br /><br />Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.<br /><br />snip...<br /><br />76/10.12/4.6<br /><br /><a href="http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf">http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br /><br /><br />Epidemiology of Scrapie in the United States 1977<br /><br /><a href="http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf">http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a><br /><br /><br />SCRAPIE PROGRAM FY REPORT 2007<br /><br />Prepared by National Center for Animal Health Programs Ruminant Health Programs Team November 15, 2007<br /><br />snip...<br /><br />Infected and Source Flocks<br /><br />During FY 2007, there were a total of 76 new infected or source flocks identified. Of those new flocks identified, 30 were infected flocks and 46 were source flocks (Figure 2). As of September 30, 2007, there were 38 scrapie infected and source flocks with open statuses (Figure 3). ...<br /><br />snip...<br /><br />In FY 2007, 331 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), including 59* Regulatory Scrapie Slaughter Surveillance (RSSS) cases (Figure 5 and Slide 16). In FY 2007, two field cases, one validation case, and two RSSS cases were consistent with Nor-98 scrapie. The Nor98-like cases originated from flocks in California, Minnesota, Colorado, Wyoming and Indiana respectively. Nineteen cases of scrapie in goats have been reported since 1990 (Figure 6). The last goat case was reported in September 2007.<br /><br />snip...<br /><br />see full report here ;<br /><br /><a href="http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/yearly_report.pps">http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/yearly_report.pps</a><br /><br /><br />Friday, February 15, 2008<br /><br />SCRAPIE and TSE to human UPDATE 2008 (ambiguous terms of transition and reality set in)<br /><br /><a href="http://nor-98.blogspot.com/2008/02/scrapie-and-tse-to-human-update-2008.html">http://nor-98.blogspot.com/2008/02/scrapie-and-tse-to-human-update-2008.html</a><br /><br /><br />TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-73916026081841214152008-01-25T09:18:00.000-08:002008-01-25T09:52:47.669-08:00January 2008 Update on Feed Enforcement Activities to Limit the Spread of BSEJanuary 24, 2008<br /><br />January 2008 Update on Feed Enforcement Activities to Limit the Spread of BSE<br /><br />To help prevent the establishment and amplification of Bovine Spongiform Encephalophathy (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.<br /><br />The following is an update on FDA enforcement activities regarding the ruminant feed ban. FDA's Center for Veterinary Medicine (CVM) has assembled data from the inspections that have been conducted AND whose final inspection report has been recorded in the FDA's inspection database as of January 12, 2008. As of January 12, 2008, FDA had received over 59,000 inspection reports. The majority of these inspections (approximately 70%) were conducted by State feed safety officials, with the remainder conducted by FDA officials.<br /><br />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).<br /><br />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.<br /><br />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.<br /><br />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.<br /><br />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.<br /><br />RENDERERS<br /><br />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.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 267<br /><br />Number of active firms handling materials prohibited from use in ruminant feed – 165 (62 % of those active firms inspected)<br /><br />Of the 165 active firms handling prohibited materials, their most recent inspection revealed that:<br /><br />0 firms (0%) were classified as OAI<br /><br />5 firms (3.0 %) were classified as VAI<br /><br />LICENSED FEED MILLS<br /><br />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.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 1,077<br /><br />Number of active firms handling materials prohibited from use in ruminant feed – 473 (44 % of those active firms inspected)<br /><br />Of the 473 active firms handling prohibited materials, their most recent inspection revealed that:<br /><br />0 firms (0%) were classified as OAI<br /><br />8 firms (1.7 %) were classified as VAI<br /><br />FEED MILLS NOT LICENSED BY FDA<br /><br />These feed mills are not licensed by the FDA to produce medicated feeds.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 5,207<br /><br />Number of active firms handling materials prohibited from use in ruminant feed – 2,544 (49 % of those active firms inspected)<br /><br />Of the 2,544 active firms handling prohibited materials, their most recent inspection revealed that:<br /><br />0 firms (0%) were classified as OAI<br /><br />43 firms (1.7 %) were classified as VAI<br /><br />PROTEIN BLENDERS<br /><br />These firms blend rendered animal protein for the purpose of producing quality feed ingredients that will be used by feed mills.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 398<br /><br />Number of active firms handling materials prohibited from use in ruminant feed – 191 (48 % of those active firms inspected)<br /><br />Of the 191 active firms handling prohibited materials, their most recent inspection revealed that:<br /><br />0 firm (0%) was classified as OAI<br /><br />3 firms (1.6 %) were classified as VAI<br /><br />RENDERERS, FEED MILLS, AND PROTEIN BLENDERS MANUFACTURING WITH PROHIBITED MATERIAL<br /><br />This category includes only those firms that actually use prohibited material to manufacture, process, or blend animal feed or feed ingredients.<br /><br />Total number of active renderers, feed mills, and protein blenders whose initial inspection has been reported to FDA – 6,628<br /><br />Number of active renderers, feed mills, and protein blenders processing with prohibited materials – 505 (7.6 %)<br /><br />Of the 505 active renderers, feed mills, and protein blenders processing with prohibited materials, their most recent inspection revealed that:<br /><br />0 firms (0%) were classified as OAI<br /><br />22 firms (4.4 %) were classified as VAI<br /><br />OTHER FIRMS INSPECTED<br /><br />Examples of such firms include ruminant feeders, on-farm mixers, pet food manufacturers, animal feed salvagers, distributors, retailers, and animal feed transporters.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 19,481<br /><br />Number of active firms handling materials prohibited from use in ruminant feed – 6,275 (32 % of those active firms inspected)<br /><br />Of the 6,275 active firms handling prohibited materials, their most recent inspection revealed that:<br /><br /><br />0 firms (0%) were classified as OAI<br /><br />155 firms (2.5 %) were classified as VAI<br /><br />TOTAL FIRMS<br /><br />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.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 21,630<br /><br />Number of active firms handling materials prohibited from use in ruminant feed – 6,927 (32 % of those active firms inspected)<br /><br />Of the 6,927 active firms handling prohibited materials, their most recent inspection revealed that:<br /><br />0 firms (0%) were classified as OAI<br /><br />162 firms (2.3 %) were classified as VAI<br /><br /><br /><a href="http://www.fda.gov/cvm/BSE0108.htm">http://www.fda.gov/cvm/BSE0108.htm</a><br /><br /><br /><br />Greetings,<br /><br />VAI violations can consist of many breaches, that in the end, could cause tainted product to be distributed.<br /><br />im just goint to pick out one from last year, and i just ponder how they would have classified this ;<br /><br /><br />10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA<br />2007<br /><br /><br />Date: March 21, 2007 at 2:27 pm PST<br />RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II<br />___________________________________<br />PRODUCT<br />Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried,<br />Recall # V-024-2007<br />CODE<br />Cattle feed delivered between 01/12/2007 and 01/26/2007<br />RECALLING FIRM/MANUFACTURER<br />Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.<br />Firm initiated recall is ongoing.<br />REASON<br />Blood meal used to make cattle feed was recalled because it was<br />cross-contaminated with prohibited bovine meat and bone meal that had been<br />manufactured on common equipment and labeling did not bear cautionary BSE<br />statement.<br />VOLUME OF PRODUCT IN COMMERCE<br />42,090 lbs.<br />DISTRIBUTION<br />WI<br /><br />___________________________________<br />PRODUCT<br />Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL<br />Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal,<br />TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY<br />Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST<br />POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL<br />DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK<br />CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC<br />MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY,<br />A-BYPASS ML W/SMARTA, Recall # V-025-2007<br />CODE<br />The firm does not utilize a code - only shipping documentation with<br />commodity and weights identified.<br />RECALLING FIRM/MANUFACTURER<br />Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm<br />initiated recall is complete.<br />REASON<br />Products manufactured from bulk feed containing blood meal that was cross<br />contaminated with prohibited meat and bone meal and the labeling did not<br />bear cautionary BSE statement.<br />VOLUME OF PRODUCT IN COMMERCE<br />9,997,976 lbs.<br />DISTRIBUTION<br />ID and NV<br /><br />END OF ENFORCEMENT REPORT FOR MARCH 21, 2007<br /><br /><br /><a href="http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html">http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html</a><br /><br /><br /><br />FC5.5.1<br /><br />BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc<br /><br />C-terminal Truncated Fragments Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux, MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4; Monaco, S31University of Verona, of Neurological and Visual Sciences, Italy; 2CEA, IMETI/SEPIA,France; 3University of Verona, Neurological and Visual Sciences, Italy; 4IMETI/SEPIA,France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA<br /><br />The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent humanprion disease, remains still unknown. The marked disease phenotype heterogeneity observed in sCJD is thought to be influenced by the type of proteinase K-resistantprion protein, or PrPSc (type 1 or type 2 according to the electrophoretic mobility ofthe unglycosylated backbone), and by the host polymorphic Methionine/Valine (M/V)codon 129 of the PRNP. By using a two-dimensional gel electrophoresis (2D-PAGE)and imunoblotting we previously showed that in sCJD, in addition to the PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1 of all genotypes,;(ii) the second was found in M/M-2 (cortical form); (iii) the third in amyloidogenic M/V-2 and V/V-2 subtypes (Zanusso et al., JBC 2004) . Recently, we showed that sCJD subtype M/V-2 shared molecular and pathological features with an atypical form of BSE, named BASE, thus suggesting a potential link between the two conditions. This connection was further confirmed after 2D-PAGE analysis, which showed an identical PrPSc signature, including the biochemical pattern of CTFs. To pursue this issue, we obtained brain homogenates from Cynomolgus macaques intracerebrally inoculatedwith brain homogenates from BASE. Samples were separated by using a two dimensional electrophoresis (2D-PAGE) followed by immunoblotting. We here show that the PrPSc pattern obtained in infected primates is identical to BASE and sCJDMV-2 subtype. These data strongly support the link, or at least a common ancestry, between a sCJD subtype and BASE.<br /><br />This work was supported by Neuroprion (FOOD-CT-2004-506579)<br /><br /><br /><br />FC5.5.2<br /><br />Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease<br /><br />Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2;Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati,M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L21University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA,Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy<br /><br />The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecularbasis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinctconformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported twoItalian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. Amajor limitation of transmission studies to mice is the lack of reliable information onclinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolatesby i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and inexperimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle and insome subtypes of inherited and sporadic Creutzfeldt-Jakob disease.<br /><br /><br /><br />P04.27<br /><br />Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route<br /><br />Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3;Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J11Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France;3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Diseasecontrol, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany<br /><br />Background:<br /><br />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.<br /><br />Aims:<br /><br />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.<br /><br />Methods:<br /><br />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).<br /><br />Results:<br /><br />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.<br /><br />Conclusions:<br /><br />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 4years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.<br /><br />The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).<br /><br /><a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a><br /><br /><br /><br />ALSO, 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;<br /><br />Risk of oral infection with bovine spongiform encephalopathy agent inprimates<br /><br />Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, NathalieLescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-PhilippeDeslys<br /><br />Summary<br /><br />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 diseaseat 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.<br /><br />snip...<br /><br /><br />BSE bovine brain inoculum<br /><br />100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg<br /><br />Primate (oral route)* 1/2 (50%)<br /><br />Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)1/15 (7%)<br /><br />RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)<br /><br />PrPres biochemical detection<br /><br />The comparison is made on the basis of calibration of the bovine inoculumused in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was<br />inoculated into mice and cattle.8 *Data are number of animalspositive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of<br />bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.<br /><br /><br />Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula<br /><br />Published online January 27, 2005<br /><br /><a href="http://www.thelancet.com/journal/journal.isa">http://www.thelancet.com/journal/journal.isa</a><br /><br /><br /><br />It is clear that the designing scientists must<br /><br />also have shared Mr Bradley’s surprise at the results because all the dose<br /><br />levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s145d.pdf">http://www.bseinquiry.gov.uk/files/ws/s145d.pdf</a><br /><br /><br /><br />6. It also appears to me that Mr Bradley’s answer (that it would take lessthan say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attackrate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s147f.pdf">http://www.bseinquiry.gov.uk/files/ws/s147f.pdf</a><br /><br /><br /><br />APHIS-2006-0041-0006 TSE advisory committee for the meeting December 15, 2006<br /><br /><a href="http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8">http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8</a><br /><br /><br /><br />PDF]Freas, William TSS SUBMISSION<br />File Format: PDF/Adobe Acrobat -<br />Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary<br />Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...<br /><br /><a href="http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf">http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf</a><br /><br /><br /><br />Attachment to Singletary comment<br /><br />January 28, 2007<br /><br /><br />Greetings APHIS,<br /><br /><br />I would kindly like to submit the following to ;<br /><br /><br />BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES<br />[Docket No. APHIS-2006-0041] RIN 0579-AC01<br /><br /><br />[Federal Register: January 9, 2007 (Volume 72, Number 5)]<br />[Proposed Rules]<br />[Page 1101-1129]<br />From the Federal Register Online via GPO Access [wais.access.gpo.gov]<br />[DOCID:fr09ja07-21]<br /><br /><a href="http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8152">http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8152</a><br /><br /><br /><br />BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS<br />DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01<br />Date: January 9, 2007 at 9:08 am PST<br /><br /><br /><a href="http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f3412">http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f3412</a><br /><br /><br /><br />[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine<br />Spongiform Encephalopathy (BSE)<br /><br /><br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf">http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf</a><br /><br /><br /><br />[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />03-025IFA<br />03-025IFA-2<br />Terry S. Singeltary<br /><br /><br />Page 1 of 17<br /><br /><br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a><br /><br /><br /><br />Thursday, January 3, 2008<br /><br />ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)<br /><br /><a href="http://animalhealthreport2006.blogspot.com/2008/01/animal-health-report-2006-bse-h-base.html">http://animalhealthreport2006.blogspot.com/2008/01/animal-health-report-2006-bse-h-base.html</a><br /><br /><br /><br />BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA<br /><br /><a href="http://madcowtesting.blogspot.com/">http://madcowtesting.blogspot.com/</a><br /><br /><br /><br />CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA<br /><br /><a href="http://cjdmadcowbaseoct2007.blogspot.com/">http://cjdmadcowbaseoct2007.blogspot.com/</a><br /><br /><br /><br />Archive Number 20071105.3602<br />Published Date 05-NOV-2007<br />Subject PRO/AH/EDR> Prion disease update 2007 (07)<br /><br />PRION DISEASE UPDATE 2007 (07)<br /><br />snip...<br /><br />[In submitting these data, Terry S. Singeltary Sr. draws attention to the<br />steady increase in the "type unknown" category, which, according to their<br />definition, comprises cases in which vCJD could be excluded. The total of 26<br />cases for the current year (2007) is disturbing, possibly symptomatic of the<br />circulation of novel agents. Characterization of these agents should be<br />given a high priority. - Mod.CP]<br /><br /><a href="http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963">http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963</a><br /><br /><br />There is a growing number of human CJD cases, and they were presented last<br />week in San Francisco by Luigi Gambatti(?) from his CJD surveillance<br />collection.<br /><br />He estimates that it may be up to 14 or 15 persons which display selectively<br />SPRPSC and practically no detected RPRPSC proteins.<br /><br /><br /><a href="http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm">http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm</a><br /><br /><br /><br /><a href="http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf">http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf</a><br /><br /><br /><br /><br />full text ;<br /><br />Friday, January 11, 2008<br />CJD HUMAN TSE REPORT UK, USA, CANADA, and Mexico JANUARY 2008<br /><br /><a href="http://cjdmadcowbaseoct2007.blogspot.com/2008/01/cjd-human-tse-report-uk-usa-canada-and.html">http://cjdmadcowbaseoct2007.blogspot.com/2008/01/cjd-human-tse-report-uk-usa-canada-and.html</a><br /><br /><br /><br /><br />Terry S. Singeltary Sr.<br />P.O. Box 42<br />Bacliff, Texas USA 77518Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-1169334957143211942007-01-20T15:12:00.000-08:002009-11-16T17:38:33.208-08:00MAD COW FEED IN COMMERCE UPDATE FDA JANUARY 2007Subject: Re: January 2007 Update on Feed Enforcement Activities to Limit the<br />Spread of BSE<br />Date: January 15, 2007 at 8:12 pm PST<br /><br /><br />REPORT OF THE COMMITTEE ON FEED SAFETY Chair: Kevin G. Custer, Des Moines, IA Vice Chair: Richard Sellers, Arlington, VA David C. Ailor, DC; Roy D. Brister, AR; Eric C. Gonder, NC; C. Ross Hamilton, TX; Jay Hawley, IN; Larry E. Hendricks, IL; Tom Holder, MD; Rex D. Holt, GA; David C. Kradel, PA; Elizabeth A. Lautner, IA; Gerald G. May, OH; David L. Meeker, VA; Gary D. Osweiler, IA; Jane F. Robens, MD; James E. Stocker, NC; H. Wesley Towers, DE; Elizabeth K. Wagstrom, IA; W. Douglas Waltman, GA; Gary L. Waters, MT. The Committee met at the Minneapolis Hilton Hotel, Minneapolis, Minnesota, Monday, October 16, 2006, 1:00-6:00 p.m., LaSalle Room. Twenty-three members and quest were present. Dr. Burt Pritchett, Center for Veterinary Medicine (CVM), Food and Drug Administration (FDA), gave an update on agency activities relative to bovine spongiform encephalopathy (BSE), the Animal Feed Safety System (AFSS) and contaminant limits. • BSE – The proposed rule (589.2001) to enhance the “feed rule” was published on October 6, 2005. CVM remains committed to publishing a final rule, but it is unlikely that publication will take place this year. FDA agrees that the economic impact was under estimated and is conducting a new economic evaluation. Carcass disposal is a major issue and revisions are needed relative to the environmental assessment. • AFSS – is a comprehensive, risk-based system for feed manufacture and distribution to minimize risks to animal and human health. It is intended to tie together regulation, policy and guidance. The goal is to complete the AFSS by the end of 2007. • Contaminant Limits – There is a lack of process for distinguishing feed hazards based upon their relative risks (Risk = Hazard x Exposure). The Feed Contaminants Program is scheduled for completion in 2010. Dr. Aaron Scott, Veterinary Services (VS), Animal and Plant Health Inspection Service (APHIS), United States Department of Agriculture (USDA) gave an update on BSE surveillance activities. To date, 189,000+ cases of BSE have been diagnosed. Of those, 89 percent occurred prior to 1997, and more than 96 percent have occurred in the United Kingdom (UK). USDA has conducted active surveillance since 1990. Surveillance is to monitor the presence of the disease in cattle, not to identify every case. The enhanced surveillance program began in June 2004 and ended in August 2006. More than 785,000 samples were analyzed. Two positive samples were identified. The conclusion of the enhanced surveillance program is that BSE prevalence is less than one infected animal per one million adult cattle. Dr. Scott emphasized the importance of clinical history accompanying samples, as those samples will carry more relative weight in the analysis of the data. Dr. Eric Nelson, President, American Association of Feed Control Officials (AAFCO), gave an update on association activities. AAFCO’s Model Feed Safety Program is designed to elevate the scope and effectiveness of current laws and regulations, and emerging systems and practices. The program will fill in the gaps of regulations and increase stakeholder participation. Richard Sellers, Vice President, American Feed Industry Association (AFIA), gave an update on the association’s Safe Feed/Safe Food program. The association is also monitoring European Union (EU) 183, which could put Hazard Analysis and Critical Control Point (HACCP) requirements on feed ingredients imported into the EU. Dr. David Meeker, Vice President, National Renderers Association (NRA), gave an update on the association’s Code of Practice Certification for rendering facilities, and rendered animal product blending facilities. Mr. Richard Sellers, AFIA introduced a new business item questioning the relevancy of the Committee on Feed Safety? Chair Custer responded that the relevance of a Committee is based upon issues addressed and resolutions generated. Only six of the twenty-two committee members attended the meeting. Discussions included the importance and need for a standing Committee on Feed Safety or could the Committee issues be distributed to another Committee. The Chair will be working with USAHA’s Executive Committee in reviewing how best to address the feed safety issues at USAHA.<br /><br /><a href="http://www.usaha.org/committees/reports/2006/report-fes-2006.pdf">http://www.usaha.org/committees/reports/2006/report-fes-2006.pdf</a><br /><br /><br />SRM TASK FORCE<br /><br /><a href="http://www.usaha.org/committees/resolutions/2005/resolution38-2005.pdf">http://www.usaha.org/committees/resolutions/2005/resolution38-2005.pdf</a><br /><br /><br />IMPORT AND EXPORT<br /><br /><a href="http://www.usaha.org/committees/reports/2006/report-ie-2006.pdf">http://www.usaha.org/committees/reports/2006/report-ie-2006.pdf</a><br /><br /><br />TSS<br /><br />----- Original Message ----- From: "Terry S. Singeltary Sr." To: Sent: Saturday, January 13, 2007 1:51 PM Subject: January 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE<br /><br />CVM Update January 12, 2007<br /><br />January 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE<br /><br />To help prevent the establishment and amplification of BSE through feed in the United States, 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, called the Ruminant Feed Ban, became effective on August 4, 1997.<br /><br />The following information is an update on FDA enforcement activities regarding the ruminant feed ban. FDA's Center for Veterinary Medicine (CVM) has assembled data from the inspections that have been conducted and whose final inspection report has been recorded in the FDA's inspection database as of January 6, 2007. As of January 6, 2007, FDA had received over 50,000 inspection reports. The majority of these inspections (around 68%) were conducted by State feed safety officials, with the remainder conducted by FDA officials.<br /><br />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).<br /><br />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.<br /><br />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.<br /><br />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.<br /><br />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.<br /><br />RENDERERS<br /><br />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.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 271 Number of active firms handling materials prohibited from use in ruminant feed – 169 (62% of those active firms inspected) Of the 169 active firms handling prohibited materials, their most recent inspection revealed that: 1 firm (0.6%) was classified as OAI 2 firms (1.2%) were classified as VAI FEED MILLS NOT LICENSED BY FDA<br /><br />These feed mills are not licensed by the FDA to produce medicated feeds.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 5,211 Number of active firms handling materials prohibited from use in ruminant feed – 2,360 (45% of those active firms inspected) Of the 2,360 active firms handling prohibited materials, their most recent inspection revealed that: 3 firms (0.1%) were classified as OAI 48 firms (2.0%) were classified as VAI PROTEIN BLENDERS<br /><br />These firms blend rendered animal protein for the purpose of producing quality feed ingredients that will be used by feed mills.<br /><br />Number of active firms whose initial inspection has been reported to FDA -- 362 Number of active firms handling materials prohibited from use in ruminant feed – 187 (52% of those active firms inspected) Of the 187 active firms handling prohibited materials, their most recent inspection revealed that: 2 firms (1.1%) were classified as OAI 2 firms (1.1%) were classified as VAI RENDERERS, FEED MILLS, AND PROTEIN BLENDERS MANUFACTURING WITH PROHIBITED MATERIAL<br /><br />This category includes only those firms that actually use prohibited material to manufacture, process, or blend animal feed or feed ingredients.<br /><br />Total number of active renderers, feed mills, and protein blenders whose initial inspection has been reported to FDA – 6,636 Number of active renderers, feed mills, and protein blenders processing with prohibited materials – 497 (7.5%) Of the 497 active renderers, feed mills, and protein blenders processing with prohibited materials, their most recent inspection revealed that: 6 firms (1.2%) were classified as OAI 16 firms (3.2%) were classified as VAI OTHER FIRMS INSPECTED<br /><br />Examples of such firms include ruminant feeders, on-farm mixers, pet food manufacturers, animal feed salvagers, distributors, retailers, and animal feed transporters.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 16,653 Number of active firms handling materials prohibited from use in ruminant feed – 5,227 (31% of those active firms inspected) Of the 5,227 active firms handling prohibited materials, their most recent inspection revealed that: 4 firms (0.1%) were classified as OAI 178 firms (3.4%) were classified as VAI TOTAL FIRMS<br /><br />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.<br /><br />Number of active firms whose initial inspection has been reported to FDA – 19,492 Number of active firms handling materials prohibited from use in ruminant feed – 5,905 (30% of those active firms inspected) Of the 5,905 active firms handling prohibited materials, their most recent inspection revealed that: 7 firms (0.1%) were classified as OAI 188 firms (3.2%) were classified as VAI<br /><br />---------------------------------------------------------------------------- ----<br /><br />Issued by: FDA, Center for Veterinary Medicine, Communications Staff, HFV-12 7519 Standish Place, Rockville, MD 20855 Telephone: (240) 276-9300 FAX: (240) 276-9115 Internet Web Site: http://www.fda.gov/cvm<br /><br /><a href="http://www.fda.gov/cvm/CVM_Updates/BSE0107.htm">http://www.fda.gov/cvm/CVM_Updates/BSE0107.htm</a><br /><br /><br />[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle<br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a><br /><br /><br />[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)<br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf">http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf</a><br /><br /><br />THE SEVEN SCIENTIST REPORT ***<br /><br /><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf">http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf</a><br /><br /><br />USA BSE OIG 2006<br /><br /><a href="http://www.usda.gov/oig/webdocs/50601-10-KC.pdf">http://www.usda.gov/oig/webdocs/50601-10-KC.pdf</a><br /><br /><br />CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006<br /><br />The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.<br /><br />The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.<br /><br />These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.<br /><br />"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."<br /><br />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.<br /><br />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.<br /><br />"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end<br /><br /><a href="http://www.upi.com/">http://www.upi.com/</a><br /><br /><br />CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...<br /><br /><a href="http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm">http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm</a><br /><br /><br />PAUL BROWN M.D.<br /><br /><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf">http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf</a><br /><br /><br />9 December 2005 Division of Dockets Management (RFA-305)<br /><br />SEROLOGICALS CORPORATION James J. Kramer, Ph.D. Vice President, Corporate Operations<br /><br /><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf">http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf</a><br /><br /><br />Embassy of Japan<br /><br /><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm">http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm</a><br /><br /><br />Dockets Entered on December 22, 2005 2005D-0330, Guidance for Industry and FDA Review Staff on Collection of Platelets by Automated ... EC 203, McDonald's Restaurants Corporation, Vol #:, 34 ... http://www.fda.gov/ohrms/dockets/dailys/05/Dec05/122205/122205.htm<br /><br />03-025IF 03-025IF-631 Linda A. Detwiler [PDF] Page 1. 03-025IF 03-025IF-631 Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8. Page 9. Page 10. Page 11. Page 12. http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-631.pdf<br /><br />03-025IF 03-025IF-634 Linda A. Detwiler [PDF] Page 1. 03-025IF 03-025IF-634 Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8. http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-634.pdf<br /><br />Page 1 of 17 9/13/2005 [PDF] ... 2005 6:17 PM To: fsis.regulationscomments@fsis.usda.gov Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food ... http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf<br /><br />03-025IFA 03-025IFA-6 Jason Frost [PDF] ... Zealand Embassy COMMENTS ON FEDERAL REGISTER 9 CFR Parts 309 et al [Docket No. 03- 025IF] Prohibition of the Use of Specified Risk Materials for Human Food and ... http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-6.pdf<br /><br />In its opinion of 7-8 December 2000 (EC 2000), the SSC ... [PDF] Page 1. Linda A. Detwiler, DVM 225 Hwy 35 Red Bank, New Jersey 07701 Phone: 732-741-2290 Cell: 732-580-9391 Fax: 732-741-7751 June 22, 2005 FSIS Docket Clerk US ...<br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-589.pdf">http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-589.pdf</a><br /><br /><br />Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)<br /><br /><a href="https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument">https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument</a><br /><br /><br />Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA<br /><br /><a href="https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed">https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed</a><br /><br /><br />Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]<br /><br /><a href="http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt">http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt</a><br /><br /><br />Docket Management Docket: 02N-0273 - Substances Prohibited From Use in<br /><br />Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed<br /><br />Comment Number: EC -10<br /><br />Accepted - Volume 2<br /><br /><a href="http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html">http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html</a><br /><br /><br />PART 2<br /><br /><a href="http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html">http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html</a><br /><br /><br />18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.<br /><br />snip...<br /><br />4. Members had received information about the notification by the Health Protection Agency (HPA) of recipients of four batches of plasma products that had been produced from blood donated by individuals that had later developed variant Creutzfeldt Jakob Disease (vCJD). THESE batches HAD NOT been included in a similar notification exercise in 2004, as the fate of these products COULD NOT BE TRACED at that time. The fourteenth annual report of the National CJD Surveillance Unit had been published. The European Food Safety Authority (EFSA) had issued a consultation on a revised methodology for geographical bovine spongiform encephalopathy (BSE) risk assessment. Members could submit individual responses. Submission of a SEAC response was under consideration.<br /><br />snip...<br /><br />ITEM 9 - ANY OTHER BUSINESS<br /><br />snip...<br /><br />64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a mouse model it was possible to alleviate the pathological changes of prion disease by suppressing expression of the prion protein gene after infection.<br /><br /><a href="http://www.seac.gov.uk/minutes/95.pdf">http://www.seac.gov.uk/minutes/95.pdf</a><br /><br /><br />Terry S. Singeltary SR. P.O. Box 42 Bacliff, Texas USA 77518Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-1156281283875089492006-08-22T14:14:00.000-07:002009-11-16T17:34:34.981-08:00BSE News atypical BSE USA***UPDATE JANUARY 20, 2007<br /><br /><br />18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7<br />December 2006 are now available.<br /><br /><br /><br />snip...<br /><br />4. Members had received information about the notification by the Health Protection Agency (HPA) of recipients of four batches of plasma products that had been produced from blood donated by individuals that had later developed variant Creutzfeldt Jakob Disease (vCJD). THESE batches HAD NOT been included in a similar notification exercise in 2004, as the fate of these products COULD NOT BE TRACED at that time. The fourteenth annual report of the National CJD Surveillance Unit had been published. The European Food Safety Authority (EFSA) had issued a consultation on a revised methodology for geographical bovine spongiform encephalopathy (BSE) risk assessment. Members could submit individual responses. Submission of a SEAC response was under consideration.<br /><br />snip...<br /><br />ITEM 9 - ANY OTHER BUSINESS<br /><br />snip...<br /><br />64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a mouse model it was possible to alleviate the pathological changes of prion disease by suppressing expression of the prion protein gene after infection.<br /><br />http://www.seac.gov.uk/minutes/95.pdf<br /><br />TSS<br /><br />##################### Bovine Spongiform Encephalopathy #####################<br /><br />Subject: SEAC Draft minutes of the open session of the 93rd meeting held on 6th July 2006 (atypical BSE USA) Date: August 22, 2006 at 3:03 pm PST SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE<br /><br />Draft minutes of the open session of the 93rd meeting held on 6th July 2006<br /><br />snip...<br /><br />The Chair noted that recent reports described two cases of BSE in cattle in the United States of America (USA) as being similar to atypical cases of BSE found in a number of European countries. The Chair suggested that the term "atypical BSE", used in the USA report, is potentially confusing and that this would be discussed under any other business. Dr Danny Matthews (Veterinary Laboratories Agency [VLA]) explained that data from western blots of the USA cases resembled that of a small number of atypical cases of BSE in France. A study of the French cases had shown the condition to be transmissible to mice by intracerebral (ic) inoculation with the neuropathological phenotype maintained on transmission3. Claims have been made about the existence of atypical cases of BSE in other countries but these have yet to be confirmed. No study has yet examined the tissue distribution of abnormal prion protein (PrPSc) or infectivity in such atypical cases of BSE.<br /><br />3 Baron et al. (2006) Transmission of new bovine prion to mice. Emerging. Infect. Diseases. 12, 1125-1128.<br /><br />snip...<br /><br /><a href="http://www.seac.gov.uk/minutes/draft93.pdf">http://www.seac.gov.uk/minutes/draft93.pdf</a><br /><br /><br />However, based on analysis of molecular features of prion<br /><br />diseases in cattle, this situation is similar to that in humans<br /><br />(5), in which different subtypes of sporadic Creutzfeldt-<br /><br />Jakob disease agents are found.<br /><br />DISPATCHES<br /><br />1126 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 12, No. 7, July 2006<br /><br /><a href="http://www.cdc.gov/ncidod/EID/vol12no07/pdfs/vol12no07.pdf">http://www.cdc.gov/ncidod/EID/vol12no07/pdfs/vol12no07.pdf</a><br /><br /><br />Medical Sciences Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease<br /><br />Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco , and Maria Caramelli * *Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy<br /><br />Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)<br /><br />Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.<br /><br />--------------------------------------------------------------------------------<br /><br />C.C. and G.Z. contributed equally to this work.<br /><br />To whom correspondence should be addressed.<br /><br />E-mail: salvatore.monaco@mail.univr.it. www.pnas.org/cgi/doi/10.1073/pnas.0305777101<br /><br /><a href="http://www.pnas.org/cgi/content/abstract/0305777101v1">http://www.pnas.org/cgi/content/abstract/0305777101v1</a><br /><br /><br />PLEASE NOTE!<br /><br />SINCE spontaneous scrapie or CWD does not occur, then why is it that only BSE and sproadic CJD are capable of spontaneous mutation $$$<br /><br />confusious is confused again;-) ...TSS<br /><br />Science 24 September 2004: Vol. 305. no. 5692, pp. 1918 - 1921 DOI: 10.1126/science.1103581<br /><br />Perspectives BIOMEDICINE:<br /><br />A Fresh Look at BSE<br /><br />Bruce Chesebro*<br /><br />Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle form of a family of progressive brain diseases. These diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease (CWD) in deer and elk. They are also known as either "prion diseases" because of the association of a misfolded cellular prion protein in pathogenesis or "transmissible spongiform encephalopathies" (TSEs) because of the spongelike nature of the damaged brain tissue (1).<br /><br />The recent discovery of two BSE-infected cows, one in Canada and one in the United States, has dramatically increased concern in North America among meat producers and consumers alike over the extent to which BSE poses a threat to humans as well as to domestic and wild animals. The European BSE epidemic of the late-1980s seems to have been initiated a decade earlier in the United Kingdom by changes in the production of meat and bone meal (MBM) from rendered livestock, which led to contamination of MBM with the BSE infectious agent. Furthermore, the fact that UK farmers fed this rendered MBM to younger animals and that this MBM was distributed to many countries may have contributed to the ensuing BSE epidemic in the United Kingdom and internationally (2).<br /><br />Despite extensive knowledge about the spread of BSE through contaminated MBM, the source of BSE in Europe remains an unsolved mystery (2). It has been proposed that BSE could be derived from a cross-species infection, perhaps through contamination of MBM by scrapie-infected sheep tissues (see the figure). Alternatively, BSE may have been an endemic disease in cattle that went unnoticed because of its low level of horizontal transmission. Lastly, BSE might have originated by "spontaneous" misfolding of the normal cellular prion protein into the disease-associated abnormal isoform (3), which is postulated to be the infectious agent or "prion."<br /><br />Five possible sources of BSE in North American cattle. Sheep, deer, and elk could spread prion diseases (TSEs) to cattle through direct animal contact or contamination of pastures. Endemic BSE has not been proven to exist anywhere in the world, but it is difficult to exclude this possibility because of the inefficient spread of BSE infectivity between individual animals (2). BSE caused by spontaneous misfolding of the prion protein has not been proven. CREDIT: KATHARINE SUTLIFF/SCIENCE<br /><br />Spontaneous protein misfolding is not a new phenomenon as proteins are known to sometimes misfold after synthesis. Cells in turn have devised ingenious ways to deal with this problem. These include molecular chaperone proteins that bind to misfolded proteins and help them to unfold, and organelles called proteosomes that degrade misfolded or unwanted proteins. However, although misfolded prion proteins have been generated in test tubes as well as in cultured cells, it has been difficult to demonstrate that such misfolded abnormal prion proteins are infectious (4, 5). Even the most recent data do not prove conclusively that infectivity has been generated in vitro because misfolded synthetic prion proteins were not able to transfer disease directly to wild-type mice (6). To obtain infectivity and subsequent prion disease, the misfolded proteins had to be inoculated and incubated for 1 to 2 years in transgenic mice that overexpressed a mutant version of the prion protein. Previous data from this group showed that transgenic mice expressing high amounts of prion protein developed neurological disease without inoculation of misfolded prion protein (7). Thus, at the biochemical level, the critical attributes of the misfolded prion protein required for infectivity are not known, and misfolding of prion protein alone may not be sufficient to generate an infectious agent (8). Nevertheless, the idea that BSE might originate due to the spontaneous misfolding of prion proteins has received renewed interest in the wake of reports suggesting the occurrence of atypical BSE (9-11). These results imply that new strains of cattle BSE might have originated separately from the main UK outbreak. Where and how might such strains have originated? Although such rare events cannot be studied directly, any number of sources of the original BSE strain could also explain the discovery of additional BSE strains in cattle (see the figure). However, it would be worrisome if spontaneous BSE were really a valid etiology because such a mechanism would be impossible to prevent--unlike other possible scenarios that could be controlled by large-scale eradication of TSE-positive animals.<br /><br />Another way to look at this problem is to examine evidence for possible spontaneous TSE disease in other animals besides cattle. Spontaneous BSE would be extremely difficult to detect in cattle, where horizontal spread is minimal. However, in the case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at birth as well as between adults, spontaneous disease should be detectable as new foci of clinical infection. In the early 1950s scrapie was eradicated in both Australia and New Zealand, and the mainland of both these countries has remained scrapie-free ever since. This scrapie-free status is not the result of selection of sheep resistant to scrapie because sheep from New Zealand are as susceptible as their UK counterparts to experimental scrapie infection (12). These experiments of man and nature appear to indicate that spontaneous clinical scrapie does not occur in sheep. Similarly, because CWD is known to spread horizontally, the lack of CWD in the deer or elk of eastern North America but its presence in western regions would also argue against a spontaneous disease mechanism. This is particularly noteworthy in New Zealand, where there are large numbers of deer and elk farms and yet no evidence of spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer, this would suggest that spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are unlikely to be found in cattle or humans. The main caveat to this notion is that spontaneous disease may arise in some animal species but not others. In humans, sCJD--which is considered by some researchers to begin by spontaneous misfolding of the prion protein--usually takes more than 50 years to appear. Thus, in animals with a shorter life-span, such as sheep, deer, and cattle, an analogous disease mechanism might not have time to develop.<br /><br />What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? "Sporadic" pertains to the rarity of disease occurrence. "Spontaneous" pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE of unknown etiology--might be a better term to describe the origin of this malady.<br /><br />What does all this imply about testing cattle for BSE in North America? Current testing in the United States indicates that BSE is rare (one positive result in 40,000 cattle tested). However, additional testing of 200,000 head of slaughtered cattle over the next 1 to 2 years, as recently proposed by the U.S. Department of Agriculture (USDA), should tell us the incidence more precisely. Nevertheless, if any rare cases are detected, we may still not know their origin. If evidence arises of a focal occurrence of BSE, we might gain important insight into unexpected sources of contamination. However, because current tests do not seem to be able to detect BSE in infected animals less than 30 months of age, even more extensive testing will not completely guarantee the negative status of younger animals in the food chain. Therefore, the alternative option of testing all slaughtered cattle, as implemented in some countries such as Japan, would appear to provide little additional benefit. This fact has been acknowledged as the basis for a new agreement between the United States and Japan aimed at reestablishing the beef trade between the two countries.<br /><br />One problem with the current U.S. testing program was the announcement a few months ago of unconfirmed positive BSE tests in two additional North American animals that were subsequently found to be negative when tested with the more accurate method of Western blotting. The public release of information about unconfirmed positive tests detected by the rapid test used for mass screening may be a good idea in the interest of openness, but it has the potential to create unwarranted anxiety. If unconfirmed positives are a frequent occurrence, it would seem reasonable to follow a more cautious approach and wait until confirmatory testing is complete before publicly announcing the details.<br /><br />Based on the experience of many European countries, the mainstays of controlling BSE in cattle and avoiding spread to humans are threefold: first, eliminate feeding of ruminant tissues to ruminants; second, remove high-risk cattle tissues from human food; and third, continue to test for BSE in cattle in order to monitor progress with the elimination of the disease on a local and national basis. In the next 12 months, after extensive USDA test results are available, the extent of any possible BSE spread in the United States will be better documented. But, in fact, the United States and Canada have already instituted the most important steps to prevent the spread of cattle BSE in advance of the results--that is, a ban on feeding ruminant MBM to other ruminants and removal of high-risk tissues from meat for human consumption. It is hoped that the new data will not deviate enough from previous predictions to require further measures for management of this problem. The most important line of defense against any possible spread of BSE will be to maintain strict vigilance in the implementation of the current regulations.<br /><br />References<br /><br />S. B. Prusiner, Proc. Natl. Acad. Sci. U.S.A 95, 13363 (1998) [Medline]. P. G. Smith, R. Bradley, Br. Med. Bull. 66, 185 (2003) [Medline]. C. Weissmann, A. Aguzzi, Curr. Opin. Neurobiol. 7, 695 (1997) [Medline]. A. F. Hill et al., J. Gen. Virol. 80, 11 (1999) [Medline]. R. Chiesa et al., J. Virol. 77, 7611 (2003) [Medline]. G. Legname et al., Science 305, 673 (2004). D. Westaway et al., Cell 76, 117 (1994) [Medline]. B. Chesebro, Science 279, 42 (1998). A. G. Biacabe et al., EMBO Rep. 5, 110 (2004) [Medline]. Y. Yamakawa et al., Jpn. J. Infect. Dis. 56, 221 (2003) [Medline]. C. Casalone et al., Proc. Natl. Acad. Sci. U.S.A. 101, 3065 (2004) [Medline]. E. F. Houston et al., J. Gen. Virol. 83, 1247 (2002) [Medline].<br /><br /><a href="http://www.sciencemag.org/cgi/content/full/305/5692/1918">http://www.sciencemag.org/cgi/content/full/305/5692/1918</a><br /><br /><br />US atypical BSE – further details<br /><br />As reported in the last BSE Report (Which? BSE May 2006) French research findings<br /><br />concerning the two most recent cases of BSE in the USA suggest that these cases were<br /><br />not typical of BSE in cattle and may reflect a sporadic form of the disease.<br /><br />I<br /><br />n the two US cases, discovered in herds in Texas and Alabama, threre was an absence<br /><br />of telltale spongy lesions caused by prions. In addition, the prions in brain tissue<br /><br />samples from these cows seemed to be distributed differently from the classic form.<br /><br />Laboratory studies on mice in France showed that both the classic and atypical strains<br /><br />could be spread from one animal to another, but the atypical strain might happen<br /><br />spontaneously in cattle. The Texas and Alabama cows were older animals, as were<br /><br />some of the other animals in Europe with seemingly atypical forms of BSE.31<br /><br />Linda Detwiler, a former Agriculture Department veterinarian who consults for major<br /><br />food companies, cautioned against making that assumption. "I think it's kind of early to<br /><br />say that would be the case," Detwiler said. Other theories, she said, suggest the<br /><br />atypical strain might come from a mutation of BSE or even from a related disease in<br /><br />sheep.<br /><br />The US Agriculture Department has stated that whatever the cause there is no reason<br /><br />to change federal testing or control measures. "It's most important right now, till the<br /><br />science tells us otherwise, that we treat this as BSE regardless," the department's chief<br /><br />veterinarian, John Clifford, said in an interview. ...<br /><br /><a href="http://www.which.co.uk/files/application/pdf/bserep0606-445-89308.pdf">http://www.which.co.uk/files/application/pdf/bserep0606-445-89308.pdf</a><br /><br /><br />BSE, BOVINE - USA: ATYPICAL STRAIN (02) *************************************** A ProMED-mail post<br /><br />ProMED-mail is a program of the International Society for Infectious Diseases<br /><br />[1] Date: Tue 6 Jun 2006 From: Terry Singeltary Source: News.Farmpage.com [edited]<br /><br />USDA Confirms BSE Tests On U.S. Cows Found Identical To Atypical Cases In France ----------------------------------------------- A USDA official confirmed that the positive BSE tests in 2 U.S.-born cattle were indeed an "atypical" type of the disease.<br /><br />A USDA spokesman acknowledged Friday [2 Jun 2006] that positive BSE tests from 2 domestic-born cattle were from a rare strain of the disease found in a small number of European cases.<br /><br />BSE, scientifically known as bovine spongiform encephalopathy and commonly known as mad cow disease, is a degenerative, fatal disease affecting the central nervous system of adult cattle.<br /><br />USDA officials have declined in the past to provide such details, but released information Friday [2 Jun 2006] after a French researcher revealed earlier this week that the cases in Texas last year 2005 and Alabama last spring 2006 were identical to "atypical" cases of BSE found in France.<br /><br />Scientists from around the world are trying to quantify the significance of these rare cases. They also want to know whether these cases may be sporadic.<br /><br />In an e-mail, a USDA spokesman said the cases raise "many unanswered questions about these unusual findings, and additional research is needed to help characterize the significance -- or lack of significance -- of any of these findings."<br /><br />The USDA spokesperson said nothing in the test results of the 2 cattle justifies any changes in surveillance, disease control or public-health measures already being taken in the U.S.<br /><br />-- Terry Singeltary<br /><br />****** [2] Date: Tue 6 Jun 2006 From: Terry Singeltary Source: Farmers Weekly [edited]<br /><br />Cattle disease might be unknown strain of BSE ----------------------------------------------- Scientists across Europe and the United States are following the emergence of a new Transmissible Spongiform Encephalopathy (TSE) in cattle that could be a new strain of BSE.<br /><br />Speaking last weekend at an international conference on prion diseases in domestic livestock (such as BSE in cows and scrapie in sheep and goats), scientists from France and Italy described how the disease had been detected in a small number of cattle ranging from 5 to 15 years old.<br /><br />The strain differs from BSE in that it has a longer incubation time and is consequently being found in older cattle.<br /><br />The new strain also demonstrates different characteristics from BSE in laboratory tests and was originally detected through active surveillance of live animals rather than during inspection of a suspect fallen animal.<br /><br />Marion Simmons of the Veterinary Laboratory Agency at Weybridge urged caution, saying there are not yet sufficient supporting data to suggest that the disease is a new strain of BSE.<br /><br />-- Terry Singeltary<br /><br />[It has long been debated whether this atypical form is sporadic or whether the sporadic appearance was an atypical form. There does not seem to be a good explanation, which simply highlights the need for more research and understanding of this disease. - Mod.TG]<br /><br />[see also: BSE, bovine - USA: atypical strain 20060601.1525] ..........tg/msp/dk<br /><br />*##########################################################* ************************************************************ ProMED-mail makes every ************************************************************<br /><br />Visit ProMED-mail's web site at . Send all items for posting to: promed@promedmail.org (NOT to an individual moderator). If you do not give your full name and affiliation, it may not be posted. Send commands to subscribe/unsubscribe, get archives, help, etc. to: majordomo@promedmail.org. For assistance from a human being send mail to: <a href="mailto:owner-promed@promedmail.org">owner-promed@promedmail.org</a>.<br /><br />############################################################<br /><br />Order Code RS22345<br /><br />Updated July 18, 2006<br /><br />CRS REPORT FOR CONGRESS<br /><br />BSE (“Mad Cow Disease”): A Brief Overview<br /><br />Geoffrey S. Becker<br /><br />Specialist in Agricultural Policy<br /><br />Resources, Science, and Industry Division<br /><br />snip...<br /><br />1 This report, which replaces CRS Issue Brief IB10127, Mad Cow Disease: Agricultural Issues<br /><br />for Congress, summarizes and updates information in other CRS reports, listed on page 6.<br /><br />Sources for facts and citation to reports and studies can be found in these CRS reports.<br /><br />Congressional Research Service ˜ The Library of Congress<br /><br />CRS Report for Congress<br /><br />Received through the CRS Web<br /><br />Order Code RS22345<br /><br />Updated July 18, 2006<br /><br />BSE (“Mad Cow Disease”): A Brief Overview<br /><br />Geoffrey S. Becker<br /><br />Specialist in Agricultural Policy<br /><br />Resources, Science, and Industry Division<br /><br />Summary<br /><br />The appearance of BSE (bovine spongiform encephalopathy or “mad cow disease”)<br /><br />in North America in 2003 raised meat safety concerns and disrupted trade for cattle and<br /><br />beef producers. A major issue for Congress has been how to rebuild foreign confidence<br /><br />in the safety of U.S. beef and regain lost markets like Japan and Korea. Among other<br /><br />issues are whether additional measures are needed to further protect the public and cattle<br /><br />herd, and concerns over the relative costs and benefits of such measures for consumers,<br /><br />taxpayers and industry. This report will be updated if significant developments ensue.1<br /><br />What Is BSE?<br /><br />BSE (bovine spongiform encephalopathy or “mad cow disease”) is a fatal<br /><br />neurological disease of cattle, believed to be transmitted mainly by feeding infected cattle<br /><br />parts back to cattle. More than 187,000 cases have been reported worldwide, 183,000 of<br /><br />them in the United Kingdom (UK) where BSE was first identified in 1986. The annual<br /><br />number of new cases has declined steeply since 1992. Humans who eat contaminated<br /><br />beef are believed susceptible to a rare but fatal brain wasting disease, variant Creutzfeldt-<br /><br />Jakob disease (vCJD). About 160 people, most in the UK, have been diagnosed with<br /><br />vCJD since 1986, but none has been linked to any Canadian or U.S. meat consumption.<br /><br />BSE in North America<br /><br />BSE has been reported in 11 North American cattle, 10 born here and one imported<br /><br />from the UK. The first native case was an Alberta, Canada, beef cow reported in May<br /><br />2003. Canada has since reported six more cases, most recently in July 2006 in a 50-<br /><br />month-old dairy cow in Manitoba. The first U.S. case was in a Canadian-born dairy cow<br /><br />found in Washington state in December 2003. The other two U.S. cases were a 12-yearold<br /><br />Texas-born and -raised beef cow, found in November 2004 but not confirmed until<br /><br />June 2005, and a 10-year-old Alabama beef cow found in late February 2006.<br /><br />CRS-2<br /><br />In epidemiological investigations of the three U.S. cases, the U.S. Department of<br /><br />Agriculture (USDA) was unable to track down all related animals of interest, but those<br /><br />that were located tested negative for the disease. Despite a beef recall, some meat from<br /><br />the first U.S. BSE cow may have been consumed, USDA said, adding, however, that the<br /><br />highest-risk tissues never entered the food supply. No materials from the other two U.S.<br /><br />cows entered the food supply, USDA also said. In the recent Alabama case, authorities<br /><br />were unable to determine the cow’s herd of origin. Animal health officials initially<br /><br />indicated that all of the North American cases were caused by the consumption of BSEcontaminated<br /><br />feed. However, USDA reportedly now believes that the two native-born<br /><br />U.S. cattle had “atypical” BSE, which differs from other cases. If these cases are<br /><br />determined to be “spontaneous,” that may affect future control strategies.<br /><br />snip...<br /><br /><a href="http://ncseonline.org/NLE/CRSreports/06Jul/RS22345.pdf">http://ncseonline.org/NLE/CRSreports/06Jul/RS22345.pdf</a><br /><br /><br />Research Project: Study of Atypical Bse<br /><br />Location: Virus and Prion Diseases of Livestock<br /><br />Project Number: 3625-32000-073-07 Project Type: Specific C/A<br /><br />Start Date: Sep 15, 2004 End Date: Sep 14, 2007<br /><br />Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.<br /><br />Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.<br /><br /><a href="http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490">http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490</a><br /><br /><br />Research Project: Study of Atypical Bse<br /><br />Location: Virus and Prion Diseases of Livestock<br /><br />2005 Annual Report<br /><br />This report serves to document research conducted under a specific cooperative agreement between ARS and the Italian Reference Centre for Animal TSE (CEA) at the Istituto Zooprofilattico Sperimentale, Turin, Italy. Additional details of research can be found in then report for the parent project 3625-32000-073-00D, Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies. The aim of the cooperative research project conducted by the CEA and ARS is to compare the U.S. bovine spongiform encephalopathy (BSE) isolate and the bovine amyloidotic spongiform encephalopathy isolates (BASE) identified in Italy. The first objective was to determine whether diagnostic methods routinely used by USDA are able to identify the Italian BASE cases. For this purpose, CEA received the immunohistochemistry (IHC) protocol developed by APHIS-USDA. The IHC protocol was reproduced and standardized in the CEA laboratory and will be applied to the Italian BSE and BASE cases. Furthermore, fixed brainstem sections and frozen brainstem material from Italian BSE and BASE cases will be sent to ARS for analysis using USDA IHC and Western blot (WB) methods. These studies will enable us to determine whether the present diagnostic tools (IHC and WB) employed at the USDA will be able to detect the Italian BASE cases and also enable us to compare Italian BSE and BASE with the U.S. BSE cases.<br /><br /><a href="http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2005">http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2005</a><br /><br /><br />Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies<br /><br />Location: Virus and Prion Diseases of Livestock<br /><br />Title: Where We've Been and Where We're Going with Bse Testing in the United States<br /><br />Authors item Hall, Mark - NVSL-APHIS-USDA item Richt, Juergen item Davis, Arthur - NVSL-APHIS-USDA item Levings, Randall - NVSL-APHIS-USDA<br /><br />Submitted to: American Association of Veterinary Laboratory Diagnosticians Publication Type: Abstract Publication Acceptance Date: September 1, 2005 Publication Date: November 3, 2005 Citation: Hall, M.S., Richt, J.A., Davis, A.J., Levings, R.L. 2005. Where We've Been and Where We're Going with Bse Testing in the United States [abstract]. 48th Annual Meeting of the American Association of Veterinary Laboratory Diagnosticians. P. 20.<br /><br />Technical Abstract: A review of the laboratory aspects of the United States Department of Agriculture's (USDA) Bovine Spongiform Encephalopathy (BSE) Surveillance Program from its beginning to the present day will be provided. Validated diagnostic tests for BSE require brain tissue. There are no ante mortem (blood/serum) tests for BSE available at present. From a historical perspective, diagnostic tests for BSE continue to evolve. The original diagnostic test method was histopathology in which sections of brain were examined under a microscope, and the classical vacuoles and spongiform change in specific areas of the brain would allow a diagnosis to be made. This method was accurate but only allowed a diagnosis to be made relatively late in the course of the disease. In the mid-1990s, immunohistochemistry (IHC) and Western blotting were developed which allow the detection of the abnormal form of the prion protein (PrPSc) and a diagnosis could be made prior to the development of spongiform changes and clinical signs. In the past decade, so-called "rapid tests" have been introduced commercially for BSE. Five commercial tests are currently licensed/permitted in the United States for BSE. These licensed tests include the Prionics Western blot, Prionics ELISA, Enfer/Abbott ELISA, IDEXX ELISA, and the BioRad ELISA. This presentation will discuss various attributes of the validated test methods available today. Both IHC and Western blot are considered confirmatory tests for BSE by the World Organisation of Animal Health (OIE). IHC provides for a specific immunological detection of PrPSc and enables the specific anatomical location to be determined. Western blot provides both immunological detection of PrPSc as well as specific molecular weight characterizations; certain Western blot procedures can be extremely sensitive due to various concentration procedures before analysis of the sample. The OIE recommended Western blot and IHC methods for confirmatory diagnosis of BSE used by USDA and the Veterinary Laboratories Agency in Weybridge, England, will be discussed. The overall enhanced testing plan that has been used for the past 18 months will be described including changes that have occurred during this time. The USDA's BSE enhanced surveillance plan has been a very successful national surveillance testing program that has been a shared effort between state veterinary diagnostic laboratories as part of the National Animal Health Laboratory Network and the National Veterinary Services Laboratories.<br /><br /><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=183829">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=183829</a><br /><br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a><br /><br /><br />3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.<br /><br /><a href="http://www.bseinquiry.gov.uk/">http://www.bseinquiry.gov.uk/</a><br /><br /><br />The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33<br /><br /><a href="http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf">http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a><br /><br /><br /><a href="http://www.bseinquiry.gov.uk/">http://www.bseinquiry.gov.uk/</a><br /><br /><br />The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.<br /><br />3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988, 35 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988-89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA. 36 It was also felt that the results of such an experiment would be hard to interpret. While a negative result would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE. 37 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest. 38<br /><br /><a href="http://www.bseinquiry.gov.uk/">http://www.bseinquiry.gov.uk/</a><br /><br /><br />REPORT OF THE COMMITTEE ON SCRAPIE<br /><br />Chair: Dr. Jim Logan, Cheyenne, WY<br /><br />Vice Chair: Dr. Joe D. Ross, Sonora, TX<br /><br />Dr. Deborah L. Brennan, MS; Dr. Beth Carlson, ND; Dr. John R. Clifford, DC; Dr. Thomas F. Conner, OH; Dr. Walter E. Cook, WY; Dr. Wayne E. Cunningham, CO; Dr. Jerry W. Diemer, TX; Dr. Anita J. Edmondson, CA; Dr. Dee Ellis, TX; Dr. Lisa A. Ferguson, MD; Dr. Keith R. Forbes, NY; Dr. R. David Glauer, OH; Dr. James R. Grady, CO; Dr. William L. Hartmann, MN; Dr. Carolyn Inch, CAN; Dr. Susan J. Keller, ND; Dr. Allen M. Knowles, TN; Dr. Thomas F. Linfield, MT; Dr. Michael R. Marshall, UT; Dr. Cheryl A. Miller, In; Dr. Brian V. Noland, CO; Dr. Charles Palmer, CA; Dr. Kristine R. Petrini, MN; Mr. Stan Potratz, IA; Mr. Paul E. Rodgers, CO; Dr. Joan D. Rowe, CA; Dr. Pamela L. Smith, IA; Dr. Diane L. Sutton, MD; Dr. Lynn Anne Tesar, SD; Dr. Delwin D. Wilmot, NE; Dr. Nora E. Wineland, CO; Dr. Cindy B. Wolf, MN.<br /><br />The Committee met on November 9, 2005, from 8:00am until 11:55am, Hershey Lodge and Convention Center, Hershey, Pennsylvania. The meeting was called to order by Dr. Jim Logan, chair, with vice chairman Dr. Joe D. Ross attending. There were 74 people in attendance.<br /><br />The Scrapie Program Update was provided by Dr. Diane Sutton, National Scrapie Program Coordinator, United States Department of Agriculture (USDA), Animal and Plant Health Inspection Services (APHIS), Veterinary Services (VS). The complete text of the Status Report is included in these Proceedings.<br /><br />Dr. Patricia Meinhardt, USDA-APHIS-VS-National Veterinary Services Laboratory (NVSL) gave the Update on Genotyping Labs and Discrepancies in Results. NVSL conducts investigations into discrepancies on genotype testing results associated with the Scrapie Eradication Program. It is the policy of the Program to conduct a second genotype test at a second laboratory on certain individual animals. Occasionally, there are discrepancies in those results. The NVSL conducts follow-up on these situations through additional testing on additional samples from the field and archive samples from the testing laboratories.<br /><br />For the period of time from January 1, 2005, until October 15, 2005, there were 23 instances of discrepancies in results from 35 flocks. Of those 23 instances, 14 were caused by laboratory error (paperwork or sample mix-up), 3 results from field error, 5 were not completely resolved, and 1 originated from the use of a non-approved laboratory for the first test. As a result of inconsistencies, one laboratory’s certification was revoked by APHIS-VS.<br /><br />snip...<br /><br />Infected and Source Flocks<br /><br />As of September 30, 2005, there were 105 scrapie infected and source flocks. There were a total of 165** new infected and source flocks reported for FY 2005. The total infected and source flocks that have been released in FY 2005 was 128. The ratio of infected and source flocks cleaned up or placed on clean up plans vs. new infected and source flocks discovered in FY 2005 was 1.03 : 1*. In addition 622 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2005, of which 130 were RSSS cases. Fifteen cases of scrapie in goats have been reported since 1990. The last goat case was reported in May 2005. Approximately 5,626 animals were indemnified comprised of 49% non-registered sheep, 45% registered sheep, 1.4% non-registered goats and 4.6% registered goats.<br /><br />Regulatory Scrapie Slaughter Surveillance (RSSS)<br /><br />RSSS was designed to utilize the findings of the Center for Epidemiology and Animal Health (CEAH) Scrapie: Ovine Slaughter Surveillance (SOSS) study. The results of SOSS can be found at <a href="http://www.aphis.usda.gov/vs/ceah/cahm/Sheep/sheep.htm">http://www.aphis.usda.gov/vs/ceah/cahm/Sheep/sheep.htm</a><br />. RSSS started April 1,<br /><br />2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks for clean-up. During FY 2005 collections increased by 32% overall and by 90% for black and mottled faced sheep improving overall program effectiveness and efficiency as demonstrated by the 26% decrease in percent positive black faced sheep compared to FY 2004. Samples have been collected from 62,864 sheep since April 1, 2003, of which results have been reported for 59,105 of which 209 were confirmed positive. During FY 2005, 33,137 samples were collected from 81 plants. There have been 130 NVSL confirmed positive cases (30 collected in FY 2004 and confirmed in FY 2005 and 100 collected and confirmed in FY 2005) in FY 2005. Face colors of these positives were 114 black, 14 mottled, 1 white and 1 unknown. The percent positive by face color is shown in the chart below.<br /><br />Scrapie Testing<br /><br />In FY 2005, 35,845 animals have been tested for scrapie: 30,192 RSSS; 4,742 regulatory field cases; 772 regulatory third eyelid biopsies; 10 third eyelid validations; and 129 necropsy validations (chart 9).<br /><br />Animal ID<br /><br />As of October 04, 2005, 103,580 sheep and goat premises have been assigned identification numbers in the Scrapie National Generic Database. Official eartags have been issued to 73,807 of these premises.<br /><br />*This number based on an adjusted 12 month interval to accommodate the 60 day period for setting up flock plans.<br /><br /><a href="http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf">http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf</a><br /><br /><br />Published online before print October 20, 2005<br /><br />Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102 Medical Sciences<br /><br />A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes<br /><br />( sheep prion transgenic mice )<br /><br />Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *, Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte , Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude * *Virologie Immunologie Moléculaires and Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway<br /><br />Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)<br /><br />Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.<br /><br />--------------------------------------------------------------------------------<br /><br />Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B. contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data; and H.L. wrote the paper.<br /><br />A.L.D. and V.B. contributed equally to this work.<br /><br />To whom correspondence should be addressed.<br /><br />Hubert Laude, E-mail: laude@jouy.inra.fr<br /><br /><a href="http://www.pnas.org/cgi/doi/10.1073/pnas.0502296102">www.pnas.org/cgi/doi/10.1073/pnas.0502296102</a><br /><br /><br /><a href="http://www.pnas.org/cgi/content/abstract/0502296102v1">http://www.pnas.org/cgi/content/abstract/0502296102v1</a><br /><br /><br />12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY<br /><br />snip...<br /><br />A The Present Position with respect to Scrapie A] The Problem<br /><br />Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries.<br /><br />The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep.<br /><br />It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible.<br /><br />Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"<br /><br />Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.<br /><br />snip...<br /><br />76/10.12/4.6<br /><br /><a href="http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf">http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br /><br /><br />Subject: SCRAPIE and CWD USA UPDATE July 19, 2006 Date: July 19, 2006 at 12:06 pm PST SCRAPIE USA UPDATE MAY 31, 2006<br /><br />Infected and Source Flocks<br /><br />As of May 31, 2006, there were 93 scrapie infected and source flocks (Figure 3). There were 12 new infected and source flocks reported in May (Figure 4) with a total of 67 flocks reported for FY 2006 (Figure 5). The total infected and source flocks that have been released in FY 2006 are 53 (Figure 6), with 7 flocks released in May. The ratio of infected and source flocks released to newly infected and source flocks for FY 2006 = 0.79 : 1. In addition, as of May 31, 2006, 216 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 33 were RSSS cases (Figure 7). This includes 33 newly confirmed cases in May 2006 (Figure 8). Eighteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat case was reported in March 2006. New infected flocks, source flocks, and flocks released for FY 2006 are depicted in Chart 3. New infected and source statuses from 1997 to 2006 are depicted in Chart 4.<br /><br />snip...<br /><br />Scrapie Testing<br /><br />In FY 2006, 26,185 animals have been tested for scrapie : 22,634 RSSS*; 2063 regulatory field cases; 61 necropsy validations, 5 rectal biopsy and 1427 regulatory third eyelid biopsies (Chart 9). ...<br /><br />snip...END<br /><br /><a href="http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html">http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html</a><br /><br /><br />TSS<br /><br />#################### https://lists.aegee.org/bse-l.html ####################Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-30008838.post-1150851573990278902006-06-20T17:57:00.000-07:002009-11-16T17:02:09.824-08:00MAD COW FEED RECALL USA Albertville, AL -- June 16, 2006 -- H.J. Baker & Bro.Tuesday, June 20, 2006<br /><br /><br />MAD COW FEED RECALL USA Albertville, AL -- June 16, 2006 -- H.J. Baker & Bro.<br /><br />Subject: MAD COW FEED RECALL USA Albertville, AL -- June 16, 2006 -- H.J. Baker & Bro. Date: June 20, 2006 at 6:55 am PST MAD COW FEED RECALL USA Albertville, AL -- June 16, 2006 -- H.J. Baker & Bro.<br /><br />Recall -- Firm Press Release<br /><br />FDA posts press releases and other notices of recalls and market withdrawals from the firms involved as a service to consumers, the media, and other interested parties. FDA does not endorse either the product or the company. This listserv covers mainly Class I (life-threatening) recalls. A complete listing of recalls can be found in the FDA Enforcement Report at: http://www.fda.gov/opacom/Enforce.html<br /><br />HJ Baker and Bro., Inc. Announces National Recall of Three Animal Feed Products Containing Prohibited Ingredients Contact: Mark Hohnbaum 501-664-4870<br /><br />FOR IMMEDIATE RELEASE -- Albertville, AL -- June 16, 2006 -- H.J. Baker & Bro. has announced today that in cooperation with the US Food & Drug Administration (FDA) it has begun efforts to retrieve PRO-PAK WITH PORCINE MEAT AND BONE, PRO-LAK, AND PRO-AMINO II produced at its Albertville, AL facility. These products are used as an ingredient in the manufacturing of livestock feed, including feed for dairy animals. This action is being taken to address potential risk of unintentional contamination with ruminant derived protein that may have occurred at this facility from August 2005 to June 2006. Certain mammalian protein is prohibited for use in ruminant feed. These products were distributed in bulk or bags to feed manufacturers and dairy farms in Georgia, Kentucky, Michigan, Florida, Alabama, Tennessee, Mississippi, California, and Louisiana.<br /><br />If you have received any of these products, discontinue their use immediately. Quarantine the product so that it cannot be inadvertently used in the manufacture of feeds and contact the manufacturer at 501-664-4870 for further instructions.<br /><br />"All production and shipment of these products from the Albertville mill have ceased and all of our customers are being notified of the potential contamination. With the advice and support of the FDA, we were able to respond rapidly to address this matter," said Christopher Smith, President & CEO.<br /><br />H.J. Baker & Bro., Inc., headquartered in Westport, CT, has served the fertilizer and animal feed industries since the Company was founded in 1850.<br /><br />####<br /><br />FDA's Recalls, Market Withdrawals and Safety Alerts Page: <a href="http://www.fda.gov/opacom/7alerts.html">http://www.fda.gov/opacom/7alerts.html</a><br /><br /><br />lets see here now, we have mad cows in Alabama, we have mad cow feed in Alabama, however JUST another spontaneous event of more BSe. ...TSS<br /><br />#################### https://lists.aegee.org/bse-l.html ####################<br /><br />June 20, 2006, 5:13PM Feed Recalled Over Mad Cow Violation<br /><br />© 2006 The Associated Press<br /><br />WASHINGTON — Livestock feed ingredients shipped to nine states may have been contaminated with cattle remains in violation of a 1997 ban to protect against mad cow disease, a manufacturer said Tuesday.<br /><br />H.J. Baker & Bro. Inc. said it was recalling three livestock feed ingredients, including two used to supplement feed given to dairy cows. A sample tested by the Food and Drug Administration was positive for cattle meat and bone meal, said Mark Hohnbaum, president of the Westport, Conn.-based company's feed products group.<br /><br />"This is very concerning to us. This isn't something that happens to us. We are very serious about food safety," Hohnbaum said.<br /><br />Mad cow disease is only known to spread when cows eat feed containing brain and other nerve tissue from infected cattle. Protein from cattle was commonly added to cattle feed to speed growth until the ban largely outlawed the practice.<br /><br />Cattle tissue may have contaminated two feed ingredients given to dairy cows _ Pro-Lak and Pro-Amino II _ made by H.J. Baker between August 2005 and June. The third of the recalled ingredients, Pro-Pak with Porcine Meat and Bone, was mislabeled. It is used in poultry feed.<br /><br />The company announced the recall in the wake of ongoing FDA inspections of its Albertville, Ala. plant, Hohnbaum said. The inspections have found manufacturing and clerical issues, he added.<br /><br />The company shipped the ingredients to feed manufacturers and dairy farms in the following states: Alabama, California, Florida, Georgia, Kentucky, Louisiana, Michigan, Mississippi and Tennessee. The company is notifying its customers of the voluntary recall. It does not know how much of the feed ingredients it sold, Hohnbaum said.<br /><br />___<br /><br />On the Net:<br /><br />Food and Drug Administration animal feed information:<br /><br /><a href="http://www.fda.gov/cvm/animalfeed.htm">http://www.fda.gov/cvm/animalfeed.htm</a><br /><br /><br /><a href="http://www.chron.com/disp/story.mpl/ap/fn/3987413.html">http://www.chron.com/disp/story.mpl/ap/fn/3987413.html</a><br /><br /><br />Subject: USDA, SPONTANEOUS MAD COW DISEASE, THE TOOTH FAIRY AND SANTA CLAUS<br /><br />Date: June 12, 2006 at 5:18 am PST<br /><br />IF we all believe the BSe that the USDA is trying to put out now about atypical BSE in USA cattle just arising spontaneously, then we all should believe in the tooth fairy and santa claus as well.<br /><br />IF USA scrapie transmitted to USA cattle long ago in experiments in a lab in Mission Texas did not produce UK BSE, but something very different, then why would USA TSE cattle produce the UK human version of mad cow i.e. nvCJD? IT wouldn't. USA sporadic cjd is increasing, the USA also has atypical human cases of unknown origin as well?<br /><br />THERE are over 20 strains of scrapie, plus the atypical in sheep, and these strains are increasing in numbers.<br /><br />SCRAPIE, CWD, AND TSE IN CATTLE i.e. ANIMAL TSE RAMPANT IN USA FOR DECADES, and amplified via rendering and feeding practices, where USDA triple firewalls against BSE were nothing more than a mere smoke screen.<br /><br />NO test tube TSE by either Prusiner or Soto, to date, have ever produced a TSE identical to the sporadic CJD. IN fact, no test tube TSE has ever been produced that resembles _any_ natural field TSE.<br /><br />IF you feed BSE tainted materials to cattle and primate, you have BSE and nvCJD. IF you feed USA sheep strain to USA cattle, you get USA TSE. IF you feed USA tainted cattle to humans, you get USA mad cow disease. IF you feed sporadic CJD to primate you get a CJD infected primate. NOTHING spontaneous about it at all.<br /><br />USA is in a very unique situation. there are more documented TSE in different species than any other country, all of which have been rendered and fed back to animals for human and animal consumption, for decades. Millions exposed, and of these Millions, how many surgical and dental procedures have been done on these exposed, to pass on to others, via the 'friendly fire' mode of transmission?<br /><br />IF, the spontaneous TSE was true, then this would be Prusiner and everyone else that is trying to cash in on this agent with there TSE rapid test, this would be there dream come true. IT would require mandatory BSE/TSE testing of all species, due to the fact you could not ever eradicate it through any intervention. BUT, then again, the spontaneous TSE is like believing in the tooth fairy or santa claus will be arriving at your house this year.<br /><br />How long can this sharade continue $<br /><br />How many more will become exposed and have to die $<br /><br />Medical Sciences Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease<br /><br />Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco , and Maria Caramelli * *Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy<br /><br />Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)<br /><br />Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.<br /><br />--------------------------------------------------------------------------------<br /><br />C.C. and G.Z. contributed equally to this work.<br /><br />To whom correspondence should be addressed.<br /><br />E-mail: salvatore.monaco@mail.univr.it. www.pnas.org/cgi/doi/10.1073/pnas.0305777101<br /><br /><a href="http://www.pnas.org/cgi/content/abstract/0305777101v1">http://www.pnas.org/cgi/content/abstract/0305777101v1</a><br /><br /><br />: J Infect Dis 1980 Aug;142(2):205-8<br /><br />Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.<br /><br />Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.<br /><br />Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.<br /><br />PMID: 6997404<br /><br /><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br /><br /><br />Atypical cases of TSE in cases of TSE in cattle and sheep cattle and sheep H. De H. De Bosschere Bosschere CODA/CERVA CODA/CERVA Nat. Ref. Lab. Vet. Nat. Ref. Lab. Vet. TSEs TSEs Belgium<br /><br /><a href="http://www.var.fgov.be/pdf/1100_TSEDAY.pdf">http://www.var.fgov.be/pdf/1100_TSEDAY.pdf</a><br /><br /><br />USDA 2004 ENHANCED BSE SURVEILLANCE PROGRAM AND HOW NOT TO FIND BSE CASES (OFFICIAL DRAFT OIG REPORT)<br /><br />snip...<br /><br />CATTLE With CNS Symptoms Were NOT Always Tested<br /><br />snip...<br /><br />Between FYs 2002 and 2004, FSIS condemned 680 cattle of all ages due to CNS symptoms. About 357 of these could be classified as adult. We could validate that ONLY 162 were tested for BSE (per APHIS records. ...<br /><br />snip...<br /><br />WE interviewed officials at five laboratories that test for rabies. Those officials CONFIRMED THEY ARE NOT REQUIRED TO SUBMIT RABIES-NEGATIVE SAMPLES TO APHIS FOR BSE TESTING. A South Dakota laboratory official said they were not aware they could submit rabies-negative samples to APHIS for BSE testing. A laboratory official in another State said all rabies-negative cases were not submitted to APHIS because BSE was ''NOT ON THEIR RADAR SCREEN." Officials from New York, Wisconsin, TEXAS, and Iowa advised they would NOT submit samples from animals they consider too young. Four of the five States contacted defined this age as 24 months; Wisconsin defined it as 30 months. TEXAS officials also advised that they do not always have sufficient tissue remaining to submit a BSE sample. ...<br /><br />snip...<br /><br />FULL TEXT 54 PAGES OF HOW NOT TO FIND BSE IN USA ;<br /><br /><a href="http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_july_13_ig_rep.pdf">http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_july_13_ig_rep.pdf</a><br /><br /><br />HUMAN TSE USA 2005<br /><br />Animal Prion Diseases Relevant to Humans (unknown types?) Thu Oct 27, 2005 12:05 71.248.128.109<br /><br />About Human Prion Diseases / Animal Prion Diseases Relevant to Humans<br /><br />Bovine Spongiform Encephalopathy (BSE) is a prion disease of cattle. Since 1986, when BSE was recognized, over 180,000 cattle in the UK have developed the disease, and approximately one to three million are likely to have been infected with the BSE agent, most of which were slaughtered for human consumption before developing signs of the disease. The origin of the first case of BSE is unknown, but the epidemic was caused by the recycling of processed waste parts of cattle, some of which were infected with the BSE agent and given to other cattle in feed. Control measures have resulted in the consistent decline of the epidemic in the UK since 1992. Infected cattle and feed exported from the UK have resulted in smaller epidemics in other European countries, where control measures were applied later.<br /><br />Compelling evidence indicates that BSE can be transmitted to humans through the consumption of prion contaminated meat. BSE-infected individuals eventually develop vCJD with an incubation time believed to be on average 10 years. As of November 2004, three cases of BSE have been reported in North America. One had been imported to Canada from the UK, one was grown in Canada, and one discovered in the USA but of Canadian origin. There has been only one case of vCJD reported in the USA, but the patient most likely acquired the disease in the United Kingdom. If current control measures intended to protect public and animal health are well enforced, the cattle epidemic should be largely under control and any remaining risk to humans through beef consumption should be very small. (For more details see Smith et al. British Medical Bulletin, 66: 185. 2003.)<br /><br />Chronic Wasting Disease (CWD) is a prion disease of elk and deer, both free range and in captivity. CWD is endemic in areas of Colorado, Wyoming, and Nebraska, but new foci of this disease have been detected in Nebraska, South Dakota, New Mexico, Wisconsin, Mississippi Kansas, Oklahoma, Minnesota, Montana, and Canada. Since there are an estimated 22 million elk and deer in the USA and a large number of hunters who consume elk and deer meat, there is the possibility that CWD can be transmitted from elk and deer to humans. As of November 2004, the NPDPSC has examined 26 hunters with a suspected prion disease. However, all of them appeared to have either typical sporadic or familial forms of the disease. The NPDPSC coordinates with the Centers for Disease Control and state health departments to monitor cases from CWD-endemic areas. Furthermore, it is doing experimental research on CWD transmissibility using animal models. (For details see Sigurdson et al. British Medical Bulletin. 66: 199. 2003 and Belay et al. Emerging Infectious Diseases. 10(6): 977. 2004.)<br /><br /><a href="http://www.cjdsurveillance.com/abouthpd-animal.html">http://www.cjdsurveillance.com/abouthpd-animal.html</a><br /><br /><br />SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is with a human TSE surveillance system that is terrible flawed. in 1997 cases of the _reported_ cases of cjd were at 54, to 163 _reported_ cases in 2004. see stats here;<br /><br />p.s. please note the 47 PENDING CASES to Sept. 2005<br /><br />p.s. please note the 2005 Prion D. total 120(8) 8=includes 51 type pending, 1 TYPE UNKNOWN ???<br /><br />p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???<br /><br />p.s. please note 2004 prion disease (6) 6=7 TYPE UNKNOWN???<br /><br />http://www.cjdsurveillance.com/resources-casereport.html<br /><br />CWD TO HUMANS = sCJD ???<br /><br />AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.<br /><br />snip...<br /><br /><a href="http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf">http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf</a><br /><br /><br />snip...end full text ;<br /><br /><a href="http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf">http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a><br /><br /><br />VERY VERY IMPORTANT THING TO REMEMBER<br /><br />Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.<br /><br />Research Project: Study of Atypical Bse<br /><br />Location: Virus and Prion Diseases of Livestock<br /><br />Project Number: 3625-32000-073-07 Project Type: Specific C/A<br /><br />Start Date: Sep 15, 2004 End Date: Sep 14, 2007<br /><br />Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.<br /><br />Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.<br /><br /><a href="http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490">http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490</a><br /><br /><br />3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.<br /><br /><a href="http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820543">http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820543</a><br /><br /><br />The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33<br /><br /><a href="http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf">http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a><br /><br /><br /><a href="http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546">http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546</a><br /><br /><br />The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.<br /><br />3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988, 35 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988-89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA. 36 It was also felt that the results of such an experiment would be hard to interpret. While a negative result would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE. 37 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest. 38<br /><br /><a href="http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820550">http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820550</a><br /><br /><br /><a href="http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm">http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm</a><br /><br /><br />REPORT OF THE COMMITTEE ON SCRAPIE<br /><br /><br />Chair: Dr. Jim Logan, Cheyenne, WY<br /><br />Vice Chair: Dr. Joe D. Ross, Sonora, TX<br /><br />Dr. Deborah L. Brennan, MS; Dr. Beth Carlson, ND; Dr. John R. Clifford, DC; Dr. Thomas F. Conner, OH; Dr. Walter E. Cook, WY; Dr. Wayne E. Cunningham, CO; Dr. Jerry W. Diemer, TX; Dr. Anita J. Edmondson, CA; Dr. Dee Ellis, TX; Dr. Lisa A. Ferguson, MD; Dr. Keith R. Forbes, NY; Dr. R. David Glauer, OH; Dr. James R. Grady, CO; Dr. William L. Hartmann, MN; Dr. Carolyn Inch, CAN; Dr. Susan J. Keller, ND; Dr. Allen M. Knowles, TN; Dr. Thomas F. Linfield, MT; Dr. Michael R. Marshall, UT; Dr. Cheryl A. Miller, In; Dr. Brian V. Noland, CO; Dr. Charles Palmer, CA; Dr. Kristine R. Petrini, MN; Mr. Stan Potratz, IA; Mr. Paul E. Rodgers, CO; Dr. Joan D. Rowe, CA; Dr. Pamela L. Smith, IA; Dr. Diane L. Sutton, MD; Dr. Lynn Anne Tesar, SD; Dr. Delwin D. Wilmot, NE; Dr. Nora E. Wineland, CO; Dr. Cindy B. Wolf, MN.<br /><br />The Committee met on November 9, 2005, from 8:00am until 11:55am, Hershey Lodge and Convention Center, Hershey, Pennsylvania. The meeting was called to order by Dr. Jim Logan, chair, with vice chairman Dr. Joe D. Ross attending. There were 74 people in attendance.<br /><br />The Scrapie Program Update was provided by Dr. Diane Sutton, National Scrapie Program Coordinator, United States Department of Agriculture (USDA), Animal and Plant Health Inspection Services (APHIS), Veterinary Services (VS). The complete text of the Status Report is included in these Proceedings.<br /><br />Dr. Patricia Meinhardt, USDA-APHIS-VS-National Veterinary Services Laboratory (NVSL) gave the Update on Genotyping Labs and Discrepancies in Results. NVSL conducts investigations into discrepancies on genotype testing results associated with the Scrapie Eradication Program. It is the policy of the Program to conduct a second genotype test at a second laboratory on certain individual animals. Occasionally, there are discrepancies in those results. The NVSL conducts follow-up on these situations through additional testing on additional samples from the field and archive samples from the testing laboratories.<br /><br />For the period of time from January 1, 2005, until October 15, 2005, there were 23 instances of discrepancies in results from 35 flocks. Of those 23 instances, 14 were caused by laboratory error (paperwork or sample mix-up), 3 results from field error, 5 were not completely resolved, and 1 originated from the use of a non-approved laboratory for the first test. As a result of inconsistencies, one laboratory’s certification was revoked by APHIS-VS.<br /><br />snip...<br /><br />Infected and Source Flocks<br /><br />As of September 30, 2005, there were 105 scrapie infected and source flocks. There were a total of 165** new infected and source flocks reported for FY 2005. The total infected and source flocks that have been released in FY 2005 was 128. The ratio of infected and source flocks cleaned up or placed on clean up plans vs. new infected and source flocks discovered in FY 2005 was 1.03 : 1*. In addition 622 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2005, of which 130 were RSSS cases. Fifteen cases of scrapie in goats have been reported since 1990. The last goat case was reported in May 2005. Approximately 5,626 animals were indemnified comprised of 49% non-registered sheep, 45% registered sheep, 1.4% non-registered goats and 4.6% registered goats.<br /><br />Regulatory Scrapie Slaughter Surveillance (RSSS)<br /><br />RSSS was designed to utilize the findings of the Center for Epidemiology and Animal Health (CEAH) Scrapie: Ovine Slaughter Surveillance (SOSS) study. The results of SOSS can be found at http://www.aphis.usda.gov/vs/ceah/cahm/Sheep/sheep.htm . RSSS started April 1,<br /><br />2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks for clean-up. During FY 2005 collections increased by 32% overall and by 90% for black and mottled faced sheep improving overall program effectiveness and efficiency as demonstrated by the 26% decrease in percent positive black faced sheep compared to FY 2004. Samples have been collected from 62,864 sheep since April 1, 2003, of which results have been reported for 59,105 of which 209 were confirmed positive. During FY 2005, 33,137 samples were collected from 81 plants. There have been 130 NVSL confirmed positive cases (30 collected in FY 2004 and confirmed in FY 2005 and 100 collected and confirmed in FY 2005) in FY 2005. Face colors of these positives were 114 black, 14 mottled, 1 white and 1 unknown. The percent positive by face color is shown in the chart below.<br /><br />Scrapie Testing<br /><br />In FY 2005, 35,845 animals have been tested for scrapie: 30,192 RSSS; 4,742 regulatory field cases; 772 regulatory third eyelid biopsies; 10 third eyelid validations; and 129 necropsy validations (chart 9).<br /><br />Animal ID<br /><br />As of October 04, 2005, 103,580 sheep and goat premises have been assigned identification numbers in the Scrapie National Generic Database. Official eartags have been issued to 73,807 of these premises.<br /><br />*This number based on an adjusted 12 month interval to accommodate the 60 day period for setting up flock plans.<br /><br /><a href="http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf">http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf</a><br /><br /><br />Date: April 30, 2006 at 4:49 pm PST SCRAPIE USA UPDATE AS of March 31, 2006<br /><br />2 NEW CASES IN GOAT, 82 INFECTED SOURCE FLOCKS, WITH 4 NEW INFECTED SOURCE FLOCKS IN MARCH, WITH 19 SCRAPIE INFECTED RSSS REPORTED BY NVSL<br /><br /><a href="http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html">http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html</a><br /><br /><br />Published online before print October 20, 2005<br /><br />Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102 Medical Sciences<br /><br />A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes<br /><br />( sheep prion transgenic mice )<br /><br />Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *, Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte , Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude * *Virologie Immunologie Moléculaires and Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway<br /><br />Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)<br /><br />Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.<br /><br />--------------------------------------------------------------------------------<br /><br />Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B. contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data; and H.L. wrote the paper.<br /><br />A.L.D. and V.B. contributed equally to this work.<br /><br />To whom correspondence should be addressed.<br /><br />Hubert Laude, E-mail: laude@jouy.inra.fr<br /><br /><a href="http://www.pnas.org/cgi/doi/10.1073/pnas.0502296102">www.pnas.org/cgi/doi/10.1073/pnas.0502296102</a><br /><br /><br /><a href="http://www.pnas.org/cgi/content/abstract/0502296102v1">http://www.pnas.org/cgi/content/abstract/0502296102v1</a><br /><br /><br />12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY<br /><br />snip...<br /><br />A The Present Position with respect to Scrapie A] The Problem<br /><br />Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries.<br /><br />The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep.<br /><br />It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible.<br /><br />Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"<br /><br />Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.<br /><br />snip...<br /><br />76/10.12/4.6<br /><br /><a href="http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf">http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br /><br /><br />Like lambs to the slaughter 31 March 2001 Debora MacKenzie Magazine issue 2284<br /><br />What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie? FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.<br /><br />Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.<br /><br />Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in ...<br /><br />The complete article is 889 words long.<br /><br />full text;<br /><br /><a href="http://www.newscientist.com/article.ns?id=mg16922840.300">http://www.newscientist.com/article.ns?id=mg16922840.300</a><br /><br /><br />Neurobiology Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt- Jakob disease: Implications for human health<br /><br /><br />Corinne Ida Lasmézas*,, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp, Jean-Jacques Hauw§, James Ironside¶, Moira Bruce, Dominique Dormont*, and Jean-Philippe Deslys* * Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction des Sciences du Vivant/Département de Recherche Medicale, Centre de Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; § Laboratoire de Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital, 75013 Paris, France; ¶ Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and Institute for Animal Health, Neuropathogenesis Unit, West Mains Road, Edinburgh EH9 3JF, United Kingdom<br /><br />Edited by D. Carleton Gajdusek, Centre National de la Recherche Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000 (received for review October 16, 2000)<br /><br />Abstract<br /><br />There is substantial scientific evidence to support the notion that bovine spongiform encephalopathy (BSE) has contaminated human beings, causing variant Creutzfeldt-Jakob disease (vCJD). This disease has raised concerns about the possibility of an iatrogenic secondary transmission to humans, because the biological properties of the primate-adapted BSE agent are unknown. We show that (i) BSE can be transmitted from primate to primate by intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD to humans could be readily recognized pathologically, whether it occurs by the central or peripheral route. Strain typing in mice demonstrates that the BSE agent adapts to macaques in the same way as it does to humans and confirms that the BSE agent is responsible for vCJD not only in the United Kingdom but also in France. The agent responsible for French iatrogenic growth hormone-linked CJD taken as a control is very different from vCJD but is similar to that found in one case of sporadic CJD and one sheep scrapie isolate. These data will be key in identifying the origin of human cases of prion disease, including accidental vCJD transmission, and could provide bases for vCJD risk assessment.<br /><br /><a href="http://www.pnas.org/cgi/content/full/041490898v1">http://www.pnas.org/cgi/content/full/041490898v1</a><br /><br /><br />USDA CWD PROGRAM<br /><br /><a href="http://www.aphis.usda.gov/vs/nahps/cwd/">http://www.aphis.usda.gov/vs/nahps/cwd/</a><br /><br /><br />USDA CWD MAP (slow to update)<br /><br /><a href="http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html">http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html</a><br /><br /><br />DRAFT<br /><br />WYOMING GAME AND FISH DEPARTMENT<br /><br />CHRONIC WASTING DISEASE MANAGEMENT PLAN<br /><br />February 17, 2006<br /><br />snip...<br /><br />5. Predicted population effects on free-ranging elk based on captive elk chronically exposed to the CWD prion. Forty-three female elk calves were trapped at the National Elk Refuge and transported to Sybille in February 2002. Elk were housed in pens, assumed to be environmentally contaminated with the CWD prion. Elk will be held throughout their lifetimes. Elk dying will be examined and cause of death determined. From these data, it will should be possible to model free-ranging elk mortality and population dynamics under extreme circumstances of CWD prion exposure and transmission. As of December 2005 (46 months post capture), 11 of 43 elk have died due to CWD. This compares to 100% mortality in less than 25 months in elk orally inoculated with different dosages of the CWD prion.<br /><br />REVISED DRAFT<br /><br /><a href="http://gf.state.wy.us/downloads/pdf/CWD2005reviseddraft.pdf">http://gf.state.wy.us/downloads/pdf/CWD2005reviseddraft.pdf</a><br /><br /><br />Prions in Skeletal Muscles of Deer with Chronic Wasting Disease<br /><br />Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J. Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§<br /><br />1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA.<br /><br />*These authors contributed equally to this work.<br /><br />†Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA.<br /><br />‡Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland.<br /><br />§To whom correspondence should be addressed: E-mail: gtell2@uky.edu<br /><br />Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD.<br /><br />To test whether skeletal muscle of diseased cervids contained prion infectivity, Tg(CerPrP)1536 mice (2) expressing cervid prion protein (CerPrP), were inoculated intracerebrally with extracts prepared from the semitendinosus/semimembranosus muscle group of CWD-affected mule deer or from CWD-negative deer. The availability of CNS materials also afforded direct comparisons of prion infectivity in skeletal muscle and brain. All skeletal muscle extracts from CWD-affected deer induced progressive neurological dysfunction in Tg(CerPrP)1536 mice with mean incubation times ranging between 360 and ~490 d, whereas the incubation times of prions from the CNS ranged from ~230 to 280 d (Table 1). For each inoculation group, the diagnosis of prion disease was confirmed by the presence of PrPSc in the brains of multiple infected Tg(CerPrP)1536 mice (see supporting online material for examples). In contrast, skeletal muscle and brain material from CWD-negative deer failed to induce disease in Tg(CerPrP)1536 mice (Table 1) and PrPSc was not detected in the brains of sacrificed asymptomatic mice as late as 523 d after inoculation (supporting online material).<br /><br />Our results show that skeletal muscle as well as CNS tissue of deer with CWD contains infectious prions. Similar analyses of skeletal muscle BSE-affected cattle did not reveal high levels of prion infectivity (3). It will be important to assess the cellular location of PrPSc in muscle. Notably, while PrPSc has been detected in muscles of scrapie-affected sheep (4), previous studies failed to detect PrPSc by immunohistochemical analysis of skeletal muscle from deer with natural or experimental CWD (5, 6). Since the time of disease onset is inversely proportional to prion dose (7), the longer incubation times of prions from skeletal muscle extracts compared to matched brain samples indicated that prion titers were lower in muscle than in CNS where infectivity titers are known to reach high levels. Although possible effects of CWD strains or strain mixtures on these incubation times cannot be excluded, the variable 360 to ~490 d incubation times suggested a range of prion titers in skeletal muscles of CWD-affected deer. Muscle prion titers at the high end of the range produced the fastest incubation times that were ~30% longer than the incubation times of prions from the CNS of the same animal. Since all mice in each inoculation group developed disease, prion titers in muscle samples producing the longest incubation times were higher than the end point of the bioassay, defined as the infectious dose at which half the inoculated mice develop disease. Studies are in progress to accurately assess prion titers.<br /><br />While the risk of exposure to CWD infectivity following consumption of prions in muscle is mitigated by relatively inefficient prion transmission via the oral route (8), these<br /><br />results show that semitendinosus/semimembranosus muscle, which is likely to be consumed by humans, is a significant source of prion infectivity. Humans consuming or handling meat from CWD-infected deer are therefore at risk to prion exposure.<br /><br />References and Notes<br /><br />1. P. J. Bosque et al., Proc. Natl. Acad. Sci. U.S.A. 99, 3812 (2002).<br /><br />2. S. R. Browning et al., J. Virol. 78, 13345 (2004).<br /><br />3. A. Buschmann, M. H. Groschup, J. Infect. Dis. 192, 934 (2005).<br /><br />4. O. Andreoletti et al., Nat. Med. 10, 591 (2004).<br /><br />5. T. R. Spraker et al., Vet. Pathol. 39, 110 (2002).<br /><br />6. A. N. Hamir, J. M. Miller, R. C. Cutlip, Vet. Pathol. 41, 78 (2004).<br /><br />7. S. B. Prusiner et al., Biochemistry 21, 4883 (1980).<br /><br />8. M. Prinz et al., Am. J. Pathol. 162, 1103 (2003).<br /><br />9. This work was supported by grants from the U.S. Public Health Service 2RO1 NS040334-04 from the National Institute of Neurological Disorders and Stroke and N01-AI-25491 from the National Institute of Allergy and Infectious Diseases.<br /><br />Supporting Online Material<br /><br />www.sciencemag.org/<br /><br />Materials and Methods<br /><br />Fig. S1<br /><br />21 November 2005; accepted 13 January 2006 Published online 26 January 2006; 10.1126/science.1122864 Include this information when citing this paper.<br /><br />Table 1. Incubation times following inoculation of Tg(CerPrP)1536 mice with prions from skeletal muscle and brain samples of CWD-affected deer.<br /><br />Inocula Incubation time, mean d ± SEM (n/n0)*<br /><br />Skeletal muscle Brain<br /><br />CWD-affected deer<br /><br />H92 360 ± 2 d (6/6) 283 ± 7 d (6/6)<br /><br />33968 367 ± 9 d (8/8) 278 ± 11 d (6/6)<br /><br />5941 427 ± 18 d (7/7)<br /><br />D10 483 ± 8 d (8/8) 231 ± 17 d (7/7)<br /><br />D08 492 ± 4 d (7/7)<br /><br />Averages 426 d 264 d<br /><br />Non-diseased deer<br /><br />FPS 6.98 >523 d (0/6)<br /><br />FPS 9.98 >454 d (0/7) >454 d (0/6)<br /><br />None >490 d (0/6)<br /><br />PBS >589 d (0/5)<br /><br />*The number of mice developing prion disease divided by the original number of inoculated mice is shown in parentheses. Mice dying of intercurrent illnesses were excluded.<br /><br /><a href="http://www.sciencemag.org/">http://www.sciencemag.org/</a><br /><br /><br /><a href="http://www.sciencemag.org/">www.sciencemag.org/</a><br /><br /><br />Supporting Online Material for<br /><br />Prions in Skeletal Muscles of Deer with Chronic Wasting Disease<br /><br />Rachel C. Angers, Shawn R. Browning, Tanya S. Seward, Christina J. Sigurdson,<br /><br />Michael W. Miller, Edward A. Hoover, Glenn C. Telling§<br /><br />§To whom correspondence should be addressed: E-mail: gtell2@uky.edu<br /><br />Published 26 January 2006 on Science Express<br /><br />DOI: 10.1126/science.1122864<br /><br />This PDF file includes:<br /><br />Materials and Methods<br /><br />Fig. S1<br /><br />Supporting Online Materials<br /><br />Materials and Methods<br /><br />Homogenates of semitendinosus/semimembranosus muscle (10% w/v in phosphate<br /><br />buffered saline) were prepared from five emaciated and somnolent mule deer, naturally<br /><br />infected with CWD at the Colorado Division of Wildlife, Wildlife Research Center.<br /><br />These deer were identified as D10, D08, 33968, H92, and 5941. CWD infection was<br /><br />confirmed in all cases by the presence of histologic lesions in the brain including<br /><br />spongiform degeneration of the perikaryon, the immunohistochemical detection of<br /><br />disease-associated PrP in brain and tonsil, or by immunoblotting of protease-resistant,<br /><br />disease associated PrP (CerPrPSc). Semitendinosus/semimembranosus muscle was also<br /><br />obtained from two asymptomatic, mock inoculated deer, referred to as FPS 6.68 and 9.98,<br /><br />that originated from a CWD non-endemic area and which were held indoors at Colorado<br /><br />State University from ten days of age. These control deer were confirmed negative for<br /><br />CWD by histopathological and immunohistochemical analysis of brain tissue at autopsy.<br /><br />The utmost care was taken to avoid inclusion of obvious nervous tissue when muscle<br /><br />biopsies were prepared and to ensure that contamination of skeletal muscle samples with<br /><br />CNS tissue did not occur. Fresh, single-use instruments were used to collect each sample<br /><br />biopsy and a central piece from each sample was prepared with fresh, disposable<br /><br />instruments to further isolate muscle tissue for inoculum preparation. Brain samples for<br /><br />transmission were prepared separately from muscle as additional insurance against cross<br /><br />contamination.<br /><br />1<br /><br />Groups of anesthetized Tg(CerPrP)1536 mice were inoculated intracerebrally with 30 µl<br /><br />of 1 % skeletal muscle or brain extracts prepared in phosphate buffered saline (PBS).<br /><br />Inoculated Tg(CerPrP) mice were diagnosed with prion disease following the progressive<br /><br />development of at least three neurologic symptoms including truncal ataxia, ‘plastic’ tail,<br /><br />loss of extensor reflex, difficultly righting, and slowed movement. The time from<br /><br />inoculation to the onset of clinical signs is referred to as the incubation time.<br /><br />For PrP analysis in brain extracts of Tg(CerPrP)1536 mice, 10 % homogenates prepared<br /><br />in PBS were either untreated (-) or treated (+) with 40 µg/ml proteinase K (PK) for one<br /><br />hour at 37oC in the presence of 2% sarkosyl. Proteins were separated by sodium dodecyl<br /><br />sulfate polyacrylamide gel electrophoresis, analyzed by immunoblotting using anti PrP<br /><br />monoclonal antibody 6H4 (Prionics AG, Switzerland), incubated with appropriate<br /><br />secondary antibody, developed using ECL-plus detection (Amersham), and analyzed<br /><br />using a FLA-5000 scanner (Fuji).<br /><br />2<br /><br />Fig. S1<br /><br />PrP in brain extracts from representative Tg(CerPrP)1536 mice receiving muscle or CNS<br /><br />tissue inocula from CWD-affected or CWD-negative deer. Extracts were either treated<br /><br />(+) or untreated (-) with proteinase K (PK) as indicated. The positions of protein<br /><br />molecular weight markers at 21.3, 28.7, 33.5 kDa (from bottom to top) are shown to the<br /><br />left of the immunoblot.<br /><br />3<br /><br /><a href="http://www.sciencemag.org/">http://www.sciencemag.org/</a><br /><br /><br />Chronic Wasting Disease and Potential Transmission to Humans<br /><br />Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W. Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger* *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †University of Wyoming, Laramie, Wyoming, USA; ‡Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA<br /><br />Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:<br /><br /><a href="http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm">http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm</a><br /><br /><br /><a href="http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm">http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm</a><br /><br /><br />Research<br /><br />Environmental Sources of Prion Transmission in Mule Deer Michael W. Miller,* Elizabeth S. Williams,† N. Thompson Hobbs,‡ and Lisa L. Wolfe* *Colorado Division of Wildlife, Fort Collins, Colorado, USA; †University of Wyoming, Laramie, Wyoming, USA; and ‡Colorado State University, Fort Collins, Colorado, USA<br /><br />Suggested citation for this article: Miller MW, Williams ES, Hobbs NT, Wolfe LL. Environmental sources of prion transmission in mule deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm<br /><br /><a href="http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm">http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm</a><br /><br /><br />ATYPICAL TSEs in USA CATTLE AND SHEEP ?<br /><br /><a href="http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf">http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf</a><br /><br /><br />UKBSEnvCJD only theory Singeltary et al 2006 (please note, et al in this term means all victims and familes of the sporadic CJD that are still looking for answers. ...TSS)<br /><br /><a href="http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13">http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13</a><br /><br /><br /><a href="http://www.microbes.info/forums/index.php?showtopic=306">http://www.microbes.info/forums/index.php?showtopic=306</a><br /><br /><br />NEW STRAIN OF TSE USA CATTLE OR JUST INCOMPETENCE IN TESTING???<br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a><br /><br /><br />CJD WATCH<br /><br /><a href="http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm">http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm</a><br /><br /><br />CJD WATCH MESSAGE BOARD<br /><br /><a href="http://disc.server.com/Indices/167318.html">http://disc.server.com/Indices/167318.html</a><br /><br /><br />Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518<br /><br />posted by Terry S. Singeltary Sr. 5:57 PM<br /><br />4 Comments: Terry S. Singeltary Sr. said...<br /><br /><br />##################### Bovine Spongiform Encephalopathy #####################<br /><br />Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006<br />Date: June 27, 2006 at 7:42 am PST<br />Public Health Service Food and Drug Administration<br /><br />New Orleans District 297 Plus Park Blvd. Nashville, TN 37217<br /><br />Telephone: 615-781-5380 Fax: 615-781-5391<br /><br />May 17, 2006<br /><br />WARNING LETTER NO. 2006-NOL-06<br /><br />FEDERAL EXPRESS OVERNIGHT DELIVERY<br /><br />Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204<br /><br />Dear Mr. Shirley:<br /><br />On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).<br /><br />Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:<br /><br />You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.<br /><br />You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.<br /><br />As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.<br /><br />This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.<br /><br />You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.<br /><br />Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.<br /><br />Sincerely,<br /><br />/S<br /><br />Carol S. Sanchez Acting District Director New Orleans District<br /><br /><a href="http://www.fda.gov/foi/warning_letters/g5883d.htm">http://www.fda.gov/foi/warning_letters/g5883d.htm</a><br /><br /><br />AHH, with all the bad news about FDA et al on there lack of enforcement, I would have expected a token mad cow feed ban warning letter or two to pop up now. what would really be interesting would be to see all violations of the mad cow feed ban, large and small, from all states. ...tss<br /><br />#################### https://lists.aegee.org/bse-l.html ####################<br /><br />Subject: [Docket No. 03-025IFA] SRMs and Non-Ambulatory disabled cattle[TSS] Date: October 6, 2005 at 2:28 pm PST<br /><br />[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />03-025IFA 03-025IFA-2 Terry S. Singeltary<br /><br />Page 1 of 17<br /><br />From: Terry S. Singeltary Sr. [flounder9@verizon.net]<br /><br />Sent: Thursday, September 08, 2005 6:17 PM<br /><br />To: fsis.regulationscomments@fsis.usda.gov<br /><br />Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements<br /><br />for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />Greetings FSIS,<br /><br />I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and<br /><br />Requirements for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle<br /><br />Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;<br /><br />SUB CLINICAL PRION INFECTION<br /><br />MRC-43-00<br /><br />Issued: Monday, 28 August 2000<br /><br />NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH<br /><br />FINDINGS RELEVANT TO CJD AND BSE<br /><br />Terry S. Singeltary Sr.<br /><br />P.O. Box 42<br /><br />Bacliff, Texas USA 77518<br /><br />9/13/2005<br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a><br /><br /><br />TSS<br /><br />6:48 PM Terry S. Singeltary Sr. said... ##################### Bovine Spongiform Encephalopathy #####################<br /><br />CJD WATCH MESSAGE BOARD TSS Monthly Creutzfeldt Jakob disease statistics July 3, 2006 Mon Jul 3, 2006 11:47 68.238.110.55<br /><br />Date: July 03, 2006 Time: 15:15 Monthly Creutzfeldt Jakob disease statistics published<br /><br />The Department of Health is today issuing the latest information about the numbers of known cases of Creutzfeldt Jakob disease. This includes cases of variant Creutzfeldt Jakob disease (vCJD) - the form of the disease thought to be linked to BSE. The position is as follows:<br /><br />Definite and probable CJD cases in the UK:<br /><br />As at 30 June 2006<br /><br />Summary of vCJD cases<br /><br />Deaths<br /><br />Deaths from definite vCJD (confirmed): 111<br /><br />Deaths from probable vCJD (without neuropathological confirmation): 44<br /><br />Deaths from probable vCJD (neuropathological confirmation pending): 1<br /><br />Number of deaths from definite or probable vCJD (as above): 156<br /><br />Alive<br /><br />Number of probable vCJD cases still alive: 5<br /><br />Total number of definite or probable vCJD (dead and alive): 161<br /><br />The next table will be published on Monday 7th August 2006<br /><br />Referrals: a simple count of all the cases which have been referred to the National CJD Surveillance Unit for further investigation in the year in question. CJD may be no more than suspected; about half the cases referred in the past have turned out not to be CJD. Cases are notified to the Unit from a variety of sources including neurologists, neuropathologists, neurophysiologists, general physicians, psychiatrists, electroencephalogram (EEG) departments etc. As a safety net, death certificates coded under the specific rubrics 046.1 and 331.9 in the 9th ICD Revisions are obtained from the Office for National Statistics in England and Wales, the General Register Office for Scotland and the General Register Office for Northern Ireland.<br /><br />Deaths: All columns show the number of deaths that have occurred in definite and probable cases of all types of CJD and GSS in the year shown. The figures include both cases referred to the Unit for investigation while the patient was still alive and those where CJD was only discovered post mortem (including a few cases picked up by the Unit from death certificates). There is therefore no read across from these columns to the referrals column. The figures will be subject to retrospective adjustment as diagnoses are confirmed.<br /><br />Definite cases: this refers to the diagnostic status of cases. In definite cases the diagnosis will have been pathologically confirmed, in most cases by post mortem examination of brain tissue (rarely it may be possible to establish a definite diagnosis by brain biopsy while the patient is still alive).<br /><br />Probable vCJD cases: are those who fulfil the 'probable' criteria set out in the Annex and are either still alive, or have died and await post mortem pathological confirmation. Those still alive will always be shown within the current year's figures.<br /><br />Sporadic: Classic CJD cases with typical EEG and brain pathology. Sporadic cases appear to occur spontaneously with no identifiable cause and account for 85% of all cases.<br /><br />Probable sporadic: Cases with a history of rapidly progressive dementia, typical EEG and at least two of the following clinical features; myoclonus, visual or cerebellar signs, pyramidal/extrapyramidalsigns or akinetic mutism.<br /><br />Iatrogenic: where infection with classic CJD has occurred accidentally as the result of a medical procedure. All UK cases have resulted from treatment with human derived pituitary growth hormones or from grafts using dura mater (a membrane lining the skull).<br /><br />Familial: cases occurring in families associated with mutations in the PrP gene (10 - 15% of cases).<br /><br />GSS: Gerstmann-Straussler-Scheinker syndrome - an exceedingly rare inherited autosomal dominant disease, typified by chronic progressive ataxia and terminal dementia. The clinical duration is from 2 to 10 years, much longer than for CJD.<br /><br />vCJD: Variant CJD, the hitherto unrecognised variant of CJD discovered by the National CJD Surveillance Unit and reported in The Lancet on 6 April 1996. This is characterised clinically by a progressive neuropsychiatric disorder leading to ataxia, dementia and myoclonus (or chorea) without the typical EEG appearance of CJD. Neuropathology shows marked spongiform change and extensive florid plaques throughout the brain.<br /><br />Definite vCJD cases still alive: These will be cases where the diagnosis has been pathologically confirmed (by brain biopsy).<br /><br />Related links<br /><br />Download cjd annual stats (PDF, 145K)<br /><br />Notes to editor<br /><br />ANNEX<br /><br />DIAGNOSTIC CRITERIA FOR VARIANT CJD<br /><br />I A) PROGRESSIVE NEUROPSYCHIATRIC DISORDER<br /><br />B) DURATION OF ILLNESS > 6 MONTHS<br /><br />C) ROUTINE INVESTIGATIONS DO NOT SUGGEST AN ALTERNATIVE DIAGNOSIS<br /><br />D) NO HISTORY OF POTENTIAL IATROGENIC EXPOSURE<br /><br />II A) EARLY PSYCHIATRIC SYMPTOMS *<br /><br />B) PERSISTENT PAINFUL SENSORY SYMPTOMS **<br /><br />C) ATAXIA<br /><br />D) MYOCLONUS OR CHOREA OR DYSTONIA<br /><br />E) DEMENTIA<br /><br />III A) EEG DOES NOT SHOW THE TYPICAL APPEARANCE OF SPORADIC<br /><br />CJD *** (OR NO EEG PERFORMED)<br /><br />B) BILATERAL PULVINAR HIGH SIGNAL ON MRI SCAN<br /><br />IV A) POSITIVE TONSIL BIOPSY<br /><br />DEFINITE: IA (PROGRESSIVE NEUROPSYCHIATRIC DISORDER) and NEUROPATHOLOGICAL CONFIRMATION OF vCJD ****<br /><br />PROBABLE: I and 4/5 OF II and III A and III B<br /><br />or I and IV A<br /><br />* depression, anxiety, apathy, withdrawal, delusions.<br /><br />** this includes both frank pain and/ or unpleasant dysaesthesia<br /><br />*** generalised triphasic periodic complexes at approximately one per second<br /><br />****spongiform change and extensive PrP deposition with florid plaques, throughout the cerebrum and cerebellum.<br /><br /><a href="http://www.wired-gov.net/WGLaunch.aspx?ARTCL=39920">http://www.wired-gov.net/WGLaunch.aspx?ARTCL=39920</a><br /><br /><br />TOTAL CASES OF SPORADIC CJD (DEATHS)<br /><br /><a href="http://www.eurocjd.ed.ac.uk/sporadic.htm">http://www.eurocjd.ed.ac.uk/sporadic.htm</a><br /><br /><br />TOTAL CASES OF FAMILIAL/GENETIC CJD AND IATROGENIC CJD DEATHS TO 31 MARCH 2006<br /><br /><a href="http://www.eurocjd.ed.ac.uk/genetic.htm">http://www.eurocjd.ed.ac.uk/genetic.htm</a><br /><br /><br />CJD USA<br /><br />(please note steady increase in sporadic cjd from 1997 to 2004 with steady increase in type 'UNKNOWN' CJD? also, seems like they could come up with a better, more readable chart. ...TSS)<br /><br /><a href="http://www.cjdsurveillance.com/resources-casereport.html">http://www.cjdsurveillance.com/resources-casereport.html</a><br /><br /><br />HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory<br /><br />TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2005. With all the science to date refuting it, to continue to validate this myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, surgical, blood, medical, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Tranmissible 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. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from subclinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. BUT, to continue with this myth that the U.K. strain of BSE one strain in cows, and the nv/v CJD, one strain in humans, and that all the rest of human TSE is one single strain i.e. sporadic CJD (when to date there are 6 different phenotypes of sCJD), and that no other animal TSE transmits to humans, to continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...<br /><br />TSS<br /><br />Coexistence of multiple PrPSc types in individuals with<br /><br />Creutzfeldt-Jakob disease<br /><br />Magdalini Polymenidou, Katharina Stoeck, Markus Glatzel, Martin Vey, Anne Bellon, and Adriano Aguzzi<br /><br />Summary<br /><br />Background The molecular typing of sporadic Creutzfeldt-Jakob disease (CJD) is based on the size and glycoform ratio of protease-resistant prion protein (PrPSc), and on PRNP haplotype. On digestion with proteinase K, type 1 and type 2 PrPSc display unglycosylated core fragments of 21 kDa and 19 kDa, resulting from cleavage around amino acids 82 and 97, respectively.<br /><br />Methods We generated anti-PrP monoclonal antibodies to epitopes immediately preceding the differential proteinase K cleavage sites. These antibodies, which were designated POM2 and POM12, recognise type 1, but not type 2, PrPSc.<br /><br />Findings We studied 114 brain samples from 70 patients with sporadic CJD and three patients with variant CJD.<br /><br />Every patient classified as CJD type 2, and all variant CJD patients, showed POM2/POM12 reactivity in the cerebellum and other PrPSc-rich brain areas, with a typical PrPSc type 1 migration pattern.<br /><br />Interpretation The regular coexistence of multiple PrPSc types in patients with CJD casts doubts on the validity of electrophoretic PrPSc mobilities as surrogates for prion strains, and questions the rational basis of current CJD<br /><br />classifications. ...<br /><br /><a href="http://neurology.thelancet.com/">http://neurology.thelancet.com</a><br /><br /><br />J Neuropsychiatry Clin Neurosci 17:489-495, November 2005 doi: 10.1176/appi.neuropsych.17.4.489 © 2005 American Psychiatric Publishing, Inc.<br /><br />Psychiatric Manifestations of Creutzfeldt-Jakob Disease: A 25-Year Analysis Christopher A. Wall, M.D., Teresa A. Rummans, M.D., Allen J. Aksamit, M.D., Lois E. Krahn, M.D. and V. Shane Pankratz, Ph.D. Received April 20, 2004; revised September 9, 2004; accepted September 13, 2004. From the Mayo Clinic, Department of Psychiatry and Psychology, Rochester, Minnesota; Mayo Clinic, Department of Neurology, Rochester, Minnesota. Address correspondence to Dr. Wall, Mayo Clinic, Department of Psychiatry and Psychology, Mayo Building-W11A, 200 First St., SW, Rochester, MN 55905; wall.chris@mayo.edu (E-mail).<br /><br />This study characterizes the type and timing of psychiatric manifestations in sporadic Creutzfeldt-Jakob disease (sCJD). Historically, sCJD has been characterized by prominent neurological symptoms, while the variant form (vCJD) is described as primarily psychiatric in presentation and course: A retrospective review of 126 sCJD patients evaluated at the Mayo Clinic from 1976-2001 was conducted. Cases were reviewed for symptoms of depression, anxiety, psychosis, behavior dyscontrol, sleep disturbances, and neurological signs during the disease course. Eighty percent of the cases demonstrated psychiatric symptoms within the first 100 days of illness, with 26% occurring at presentation. The most commonly reported symptoms in this population included sleep disturbances, psychotic symptoms, and depression. Psychiatric manifestations are an early and prominent feature of sporadic CJD, often occurring prior to formal diagnosis.<br /><br />snip...<br /><br />CONCLUSIONS<br /><br />Historically, psychiatric manifestations have been described as a relatively infrequent occurrence in the sporadic form of creutzfeldt-Jakob disease. However, our findings suggest otherwise. In this study, a vast majority of the cases were noted to have at least one psychiatric symptom during the course of illness, with nearly one-quarter occurring in the prodromal or presenting phase of the illness. After comparing the frequency of neuropsychiatric symptoms in sporadic CJD to studies describing the variant form of CJD, we found that there are fewer clinical differences than previously reported.5-7 While the age of patients with vCJD presentation is significantly younger and the course of illness is longer, the type and timing of psychiatric manifestations appear similar between these two diseases. ...snip...<br /><br /><a href="http://neuro.psychiatryonline.org/cgi/content/abstract/17/4/489">http://neuro.psychiatryonline.org/cgi/content/abstract/17/4/489</a><br /><br /><br />Personal Communication<br /><br />-------- Original Message --------<br /><br />Subject: re-BSE prions propagate as<br /><br />either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43<br /><br />-0000 From: "Asante, Emmanuel A" To: "'flounder@wt.net'"<br /><br />Dear Terry,<br /><br />I have been asked by Professor Collinge to respond to your request. I am<br /><br />a Senior Scientist in the MRC Prion Unit and the lead author on the<br /><br />paper. I have attached a pdf copy of the paper for your attention. Thank<br /><br />you for your interest in the paper.<br /><br />In respect of your first question, the simple answer is, yes. As you<br /><br />will find in the paper, we have managed to associate the alternate<br /><br />phenotype to type 2 PrPSc, the commonest sporadic CJD.<br /><br />It is too early to be able to claim any further sub-classification in<br /><br />respect of Heidenhain variant CJD or Vicky Rimmer's version. It will<br /><br />take further studies, which are on-going, to establish if there are<br /><br />sub-types to our initial finding which we are now reporting. The main<br /><br />point of the paper is that, as well as leading to the expected new<br /><br />variant CJD phenotype, BSE transmission to the 129-methionine genotype<br /><br />can lead to an alternate phenotype which is indistinguishable from type<br /><br />2 PrPSc.<br /><br />I hope reading the paper will enlighten you more on the subject. If I<br /><br />can be of any further assistance please to not hesitate to ask. Best wishes.<br /><br />Emmanuel Asante<br /><br /><> ____________________________________<br /><br />Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial<br /><br />College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG<br /><br />Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:<br /><br />e.asante@ic.ac.uk (until 9/12/02)<br /><br />New e-mail: e.asante@prion.ucl.ac.uk (active from now)<br /><br />____________________________________<br /><br />Full Text Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734<br /><br /><a href="http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama">http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama</a><br /><br /><br />TSS<br /><br />#################### https://lists.aegee.org/bse-l.html ####################<br /><br />6:53 PM Terry S. Singeltary Sr. said... Latest Information (as of July 4, 2006 - 17:30 EST) Final test results have confirmed bovine spongiform encephalopathy (BSE) in a mature cross-bred beef cow from Manitoba. The Canadian Food Inspection Agency (CFIA) is conducting a comprehensive investigation. Officials have confirmed the animal was purchased by the owner as part of an assembled group of cattle in 1992. This means that the animal was at least 15 years of age and would have been born well before the 1997 introduction of Canada’s feed ban. As a priority, investigators are attempting to locate the birth farm, which will provide the basis needed to identify the animal’s herdmates and feed to which it may have been exposed at a young age. Given the animal’s age, investigative efforts may be constrained by few surviving animals and limited sources of information, such as detailed records. A calf born to the affected animal in 2004 is also being traced.<br /><br />---------------------------------------------------------------------------- ----<br /><br /><a href="http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/situatione.shtml">http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/situatione.shtml</a><br /><br /><br />TSS<br /><br />6:55 PM Terry S. Singeltary Sr. said... ##################### Bovine Spongiform Encephalopathy #####################<br /><br />Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS Date: August 16, 2006 at 9:19 am PST<br /><br />RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II ______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-115-6 CODE None RECALLING FIRM/MANUFACTURER Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE Approximately 2,223 tons DISTRIBUTION KY<br /><br />______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-116-6 CODE None RECALLING FIRM/MANUFACTURER Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 1,220 tons DISTRIBUTION KY<br /><br />______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-117-6 CODE None RECALLING FIRM/MANUFACTURER Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed. REASON Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 40 tons DISTRIBUTION LA and MS<br /><br />______________________________ PRODUCT Bulk Dairy Feed, Recall V-118-6 CODE None RECALLING FIRM/MANUFACTURER Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete. REASON Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 7,150 tons DISTRIBUTION MS<br /><br />______________________________ PRODUCT Bulk custom dairy pre-mixes, Recall # V-119-6 CODE None RECALLING FIRM/MANUFACTURER Walthall County Co-op, Tylertown, MS, by telephone on June 26, 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 87 tons DISTRIBUTION MS<br /><br />______________________________ 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<br /><br />______________________________ 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<br /><br />END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006<br /><br />###<br /><br /><a href="http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html">http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html</a><br /><br /><br />GOTTA LOVE THOSE FDA/USDA TRIPLE BSE FIREWALLS. ...TSS<br /><br />WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows ;<br /><br /><a href="http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html">http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html</a><br /><br /><br />NOT TO FORGET THE TEXAS MAD COW THAT DID GET AWAY ;<br /><br /><a href="http://www.fda.gov/bbs/topics/news/2004/NEW01061.html">http://www.fda.gov/bbs/topics/news/2004/NEW01061.html</a><br /><br /><br />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;<br /><br />Risk of oral infection with bovine spongiform encephalopathy agent in primates<br /><br />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.<br /><br />snip...<br /><br />BSE bovine brain inoculum<br /><br />100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg<br /><br />Primate (oral route)* 1/2 (50%)<br /><br />Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)<br /><br />RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)<br /><br />PrPres biochemical detection<br /><br />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<br /><br />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<br /><br />bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.<br /><br />Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula<br /><br />Published online January 27, 2005<br /><br /><a href="http://www.thelancet.com/journal/journal.isa">http://www.thelancet.com/journal/journal.isa</a><br /><br /><br />It is clear that the designing scientists must<br /><br />also have shared Mr Bradley’s surprise at the results because all the dose<br /><br />levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s145d.pdf">http://www.bseinquiry.gov.uk/files/ws/s145d.pdf</a><br /><br /><br />2<br /><br />6. It also appears to me that Mr Bradley’s answer (that it would take less than say 100<br /><br />grams) was probably given with the benefit of hindsight; particularly if one<br /><br />considers that later in the same answer Mr Bradley expresses his surprise that it<br /><br />could take as little of 1 gram of brain to cause BSE by the oral route within the<br /><br />same species. This information did not become available until the "attack rate"<br /><br />experiment had been completed in 1995/96. This was a titration experiment<br /><br />designed to ascertain the infective dose. A range of dosages was used to ensure<br /><br />that the actual result was within both a lower and an upper limit within the study<br /><br />and the designing scientists would not have expected all the dose levels to trigger<br /><br />infection. The dose ranges chosen by the most informed scientists at that time<br /><br />ranged from 1 gram to three times one hundred grams. It is clear that the designing<br /><br />scientists must have also shared Mr Bradley’s surprise at the results because all the<br /><br />dose levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s147f.pdf">http://www.bseinquiry.gov.uk/files/ws/s147f.pdf</a><br /><br /><br />Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts<br /><br />[BBC radio 4 FARM news]<br /><br /><br /><a href="http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram">http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram</a><br /><br /><br /><a href="http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm">http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm</a><br /><br /><br />2) Infectious dose:<br /><br />To cattle: 1 gram of infected brain material (by oral ingestion)<br /><br /><a href="http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml">http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml</a><br /><br /><br />Terry S. Singeltary Sr.<br /><br />P.O. Box 42<br /><br />Bacliff, Texas USA 77518<br /><br />[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />03-025IFA 03-025IFA-2 Terry S. Singeltary<br /><br />Page 1 of 17<br /><br />From: Terry S. Singeltary Sr. [flounder9@verizon.net]<br /><br />Sent: Thursday, September 08, 2005 6:17 PM<br /><br />To: fsis.regulationscomments@fsis.usda.gov<br /><br />Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements<br /><br />for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />Greetings FSIS,<br /><br />I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and<br /><br />Requirements for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle<br /><br />Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;<br /><br />SUB CLINICAL PRION INFECTION<br /><br />MRC-43-00<br /><br />Issued: Monday, 28 August 2000<br /><br />NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH<br /><br />FINDINGS RELEVANT TO CJD AND BSE<br /><br />Terry S. Singeltary Sr.<br /><br />P.O. Box 42<br /><br />Bacliff, Texas USA 77518<br /><br />9/13/2005<br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a><br /><br /><br />TSS<br /><br />#################### https://lists.aegee.org/bse-l.html #################### Labels: MAD COW FEED IN COMMERCE USA<br /><br />posted by Terry S. Singeltary Sr. 5:57 PM<br /><br />4 Comments: Terry S. Singeltary Sr. said... ##################### Bovine Spongiform Encephalopathy #####################<br /><br />Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006 Date: June 27, 2006 at 7:42 am PST Public Health Service Food and Drug Administration<br /><br />New Orleans District 297 Plus Park Blvd. Nashville, TN 37217<br /><br />Telephone: 615-781-5380 Fax: 615-781-5391<br /><br />May 17, 2006<br /><br />WARNING LETTER NO. 2006-NOL-06<br /><br />FEDERAL EXPRESS OVERNIGHT DELIVERY<br /><br />Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204<br /><br />Dear Mr. Shirley:<br /><br />On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).<br /><br />Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:<br /><br />You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.<br /><br />You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.<br /><br />As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.<br /><br />This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.<br /><br />You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.<br /><br />Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.<br /><br />Sincerely,<br /><br />/S<br /><br />Carol S. Sanchez Acting District Director New Orleans District<br /><br /><a href="http://www.fda.gov/foi/warning_letters/g5883d.htm">http://www.fda.gov/foi/warning_letters/g5883d.htm</a><br /><br /><br />AHH, with all the bad news about FDA et al on there lack of enforcement, I would have expected a token mad cow feed ban warning letter or two to pop up now. what would really be interesting would be to see all violations of the mad cow feed ban, large and small, from all states. ...tss<br /><br />#################### https://lists.aegee.org/bse-l.html ####################<br /><br />Subject: [Docket No. 03-025IFA] SRMs and Non-Ambulatory disabled cattle[TSS] Date: October 6, 2005 at 2:28 pm PST<br /><br />[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />03-025IFA 03-025IFA-2 Terry S. Singeltary<br /><br />Page 1 of 17<br /><br />From: Terry S. Singeltary Sr. [flounder9@verizon.net]<br /><br />Sent: Thursday, September 08, 2005 6:17 PM<br /><br />To: fsis.regulationscomments@fsis.usda.gov<br /><br />Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements<br /><br />for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />Greetings FSIS,<br /><br />I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and<br /><br />Requirements for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle<br /><br />Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;<br /><br />SUB CLINICAL PRION INFECTION<br /><br />MRC-43-00<br /><br />Issued: Monday, 28 August 2000<br /><br />NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH<br /><br />FINDINGS RELEVANT TO CJD AND BSE<br /><br />Terry S. Singeltary Sr.<br /><br />P.O. Box 42<br /><br />Bacliff, Texas USA 77518<br /><br />9/13/2005<br /><br /><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a><br /><br /><br />TSS<br /><br />6:48 PM Terry S. Singeltary Sr. said... ##################### Bovine Spongiform Encephalopathy #####################<br /><br />CJD WATCH MESSAGE BOARD TSS Monthly Creutzfeldt Jakob disease statistics July 3, 2006 Mon Jul 3, 2006 11:47 68.238.110.55<br /><br />Date: July 03, 2006 Time: 15:15 Monthly Creutzfeldt Jakob disease statistics published<br /><br />The Department of Health is today issuing the latest information about the numbers of known cases of Creutzfeldt Jakob disease. This includes cases of variant Creutzfeldt Jakob disease (vCJD) - the form of the disease thought to be linked to BSE. The position is as follows:<br /><br />Definite and probable CJD cases in the UK:<br /><br />As at 30 June 2006<br /><br />Summary of vCJD cases<br /><br />Deaths<br /><br />Deaths from definite vCJD (confirmed): 111<br /><br />Deaths from probable vCJD (without neuropathological confirmation): 44<br /><br />Deaths from probable vCJD (neuropathological confirmation pending): 1<br /><br />Number of deaths from definite or probable vCJD (as above): 156<br /><br />Alive<br /><br />Number of probable vCJD cases still alive: 5<br /><br />Total number of definite or probable vCJD (dead and alive): 161<br /><br />The next table will be published on Monday 7th August 2006<br /><br />Referrals: a simple count of all the cases which have been referred to the National CJD Surveillance Unit for further investigation in the year in question. CJD may be no more than suspected; about half the cases referred in the past have turned out not to be CJD. Cases are notified to the Unit from a variety of sources including neurologists, neuropathologists, neurophysiologists, general physicians, psychiatrists, electroencephalogram (EEG) departments etc. As a safety net, death certificates coded under the specific rubrics 046.1 and 331.9 in the 9th ICD Revisions are obtained from the Office for National Statistics in England and Wales, the General Register Office for Scotland and the General Register Office for Northern Ireland.<br /><br />Deaths: All columns show the number of deaths that have occurred in definite and probable cases of all types of CJD and GSS in the year shown. The figures include both cases referred to the Unit for investigation while the patient was still alive and those where CJD was only discovered post mortem (including a few cases picked up by the Unit from death certificates). There is therefore no read across from these columns to the referrals column. The figures will be subject to retrospective adjustment as diagnoses are confirmed.<br /><br />Definite cases: this refers to the diagnostic status of cases. In definite cases the diagnosis will have been pathologically confirmed, in most cases by post mortem examination of brain tissue (rarely it may be possible to establish a definite diagnosis by brain biopsy while the patient is still alive).<br /><br />Probable vCJD cases: are those who fulfil the 'probable' criteria set out in the Annex and are either still alive, or have died and await post mortem pathological confirmation. Those still alive will always be shown within the current year's figures.<br /><br />Sporadic: Classic CJD cases with typical EEG and brain pathology. Sporadic cases appear to occur spontaneously with no identifiable cause and account for 85% of all cases.<br /><br />Probable sporadic: Cases with a history of rapidly progressive dementia, typical EEG and at least two of the following clinical features; myoclonus, visual or cerebellar signs, pyramidal/extrapyramidalsigns or akinetic mutism.<br /><br />Iatrogenic: where infection with classic CJD has occurred accidentally as the result of a medical procedure. All UK cases have resulted from treatment with human derived pituitary growth hormones or from grafts using dura mater (a membrane lining the skull).<br /><br />Familial: cases occurring in families associated with mutations in the PrP gene (10 - 15% of cases).<br /><br />GSS: Gerstmann-Straussler-Scheinker syndrome - an exceedingly rare inherited autosomal dominant disease, typified by chronic progressive ataxia and terminal dementia. The clinical duration is from 2 to 10 years, much longer than for CJD.<br /><br />vCJD: Variant CJD, the hitherto unrecognised variant of CJD discovered by the National CJD Surveillance Unit and reported in The Lancet on 6 April 1996. This is characterised clinically by a progressive neuropsychiatric disorder leading to ataxia, dementia and myoclonus (or chorea) without the typical EEG appearance of CJD. Neuropathology shows marked spongiform change and extensive florid plaques throughout the brain.<br /><br />Definite vCJD cases still alive: These will be cases where the diagnosis has been pathologically confirmed (by brain biopsy).<br /><br />Related links<br /><br />Download cjd annual stats (PDF, 145K)<br /><br />Notes to editor<br /><br />ANNEX<br /><br />DIAGNOSTIC CRITERIA FOR VARIANT CJD<br /><br />I A) PROGRESSIVE NEUROPSYCHIATRIC DISORDER<br /><br />B) DURATION OF ILLNESS > 6 MONTHS<br /><br />C) ROUTINE INVESTIGATIONS DO NOT SUGGEST AN ALTERNATIVE DIAGNOSIS<br /><br />D) NO HISTORY OF POTENTIAL IATROGENIC EXPOSURE<br /><br />II A) EARLY PSYCHIATRIC SYMPTOMS *<br /><br />B) PERSISTENT PAINFUL SENSORY SYMPTOMS **<br /><br />C) ATAXIA<br /><br />D) MYOCLONUS OR CHOREA OR DYSTONIA<br /><br />E) DEMENTIA<br /><br />III A) EEG DOES NOT SHOW THE TYPICAL APPEARANCE OF SPORADIC<br /><br />CJD *** (OR NO EEG PERFORMED)<br /><br />B) BILATERAL PULVINAR HIGH SIGNAL ON MRI SCAN<br /><br />IV A) POSITIVE TONSIL BIOPSY<br /><br />DEFINITE: IA (PROGRESSIVE NEUROPSYCHIATRIC DISORDER) and NEUROPATHOLOGICAL CONFIRMATION OF vCJD ****<br /><br />PROBABLE: I and 4/5 OF II and III A and III B<br /><br />or I and IV A<br /><br />* depression, anxiety, apathy, withdrawal, delusions.<br /><br />** this includes both frank pain and/ or unpleasant dysaesthesia<br /><br />*** generalised triphasic periodic complexes at approximately one per second<br /><br />****spongiform change and extensive PrP deposition with florid plaques, throughout the cerebrum and cerebellum.<br /><br /><a href="http://www.wired-gov.net/WGLaunch.aspx?ARTCL=39920">http://www.wired-gov.net/WGLaunch.aspx?ARTCL=39920</a><br /><br /><br />TOTAL CASES OF SPORADIC CJD (DEATHS)<br /><br />http://www.eurocjd.ed.ac.uk/sporadic.htm<br /><br />TOTAL CASES OF FAMILIAL/GENETIC CJD AND IATROGENIC CJD DEATHS TO 31 MARCH 2006<br /><br /><a href="http://www.eurocjd.ed.ac.uk/genetic.htm">http://www.eurocjd.ed.ac.uk/genetic.htm</a><br /><br /><br />CJD USA<br /><br />(please note steady increase in sporadic cjd from 1997 to 2004 with steady increase in type 'UNKNOWN' CJD? also, seems like they could come up with a better, more readable chart. ...TSS)<br /><br />http://www.cjdsurveillance.com/resources-casereport.html<br /><br />HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory<br /><br />TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2005. With all the science to date refuting it, to continue to validate this myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, surgical, blood, medical, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Tranmissible 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. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from subclinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. BUT, to continue with this myth that the U.K. strain of BSE one strain in cows, and the nv/v CJD, one strain in humans, and that all the rest of human TSE is one single strain i.e. sporadic CJD (when to date there are 6 different phenotypes of sCJD), and that no other animal TSE transmits to humans, to continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...<br /><br />TSS<br /><br />Coexistence of multiple PrPSc types in individuals with<br /><br />Creutzfeldt-Jakob disease<br /><br />Magdalini Polymenidou, Katharina Stoeck, Markus Glatzel, Martin Vey, Anne Bellon, and Adriano Aguzzi<br /><br />Summary<br /><br />Background The molecular typing of sporadic Creutzfeldt-Jakob disease (CJD) is based on the size and glycoform ratio of protease-resistant prion protein (PrPSc), and on PRNP haplotype. On digestion with proteinase K, type 1 and type 2 PrPSc display unglycosylated core fragments of 21 kDa and 19 kDa, resulting from cleavage around amino acids 82 and 97, respectively.<br /><br />Methods We generated anti-PrP monoclonal antibodies to epitopes immediately preceding the differential proteinase K cleavage sites. These antibodies, which were designated POM2 and POM12, recognise type 1, but not type 2, PrPSc.<br /><br />Findings We studied 114 brain samples from 70 patients with sporadic CJD and three patients with variant CJD.<br /><br />Every patient classified as CJD type 2, and all variant CJD patients, showed POM2/POM12 reactivity in the cerebellum and other PrPSc-rich brain areas, with a typical PrPSc type 1 migration pattern.<br /><br />Interpretation The regular coexistence of multiple PrPSc types in patients with CJD casts doubts on the validity of electrophoretic PrPSc mobilities as surrogates for prion strains, and questions the rational basis of current CJD<br /><br />classifications. ...<br /><br /><a href="http://neurology.thelancet.com/">http://neurology.thelancet.com</a><br /><br /><br />J Neuropsychiatry Clin Neurosci 17:489-495, November 2005 doi: 10.1176/appi.neuropsych.17.4.489 © 2005 American Psychiatric Publishing, Inc.<br /><br />Psychiatric Manifestations of Creutzfeldt-Jakob Disease: A 25-Year Analysis Christopher A. Wall, M.D., Teresa A. Rummans, M.D., Allen J. Aksamit, M.D., Lois E. Krahn, M.D. and V. Shane Pankratz, Ph.D. Received April 20, 2004; revised September 9, 2004; accepted September 13, 2004. From the Mayo Clinic, Department of Psychiatry and Psychology, Rochester, Minnesota; Mayo Clinic, Department of Neurology, Rochester, Minnesota. Address correspondence to Dr. Wall, Mayo Clinic, Department of Psychiatry and Psychology, Mayo Building-W11A, 200 First St., SW, Rochester, MN 55905; wall.chris@mayo.edu (E-mail).<br /><br />This study characterizes the type and timing of psychiatric manifestations in sporadic Creutzfeldt-Jakob disease (sCJD). Historically, sCJD has been characterized by prominent neurological symptoms, while the variant form (vCJD) is described as primarily psychiatric in presentation and course: A retrospective review of 126 sCJD patients evaluated at the Mayo Clinic from 1976-2001 was conducted. Cases were reviewed for symptoms of depression, anxiety, psychosis, behavior dyscontrol, sleep disturbances, and neurological signs during the disease course. Eighty percent of the cases demonstrated psychiatric symptoms within the first 100 days of illness, with 26% occurring at presentation. The most commonly reported symptoms in this population included sleep disturbances, psychotic symptoms, and depression. Psychiatric manifestations are an early and prominent feature of sporadic CJD, often occurring prior to formal diagnosis.<br /><br />snip...<br /><br />CONCLUSIONS<br /><br />Historically, psychiatric manifestations have been described as a relatively infrequent occurrence in the sporadic form of creutzfeldt-Jakob disease. However, our findings suggest otherwise. In this study, a vast majority of the cases were noted to have at least one psychiatric symptom during the course of illness, with nearly one-quarter occurring in the prodromal or presenting phase of the illness. After comparing the frequency of neuropsychiatric symptoms in sporadic CJD to studies describing the variant form of CJD, we found that there are fewer clinical differences than previously reported.5-7 While the age of patients with vCJD presentation is significantly younger and the course of illness is longer, the type and timing of psychiatric manifestations appear similar between these two diseases. ...snip...<br /><br /><a href="http://neuro.psychiatryonline.org/cgi/content/abstract/17/4/489">http://neuro.psychiatryonline.org/cgi/content/abstract/17/4/489</a><br /><br /><br />Personal Communication<br /><br />-------- Original Message --------<br /><br />Subject: re-BSE prions propagate as<br /><br />either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43<br /><br />-0000 From: "Asante, Emmanuel A" To: "'flounder@wt.net'"<br /><br />Dear Terry,<br /><br />I have been asked by Professor Collinge to respond to your request. I am<br /><br />a Senior Scientist in the MRC Prion Unit and the lead author on the<br /><br />paper. I have attached a pdf copy of the paper for your attention. Thank<br /><br />you for your interest in the paper.<br /><br />In respect of your first question, the simple answer is, yes. As you<br /><br />will find in the paper, we have managed to associate the alternate<br /><br />phenotype to type 2 PrPSc, the commonest sporadic CJD.<br /><br />It is too early to be able to claim any further sub-classification in<br /><br />respect of Heidenhain variant CJD or Vicky Rimmer's version. It will<br /><br />take further studies, which are on-going, to establish if there are<br /><br />sub-types to our initial finding which we are now reporting. The main<br /><br />point of the paper is that, as well as leading to the expected new<br /><br />variant CJD phenotype, BSE transmission to the 129-methionine genotype<br /><br />can lead to an alternate phenotype which is indistinguishable from type<br /><br />2 PrPSc.<br /><br />I hope reading the paper will enlighten you more on the subject. If I<br /><br />can be of any further assistance please to not hesitate to ask. Best wishes.<br /><br />Emmanuel Asante<br /><br /><> ____________________________________<br /><br />Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial<br /><br />College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG<br /><br />Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:<br /><br />e.asante@ic.ac.uk (until 9/12/02)<br /><br />New e-mail: e.asante@prion.ucl.ac.uk (active from now)<br /><br />____________________________________<br /><br />Full Text Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734<br /><br /><a href="http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama">http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama</a><br /><br /><br />TSS<br /><br />#################### https://lists.aegee.org/bse-l.html ####################<br /><br />6:53 PM Terry S. Singeltary Sr. said... Latest Information (as of July 4, 2006 - 17:30 EST) Final test results have confirmed bovine spongiform encephalopathy (BSE) in a mature cross-bred beef cow from Manitoba. The Canadian Food Inspection Agency (CFIA) is conducting a comprehensive investigation. Officials have confirmed the animal was purchased by the owner as part of an assembled group of cattle in 1992. This means that the animal was at least 15 years of age and would have been born well before the 1997 introduction of Canada’s feed ban. As a priority, investigators are attempting to locate the birth farm, which will provide the basis needed to identify the animal’s herdmates and feed to which it may have been exposed at a young age. Given the animal’s age, investigative efforts may be constrained by few surviving animals and limited sources of information, such as detailed records. A calf born to the affected animal in 2004 is also being traced.<br /><br />---------------------------------------------------------------------------- ----<br /><br /><a href="http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/situatione.shtml">http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/situatione.shtml</a><br /><br /><br />TSS<br /><br />6:55 PM Terry S. Singeltary Sr. said... ##################### Bovine Spongiform Encephalopathy #####################<br /><br />Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS Date: August 16, 2006 at 9:19 am PST<br /><br />RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II ______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-115-6 CODE None RECALLING FIRM/MANUFACTURER Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE Approximately 2,223 tons DISTRIBUTION KY<br /><br />______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-116-6 CODE None RECALLING FIRM/MANUFACTURER Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 1,220 tons DISTRIBUTION KY<br /><br />______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-117-6 CODE None RECALLING FIRM/MANUFACTURER Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed. REASON Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 40 tons DISTRIBUTION LA and MS<br /><br />______________________________ PRODUCT Bulk Dairy Feed, Recall V-118-6 CODE None RECALLING FIRM/MANUFACTURER Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete. REASON Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 7,150 tons DISTRIBUTION MS<br /><br />______________________________ PRODUCT Bulk custom dairy pre-mixes, Recall # V-119-6 CODE None RECALLING FIRM/MANUFACTURER Walthall County Co-op, Tylertown, MS, by telephone on June 26, 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 87 tons DISTRIBUTION MS<br /><br />______________________________ 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<br /><br />______________________________ 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<br /><br />END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006<br /><br />###<br /><br /><a href="http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html">http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html</a><br /><br /><br />GOTTA LOVE THOSE FDA/USDA TRIPLE BSE FIREWALLS. ...TSS<br /><br />WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows ;<br /><br />http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html<br /><br />NOT TO FORGET THE TEXAS MAD COW THAT DID GET AWAY ;<br /><br /><a href="http://www.fda.gov/bbs/topics/news/2004/NEW01061.html">http://www.fda.gov/bbs/topics/news/2004/NEW01061.html</a><br /><br /><br />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;<br /><br />Risk of oral infection with bovine spongiform encephalopathy agent in primates<br /><br />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.<br /><br />snip...<br /><br />BSE bovine brain inoculum<br /><br />100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg<br /><br />Primate (oral route)* 1/2 (50%)<br /><br />Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)<br /><br />RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)<br /><br />PrPres biochemical detection<br /><br />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<br /><br />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<br /><br />bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.<br /><br />Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula<br /><br />Published online January 27, 2005<br /><br /><a href="http://www.thelancet.com/journal/journal.isa">http://www.thelancet.com/journal/journal.isa</a><br /><br /><br />It is clear that the designing scientists must<br /><br />also have shared Mr Bradley’s surprise at the results because all the dose<br /><br />levels right down to 1 gram triggered infection.<br /><br /><a href="http://www.bseinquiry.gov.uk/files/ws/s145d.pdf">http://www.bseinquiry.gov.uk/files/ws/s145d.pdf</a><br /><br /><br />2<br /><br />6. It also appears to me that Mr Bradley’s answer (that it would take less than say 100<br /><br />grams) was probably given with the benefit of hindsight; particularly if one<br /><br />considers that later in the same answer Mr Bradley expresses his surprise that it<br /><br />could take as little of 1 gram of brain to cause BSE by the oral route within the<br /><br />same species. This information did not become available until the "attack rate"<br /><br />experiment had been completed in 1995/96. This was a titration experiment<br /><br />designed to ascertain the infective dose. A range of dosages was used to ensure<br /><br />that the actual result was within both a lower and an upper limit within the study<br /><br />and the designing scientists would not have expected all the dose levels to trigger<br /><br />infection. The dose ranges chosen by the most informed scientists at that time<br /><br />ranged from 1 gram to three times one hundred grams. It is clear that the designing<br /><br />scientists must have also shared Mr Bradley’s surprise at the results because all the<br /><br />dose levels right down to 1 gram triggered infection.<br /><br />http://www.bseinquiry.gov.uk/files/ws/s147f.pdf<br /><br />Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts<br /><br />[BBC radio 4 FARM news]<br /><br />http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram<br /><br />http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm<br /><br />2) Infectious dose:<br /><br />To cattle: 1 gram of infected brain material (by oral ingestion)<br /><br />http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml<br /><br />Terry S. Singeltary Sr.<br /><br />P.O. Box 42<br /><br />Bacliff, Texas USA 77518<br /><br />[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />03-025IFA 03-025IFA-2 Terry S. Singeltary<br /><br />Page 1 of 17<br /><br />From: Terry S. Singeltary Sr. [flounder9@verizon.net]<br /><br />Sent: Thursday, September 08, 2005 6:17 PM<br /><br />To: fsis.regulationscomments@fsis.usda.gov<br /><br />Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements<br /><br />for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />Greetings FSIS,<br /><br />I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and<br /><br />Requirements for the Disposition of Non-Ambulatory Disabled Cattle<br /><br />THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle<br /><br />Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;<br /><br />SUB CLINICAL PRION INFECTION<br /><br />MRC-43-00<br /><br />Issued: Monday, 28 August 2000<br /><br />NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH<br /><br />FINDINGS RELEVANT TO CJD AND BSE<br /><br />Terry S. Singeltary Sr.<br /><br />P.O. Box 42<br /><br />Bacliff, Texas USA 77518<br /><br />9/13/2005<br /><br />http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf<br /><br />TSS<br /><br />#################### https://lists.aegee.org/bse-l.html ####################Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com4