Another Big Myth about Transmissible Spongiform Encephalopathy, is that TSE will not transmit to dogs. This is simply NOT TRUE. IT is perfectly legal to feed dogs and cats here in the USA bovine meat and bone meal. Canine dementia is real. how many dogs and cats here in the USA are tested for mad cow disease ? I just received this F.O.I.A. request, and thought I would post it here with a follow up on MAD DOG DISEASE. This is a follow up with additional data I just received on a FOIA request in 2009 ;
DEPARTMENT OF HEALTH & HUMAN SERVICES Public Health Service Food and Drug Administration Rockville MD 20857
Terry Singeltary Bacliff, TX USA 77518
Dear Requestor
In reply refer to: F2009-7430
This is in response to your Freedom of Information Act (FOIA) request received by the Food and Drug Administration (FDA) on September 10,2009 which you ask for Recall V-258-2009. I apologize for the delay in our response to you. Enclosed you will find the records you requested. The following charges will be included in a monthly invoice:
Reproduction Search Review Total 5 Pages hour $.50 $ $.50
The above charges may not reflect final charges for this request. Please DO NOT send any payment until you receive an invoice from the Agency's Freedom of Information Staff (HFI-35).
Sincerely yours,
Sandy McGeehan Paralegal Specialist Communications Staff Center for Veterinary Medicine
Memorandum
Date August 26, 2009
From CVM Animal Health Hazard Evaluation Committee
Subject Problem:
Fargam Land & Grain recalled 429,128 pounds of ground corn because it may have been contaminated with prohibited material (material prohibited for use in ruminant feed by the 1997 BSE feed regulation) and was not labeled with the cautionary statement.
The feed mill received two semi trailer loads of barley that had been recalled by Mars Petcare US because it had been contaminated by dog food, some of which is formulated to contain bovine origin meat and bone meal.
The auger used to receive the barley was used to receive two truck loads of corn before the feed mill became aware of the problem with the barley. This potentially allowed some of the dog food in the barley to be carried over into the corn.
Recall Event IDIRES #: 52103
DAF/Surveillance #: 09234
CVM Recall and Emergency Coordinator (Kathy Hemming-Thompson), HFV -234
Field/RES Report Data:
Recalling firm: Fargam Land & Grain 505 Burlington Rd Saginaw, TX 76179
Manufacturer: Mars Petcare US 1 Doane Rd Clinton, OK 73601
Product & Code: Bulk ground corn; 70AY -02
Quantity Manufactured: 429,128 pounds
Quantity Distributed: 429,128 pounds
Recall Contact: Phil Farr, Owner, Fargam Land & Grain, Saginaw, TX
FDA District: Dallas
Field Recommended Classification: Class III
Effectiveness Check Level: Direct Accounts
Page 2 of 4 - DAF 09234 - Health Hazard Evaluation
Background: The firm is a feed mill that stores and manufactures products intended for use in animal feed. Its business is commingled with Saginaw Flakes, a feed mill which is under the same ownership, and located across the street from Fargam Land & Grain. A limited inspection was conducted to determine compliance with CP 7371.009 after the firm notified the Office of the Texas State Chemist that it had received four semi trailer loads of barley that may have contained dog food.
ReView:
Sample collection:
Aseptic technique [ ] Yes [ ] No [X] NA
Number of subsamples
FDA/FACTS #
Was chain of custody documented correctly?
[ ] Yes
[ ] No Explain in narrative box:
[X] NA
Analytical method: [ ] Yes [ ] No [X] NA
[ ] Official method
[ ] FDA method
[ ] Other method, explain in narrative box:
Was analysis properly conducted? [ ]Yes [ ] No Explain in narrative box: [X] NA
Laboratory analysis: [ ] Yes [ ] No [X] NA
Done by:
[ ] FDA laboratory
[ ] State laboratory
[ ] Other laboratory
[ ] None
Have any adverse reaction reports or other indication of injuries or diseases been reported relating to this problem or for similar situations?
[X] No
[ ] Yes Attach copies or explain in narrative box:
[ ] NA
Is the problem easily identified by the user?
[X] No
[ ] Yes
What are the animal and human populations at risk?
Cattle, particularly calves, is the population that is most susceptible to BSE and at greatest risk ofexposure to the BSE agent through these shipments of ground corn that may have contained prohibited material and were not labeled with the cautionary statement. Other susceptible populations, such as humans, domestic cats, and zoo animals are best protected by keeping BSE out of the cattle population.
Page 3 of 4 - DAF 09234 - Health Hazard Evaluation
What is the hazard associated with use of the product?
[X ] Life-threatening (death has or could occur) .
[ ] Results in permanent impaiiment of a body function or permanent damage to a body structure
[ ] Necessitates medical or surgical intervention to preclude or reverse permanent damage to a body structure orpermanent impairment of a body function
[ ] Temporary-or reversible (without medical intervention)
[ ] Limited (transient, minor impairment or complaints)
[ ] No adverse health consequences
[ ] Hazard cannot be assessed with the data currently available
What is the likelihood of an adverse event occurring?
[ ] Probable
[ ] Possible
[X] Unlikely
[ ] Unknown
CVM's AHHE Committee recommends the following:
a) Recall Classification: [21 CFR 7.41(b) and RPM 5-00-20 (j)].
l-Class I [ ]
2-Class ll [ ]
3-Class III [X]
4-Market withdrawal [ ] Skip parts b & c
5-0ther [ ] Skip parts b & c.
b) Depth of Recall: [21 CFR 7 .42(b )(1) and RPM 5-00-20(k)].
l-Consumer or User Level [X]
2- Retail Level/Veterinarian [ ]
3- Wholesale Level [ ]
4-NA [ ]
c) Level of Audit Checks: [Investigations Operations Manual Chapter 7, Section 7.3.2.2]
[ ] Level A-I 00% of the total number of consignees to be contacted.
[ ] Level B - Greater than 10% but less than 100% of the total number of consignees to be contacted.
[ ] Level C - 10% of the total number of consignees to be contacted.
[ ] Level D - 2% of the total number of consignees to be contacted.
[ X] Level E - No checks.
Narrative Summary:
Fargam Land & Grain, Saginaw, TX recalled 429,128 pounds of ground corn that may have contained prohibited material. The com was not labeled with the required cautionary statement to alert users of the product that it should not be fed to ruminants or be used as an ingredient in
Page 4 of 4 - DAF 09234 - Health Hazard Evaluation
ruminant feed. The corn was shipped to eleven dairy farms in Texas and one dairy farm in Louisiana between May 13th and May 15th, 2009. This is a sub-recall of a recall by Mars Petcare US, Clinton, OK of bulk whole barley that was cross-contaminated with dog food during storage and loading at the Mars Petcare plant. A receiving auger at Fargam Land and Grain that was used to unload the contaminated barley was used to unload whole corn before the problem was discovered. This potentially allowed some of the dog food in the barley to be carried over into the corn.
BSE is a degenerative disease of the central nervous system of cattle and is always fatal. It is characterized by a long incubation period of three to eight years, followed by a much shorter course of illness. The BSE agent is also the cause of variant Creutzfeldt-Jakob disease in humans, which is also always fatal.
While the health hazard is life threatening, It is highly unlikely that deaths or illnesses would result from the use of the recalled product. The meat and bone meal ingredient of the dog food carried over into the barley as a result of cross contamination, and then potentially carried over into the corn through cross-contamination, would have to have been derived from a BSE infected animal for the BSE agent to be present in the dog food-barley, and corn. This is unlikely due to the low prevalence of BSE in the U.S. cattle population. In 2006, USDA estimated the prevalence of BSE in the United States to be less than one infected animal per million adult cattle. This estimate was based on results of 735,213 cattle tested over a seven year period. The most recent of only three BSE cases ever detected in the United States was found in March 2006.
CVM Animal Health Hazard Evaluation Committee recommends a class _III_ recall and we concur with the effectiveness check level of _100_ percent.
Animal Health Hazard Evaluation Committee
Lynn Post, DVM, Ph.D., D.A.B.V.T., Chair
Sharon Benz, Ph.D., PAS
Terry Proescholdt, Leader, Feed Safety Team
Prepared by :
Burt Pritchett, DVM
end...March 4, 2010...TSS
HISTORY F.O.I.A.
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html
Thursday, September 3, 2009
429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
http://madcowfeed.blogspot.com/2009/09/429128-lbs-feed-for-ruminant-animals.html
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
http://madcowfeed.blogspot.com/2009_09_01_archive.html
Tuesday, November 3, 2009
re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/11/re-foia-request-on-feed-recall-product.html
From: Terry S. Singeltary Sr.
To: CVMHomeP@cvm.fda.gov
Cc: FOIASTAFF@oig.usda.gov ; paffairs@oig.hhs.gov ; HHSTips@oig.hhs.gov ; phyllis.fong@oig.usda.gov
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
September 4, 2009
TO:
Food and Drug Administration
Division of Freedom of Information (HFI-35)
Office of Shared Services
Office of Public Information and Library Services
5600 Fishers Lane
Rockville, MD 20857
Or requests may be sent via fax to: fax number 301-443-1726 or 301-443-1719. If experience difficulty sending a fax, please call (301) 443-2414.
FROM:
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
Greetings FDA FOIE, and the Honorable Phyllis Fong et al @ OIG FOIA,
ANOTHER FOIA REQUEST PLEASE !
I apologize for wasting your time. this could have been handled differently if the FDA et al would just clearly identify these feed recalls with exactly what was in them, and what type recall it is.
I was told that the only way to find any more information on the following recall, i would have to submit a FOIA ? why, i do not know ?
----- Original Message -----
From: Pritchett, Burt
To: Terry S. Singeltary Sr.
Sent: Thursday, August 27, 2009 3:26 PM
Subject: RE: hello Mr. Pritchett Sir !!! mad cow feed question
Terry,
That is the extent of the public information on the recall. If you wish to obtain additional information, you should submit a freedom of information act request through our communications staff. You could send an email request to: CVMHomeP@cvm.fda.gov
Burt
================end...TSS
Greetings again FDA, OIG et al,
I am trying to find out more information on another recall, that contains possible mad cow protein? but we do not know for sure, the way the recall warning letters are being wrote up now.
I had to file FOIA last week for the same thing. see ;
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html
and I recieved 'confirmation' of my request in the postal mail with Log No. xx-xxxxx.
HOWEVER, SADLY, I requested another explaination again from Pritchett, Burt on this newest suspect mad cow feed recall this week below, explaining to him that this is rediculous to have to file a FOIA on every feed recall now, and that all he had to do was to explain exactly what we are speaking of in these recalls, and I have gotten no response to date. SO, I will continue to write these FOIA request, until we get this straightened out, even if it takes another 6+ years to find the truth.
F.O.I.A request on the following please ;
PRODUCT Bulk ground corn; distributed by Saginaw Flakes, Saginaw, TX, Recall # V-258-2009
CODE Bulk ground corn shipped between 05/13/-14/09
RECALLING FIRM/MANUFACTURER Recalling Firm: Fargam Land & Grain, Saginaw, TX, by telephone on May 21, 2009. Manufacturer: Mars Petcare US, Clinton, OK.
Firm initiated recall is ongoing.
REASON Bulk ground corn used as feed for ruminant animals may have been contaminated with prohibited material.
VOLUME OF PRODUCT IN COMMERCE 429,128 lbs.
DISTRIBUTION TX, LA
END OF ENFORCEMENT REPORT FOR SEPTEMBER 2, 2009
###
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm181251.htm
archived url link;
http://web.archive.org/web/20100309080021/http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm181251.htm
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
How to Make a FOIA Request All FOIA requests must be in writing and should include the following information:
A. Requestor's name, address, and telephone number.
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
281-xxx-xxxx
B. A description of the records being sought. The records should be identified as specifically as possible. A request for specific records that are releasable to the public can be processed much more quickly than a request for "all information" on a particular subject. Also fees for a more specific and limited request will generally be less.
SEE ABOVE FOIA SPECIFIC REQUEST OF RECORDS. ...TSS
C. Separate requests should be submitted for each firm or product involved.
DUE TO THE LACK OF INFORMATION IN THE ORIGINAL WARNING LETTER, THIS IS NOT POSSIBLE. ...TSS
D. A statement concerning willingness to pay fees, including any limitations.
I CANNOT PAY ANYTHING. I AM DISABLED AND ON FIXED INCOME. THIS INFORMATION I REQUEST IS FOR ME AND THE PUBLIC. ...TSS
Questions relating to FOI requests may be addressed to the Division of the Freedom of Information Offices at 301-827-6567.
All FOIA requests must be in writing. At this time, FDA does not accept FOIA requests sent via e-mail. Requests should be mailed to the following address:
Food and Drug Administration
Division of Freedom of Information (HFI-35)
Office of Shared Services
Office of Public Information and Library Services
5600 Fishers Lane
Rockville, MD 20857
Or requests may be sent via fax to: fax number 301-443-1726 or 301-443-1719. If experience difficulty sending a fax, please call (301) 443-2414.
FAXED AND RECIEVED TO THE ABOVE NUMBER SEPTEMBER 4, 2009...TSS
Subject: FDA BSE MAD COW and the safety of your pet, the rest of the story
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Mon, 7 Nov 2005 09:28:23 -0600
Content-Type: text/plain
Parts/Attachments: text/plain (1529 lines)
Reply
##################### Bovine Spongiform Encephalopathy #####################
From: TSS
Subject: FDA BSE MAD COW and the safety of your pet, the rest of the story
Date: November 5, 2005 at 8:09 am PST
BSE and the safety of pets
With the exception of cats, no pets (companion animals) are known to be susceptible to the infectious agent that causes BSE in cattle. No evidence of BSE has ever been found in dogs, horses, birds, or reptiles.
However, cats are susceptible. Approximately 90 cats in the UK and several cats in other European countries have been diagnosed with the feline version of BSE, or FSE. Before it was recognized that they were susceptible to the BSE agent, cats were exposed to the infectious agent through commercial cat food or through meat scraps provided by butchers. The number of reported cases of FSE in the UK and Europe has been declining annually since 1994 after implementation of feed bans in those countries.
Currently in the U.S. , animal products that are prohibited from cattle feed are acceptable for use in pet food. Such products include meat and bone meal, for example. However, FDA believes that the safeguards it has put into place (i.e. ruminant feed rule) to prevent BSE in the U.S. have also protected cats. To date, no case of FSE has been found in the U.S. FDA continues to review these safeguards to be sure they are adequate, especially in light of the BSE case found in Washington State in December, 2003.
Material from the BSE positive cow in Washington State did not pose a risk to cats in the U.S. because none of it was released into distribution. All firms involved with the incident in Washington State were found to be in compliance with the BSE rules.
In addition, when the BSE positive cow was found in Canada in May 2003, the FDA stopped imports of all pet foods made from material derived from mammalian sources, and the pet food manufacturer recalled the food it had manufactured that was thought to contain material from the infected cow.
In an Advance Notice of Proposed Rulemaking published in the Federal Register on July 14, 2004, the FDA announced that the agency intends to further strengthen the ruminant feed rule (or BSE feed regulation) by prohibiting the use of high-risk tissues, often referred to as specified risk material or SRM, in any animal feed including pet food.
CVM DOES NOT recommend one product over another or offer guidance on individual pet health issues that are normally provided by the pet’s veterinarian. Questions regarding your pets' health and/or the specific use of any veterinary drug, pet food, or other product should always be referred to your veterinarian.
The following documents contain information on the regulation, marketing and labeling of pet foods in the United States.
News Releases
http://www.fda.gov/cvm/petfoods.htm
TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS
http://www.mad-cow.org/00/aug00_late_news.html#ggg
archived url link;
http://web.archive.org/web/20100712100219/http://www.mad-cow.org/00/aug00_late_news.html#ggg
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
HOUND STUDY
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.
snip...
http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
NEW URL ;
http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
76 pages on hound study;
http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf
NEW URL ;
http://web.archive.org/web/20030327022236/http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf
I thought that in Britain dogs had contracted BSE, but perhaps not.
not so fast here;
The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.
41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).
http://www.bseinquiry.gov.uk/witness/htm/stat067.htm
It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
snip...
http://www.bseinquiry.gov.uk/files/ws/s324.pdf
archived url link ;
http://web.archive.org/web/20090506004016/http://www.bseinquiry.gov.uk/files/ws/s324.pdf
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
The signs of canine cognitive dysfunction syndrome or "old dog syndrome" commonly seen in dogs are: lose of house training increased barking or whining increased anxiety or fear signs disorientation-appearing lost or confused,getting stuck behind furniture or in corners, walking in circles, becoming forgetful,walking aimlessly,staring into space, repetitious or compulsive behavior change in sleep patterns-up at night, sleep all day
lack of responsiveness other changes,may not recognize you, their name,may become more docile, more aggressive.. You can liken it to human senility. An article at the petcenter says "CDS is not "normal aging". A number of pathophysiological changes are suspected to play a role in its development. These include: * deposition of amyloid plaques in the cerebral cortex and hippocampal part of the brain * alterations in neurotransmitters, including dopamine * increased levels of monoamine oxidase B (MAOB) in the brain * increased levels of free radicals L-DEPRENYL HYDROCHLORIDE SELEGILINE HYDROCHLORIDE,BRAND NAME: ANIPRYL OR ELDEPRYL is used to help treat canine cognitive dysfunction by increasing brain concentrations of the neurotransmitter dopamine. Hopefully you can see a difference in a month or so. If you don't see a difference in the first month, your vet might tell you to try two pills a day for the next month. ANIPRYL doesn't work for all dogs. A great writeup on L-DEPRENYL can be found at
http://www.petsinfo.org/elderlydogs1.html.
"One third of canine CD patients respond extremely well to treatment with deprenyl by regaining their youthful vigor; another one third respond reasonably well; and one third do not respond at all (perhaps there is a variant of CD with different neuropathology). The bottom line is that for any dog that is slowing down to the point that problems become apparent, treatment with deprenyl is the logical route once other organic causes for reduced mental function have been ruled out. Here is a write up on selegline " Selegiline has immune-system-boosting and anti-neurodegenerative effects. ....
Taken consistently in low doses, selegiline tends to extend the life-expectancy of rats by some 20%; enhances drive, libido and endurance; and independently improves cognitive performance in Alzheimer's patients and in some healthy normals. It is used successfully to treat canine cognitive dysfunction syndrome (CDS) in dogs...Selegiline protects the brain's dopamine cells from oxidative stress. " Some also use alpha lipoic acid and r-lipoic acid. powerful antioxidants to help slow down canine cognitive dysfunction. There is a dog food that is rich in antioxidants for CDS but I am assuming if you supplement with your own antioxidants you don't have to worry if your dog likes the food or not. I know my dog Hammy has become very picky and at least if I pill him, I know he is getting his antioxidants.
http://www.thensome.com/cds.htm
Doggie Dementia
Does 14-year-old Fido get lost in his own back yard?
Does he not respond when you call his name?
Does he generally seem confused?
According to Pulse, the official magazine of the Southern California Veterinary Medical Association, just as humans in the 21st Century are living longer, so is man’s best friends—more than 7.3 million dogs in the United States are age 10 or older. And with age dogs become prone to the same age-related diseases as their human companions, including dementia.
A disease of old age affects dogs and humans alike
Kazzy, a 17-year-old Lhasa Apso, is one of the 60 percent of dogs aged 11 to 15 who suffer from one or more symptoms of canine cognitive dysfunction syndrome (CDS), also known to veterinarians as doggie dementia. "He used to be the most incredible watchdog," says his owner, Olivia Feldman-Rich. "But he’s not like that anymore. He’s quite bewildered."
Experts like Dr. Maritza Perez, a veterinarian at West Orange (NJ) Animal Hospital, say that confusion is one of the four major signs of CDS (see sidebar). Dr. Perez says dogs may "pace around in circles, get stuck behind furniture, or they don’t know where the back door is anymore."
Often the most distressing sign of CDS is that, like human patients with Alzheimer’s disease, your pet seems to forget you and your family. "A lot of people notice that when you walk in the door, and this dog that was happy to see you doesn’t get up off the couch or off the floor to greet you," says Dr. Perez. "And he doesn’t come anymore when you call him."
These symptoms, coupled with others debilitating diseases affecting older dogs, such as arthritis, all add up to a serious loss in quality of life for your canine friend. The American Veterinary Medical Association reports that some 500,000 dogs are put to sleep each year because of CDS.
Researchers say that deposits of beta-amyloid plaques in brain tissues are likely to play a role in CDS. These plaques build up and eventually inhibit transmission of the brain’s neural signals. Still, the recognized symptoms of CDS are behavioral, so a diagnosis is exclusionary, meaning it is arrived at only after all other physical and neurological causes are ruled out.
No cure yet, but relief for some dogs
Dr. Perez with a 14 year-old beagle who is on Anipryl.
While scientists search for a permanent cure for CDS, there is one treatment currently FDA-approved for CDS. Selegiline hydrochloride, whose brand name is Anipryl, may give some dogs relief from its symptoms. Researchers speculate that Anipryl works by increasing levels of dopamine, a neurotransmitter. Other treatments are currently being investigated, including diets high in anti-oxidants as well as a new drug, Adrafinil, in one Canadian study.
Dr. Perez says that Anipryl does cause an improvement in many dogs with CDS, meaning relief from at least one of the common symptoms. "We have lots of animals on it and it does work," she says. But it’s not a sure thing—Dr. Perez tried it on her own dog with no effect.
Feldman-Rich is debating putting Kazzy on Anipryl. "I’m hoping that it will give a little more balance to his life and make him a little more aware that he’s still here and we’re still here for him," she says. "I always told him that he couldn’t leave me too soon, and he’s definitely kept up his end of it, but I’d definitely like for him to feel a little more like he’s part of the family."
by Debra Utacia Krol
http://www.sciencentral.com/articles/view.php3?article_id=218391360&cat=1_6
[Image] Research letters Volume 352, Number 9134 [Image] 3 October 1998 [Previous] [Next]
[Image][Image]
Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy
[Image]
Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, Sergio Ferrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, Salvatore Monaco
Transmissible spongiform encephalopathies (TSE) encompass inherited, acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four types of PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 in the UK.5 We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.
A 60-year-old man, with no unusual dietary habits, was admitted in November, 1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, and myoclonus. An electroencephalogram (EEG) showed diffuse theta-delta activity. A brain magnetic resonance imaging scan was unremarkable. 10 days later, he was speechless and able to follow only simple commands. Repeat EEGs showed periodic triphasic complexes. 2 weeks after admission, he was mute, akinetic, and unable to swallow. He died in early January, 1994.
His 7-year-old, neutered, female shorthaired cat presented in November, 1993, with episodes of frenzy, twitching of its body, and hyperaesthesia. The cat was usually fed on canned food and slept on its owner's bed. No bites from the cat were recalled. In the next few days, the cat became ataxic, with hindquarter locomotor dysfunction; the ataxia got worse and there was diffuse myoclonus. The cat was killed in mid-January, 1994.
No pathogenic mutations in the patient's PrP gene were found. The patient and the cat were methionine homozygous at codon 129. Histology of the patient's brain showed neocortical and cerebellar neuronal loss, astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a punctate pattern and paralleled spongiform changes (figure B). The cat's brain showed mild and focal spongiosis in deeper cortical layers of all four lobes (figure C), vacuolated cortical neurons (figure D), and mild astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed. Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and caudate nucleus (figure E). Western blot analysis of control and affected human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After digestion with proteinase K and deglycosylation, only samples from the affected patient and cat showed type-1 PrPres, with PrP glycoform ratios comparable to those observed in sporadic CJD1 (details available from author).
[Image]
Microscopic sections of patient and cat brains
A: Occipital cortex of the patient showing moderate spongiform degeneration and neuronal loss (haematoxylin and eosin) and B: punctate perineuronal pattern of PrP immunoreactivity; peroxidase immunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortex showing mild spongiform degeneration (haematoxylin and eosin).D: vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase immunohistochemistry with antibody 3F4 shows punctate perineuronal deposition of PrP in temporal cortex.
This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2 Taken together, our data suggest that the same agent strain of sporadic CJD was involved in the patient and in his cat.
It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source, or the chance occurrence of two sporadic forms.
1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypic variablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39: 767-78 [PubMed].
2 Collinge J, Sidle KCL, Meads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996; 383: 685-90 [PubMed].
3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501 [PubMed].
4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJD and BSE. Nature 1997; 389: 448-50 [PubMed].
5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiform encephalopathy: a review. Vet Annual 1993; 33: 1-10.
------------------------------------------------------------------------ Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e della Visione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy (S Monaco; e mail rizzuto@Gorgorna.univr.it); and Istituto Zooprofilattico Sperimentale della Lombardia e dell' Emilia, Brescia
=======================================
Terry S. Singeltary Sr. wrote:
######## Bovine Spongiform Encephalopathy #########
Greetings list members,
ODD that some FELINE in Italy seem to have this same or maybe very similar phenotype of TSE;
In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html
archived url link;
https://webarchive.nationalarchives.gov.uk/ukgwa/20040722121714/http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html#fse
-------- Original Message --------
Subject: FDA BSE Update - Pet Food from Canadian Manufacturer & MAD DOG DATA
Date: Tue, 27 May 2003 08:07:58 -0500
From: "Terry S. Singeltary Sr." To: Bovine Spongiform Encephalopathy
Statement
FOR IMMEDIATE RELEASE Statement May 26, 2003
Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
FDA BSE Update - Pet Food from Canadian Manufacturer
The Food and Drug Administration (FDA) has learned from the government of Canada that rendered material from a Canadian cow that last week tested positive for bovine spongiform encephalopathy (BSE, also known as mad cow disease ) may have been used to manufacture pet food, specifically dry dog food, some of which was reported to have been shipped to the United States. The Canadian government prevented the BSE positive cow from being processed for human food. Therefore, consumers can be assured that their food does not contain any remnants of the BSE positive cow.
It is also important to stress that there is no scientific evidence to date that dogs can contract BSE or any similar disease. In addition there is no evidence that dogs can transmit the disease to humans.
FDA notified the U.S. pet food firm, The Pet Pantry International, of Carson City, Nevada, when FDA learned that the pet food that the firm received may have included rendered material from the BSE positive cow. The manufacturer of the pet food is Champion Pet Food, Morinville, Alberta. Even though there is no known risk to dogs from eating this dog food, as a prudent measure to help assure that the U.S. stays BSE free The Pet Pantry International is asking its customers who may have purchased the suspect product to hold it for pickup by the distributor so that the dog food will not mistakenly be mixed into cattle or other feeds if any of the dog food is discarded or otherwise not used to feed dogs. The suspect dog food was produced by Champion Pet Food between February 4, 2003, and March 12, 2003.
The Pet Pantry products were packaged in 50 lb bags, distributed to franchises around the country, and sold by home delivery only. There was no retail distribution of the product. Consumers purchase Pet Pantry products by phone or email orders. The product is then delivered by the nearest franchisee directly to the consumer s home.
The product subject to this notification includes Maintenance Diet labeled with a use by date of 17FEB04 and Beef with Barley with a use by date of 05MAR04 . Consumers who have purchased dog food from The Pet Pantry since February of this year are asked to check their present supplies and see if any match the description of the product being removed. If so, consumers are asked to contact The Pet Pantry at 1-800-381-7387 for further information on how to return the product to The Pet Pantry for proper disposal. Consumers are asked not to destroy or discard the product themselves. The Pet Pantry will also use its sales records to contact consumers who purchased the affected product.
FDA is working closely with the Pet Pantry International to assure for proper disposal of the recovered product.
FDA will continue to provide updates on this case of BSE in Canada as additional information becomes available.
http://www.fda.gov/bbs/topics/NEWS/2003/NEW0910.html
archived url link;
http://web.archive.org/web/20030605085501/http://www.fda.gov/bbs/topics/NEWS/2003/NEW0910.html
It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994)
Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier.
Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
snip...
http://www.bseinquiry.gov.uk/files/ws/s324.pdf
archived url link;
cases have been reported in domestic cats), are characterised by long asymptomatic incubation periods followed by progressive symptoms and signs of degeneration of the brain, leading eventually to death.
http://www.bsereview.org.uk/download/draft_2.pdf
PET FOODS MAD CATS AND MAD DOGS BSE/TSEs
worse still, there is serious risk the media could get to hear of such a meeting...
snip...
Crushed heads (which inevitably involve brain and spinal cord material) are used to a limited extent but will also form one of the constituent raw materials of meat and bone meal, which is used extensively in pet food manufacturer...
http://www.bseinquiry.gov.uk/files/yb/1989/03/17004001.pdf
ARCHIVED URL LINK ;
http://web.archive.org/web/20090505225022/http://www.bseinquiry.gov.uk/files/yb/1989/03/17004001.pdf
2. The Parliamentary Secretary said that he was concerned about the possibility that countries in which BSE had not yet been detected could be exporting raw meat materials (in particular crushed heads) contaminated with the disease to the UK for use in petfood manufacture...
snip...
YOU explained that imported crushed heads were extensively used in the petfood industry...
http://www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf
ARCHIVED URL LINK ;
http://web.archive.org/web/20090505233039/http://www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf
In particular I do not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed...
http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf
ARCHIVED URL LINK ;
http://web.archive.org/web/20090505233046/http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf
BSE IN PETFOOD
1. The Secretary asked on 19 April whether I was content with the advice in para 3 of the record of the meeting on 17 March with the Parliamentary Secretary (Mr Thompson). The simple answer is ''not entirely''.
2. On occasions, material obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in petfood manufacture. Some of this material must be classified as high risk since it contains brain, spinal cord, spleen or lymphatic glands.
http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090505233052/http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf
Meldrum's notes on pet foods and materials used
http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090505233041/http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf
http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506015917/http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf
IN CONFIDENCE CJD TO CATS...
It should be noted that under experimental conditions cats succumb to an encephalopathy after intracerebral inoculation of material derived from patients affected with Creutzfeldt-Jakob Disease.
http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506055329/http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf
Confidential BSE and __________________
3. I have thought very hard about whether the Branch should carry out a similar exercise with meat and meat products for human foods. On balance I do NOT think we should undertake it, but a final decision has not been taken and you may wish to discuss this further. ...
http://www.bseinquiry.gov.uk/files/yb/1989/05/22012001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20030509205351/http://www.bseinquiry.gov.uk/files/yb/1989/05/22012001.pdf
1st case natural FSE
NATURAL SPONGIFORM ENCEPHALOPATHY IN A DOMESTIC CAT
1. We have heard from MAFF that a domestic Siamese cat from the Bristol area has had spongiform encephalopathy confirmed. Although there are previous instances of experimental infection in cats, there have been no previous natural infections reported. The assumption must be the cat became infected by scrapie/BSE agent in it's food. ...
http://www.bseinquiry.gov.uk/files/yb/1990/05/09002001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506015733/http://www.bseinquiry.gov.uk/files/yb/1990/05/09002001.pdf
FSE and pharmaceuticals
1. An analysis by MCA Professional staff of the results to the questionnaire sent out to industry to obtain additional data about the use of animal materials of any origin in the manufacture of pharmaceutical products for human use, reveals that material of feline or canine origin is used in only two licensed products. In both instances the material is sourced from outside the U.K. and from areas currently believed to be free from B.S.E.
ARCHIVED URL LINK;
http://web.archive.org/web/20090506041332/http://www.bseinquiry.gov.uk/files/yb/1990/05/10005001.pdf
CONFIDENTIAL
Confidential cats/dogs and unsatisfactory posture MAFFs failure to assure key research
3. First, I am very uneasy about the relative lack of urgency and interest that MAFF appear to hold for getting the necessary research programme on BSE and related encephalopathies started, and getting it going fast. FOR EXAMPLE, MR BRADLEY of CVL said that there were difficulties in organizing transmission experiments from the brain of the cat which died of an encephalopathy in Bristol. There were arguments going on about who should pay for this work. Should it be MAFF, the Bristol Veterinary School or someone else? Dr. Tyrrell was clearly exasperated.
snip...
11. The Committee were even LESS FORTHCOMING on what their reaction might be if an encephalopathy is found in another species, perhaps in DOGS. Their first reaction was that, as with the cats, the first step could be to investigate whether this was really a new disease, or simply one that had not previously been recognized and to see whether it has any links to BSE, scrapie or other transmissible encephalopathies. Indeed, some members of the Committee seem to regard the whole question of another species as a hypothetical question to be addressed only when it happened. A rather UNSATISFACTORY POSTURE.
12. In advance of your meeting with Dr Tyrrell on Monday morning, I have not voiced my ANXIETIES about the support the Committee is receiving from MAFF to anyone OTHER THAN DR PICKLES. ...
http://www.bseinquiry.gov.uk/files/yb/1990/06/14006001.pdf
ARCHIVED URL LINK;
CONFIDENTIAL
http://web.archive.org/web/20030605151602/http://www.bseinquiry.gov.uk/files/yb/1990/06/14006001.pdf
can't forget about the mad man and his mad cat;
Deaths of CJD man and cat linked
http://news.bbc.co.uk/1/hi/health/184558.stm
In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.
https://pubmed.ncbi.nlm.nih.gov/9798590/
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html
Image] Research letters Volume 352, Number 9134 [Image] 3 October1998[Previous] [Next] [Image][Image]
Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy
[Image] Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, SergioFerrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, SalvatoreMonaco
Transmissible spongiform encephalopathies (TSE) encompass inherited,acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four typesof PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 inthe UK.5 We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat. A 60-year-old man, with no unusual dietary habits, was admitted in November,1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, andmyoclonus. An electroencephalogram (EEG) showed diffuse theta-deltaactivity. A brain magnetic resonance imaging scan was unremarkable. 10 days later, he was speechless and able to follow only simple commands. Repeat EEGs showed periodic triphasic complexes. 2 weeks after admission, he was mute, akinetic, and unable to swallow. He died in early January, 1994. His 7-year-old, neutered, female short haired cat presented in November,1993, with episodes of frenzy, twitching of its body, and hyperaesthesia.The cat was usually fed on canned food and slept on its owner's bed. No bites from the cat were recalled. In the next few days, the cat became ataxic, with hind quarter locomotor dysfunction; the ataxia got worse and there was diffuse myoclonus. The cat was killed in mid-January, 1994. No pathogenic mutations in the patient's PrP gene were found. The patientand the cat were methionine homozygous at codon 129. Histology of thepatient's brain showed neocortical and cerebellar neuronal loss,astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a punctate pattern and paralleled spongiform changes (figure B). The cat's brain showed mild and focal spongiosis in deeper cortical layers of all four lobes (figure C), vacuolated cortical neurons (figure D), and mild astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed. Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and caudate nucleus (figure E). Western blot analysis of control and affected human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After digestion with proteinase K and deglycosylation, only samples from the affected patient and cat showed type-1 PrPres, with PrP glycoform ratios comparable to those observed in sporadic CJD1 (details available fromauthor).
[Image] Microscopic sections of patient and cat brains
A: Occipital cortex of the patient showing moderate spongiformde generation and neuronal loss (haematoxylin and eosin) and
B: punctate perineuronal pattern of PrP immunoreactivity; peroxidase immunohistochemistry with monoclonal antibody 3F4.
C: cat parietal cortex showing mild spongiform degeneration (haematoxylin and eosin).
D: vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase immunohistochemistry with antibody 3F4 shows punctate perineuronalde position of PrP in temporal cortex. This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2
Taken together, our data suggest that the same agent strain of sporadic CJDs involved in the patient and in his cat. It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source,or the chance occurrence of two sporadic forms.
http://www.ncbi.nlm.nih.gov/pubmed/9798590
http://www.lancet.com/journals/lancet/article/PIIS0140-6736(05)79756-7/fulltext
Monday, May 12, 2008
Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease
http://betaamyloidcjd.blogspot.com/2008/05/fecal-transmission-of-aa-amyloidosis-in.html
indeed there have been 4 documented cases of TSE in Lions to date.
Lion 32 December 98 Born November 86
Lion 33 May 1999 (euthanased) Born November 81.
Lion 36 Euthanased August 2000 Born July 87. Deteriorating hind limb ataxia.
Lion 37 Euthanased November 2001 Male, 14 years. Deteriorating hind limb ataxia since September 2001. (Litter mate to Ref. 36.)
http://www.defra.gov.uk/animalh/bse/index.html
ARCHIVED URL LINK;
https://webarchive.nationalarchives.gov.uk/ukgwa/20040722073834/http://www.defra.gov.uk/animalh/bse/bse-science/level-4-bse.html
go to the url above, on the bar at the top, click on _statistics_, then in middle of next page, click on _other TSEs_.
or go here;
http://www.defra.gov.uk/animalh/bse/bse-statistics/level-3-tsestat.html
ARCHIVED URL LINK;
BSE: Statistics - Other TSEs
https://webarchive.nationalarchives.gov.uk/ukgwa/20040722190045/http://www.defra.gov.uk/animalh/bse/bse-statistics/level-3-tsestat.html
and
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html
ARCHIVED URL LINK;
SPONGIFORM ENCEPHALOPATHY IN A CAPTIVE PUMA
an article in yesterday's Times (attached) which suggested that the puma concerned had never ''eaten any part of a cow or sheep which, in the opinion of Government Scientists, could transmit the species to a different species''.
3. You explained to me that this was INCORRECT. The position was as set out in the briefing for Prime Minister's questions attached to Mr Taylor's note. The puma had probably been fed low quality beef meat in the form of split carcasses. ...
http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506032628/http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf
also;
Reports on the clinical symptoms presented by these cats give a relatively homogeneous picture: Affected cats show a lack of coordination with an ataxia mainly of the hind limbs, they often fall and miss their target when jumping. Fear and increased aggressiveness against the owner and also other animals is often seen. They do not longer tolerate to be touched (stroked) and start hiding. These behavioural chances might be the result of a hypersensibility to touch and noise, but also to increased fear. Excessive salivation is another more frequently seen symptom. Cats with FSE in general show severe behavioural disturbances, restlessness and depression, and a lack of coat cleaning. Symptoms in large cats in general are comparable to those in domestic cats. A report on FSE (in german) has been presented in 2001 in the Swiss FVO Magazin. A paper on the first FSE case in a domestic cat in Switzerland is currently in press in the Journal Schweizer Archiv für Tierheilkunde (SAT).
http://www.neurocenter-bern.ch/tse_e.shtml
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Thu, 17 Oct 2002 17:04:51 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L
Greetings BSE-L,
is there any other CWD surveys/testing in the UK on their deer? what sort of testing has been done to date on UK/EU deer? any input would be helpful... thank you
DEER SPONGIFORM ENCEPHALOPATHY SURVEY
3. This will be a low key study with no publicity to avoid unnecessary media interest. It will be carried out in two stages ;
(I) A small scale examination of around 30 deer brains to establish the normal histology of the healthy brain; and
(II) A larger scale random examination of 300 or more adult deer brains drawn from both deer farms and parks to establish whether there is any evidence of a cervine spongiform encephalopathy. ...
http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
Ministry of Agriculture Fisheries and Food
Veterinary Investigation Centre
West House. Station Road. Thirsk Y07 IPZ
Telephone: 0845·522065 Fax: 0845·525224
Your reference
Our reference RJH/ASB
Date 4 November 1992
DEER SPONGIFORM ENCEPHALOPATHY SURVEY
Dear Paul
I have now found time to review the 10 deer- brains collected from Mr Walker farm··via Winchester Via Winchester
VIC. In answer to your specific question was there sufficient difference in preservation of brain tissue to warrant the extra effort involved in rapid brain removal on the farm, the answer is definitely "Yes." The original five brains (Winchester ref M487/11) showed varying degrees of autolytic vacuolation affecting both white and grey matter throughout the brain. vacuolation and separation of Purkinje cells and marked perivascular spaces. These artifacts made interpretation of subtle, specific pathological vacuolation more difficult. By contrast the second submission (Winchester reference N736/2) showed excellent preservation of white and grey matter. Any vacuolar Change present could be confidently interpreted as pathological albeit of unknown pathogenesis.
I can only reiterate the comments made by Gerald Wells and myself at the preliminary discussion at Weybridge in Autumn 1991. If the survey's purpose is an accurate histopathological interpretation of brain tissue. the material must be collected in a pristine state. This is particularly valid when looking for ar unrecognised and undefined spongiform encephalopathy in a new species. Deer brains are very large structures which take a lot of fixation and therefore must be handled sympathetically from the start. We have already seen the problems encountered in comparatively smaller hound brains where delayed fixation was a major limitation on interpretation of true pathological change.
The bottom line must be that if a pathologist's expertise is to be used, it is critical to collect artefact free brain material. If the politics or economics do not allow this, then I would suggest that an electron microscopy survey involving detection of scrapie associated fibrils would be much more appropriate.
Best wishes
Yours sincerely
R J HIGGINS VIO 92/11.4/2.1
http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506032702/http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's minute.
I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.
J W WILESMITH
Epidemiology Unit
18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20030910030852/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.
http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506043913/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf
37. Putative TSE in hounds - work started 1990 -(see para 41)
Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) dated November 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.
41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).
http://www.bseinquiry.gov.uk/witness/htm/stat067.htm
1. I have had no further submission of material or communication regarding this survey since January 1991.
http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506031340/http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf
HOUND SURVEY PATHOLOGICAL REPORT (see positive results)
http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf
ARCHIVED ULR LINK;
http://web.archive.org/web/20090506035936/http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf
kind regards, terry
###########bse-l ############
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" wt.net="">
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler<3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">===============
Incubation periods for BSE are proportional to the life expectancy of the animal affected. The disease's incubation period is 18% of a cow's life expectancy and would be expected to about double when crossing to another species [---] that is, to 36% of 70 years in humans.
Steve Dealler, consultant in medical microbiology. Burnley General Hospital, Burnley BB10 2PQ deal@airtime.co.uk
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-------- Original Message --------
Subject: Cognitive Dysfunction Syndrome (CDS) or MAD DOG DISEASE
Date: Mon, 4 Apr 2005 13:14:12 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@KALIV.UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy #####################
Greetings,
THIS is a hoot from purina, as to why your dog might be acting a bit strangely. nothing mentioned about the decades of feeding those dogs the same thing we been feeding humans, potentially tainted feed, tainted with TSEs. dog food (like cat food) is loaded with SRMs. new regulations are suppose to go into effect, but that will not help all the animals exposed over the decades. some data on dogs, cats and TSE. THE reason of bringing this up again, there was a small write-UP in question to a Dr. Michael Fox about this in the Houston Chronicle 'Easing Life of older dogs' ; 'My black Lab is 12 years old and has entered his ''Alzheimer's'' phase ... 'it's called canine cognitive dysfunction disorder ... snip... end SO, went to see what the feed sellers say about this ; Does your dog suffer from Cognitive Dysfunction Syndrome? Find out how to cope with dog dementia. Typically, an elderly dog tends to sleep longer hours and slow down in comparison to his or her younger or middle-aged years. But some older dogs exhibit behaviour changes that appear abnormal. Until recently, such changes had been attributed to normal aging, for which little could be done. However, behaviour changes in elderly dogs may be due to a disorder called Cognitive Dysfunction Syndrome. Cognitive Dysfunction Syndrome (CDS) is associated with a number of clinical signs. The diagnosis is made when dogs exhibit multiple signs which develop in old age, and which are not completely due to other medical or physical problems. Dogs with CDS may appear disoriented in familiar surroundings such as their own homes, wandering aimlessly and perhaps appearing to 'forget' to back out of corners. Those that were flawlessly housetrained throughout their lives may start to have 'accidents'. They may no longer greet their owners at the door, bring them balls to throw, or appear to care about being petted. And while they may sleep throughout the day, the night may bring restlessness and increased wandering, as though their biological clocks were reversed. Because aging dogs are increasingly susceptible to medical problems (see 'The Elderly Dog'), regular examinations by a vet are important. Only a veterinary surgeon can determine whether your dog's behaviour changes are due to CDS (rather than, for example, liver, heart, or kidney disease). If a diagnosis of CDS is made, your vet may recommend treatment. Behaviour changes in aging dogs may be responsive to treatment. Whatever, happens, after a lifetime of unconditional love and companionship, our older dogs deserve every consideration we can give them.
http://www.purina.co.uk/index.asp?frame=/dog/article.asp&id=71
ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">http://web.archive.org/web/20061007193448/http://www.purina.co.uk/index.asp?frame=/dog/article.asp&id=71
Is your dog elderly? If so, you'll have to ease their way. Here's how... Often dogs are older than we think they are. It's hard to guess-timate how old a dog is as there are considerable breed differences between dogs. Generally speaking, small dogs live the longest (a Yorkshire Terrier is considered 'old' at 10 years), while large breeds have relatively short lifespans (a Great Dane is considered 'old' at six years). Here we help you tell if your dog is old and then advise you on how to make your elderly dog's life easier& The physical signs: Physical inactivity- Difficulty getting up after lying down for a while or after a long walk can be a sign of deteriorating joints due to wear and tear through life. Some dogs may be less keen to go for walks and prefer to curl up in a warm bed. Others may be initially keen to go out but as the joints ease with gentle exercise may be tempted to do a little too much with dire consequences later in the day as joints stiffen up and become even worse. Hair loss- The skin may appear dry and scaly while the coat texture may be harsher, thinner with bald patches or white hairs. Often the coat is dull and the colour may be less vivid. Dog breath- Bad teeth or gum infections may cause bad breath or inability to eat. A common sign is of food being dropped or excessive salivation and pawing at the mouth. Swellings appearing below the eye may be signs of tooth root abscesses and need veterinary attention. Lumps and bumps- Warts, fatty lumps and even tumours may appear in old age. Check these out with your vet as early detection may save your dog's life. Loss of bladder control- Incontinence: this is sometimes associated with changes in thirst but sometimes it's associated with sore joints, which make posturing difficult. Mental alertness- Many older dogs become confused and fail to recognise their surroundings, their name or their owner! They may become less interested in food or what is happening around them. Some dogs appear dull and depressed while others become disobedient or destructive. Many older dogs get anxious if left alone for any length of time. Sleep- Many older dogs sleep more during the day but sleep less at night. Some may prowl around the house at night because of sore joints, senility or even loneliness. Ways to make your dog's life easier If your dog shows these signs, consider the following to make your dog's life easier: * Install ramps to allow your dog to get back into the house from the garden. * Dry your dog well if you've been walking in the rain. * Arthritic dogs may have trouble standing up after lying down for a period of time so gently rub the muscles to warm them up and relieve some of the stiffness. * Understand that changes in oxygen flow to the brain in old age mean dogs are likely to remember events from the past much better than if they happened yesterday. They get confused. Another change experienced by some dogs, cognitive dysfunction syndrome, may affect behaviour in more general ways, similar to the changes caused by senile dementia in humans. * Some retraining may be necessary. Often using treats is a particularly good way to retrain the older dog. Food is a great motivator but beware of obesity in a less active older dog. * Perhaps amounts at mealtimes need adjusting as elderly dogs usually become less active and require fewer calories. But conversely in some dogs, particularly the very old, more calories are needed. The main thing is to keep an eye on the dog's weight, however. * Deteriorating vision and hearing may reduce a dog's ability to respond to his environment. He/she may not greet you immediately only because he/she isn't aware that you've arrived. Take a look at how to cope with blindness and deafness. * Older dogs may also develop a fear of thunderstorms. The booming sounds of thunder may be exaggerated because of a loss of high-frequency hearing. * Ensure their bed is in a warm draught-free place to make sleep time that bit more comfortable.
http://www.purina.co.uk/index.asp?frame=/dog/article.asp&id=69
ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">http://web.archive.org/web/20061007193505/http://www.purina.co.uk/index.asp?frame=/dog/article.asp&id=69
FOR IMMEDIATE RELEASE P01-05 January 30, 2001
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">http://web.archive.org/web/20070209131251/http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
PRION 2009 CONGRESS BOOK OF ABSTRACTS
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
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Chow Down Fido - Dog Food is Safe
FDA report shows no risk from low levels of pentobarbital in dog food.
The low levels of exposure to sodium pentobarbital (pentobarbital) that dogs might receive through food is unlikely to cause them any adverse health effects, Food and Drug Administration (FDA) scientists concluded after conducting a risk assessment.
During the 1990s, FDA’s Center for Veterinary Medicine (CVM) received reports from veterinarians that pentobarbital, an anesthetizing agent used for dogs and other animals, seemed to be losing its effectiveness in dogs. Based on these reports, CVM officials decided to investigate a plausible theory that the dogs were exposed to pentobarbital through dog food, and that this exposure was making them less responsive to pentobarbital when used as a drug.
The investigation consisted of two parts. First, CVM had to determine if dog food could contain residues of the drug. Second, if residues were found, the Center had to determine what risk, if any, the residues posed to dogs. In conjunction with the investigation, the Center wanted to determine if pet food contained rendered remains of dogs and cats.
How Pentobarbital Can Get into Dog Food
Because in addition to producing anesthesia, pentobarbital is routinely used to euthanize animals, the most likely way it could get into dog food would be in rendered animal products.
Pentobarbital seems to be able to survive the rendering process. If animals are euthanized with pentobarbital and subsequently rendered, pentobarbital could be present in the rendered feed ingredients.
In order to determine if pentobarbital residues were present in animal feeds, CVM developed a sophisticated process to detect and quantify minute levels – down to two parts per billion of pentobarbital in dry dog food. To confirm that the methods they developed worked properly, CVM scientists used the methods to analyze dry commercial dog foods purchased from retail outlets near to their Laurel, MD, laboratories. The scientists purchased dog food as part of two surveys, one in 1998 and the second in 2000. They found some samples contained pentobarbital.
Dogs, Cats Not Found
Because pentobarbital is used to euthanize dogs and cats at animal shelters, finding pentobarbital in rendered feed ingredients could suggest that the pets were rendered and used in pet food.
CVM scientists, as part of their investigation, developed a test to detect dog and cat DNA in the protein of the dog food. All samples from the most recent dog food survey (2000) that tested positive for pentobarbital, as well as a subset of samples that tested negative, were examined for the presence of remains derived from dogs or cats.
The results demonstrated a complete absence of material that would have been derived from euthanized dogs or cats. The sensitivity of this method is 0.005 percent on a weight/weight basis; that is, the method can detect a minimum of five pounds of rendered remains in 50 tons of finished feed. Presently, it is assumed that the pentobarbital residues are entering pet foods from euthanized, rendered cattle or even horses.
Finding Levels of Pentobarbital Residues
Upon finding pentobarbital residues in dog food, the researchers undertook an assessment of the risk dogs might face. Dogs were given known quantities of pentobarbital for eight weeks to determine if consumption of small amounts of pentobarbital resulted in any physiological changes that could indicate potential effects on health. In short, the scientists wanted to find the level of pentobarbital dogs could be exposed to that would show no biological effects. The most sensitive indicator that pentobarbital had an effect is an increase in the production of certain enzymes collectively called cytochrome P450.
Virtually all animals produce enzymes as a normal response to metabolize naturally occurring and man-made chemicals in their environment. Barbituates, such as pentobarbital, are especially efficient at causing the liver to produce these enzymes. In dogs, the most sensitive biological response to pentobarbital is an increase in the production of cytochrome P450 enzymes, which is why the scientists chose that as the best indicator of biological effect. If a low level of pentobarbital did not cause a dog to produce additional cytochrome P450 enzymes, then scientists could assume that the pentobarbital at that low level had no significant effect on the dog.
In CVM’s study, experimental animals were each dosed orally with either 50, 150, or 500 micrograms pentobarbital/day for eight weeks. The results were compared with control animals, which were not exposed to pentobarbital.
Several significant pentobarbital-associated effects were identified in this study.
1. Dogs that received 150 and 500 micrograms pentobarbital once daily for eight weeks had statistically higher liver weights (relative to their bodyweights) than the animals in the control groups. Increased liver weights are associated with the increased production by the liver of cytochrome P450 enzymes.
2. An analysis showed that the activity of at least three liver enzymes was statistically greater than that of the controls at doses of approximately 200 micrograms pentobarbital per day or greater.
But researchers found no statistical differences in relative liver weight or liver enzyme activity between the group receiving 50 micrograms pentobarbital per day and the controls. Based on the data from this study, CVM scientists were able to determine that the no-observable-effect level – which is the highest dose at which no effects of treatment were found – for pentobarbital was 50 micrograms of pentobarbital per day.
Adverse Health Effects Unlikely
For the purposes of CVM’s assessment, the scientists assumed that at most, dogs would be exposed to no more than four micrograms/kilogram body weight/day based on the highest level of pentobarbital found in the survey of dog foods. In reality, dogs are not likely to consume that much. The high number was based on the assumption that the smallest dogs would eat dog food containing the greatest amount of pentobarbital detected in the survey of commercial pet foods – 32 parts per billion.
However, to get to the exposure level of 50 micrograms of pentobarbital per day, which is the highest level at which no biological response was seen, a dog would have to consume between 5 to 10 micrograms of pentobarbital per kilogram of body weight. But the most any dog would consume, based on the survey results, was four micrograms pentobarbital per kilogram of body weight per day.
It should be emphasized that induction of cytochrome P450 enzymes is a normal response to many substances that are naturally found in foods. It is not an indication of harm, but was selected as the most sensitive indicator to detect any biological effect due to pentobarbital.
Thus, the results of the assessment led CVM to conclude that it is highly unlikely a dog consuming dry dog food will experience any adverse effects from exposures to the low levels of pentobarbital found in CVM’s dog food surveys.
Additional information, including the survey results, can be found on CVM’s Web site at www.fda.cvm.gov under “Freedom of Information.”
April 2002 Render
http://www.rendermagazine.com/April2002/ChowDownFido.html
Reprinted with permission from Earth Island Journal (vol. 11, no. 3, Summer 1996) (vol. 5, no. 4, Fall 1990) 300 Broadway, Suite 28 San Francisco, CA 94133, USA Phone: +1 (415) 788 3666 Fax: +1 (415) 788 7324 E-mail: earthisland@igc.apc.org Web page: http://www.earthisland.org/ei/
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1. THE TRUTH ABOUT CATS AND DOGS by Ann Martin
The pet food industry, a billion-dollar, unregulated operation, feeds on the garbage that otherwise would wind up in landfills or be transformed into fertiliser. The hidden ingredients in a can of commercial pet food may include roadkill and the rendered remains of cats and dogs. The pet food industry claims that its products constitute a "complete and balanced diet" but, in reality, commercial pet food is unfit for human or animal consumption.
"Vegetable protein", the mainstay of dry dog foods, includes ground yellow corn, wheat shorts and middlings, soybean meal, rice husks, peanut meal and peanut shells (identified as "cellulose" on pet food labels). These often are little more than the sweepings from milling room floors. Stripped of their oil, germ and bran, these "proteins" are deficient in essential fatty acids, fat-soluble vitamins and antioxidants. "Animal protein" in commercial pet foods can include diseased meat, roadkill, contaminated material from slaughterhouses, faecal matter, rendered cats and dogs and poultry feathers. The major source of animal protein comes from dead-stock removal operations that supply so-called "4-D" animals - dead, diseased, dying or disabled - to "receiving plants" for hide, fat and meat removal. The meat (after being doused with charcoal and marked "unfit for human consumption") may then be sold for pet food.
Rendering plants process decomposing animal carcasses, large roadkill and euthanised dogs and cats into a dry protein product that is sold to the pet food industry. One small plant in Quebec, Ontario, renders 10 tons (22,000 pounds) of dogs and cats per week. The Quebec Ministry of Agriculture states that "the fur is not removed from dogs and cats" and that "dead animals are cooked together with viscera, bones and fat at 115° C (235° F) for 20 minutes".
The US Food and Drug Administration's Center for Veterinary Medicine (CVM) is aware of the use of rendered dogs and cats in pet foods, but has stated: "CVM has not acted to specifically prohibit the rendering of pets. However, that is not to say that the practise of using this material in pet food is condoned by the CVM."
In both the US and Canada, the pet food industry is virtually self-regulated. In the US, the Association of American Feed Control Officials (AAFCO) sets guidelines and definitions for animal feed, including pet foods. In Canada, the most prominent control is the "Labeling Act", simply requiring product labels to state the name and address of the manufacturer, the weight of the product and whether it is dog or cat food. The Canadian Veterinary Medical Association (CVMA) and the Pet Food Association of Canada (PFAC) are voluntary organisations that, for the most part, rely on the integrity of the companies they certify to assure that product ingredients do not fall below minimum standards.
The majority - 85 to 90 per cent - of the pet food sold in Canada is manufactured by US-based multinationals. Under the terms of the US-Canada Free Trade Agreement, neither the CVMA nor PFAC exercises any control over the ingredients in cans of US pet food.
Pet food industry advertising promotes the idea that, to keep pets healthy, one must feed them commercially formulated pet foods. But such a diet contributes to cancer, skin problems, allergies, hypertension, kidney and liver failure, heart disease and dental problems. One more item should be added to pet food labels: a skull-and-crossbones insignia!
(Ann Martin is an animal rights activist and leading critic of the commercial pet food industry. She lives in London, Ontario, Canada.)
2. FOOD NOT FIT FOR A PET
by Dr Wendell O. Belfield, D.V.M. The most frequently asked question in my practice is, "Which commercial pet food do you recommend?" My standard answer is "None." I am certain that pet-owners notice changes in their animals after using different batches of the same brand of pet food. Their pets may have diarrhoea, increased flatulence, a dull hair coat, intermittent vomiting or prolonged scratching. These are common symptoms associated with commercial pet foods.
In 1981, as Martin Zucker and I wrote How to Have a Healthier Dog, we discovered the full extent of negative effects that commercial pet food has on animals. In February 1990, San Francisco Chronicle staff writer John Eckhouse went even further with an exposé entitled "How Dogs and Cats Get Recycled into Pet Food".
Eckhouse wrote: "Each year, millions of dead American dogs and cats are processed along with billions of pounds of other animal materials by companies known as renderers. The finished product...tallow and meat meal...serve as raw materials for thousands of items that include cosmetics and pet food."
Pet food company executives made the usual denials. But federal and state agencies, including the Food and Drug Administration, and medical groups, such as the American Veterinary Medical Association and the California Veterinary Medical Association (CVMA), confirm that pets, on a routine basis, are rendered after they die in animal shelters or are disposed of by health authorities - and the end product frequently finds its way into pet food.
Government health officials, scientists and pet food executives argue that such open criticism of commercial pet food is unfounded. James Morris, a professor at the School of Veterinary Medicine at Davis, California, has said, "Any products not fit for human consumption are very well sterilised, so nothing can be transmitted to the animal." Individuals who make such statements know nothing of the meat and rendering business.
For seven years I was a veterinary meat inspector for the US Department of Agriculture and the State of California. I waded through blood, water, pus and faecal material, inhaled the fetid stench from the killing floor and listened to the death cries of slaughtered animals.
Prior to World War II, most slaughterhouses were all-inclusive; that is, livestock was slaughtered and processed in one location. There was a section for smoking meats, a section for processing meats into sausages, and a section for rendering. After World War II, the meat industry became more specialised. A slaughterhouse dressed the carcasses, while a separate facility made the sausages. The rendering of slaughter waste also became a separate speciality - no longer within the jurisdiction of federal meat inspectors and out of the public eye.
To prevent condemned meat from being rerouted and used for human consumption, government regulations require that meat be "denatured" before removal from the slaughterhouse and shipment to rendering facilities. In my time as a veterinary meat inspector, we denatured with carbolic acid (a potentially corrosive disinfectant) and/or creosote (used for wood-preservation or as a disinfectant). Both substances are highly toxic. According to federal meat inspection regulations, fuel oil, kerosene, crude carbolic acid and citronella (an insect repellent made from lemon grass) are all approved denaturing materials.
Condemned livestock carcasses treated with these chemicals can become meat and bone meal for the pet food industry. Because rendering facilities are not government-controlled, any animal carcasses can be rendered - even dogs and cats. As Eileen Layne of the CVMA told the Chronicle, "When you read pet food labels, and it says "meat and bone meal", that's what it is: cooked and converted animals, including some dogs and cats."
Some of these dead pets - those euthanised by veterinarians - already contain pentobarbital before treatment with the denaturing process. According to University of Minnesota researchers, the sodium pentobarbital used to euthanise pets "survives rendering without undergoing degradation". Fat stabilisers are introduced into the finished rendered product to prevent rancidity. Common chemical stabilisers include BHA (butylated hydroxyanisole) and BHT (butylated hydroxytoluene) - both known to cause liver and kidney dysfunction - and ethoxyquin, a suspected carcinogen. Many semi-moist dog foods contain propylene glycol - first cousin to the anti-freeze agent, ethylene glycol, that destroys red blood-cells. Lead frequently shows up in pet foods, even those made from livestock meat and bone meal. A Massachusetts Institute of Technology study, titled "Lead in Animal Foods", found that a nine-pound cat fed on commercial pet food ingests more lead than the amount considered potentially toxic for children.
I have been practising small-animal medicine for more than 25 years. Every day I see the casualties of pet industry propaganda. But the professors in the teaching institutions of veterinary medicine generally support an industry that has little regard for the quality of health in our companion animals.
One last word of caution: meat and bone meal from sources not fit for human consumption have found their way into poultry feed. This means that animal products rendered under questionable conditions are fed to birds that may wind up on your table. Remember this when you are eating your next piece of chicken or turkey.
(Dr Belfield is a graduate of Tuskegee Institute of Veterinary Medicine and is now in private practice in San Jose, California. Dr Belfield established the first orthomolecular veterinary hospital in the US. He is co-author of The Very Healthy Cat Book and How to Have a Healthier Dog. This article first appeared in Let's Live Magazine, May 1992.)
3. A LOOK INSIDE A RENDERING PLANT
by Gar Smith Rendering has been called "the silent industry". Each year in the US, 286 rendering plants quietly dispose of more than 12.5 million tons of dead animals, fat and meat wastes. As the public relations watchdog newsletter PR Watch observes, renderers "are thankful that most people remain blissfully unaware of their existence".
When City Paper reporter Van Smith visited Baltimore's Valley Proteins rendering plant last summer, he found that the "hoggers" (the large vats used to grind and filter animal tissues prior to deep-fat-frying) held an eclectic mix of body parts ranging from "dead dogs, cats, raccoons, possums, deer, foxes [and] snakes" to a "baby circus elephant" and the remains of Bozeman, a Police Department quarterhorse that "died in the line of duty".
In an average month, Baltimore's pound hands over 1,824 dead animals to Valley Proteins. Last year, the plant transformed 150 millions pounds of decaying flesh and kitchen grease into 80 million pounds of commercial meat and bone meal, tallow and yellow grease. Thirty years ago, most of the renderer's wastes came from small markets and slaughterhouses. Today, thanks to the proliferation of fast-food restaurants, nearly half the raw material is kitchen grease and frying oil.
Recycling dead pets and wildlife into animal food is "a very small part of the business that we don't like to advertise," Valley Proteins' President, J. J. Smith, told City Paper. The plant processes these animals as a "public service, not for profit," Smith said, since "there is not a lot of protein and fat [on pets]..., just a lot of hair you have to deal with somehow."
According to City Paper, Valley Proteins "sells inedible animal parts and rendered material to Alpo, Heinz and Ralston-Purina". Valley Proteins insists that it does not sell "dead pet by-products" to pet food firms since "they are all very sensitive to the recycled pet potential". Valley Proteins maintains two production lines - one for clean meat and bones and a second line for dead pets and wildlife. However, Van Smith reported, "the protein material is a mix from both production lines. Thus the meat and bone meal made at the plant includes materials from pets and wildlife, and about five per cent of that product goes to dry-pet-food manufacturers..."
A 1991 USDA report states that "approximately 7.9 billion pounds of meat and bone meal, blood meal and feather meal [were] produced in 1983". Of that amount, 34 per cent was used in pet food, 34 per cent in poultry feed, 20 per cent in pig food and 10 per cent in beef and dairy cattle feed.
Transmissible spongiform encephalopathy (TSE) carried in pig- and chicken-laden foods may eventually eclipse the threat of "mad cow disease". The risk of household pet exposure to TSE from contaminated pet food is more than three times greater than the risk for hamburger-eating humans.
(Gar Smith is Editor of Earth Island Journal.)
4. THE DARK SIDE OF RECYCLING [Author's name withheld]
[In February 1990, the San Francisco Chronicle carried a macabre two-part story detailing how stray dogs, cats and pound animals are routinely rounded up by meat renderers and ground up into - of all things - pet food. According to the researcher who brought the information to the Chronicle, the paper buried the story and deleted many of the charges he had documented. A report he worked on for ABC television's 20-20 was similarly watered down. In exasperation, he sent the story to Earth Island Journal. NEXUS has been asked to withhold the name of the author/researcher, who has been forced to flee San Francisco with his wife and go into hiding as a result of the threats made against his well-being. Ed.]
The rendering plant floor is piled high with "raw product": thousands of dead dogs and cats; heads and hooves from cattle, sheep, pigs and horses; whole skunks; rats and raccoons - all waiting to be processed. In the 90-degree heat, the piles of dead animals seem to have a life of their own as millions of maggots swarm over the carcasses.
Two bandana-masked men begin operating Bobcat mini-dozers, loading the "raw" into a 10-foot- deep stainless-steel pit. They are undocumented workers from Mexico, doing a dirty job. A giant auger-grinder at the bottom of the pit begins to turn. Popping bones and squeezing flesh are sounds from a nightmare you will never forget.
Rendering is the process of cooking raw animal material to remove the moisture and fat. The rendering plant works like a giant kitchen. The cooker, or "chef", blends the raw product in order to maintain a certain ratio between the carcasses of pets, livestock, poultry waste and supermarket rejects.
Once the mass is cut into small pieces, it is transported to another auger for fine shredding. It is then cooked at 280 degrees for one hour. The continuous batch cooking process goes on non-stop, 24 hours a day, seven days a week as meat is melted away from bones in the hot 'soup'. During this cooking process, the 'soup' produces a fat of yellow grease or tallow that rises to the top and is skimmed off. The cooked meat and bone are sent to a hammermill press, which squeezes out the remaining moisture and pulverises the product into a gritty powder. Shaker screens sift out excess hair and large bone chips. Once the batch is finished, all that is left is yellow grease, meat and bone meal.
A Meaty Menu As the American Journal of Veterinary Research explains, this recycled meat and bone meal is used as "a source of protein and other nutrients in the diets of poultry and swine and in pet foods, with lesser amounts used in the feed of cattle and sheep. Animal fat is also used in animal feeds as an energy source." Every day, hundreds of rendering plants across the United States truck millions of tons of this "food enhancer" to poultry ranches, cattle feed-lots, dairy and hog farms, fish-feed plants and pet-food manufacturers where it is mixed with other ingredients to feed the billions of animals that meat-eating humans, in turn, will eat.
Rendering plants have different specialities. The labelling designation of a particular "run" of product is defined by the predominance of a specific animal. Some product-label names are: meat meal, meat by-products, poultry meal, poultry by-products, fish meal, fish oil, yellow grease, tallow, beef fat and chicken fat.
Rendering plants perform one of the most valuable functions on Earth: they recycle used animals. Without rendering, our cities would run the risk of becoming filled with diseased and rotting carcasses. Fatal viruses and bacteria would spread uncontrolled through the population.
The Dark Side Death is the number one commodity in a business where the demand for feed ingredients far exceeds the supply of raw product. But this elaborate system of food production through waste management has evolved into a recycling nightmare. Rendering plants are unavoidably processing toxic waste.
The dead animals (the "raw") are accompanied by a whole menu of unwanted ingredients. Pesticides enter the rendering process via poisoned livestock, and fish oil laced with bootleg DDT and other organophosphates that have accumulated in the bodies of West Coast mackerel and tuna.
Because animals are frequently shoved into the pit with flea collars still attached, organophosphate-containing insecticides get into the mix as well. The insecticide Dursban arrives in the form of cattle insecticide patches. Pharmaceuticals leak from antibiotics in livestock, and euthanasia drugs given to pets are also included. Heavy metals accumulate from a variety of sources: pet ID tags, surgical pins and needles.
Even plastic winds up going into the pit. Unsold supermarket meats, chicken and fish arrive in styrofoam trays and shrink wrap. No one has time for the tedious chore of unwrapping thousands of rejected meat-packs. More plastic is added to the pits with the arrival of cattle ID tags, plastic insecticide patches and the green plastic bags containing pets from veterinarians.
Rendering Judgements Skyrocketing labour costs are one of the economic factors forcing the corporate flesh-peddlers to cheat. It is far too costly for plant personnel to cut off flea collars or unwrap spoiled T-bone steaks. Every week, millions of packages of plastic-wrapped meat go through the rendering process and become one of the unwanted ingredients in animal feed.
The most environmentally conscious state in the nation is California, where spot checks and testing of animal-feed ingredients happen at the wobbly rate of once every two-and-a-half months. The supervising state agency is the Department of Agriculture's Feed and Fertilizer Division of Compliance. Its main objective is to test for truth in labelling: does the percentage of protein, phosphorous and calcium match the rendering plant's claims; do the percentages meet state requirements? However, testing for pesticides and other toxins in animal feeds is incomplete.
In California, eight field inspectors regulate a rendering industry that feeds the animals that the state's 30 million people eat. When it comes to rendering plants, however, state and federal agencies have maintained a hands-off policy, allowing the industry to become largely self-regulating. An article in the February 1990 issue of Render, the industry's national magazine, suggests that the self-regulation of certain contamination problems is not working.
One policing program that is already off to a shaky start is the Salmonella Education/Reduction Program, formed under the auspices of the National Renderers Association. The magazine states that "...unless US and Canadian renderers get their heads out of the ground and demonstrate that they are serious about reducing the incidence of salmonella contamination in their animal protein meals, they are going to be faced with...new and overly stringent government regulations."
So far, the voluntary self-testing program is not working. According to the magazine, "...only about 20 per cent of the total number of companies producing or blending animal protein meal have signed up for the program..." Far fewer have done the actual testing.
The American Journal of Veterinary Research conducted an investigation into the persistence of sodium phenobarbital in the carcasses of euthanised animals at a typical rendering plant in 1985 and found "...virtually no degradation of the drug occurred during this conventional rendering processŠ" and that "...the potential of other chemical contaminants (e.g., heavy metals, pesticides and environmental toxicants, which may cause massive herd mortalities) to degrade during conventional rendering needs further evaluation."
Renderers are the silent partners in our food chain. But worried insiders are beginning to talk, and one word that continues to come up in conversation is "pesticides". The possibility of petrochemically poisoning our food has become a reality. Government agencies and the industry itself are allowing toxins to be inadvertently recycled from the streets and supermarket shelves into the food chain. As we break into a new decade of increasingly complex pollution problems, we must rethink our place in the environment. No longer hunters, we are becoming the victims of our technologically altered food chain.
The possibility of petrochemically poisoning our food has become a reality.
(First published in Earth Island Journal, Fall 1990.)
Mad cow outbreak may have been caused by animal rendering plants N.Y. Times News Service Mar 11, 1997
When cows in Britain began staggering around and dying, their brains eaten away by a mysterious disease, officials in the United States were reassuring. The disease would not be a problem here, they said. Later, when it appeared that a few people in Britain had contracted a similar lethal condition from eating affected meat, experts at the Department of Agriculture said there was no reason for Americans to worry.
Now, though, the Food and Drug Administration is starting to talk about new regulations in the aftermath of disturbing hints that something similar conceivably could appear in American animals. So far, the only affected animals are a few hundred mink in Wisconsin. Nevertheless, the agency wants to restrict the little-known agricultural practice that lies behind the problem in Britain: the use of rendered animal tissue in animal feed. In the process, they are drawing new attention to rendering -- the ancient but seldom-discussed practice of boiling down and making feed meal and other products out of slaughterhouse and restaurant scraps, dead farm animals, road kill and -- distasteful as it may seem -- cats and dogs euthanized in some animal shelters.
This quasi-cannibalism lies behind the outbreak in Britain and regulators want to be sure it will not cause problems in the United States. The disease that struck the British cows, bovine spongiform encephalopathy, may have originated as scrapie, a mysterious condition limited to sheep. Scientists believe the so-called mad cow disease results when cattle eat feed made from the brains or spinal cords of sheep suffering from scrapie. They believe the people who died were infected when they ate beef or other products from these cows, a theory that remains controversial, though evidence is accumulating.
Public health officials and agricultural experts say there are good reasons to believe that mad cow disease will not become a problem in the United States. Scrapie is less common in this country than in Britain. More importantly, the Food and Drug Administration is moving to ban the use of certain animal tissues in cattle feed. The agency recently held hearings on the effects that such a ban might have on the billion-dollar industry and hopes to decide this year whether to impose a ban.
Rendering, which dates to the early Egyptians, operates in the shadows of polite society, persisting because it provides an essential service: disposing of millions of pounds of dead animals every day.
"If you burned all the carcasses, you'd get a terrible air pollution problem," said Dr. William Heuston, associate dean of the Virginia-Maryland College of Veterinary Medicine at College Park, Md. "If you put it all into landfills, you'd have a colossal public health problem, not to mention stench. Dead animals are an ideal medium for bacterial growth."
Renderers in the United States pick up 100 million pounds of waste material every day -- a witch's brew of feet, heads, stomachs, intestines, hooves, spinal cords, tails, grease, feathers and bones. Half of every butchered cow and a third of every pig is not consumed by humans. An estimated six million to seven million dogs and cats are killed in animal shelters each year, said Jeff Frace, a spokesman for the American Society for the Prevention of Cruelty to Animals in New York City.
For example, the city of Los Angeles sends 200 tons of euthanized cats and dogs to West Coast Rendering, in Los Angeles, every month, according to Chuck Ellis, a spokesman for the city's Sanitation Department. Pet food companies try not to buy meat and bone meal from renderers who grind up cats and dogs, said Doug Anderson, president of Darling International Inc., a large rendering company in Dallas. "We do not accept companion animals," he said. "But there are still a number of small plants that will render anything."
At least 250 rendering plants operate in the United States, said Bruce Blanton, executive director of the 130-member National Renderers Association in Alexandria, Va. While there are still a few small operations on the outskirts of some cities, he said, modern rendering plants are large and centralized, and the industry's revenues amount to $2.4 billion a year.
After trucks deliver the wastes to the plants, the material is minced and fed into a vessel where it is steam-cooked to 250 degrees or more, and then the stew is cooked for 20 to 90 minutes, Blanton said. In the resulting mash, heavier material drops to the bottom and the lighter stuff floats to the top. Fat is siphoned off the top, filtered and sent through centrifuges to further refine it, Blanton said. Chemical manufacturers turn much of it into fatty acids for lubricants, lipstick, cement, polish, inks and waxes. Other fractions, including gelatinous layers, tallow and grease, go into thousands of products, including soaps, candles, pharmaceuticals, homeopathic medicines and gummy candies.
The heavier protein material on the bottom goes through a separate process, Blanton said. It is dried, squeezed to remove more fat and dried again. The resulting powder is the major ingredient in pet and animal feed. It is a cannibalistic practice that has proved highly profitable.
"We are the original recyclers," said Dr. Don A. Franco, a veterinarian and director of scientific services for the Animal Protein Producers' Industry, another trade group representing rendering firms. "We recycle 40 billion pounds of material a year."
Mad cow disease erupted in Britain because of a number of factors there, said Dr. Linda Detweiler, a veterinarian with the United States Agriculture Department's Animal and Plant Health Inspection Service in Trenton. Unlike the United States, Britain has a large sheep population relative to cows and a serious problem with scrapie, a transmissible, slowly progressive degenerative brain disease of sheep.
Many scientists who have studied the problem now believe that scrapie somehow crossed a species barrier to infect cows, possibly when the cows ate feed composed in part of brain tissue from infected sheep. The disease presumably jumped to people who ate infected cow brains. Current theory holds that some people may have genes that make them particularly susceptible.
Mad cow disease was first recognized as a cattle disorder in November 1986. Since then more than 165,000 cows have been affected. Heuston said renderers were shocked to learn that an agent like scrapie might survive the rendering process.
But British rendering practices may have helped spread the disease, said David Evans, president of Carolina Byproducts, a rendering company in Greensboro, N.C. There are people in Britain, called knackers, who make a living going around the countryside picking up dead animals and rendering them in their backyards. The fat they obtain brings good money from chemical firms, he said.
These knackers simply grind up and partly cook their daily haul to break fat cells and collect the gunk from the top of their vats. The remaining material, called greaves or crackling, was sold to farmers who then mixed it with grain and fed it to their animals. This material, some derived from sheep with scrapie or cattle with mad cow disease, was fed in large amounts to dairy herds in the late 1980s, Detweiler said.
Yet another factor lay in the way greaves were processed in conventional rendering plants, Anderson said. Until the early 1980s, many renderers had used flammable solvents to dissolve fats and the solvents may have deactivated the agent that causes mad cow disease and scrapie. But after several plant explosions, the companies switched to other methods that appear not to deactivate the agent -- a mysterious particle called a prion.
Since 1989, British renderers have tried to keep infected meat out of their products, many knackers have gone out of business and brains are no longer put into hamburger. But the incubation for the human disease is 7 to 30 years, Evans said. While only 15 cases of human disease have been confirmed, many experts fear a latent epidemic.
In 1989, the American rendering industry initiated a voluntary program under which, for example, no sheep heads were to be accepted at rendering plants. An Agriculture Department survey three years later found that 6 of 11 plants inspected still did accept sheep heads. Nevertheless, many experts feel that American shores are safe from mad cow disease, especially if scrapie is the underlying vector. In Britain, sheep account for 14 percent of raw rendering material. Here it is 0.6 percent and most of that material is free from scrapie.
The reason is that scrapie is closely monitored by United States Agriculture Department veterinarians under a federal program. There are no knackers in this country and no greaves to infect cattle, Detweiler said. Few ranchers here feed meat and bone meal to young cows and American renderers usually treat the raw material at higher temperatures.
But the key element in efforts to prevent the cow disease is a newly proposed Agriculture Department ban on feeding protein derived from ruminant animals to other ruminants. Ruminants are animals that chew cuds, including cows, sheep, goats, deer and elk. Mink are included in the ban because they can be affected by a disorder similar to mad cow disease.
If the Agriculture Department rules are adopted, cow protein might still be fed to fish, chicken or pigs in hope that if mad cow disease were to appear, a species barrier would stop it from spreading. At the same time, the Agriculture Department continues to monitor American cows for signs of mad cow disease. Scientists have examined the brains of 5,342 cows that displayed symptoms of central nervous system disease; no cases have been discovered.
But a major reason to worry is that the cow epidemic may have nothing to do with scrapie or the processing techniques used by renderers, said Dr. Richard F. Marsh, a veterinarian at the University of Wisconsin in Madison. There are reasons to believe that mad cow disease has already risen spontaneously in American cattle, he said. But it apparently has not jumped into the animal feed supply at this point.
The strongest evidence is an outbreak of mink encephalopathy (a disorder similar to mad cow disease) that occurred in 1985 in Stetsonville, Wis. The mink farmer did not feed commercial meal to his animals, Marsh said. Rather he fed them the meat from a downer cow, a cow that is down and cannot get up. It is possible that the cow had a spontaneous case of mad cow disease and passed it into mink, Marsh said.
Spontaneous cases of mad cow disease may well occur in one cow out of every million cows each year, said Dr. Joseph Gibbs, a leading expert on mad cow disease at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. There are 150 million cows in this country, which means that each year 150 of them might develop mad cow disease -- all on their own, without any exposure to tainted feed.
Renderers pick up the carcasses of 100,000 downer cows every year and mix them in with other animals, Marsh said. Although the Agriculture Department tries to test downer cows for signs of mad cow disease, it can only sample a small percentage. Moreover, animals can be quite sick and not show signs of it before they are sent to slaughter, Marsh said. Thus, try as they might to avoid the problem, renderers could unknowingly introduce infected animals into animal feed and start an epidemic.
Deer and elk also have a spontaneous mad-cow-like disease, Gibbs said. If they die in the woods, the disease would not be transmitted. But if they are killed on the road, they are sent to zoos or greyhound tracks or, more often, go straight to the rendering plant to end up as cattle feed or pet food.
http://www.mad-cow.org/~tom/render_ed.html <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">http://web.archive.org/web/20060616172055/http://www.mad-cow.org/~tom/render_ed.html
Recycled pets and potential for TSE amplification Assuming that a tiny fraction of cats with BSE-FSE ever get diagnosed as such (vestibular disorder more likely, no diagnosis at all likliest), there would be a potential for re-cycling the disease should these infected cats be non-discriminately rendered for pet food:
From Summer 1996 Earth Island Journal v11, #3 pg 27-31:
"The rendering plant floor is piled high with raw product. Thousands of dead dogs and cats; head and hooves from cattle, sheep, pigs and horses; whole skunks; rats and raccoons -- all waiting to be processed. In the 90-degree heat, the piles of dead animals seem to have a life of their own as millions of maggots swarm over the carcassess." "Rendering plants process decomposing animal carcasses, large roadkill and euthanized dogs and cats into a dry protein product that is sold in the pet food industry. One small plant in Quebec renders 22,000 pounds of dogs and cats per week... The fur is not removed and dead animals are cooked together with viscera, bones and fat at 115 C for 20 minutes."
"Each year in the US, 286 rendering plants quietly dispose of more than 12,500,000 tons of dead animals, fat and meat wasts. ... Baltimore's Valley Proteins "hogger" vat contained an eclectic mix of body parts ranging from dead dogs, cats, raccoons, possums, deer, foxes, snakes, a baby circus elephant, and a police quarterhorse.... In an average year, Baltimore's pound hands over 21,888 dead animals to Valley Proteins [which] sells inedible animal parts and rendered material to Alpo, Heinz, and Ralston-Purina [US pet food manufactureres]"
"Valley Protein maintains two production lines -- one for clean meat and bons and a second line for dead pets and wildlife. However, VP President Smith reported, that the [final] protein material is a mix from both production lines. Thus the meat and bone meal made at the plant includes materials from pets and wildlife, and are about five percent of that product goes to dry-pet-food manufacturers."
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Valley Protein responds Gerald F. Smith, Jr., President of Valley Proteins, Inc. responds to your Wednesday, October 23, 1996 transmission at 10:45 a.m. as follows:
"I was misquoted in the article you referenced. Our plant in Baltimore, MD does indeed process dead domestic house pets which have been euthanized by veterinarians, animal control officials, humane societies and other animal protection organizations. This represents less than one-half of 1% of our Baltimore plant's business on an annual basis. Valley Proteins has a total of nine rendering plants in five states. Except for one pet food producer which purchased approximately 10 tons from our Baltimore plant on three different occasions during the last 12 months, we only sell animal proteins to pet food manufacturers from our facilities which are capable of recycling poultry by-products from poultry slaughter facilities. This pet food producer purchased less than one -half of 1% of our total Baltimore Meat Meal production. Therefore, during the last 12 months approximately 300 pounds of our animal protein containing by-products from dead domestic house pets entered the pet food market."
http://www.mad-cow.org/~tom/cats_bse_rend.html
ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
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http://web.archive.org/web/20070122180434/http://www.earthisland.org/eijournal/fall97/fe_fall97petfood.html
Defense opens case Cattlemen vs. Oprah Winfrey
By CHIP CHANDLER Globe-News Staff Writer
snip...
Van Smith, a reporter with City Paper in Baltimore, testified about an article he wrote on rendering plants. Smith said he saw sheep taken to a plant despite a voluntary ban on using processed sheep in protein-enhanced feed, backing up a statement Lyman made on Winfrey's show.
Under cross-examination, Smith said he was not sure whether the sheep were used for feed or other animal-derived products.
snip...
Van Smith, a reporter with City Paper in Baltimore, testified about an article he wrote on rendering plants. Smith said he saw sheep taken to a plant despite a voluntary ban on using processed sheep in protein-enhanced feed, backing up a statement Lyman made on Winfrey's show.
Under cross-examination, Smith said he was not sure whether the sheep were used for feed or other animal-derived products.
http://www.amarillonet.com/ns-search/stories/021998/036-3052.001.shtml?NS-search-set=/3704d/aaaa2813004db0d&NS-doc-offset=5&
Web posted Wednesday, February 18, 1998 2:02 p.m. CT
Graphic pictures greet Winfrey jury
By KAY LEDBETTER Globe-News Farm and Ranch Editor
Pictures of sheep heads, euthanized pets and roadkill greeted jurors this morning as they returned to the continuation of the cattlemen vs. Oprah Winfrey lawsuit.
The lawsuit continues today in U.S. District Mary Lou Robinson's court, but in a much diminished state.
snip...
Defense lawyer Charles Babcock called Van Smith, a City Paper reporter from Baltimore who had written an article on rendering plants in September 1995.
Smith and Babcock went through more than 50 pictures taken as the reporter toured the Valley Proteins plant in Baltimore and followed a rendering truck to the local animal shelter, a sausage plant and a slaughterhouse.
The pictures showed offal being emptied from the slaughterhouses. They showed animal shelter workers in the euthanasia room; barrels of dead animals in a refrigerated room at the animal shelter; waste meat from the sausage plant; and dead sheep from the slaughterhouse.
http://www.amarillonet.com/stories/021898/graphic.shtml
Web posted Friday, January 23, 1998 5:49 a.m. CT
TSS
Witness testifies some ill cattle sent to rendering plant
By CHIP CHANDLER Globe-News Staff Writer
snip...
Mike Engler -- son of Paul Engler, the original plaintiff and owner of Cactus Feeders Inc. -- agreed that more than 10 cows with some sort of central nervous system disorder were sent to Hereford By-Products.
The younger Engler, who has a doctorate in biochemistry from Johns Hopkins University, was the only witness jurors heard Thursday in the Oprah Winfrey defamation trial. His testimony will resume this morning.
According to a U.S. Department of Agriculture report from which Winfrey attorney Charles Babcock quoted, encephalitis caused by unknown reasons could be a warning sign for bovine spongiform encephalopathy, or mad cow disease.
Encephalitis was indicated on the death certificates -- or ``dead slips'' -- of three Cactus Feeders cows discussed in court. The slips then were stamped, ``Picked up by your local used cattle dealer'' before the carcasses were taken to the rendering plant.
snip...
http://www.amarillonet.com/ns-search/stories/012398/cattle.shtml?NS-search-set=/3704d/aaaa2813004db0d&NS-doc-offset=93&
Date: Fri, 09 Jan 2004 03:12:18 -0000
Man learns he ate beef linked to Holstein with mad cow disease 01/08/2004 Associated Press
A man says it was "like getting hit by lightning" to learn that he and his family ate hamburger linked to a Holstein that was found to have mad cow disease.
Brian Weinstein, 49, a lawyer who lives in this Seattle suburb, told the Seattle Post-Intelligencer that at his request, the meat was traced by the supermarket chain where he bought it.
"I know the odds that any of us will get sick are slim," Weinstein said, "but my family's risk is greater than anyone else's in the U.S. because we actually ate it."
The trace showed the meat was among 10,410 pound of recalled beef from the Holstein and 19 other animals that were slaughtered Dec. 9 -- but not whether it came from the deceased animal or from the other cattle.
In an interview Wednesday, Weinstein said he knows there is little chance that he, his wife, their two daughters, 9 and 12, or their 14-year-old son will contract variant Cruetzfeldt-Jakob disease, which has been linked to eating brain or spinal matter from animals with bovine spongiform encephalopathy, the scientific name for mad cow disease.
The U.S. Agriculture Department has said that about 100 people, mostly from Oregon and Washington, had reported they had consumed recalled meat and were worried. The USDA said they were told the meat was safe because it was muscle meat and not affected.
Still, Weinstein said, it was a jolt to learn that the recall, issued Dec. 23, covered the meat he mixed into a ragu sauce and served his family in a spaghetti dinner Dec. 21.
"It's bad luck, really," Weinstein said. "It's like getting hit by lightning. There's one cow in the U.S. with mad cow, and my family probably ate it."
As of Wednesday, officials knew of no recalled meat still "in circulation," said Dan Puzo, a spokesman for the Agriculture Department's Food Inspection and Safety Service.
Meat that was returned, including 102 cases of beef recalled by QFC, probably will be dumped in landfills or incinerated, but non will be tested for mad cow disease because "there are no tests for BSE muscle flesh," Puzo said.
Agriculture Secretary Ann Veneman has repeatedly said there is an extremely low risk from eating muscle cuts from an infected cow.
About 150 people worldwide have been diagnosed with vCJD, a fatal brain-wasting disease.
Infected cattle have been found to harbor prions, deformed proteins that are believed to cause mad cow disease, mainly in the brain and central nervous system. Scientists believe cattle contract the disease from eating feed that contains material from infected animals.
Authorities have said the Holstein, a 6 1/2-year-old dairy cow, was born in Alberta, imported into the United States from Canada about two years ago and lived on the Sunny Dene Ranch near Mabton.
The cow became ill after delivering a calf, couldn't walk and was slaughtered at Vern's Moses Lake Meat Co. on Dec. 9.
Carcasses from that cow and 19 others that were slaughtered the same day were sent to Midway Meats in Centralia for deboning, and the processed meat -- mostly ground beef -- was then sent to two distributors in Oregon that shipped it to groceries in seven states.
Meanwhile, because the cow was ailing before slaughter, samples of its brain were sent to a laboratory in Ames, Iowa, and tested positive for BSE on Dec. 23.
That night, seeing television news reports on the discovery, "I started getting sick," Weinstein said. "I started thinking about all the times we'd eaten ground beef recently."
He dismissed the matter as the family left the next day for Hawaii, but upon returning after New Year's he learned of the recall on another trip to the store.
"Lo and behold, there was a very inconspicuous one-sheet paper posted by the meat counter that explained the recall," Weinstein said.
Soon afterward he contacted the headquarters of QFC, a division of Kroger Co., and had the meat traced through purchase records showing product codes on his frequent shopper card.
Dean Olson, a spokesman at QFC headquarters in Bellevue, said Weinstein was among a "very few customers' who had inquired and for whom the company determined whether they had bought meat subject to the recall.
Information from: Seattle Post-Intelligencer
http://www.kgw.com/sharedcontent/APStories/stories/D7VUR2483.html
AN endless cycle of greed and TSEs...TSS
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NO mad dogs? DEER, CAT and DOG SPONGIFORM ENCEPHALOPATHY SURVEY
http://www.priondata.org/data/A_deerdog.html <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">http://web.archive.org/web/20060927023250/http://www.priondata.org/data/A_deerdog.html
Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.
------------------------------------------------------------------------
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">http://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf
ARCHIVED URL LINK ;
http://web.archive.org/web/20090506032702/http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf
It is not clear that deer may well become infected with BSE although the rate at which this is taking place is unclear. DEFRA issued a document specifically to tell farmers what to do if they found a deer with potential symptoms:
http://www.defra.gov.uk/animalh/bse/bse-publications/adv-TSEs-deer.pdf
ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">https://webarchive.nationalarchives.gov.uk/ukgwa/20130822074033/http://www.defra.gov.uk/animalh/bse/bse-publications/adv-TSEs-deer.pdf
------------------------------------------------------------------------
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
Subject: Alert in Latest Mad-Cow Case Was Delayed by a Misdiagnosis (came from pet food plant in TEXAS) WSJ
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Mon, 27 Jun 2005 10:38:51 -0500
Content-Type: text/plain
Parts/Attachments: text/plain (58 lines)
Reply
##################### Bovine Spongiform Encephalopathy #####################
From: TSS
Subject: Alert in Latest Mad-Cow Case Was Delayed by a Misdiagnosis (came from pet food plant in TEXAS) WSJ
Date: June 27, 2005 at 8:33 am PST
Alert in Latest Mad-Cow Case Was Delayed by a Misdiagnosis
By SCOTT KILMAN Staff Reporter of THE WALL STREET JOURNAL June 27, 2005; Page A2
A misdiagnosis by U.S. Department of Agriculture scientists caused a seven-month delay in alerting consumers to the U.S.'s second case of mad-cow disease.
Because of the error, uncovered only at the prodding of the department's Inspector General Phyllis K. Fong and confirmed by British scientists Friday, Agriculture Secretary Mike Johanns unveiled several changes in the government's mad-cow testing program, some long sought by consumer advocates.
"Science is ever evolving.... And as we learn more, we apply the knowledge," said Mr. Johanns. He also highlighted some instances of human error in the case, including missing paperwork and sloppy handling of the beef cow's brain sample.
TALLYING MAD-COW
See a graphic that tallies world-wide cattle and human cases of mad-cow disease.
Probably no other American cow's brain has been tested so extensively as this one, which was collected at a pet-food-related plant in Texas. The female, which was at least eight years old, came to the attention of regulators in November when it was flagged by a preliminary rapid-screening test. The carcass was incinerated. After announcing a possible case of mad-cow disease, scientists at a USDA laboratory in Ames, Iowa, cleared the animal using a brain-tissue test called immunohistochemistry.
But questions persisted about the cow. Mr. Johanns, who was confirmed as agriculture secretary in January, disclosed Friday that the public wasn't told in November that an experimental test on the brain sample had detected abnormalities. "Obviously, it should have been reported," said John Clifford, the USDA's chief veterinary officer, who added that he wasn't aware until recently of the experimental work, which was designed to speed up the immunohistochemistry method, which normally takes days.
The inspector general's office, a watchdog agency within USDA that has highlighted problems in the department's testing program, learned of the conflicting test results and quietly enlisted a different group of USDA scientists to test the sample using a more-sensitive method, called Western blot, routinely employed in Europe.
When the Western blot test came up positive two weeks ago, Mr. Johanns ordered the matter settled by the world's premier mad-cow testing laboratory in Weybridge, England. The British laboratory managed to detect the abnormal prions that cause mad-cow disease using the immunohistochemistry technique, raising questions about the USDA's laboratory prowess.
Cattle prices are widely expected to drop at the start of trading today on fears that the new discovery will discourage countries such as Japan and South Korea from reopening borders they closed to American beef in December 2003. Those actions were taken after U.S. authorities found the brain-wasting disease in a Washington state dairy cow imported from Canada. So far, the U.S. has regained only one-third of that $3 billion export business.
"This case, I'm afraid, has to be taken into consideration," said Akira Chiba, spokesman for Japan's Foreign Ministry. An agreement by Japan in October to accept meat from U.S. cattle younger than 21 months has been mired in red tape there ever since. Taiwan closed its border again to U.S. beef immediately after the USDA's announcement Friday.
Mad-cow disease, or bovine spongiform encephalopathy, can trigger a rare but always-fatal brain disorder in people who eat infected meat. The USDA hasn't found any evidence that the infected cow was imported; if it is confirmed that the animal was born in the U.S., it would make the U.S. the 24th nation to find an indigenous case of mad-cow disease since the malady was discovered in Britain in the 1980s.
Cattle contract BSE by eating feed contaminated with remains of other infected animals, so it is possible other U.S. cattle were exposed. (The U.S. and Canadian governments largely banned the use of rendered cattle material in cattle rations in August 1997, although there are some loopholes.) Regulators are now trying to find and test offspring, siblings and companions that might have shared the infected cow's rations.
Beef industry officials believe the vast majority of consumers still trust the USDA's declaration that the U.S. beef supply is safe. Over the past 12 months, the department has screened 388,000 of the 455,000 cattle it deemed most likely to have the disease, and the cow that died in Texas is the only new confirmed case. But NPD Group, a consumer research firm based in Port Washington, N.Y., said that 19% of the 500 consumers it surveyed in mid-May were extremely or very concerned about mad-cow disease.
---- Janet Adamy and Andrew Morse contributed to this article.
Write to Scott Kilman at scott.kilman@wsj.com
http://online.wsj.com/article/0,,SB111963867150169044,00.html?mod=djemHL
TSS
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Subject: Canine spongiform encephalopathy?
From: J Ralph Blanchfield
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 29 Apr 1997 06:51:38 GMT
Content-Type: text/plain
Parts/Attachments: text/plain (83 lines)
Reply
Hello Everyone,
Report in Daily Telegraph, 29 April.
Tests on labrador could prove BSE has spread to dogs
By Roger Highfield, Science Editor
BRAIN sections from a dog have been sent to Britain by Norwegian pathologists to confirm that it is the first example of canine spongiform disease, akin to BSE.
The move came as Labour accused the Government of excessive secrecy for not publishing results of a 1991 study to investigate the possibility of BSE being transferred to dogs.
The 11-year-old labrador suffered nervous symptoms, lack of muscle co-ordination and seizures. A post mortem examination showed that its brain had a spongiform appearance, said Prof Jon Teige, a pathologist at the Norwegian College of Veterinary Medicine in Oslo.
"To our surprise, we saw these lesions in the brain similar to those observed in scrapie in sheep and mad cow disease," said Prof Teige. If confirmed, it would mark the first example of the disease in a dog.
Samples have had been sent to the Institute of Animal Health's neuropathogenesis unit in Edinburgh for a second opinion. "Although there are some features of the pathology in common with spongiform encephalopathies, a number of other conditions have similar aspects," said Dr Chris Bostock, of the institute.
If confirmed, it is also important to determine if it is the spontaneous form of BSE or if the dog had been infected in its diet and had a transmissible disease. About 95 per cent of Norway's dog and cat food is imported, mainly from Britain. Parts of bovine material, which could contain BSE, were removed from the animal food chain in 1990.
Scientists are interested in whether dogs are susceptible but confirmation would not change the big picture of BSE, Dr Bostock said. Dr Gavin Strang, shadow food minister, yesterday accused Douglas Hogg, the Agriculture Minister, of secrecy over BSE research. "This work on possible BSE in dogs was funded by the public," he said. "Results should have been made public."
The Government ruled out further research on dogs yesterday despite disclosures in a report six years ago that there was a possibility that they could catch a form of mad cow disease from contaminated food. "It is unnecessary," said a spokesman. "There is no threat to human or animal health."
Tests six years ago by ministry experts on the brains of 444 hunting hounds found some abnormalities called fibrils. However, some brains had started to degenerate, making the results ambiguous.
The results were passed to the Spongiform Encephalopathy Advisory Committee, which agreed that they were inconclusive and ruled out further research because there was no public health issue. "We don't eat dogs in Britain," the spokesman said.
Mr Hogg said that the research on dogs and BSE "adds nothing to human knowledge" during a tour of the North-East which included a visit to a sausage factory in marginal Stockton South.
End of Telegraph Report.
Regards
Ralph
****************************************************************** J Ralph Blanchfield Food Science, Food Technology & Food Law Consultant Chair, IFST External Affairs Web Editor, Institute of Food Science & Technology IFST Web address:******************************************************************
Subject: Re: Canine spongiform encephalopathy?
From: "Hans G. Andersson"
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 29 Apr 1997 06:02:33 -0700
Content-Type: text/plain
Parts/Attachments: text/plain (38 lines)
Reply
Hello Ralph and everybody,
Excerpt from the article you forwarded:
"The Government ruled out further research on dogs yesterday despite disclosures in a report six years ago that there was a possibility that they could catch a form of mad cow disease from contaminated food. "It is unnecessary," said a spokesman. "There is no threat to human or animal health."
Tests six years ago by ministry experts on the brains of 444 hunting hounds found some abnormalities called fibrils. However, some brains had started to degenerate, making the results ambiguous.
The results were passed to the Spongiform Encephalopathy Advisory Committee, which agreed that they were inconclusive and ruled out further research because there was no public health issue. "We don't eat dogs in Britain," the spokesman said.
Mr Hogg said that the research on dogs and BSE "adds nothing to human knowledge" during a tour of the North-East which included a visit to a sausage factory in marginal Stockton South."
I got two dogs myself, both 13 years old and fed British pet food during the period 1984-89.
The statement from the British government is tasteless!
Best regards,
Hans
Hans G. Andersson, NYC -- hasse@sprynet.com Editor, Ebola section of OUTBREAK http://www.outbreak.org/
"There is a crack in everything. That's how the light gets in." Leonard Cohen
BSE-LIST
Subject: Re: Canine Spongiform Encephalopathy?
From: Olav Hungnes
Reply-To: Bovine Spongiform Encephalopathy
Date: Wed, 23 Apr 1997 10:19:14 +0200
Content-Type: text/plain
Parts/Attachments: text/plain (47 lines)
Reply
Date: Mon, 21 Apr 1997 20:59:16 +0200 From: Torsten BrinchSubject: Canine Spongiform Encephalopathy?
Hello everyone,
I wondered if we have a Norwegian subscriber, who could brief the list on the suspected case of spongiform encephalopathy in a Norwegian dog?
Best regards,
Torsten Brinch
Torsten Brinch - Risboege, 6640, Denmark - e-mail: iaotb@inet.uni-c.dk http://inet.uni-c.dk/~iaotb/ IAO Agrochemical Pages Denmark
The story, first brought by Norwegian TV2, is that an 11 year old golden retriever was brought to the Norwegian College of Veterinary Medicine for an autopsy. The dog had shown neurological symptoms over a longer period. Microscopy of brain tissue showed spongiform encephalopathy.
Samples have been sent to another pathological laboratory in Oslo (probably at Rikshospitalet (The National Hospital)), as well as to Weybridge Central Veterinary Institute, London, for further investigation.
This is said to be the first reported case of spongiform encephalopathy in dogs.
Media focus has been on BSE-contaminated dog food as a possible cause. 95 % of dog food in this country is imported, and speculation goes that the dog could have got its disease from eating feed prepared from British meat-and-bone meal during the eighties. The possibility of genetic factors should, however, not be ignored. I would guess that investigation of the dog's PrP genotype is underway. Is anything known about polymorphism in dogs?
Source(in Norwegian, for the benefit of Torsten): Articles from NTB, appearing in the newspaper Aftenposten Saturday and Tuesday, -- __________________________________________________________________________ Olav Hungnes olavhung@idgonline.no Natl.Inst.of Public Health, Dept.of Virology ohungnes@embnet.uio.no P.O.Box 4404 Torshov, phone: (+47)22 04 25 20 N-0403 OSLO, NORWAY FAX: (+47)22 04 24 47 http://home.idgonline.no/~ohungnes/
BSE-LIST
Subject: Re: Canine Spongiform Encephalopathy
From: "Hans G. Andersson"
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 22 Apr 1997 00:15:18 -0700
Content-Type: text/plain
Parts/Attachments: text/plain (41 lines)
Reply
Hi Torsten and everybody,
Here's some additional information from media in Norway:
A Norwegian golden retriever may have died of Canine Spongiform Encephalopathy, possibly linked to BSE.
Most pet food in Norway is imported, mainly from the UK, and before 1994 there was no quality-control inspection:
"If the dog contracted the brain ailment, it probably was through dog food in the late 1980s", said Eivind Liven, Director of the National Animal Health Board.
The 11-year-old dog showed symptoms of psychiatric and neurological illness a couple of months ago, and died around Easter. An autopsy at Norway's Veterinary School showed changes in the brain consistent with those seen in the brains of cattle with late stage BSE.
Tissue samples from the brain of the dog will be studied by researchers at MAFF's Central Veterinary Laboratory, Weybridge, UK.
Source: Dagbladet in Oslo, Norway. April 20 and 21, 1997
Best regards,
Hans
Hans G. Andersson, NYC -- hasse@sprynet.com Editor, Ebola section of OUTBREAK http://www.outbreak.org/
"There is a crack in everything. That's how the light gets in." Leonard Cohen
BSE-LIST
GREETINGS AGAIN,
IT SEEMS THE USDA ET AL have taken a page, or two, from the U.K. et al on screwing up brains for the testing of Transmissible Spongiform Encephalopathy BSE i.e. mad cow disease (all strains), when they do not want to document it.
From: TSS Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE) Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf
ARCHIVED URL LINK; <3daf5023 .4080804="" wt.net="">
<3daf5023 .4080804="" wt.net="">http://web.archive.org/web/20090426161015/http://www.usda.gov/oig/webdocs/sarc070619.pdf
-MORE Office of the United States Attorney District of Arizona FOR IMMEDIATE RELEASE For Information Contact Public Affairs February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681
CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD COW DISEASE SURVEILLANCE PROGRAM
PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, “The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA’s Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law.” Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the “USDA Agreement”) to collect obex samples from cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.
Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.
Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA’s ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:
(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;
(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;
(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s testing laboratory that were false and misleading;
(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;
(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and
(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.
Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #
http://www.usdoj.gov/usao/az/press_releases/2007/2007-051(Farabee).pdf
WE can only hope that this is a single incident. BUT i have my doubts. I remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5 grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and the FDA was bragging at the time that the amount of potentially BANNED product was so little and the cattle were so big ;
"It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated."
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed. ... FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
WE now know all that was a lie. WE know that literally Thousands of TONS of BANNED and most likely tainted product is still going out to commerce. WE know now and we knew then that .005 to a gram was lethal. WE know that CWD infected deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been rendered and fed back to livestock (including cattle) for human and animal consumption.
Paul Brown, known and respected TSE scientist, former TSE expert for the CDC said he had ''absolutely no confidence in USDA tests before one year ago'', and this was on March 15, 2006 ;
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
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, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"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."
OR, what the Honorable Phyllis Fong of the OIG found ;
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
"These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS
USDA 2003
We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
snip...
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
USDA: In 9,200 cases only one type of test could be used
WASHINGTON (AP)--The U.S. Department of Agriculture acknowledged Aug. 17 that its testing options for bovine spongiform encephalopathy were limited in 9,200 cases despite its effort to expand surveillance throughout the U.S. herd.
In those cases, only one type of test was used--one that failed to detect the disease in an infected Texas cow.
The department posted the information on its website because of an inquiry from The Associated Press.
Conducted over the past 14 months, the tests have not been included in the department's running tally of BSE tests since last summer. That total reached 439,126 on Aug. 17.
"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."
Officials intended to report the tests later in an annual report, Clifford said.
These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC.
In the Texas case, officials had declared the cow free of disease in November after an IHC test came back negative. The department's inspector general ordered an additional kind of test, which confirmed the animal was infected.
Veterinarians in remote locations have used the preservative on tissue to keep it from degrading on its way to the department's laboratory in Ames, Iowa. Officials this year asked veterinarians to stop using preservative and send fresh or chilled samples within 48 hours.
The department recently investigated a possible case of BSE that turned up in a preserved sample. Further testing ruled out the disease two weeks ago.
Scientists used two additional tests--rapid screening and Western blot--to help detect BSE in the country's second confirmed case, in a Texas cow in June. They used IHC and Western blot to confirm the first case, in a Washington state cow in December 2003.
"The IHC test is still an excellent test," Clifford said. "These are not simple tests, either."
Clifford pointed out that scientists reran the IHC several times and got conflicting results. That happened, too, with the Western blot test. Both tests are accepted by international animal health officials.
Date: 8/25/05
http://www.hpj.com/archives/2005/aug05/aug29/BSEtestoptionswerelimited.cfm
""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
As for lowering standards, R-CALF has referenced the OIE (World Organization for Animal Health) as the authority on animal health issues. That's fine, as far as it goes. Trouble is, the OIE does not set standards, as R-CALF has claimed. Further, the OIE does not recommend countries ban meat imported - with SRMs removed - from countries with low or high BSE risk, contrary to R-CALF's implication.
In addition, there are no standards recognized for importing meat from minimal- or low-risk BSE countries. The U.S. is trying to set standards as precedent for trade, based on nearly 20 years of science. R-CALF wants trade only with countries who have never had a BSE case. They have not explained how many years they want the rest of the world to sit around and wait until it's okay to trust science and begin trading. Or how they would justify keeping imports out if ever a BSE case was discovered in the U.S. or export again ever.
http://www.mad-cow-facts.com/News-Commentary/r-calf-bullard-4-4-05.htm
JUST ABOUT EVERY COUNTRY THAT WENT BY THOSE FAILED OIE BSE GUIDELINES WENT DOWN WITH BSE. ...TSS
http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
see full text ;
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the USA Question number: EFSA-Q-2003-083
Adopted: 1 July 2004 Summary (0.1Mb)
Report (0.2Mb)
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594180.htm
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Canada Question number: EFSA-Q-2003-083
Adopted: 1 July 2004 Summary (0.1Mb)
Report (0.2Mb)
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked to provide an up-to-date scientific report on the GBR in Canada, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Canada. This scientific report addresses the GBR of Canada as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into the country middle of the eighties and could have reached domestic cattle in the early nineties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early 90s. It is possible that imported meat and bone meal (MBM) into Canada reached domestic cattle and led to an internal challenge in the early 90s.
A certain risk that BSE-infected cattle entered processing in Canada, and were at least partly rendered for feed, occurred in the early 1990s when cattle imported from UK in the mid 80s could have been slaughtered. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of Canada is III, i.e. it is confirmed at a lower level that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as the system remains unstable, it is expected that the GBR continues to grow, even if no additional external challenges occur.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594094.htm
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Mexico Question number: EFSA-Q-2003-083
Adopted: 1 July 2004 Summary (108 KB)
Report (168 KB)
Annex (251 KB)
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993.
It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system.
EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.
Further information
Overview of GBR assessments covering 2000-2006: list of countries and their GBR level of risk (64 KB)
Published: 20 August 2004 Last updated: 8 September 2004
http://www.efsa.europa.eu/en/scdocs/scdoc/4r.htm
Wednesday, April 16, 2008
MBM, greaves, meat offal, live cattle, imports from UK to USA vs Canada
http://madcowtesting.blogspot.com/2008/04/mbm-greaves-meat-offal-live-cattle.html
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.
http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html
MY comments/questions are as follows ;
1. SINCE the first Harvard BSE Risk Assessment was so flawed and fraught with error after the PEER REVIEW assessment assessed this fact, how do you plan on stopping this from happening again, will there be another peer review with top TSE Scientist, an impartial jury so-to-speak, to assess this new and updated Harvard BSE/TSE risk assessment and will this assessment include the Atypical TSE and SRM issues ?
*** Suppressed peer review of Harvard study October 31, 2002 ***
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
***
http://www.scribd.com/doc/1490709/USDA-200600111
***
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
***
http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
***
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
***
Response to Public Comments on the Harvard Risk Assessment of BSE USA
RESPONSE TO COMMENTS FROM TERRY S. SINGELTARY SR. Comment #1: SINCE the first Harvard BSE Risk Assessment was so flawed and fraught ...
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
IT ALL STARTED, LEGALLY, RIGHT HERE ;
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
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1
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
Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY
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.
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 ???
go figure. ...
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8151
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
January 28, 2007
Greetings APHIS,
I would kindly like to submit the following to ;
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8
Monday, October 26, 2009
MAD COW DISEASE, AND U.S. BEEF TRADE
MAD COW DISEASE, CJD, TSE, SOUND SCIENCE, COMMERCE, AND SELLING YOUR SOUL TO THE DEVIL
http://usdameatexport.blogspot.com/2009/10/mad-cow-disease-and-us-beef-trade.html
Greetings USDA/APHIS et al,
I would kindly like to comment on OIE proposed guidelines.
AS I said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. THE reason most every country around the globe came down with BSE/TSE in their cattle, were due to the failed and flawed BSE/TSE testing and surveillance policy of the O.I.E. NOW, they don't even acknowledge atypical scrapie it seems, as one for concern $
SO, chew on that !
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.
http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html
Wednesday, February 10, 2010
NAIS MAD COW TRACEABILITY DUMPED BY USDA APHIS 2010
http://naiscoolyes.blogspot.com/2010/02/nais-mad-cow-traceability-dumped-by.html
Thursday, January 07, 2010
Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008
http://scrapie-usa.blogspot.com/2010/01/scrapie-and-nor-98-scrapie-november.html
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html
Wednesday, March 3, 2010
NOR-98 ATYPICAL SCRAPIE USA 4 CASES DETECTED JANUARY 2010
http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-usa-4-cases.html
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
snip...
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.
Thanks for your interest.''
Best regards,
Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
END...TSS
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
International Society for Infectious Diseases Web: http://www.isid.org/
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Friday, February 05, 2010
New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review
http://vcjd.blogspot.com/2010/02/new-variant-creutzfelt-jakob-disease.html
Sunday, February 14, 2010
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th
ICID International Scientific Exchange Brochure -
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
TSE
http://transmissiblespongiformencephalopathy.blogspot.com/
WHO WILL WATCH THE CHILDREN FOR CJD OVER THE NEXT 5 + DECADES ???
Do you actually believe that the USDA et al jumped in on the law suit against Westland/Hallmark, at the time the largest beef recall in USA history, just because a few animals were abused on a video, or to cover their ass, for letting our children, from school district to school district, from state to state, be fed dead stock downer cows.
>>>In the papers, the government alleges the meatpacking plant slaughtered and processed downer cows for nearly four years — from January 2004 to September 2007 — at the average rate of one every six weeks... <<<>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
and there from, what will friendly fire, i.e. pass it forward, i.e. iCJD, the pathology, what will that look like pathologically?
sporadic CJD does not mean one strain of CJD. it is multiple strains, and they are growing in number ;
CJD USA RISING, with UNKNOWN PHENOTYPE ;
5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Terry S. Singeltary Sr. Bacliff, Texas USA 77518
IS this is a BSE/TSE feed ban violation of some sort, or exactly what ?
NOT KNOWING EXACTLY what this recall is about, we must assume it is just more mad cow feed in commerce, but they refuse to tell us exactly what it is.
ruminant animals may have been contaminated with prohibited material
exactly what was it ???
under regs just previously posted, if i understand this right, you now have 3
Subpart B-Listing of Specific Substances Prohibited From Use in Animal Food or Feed ;
§ 589.1000 Gentian violet.
§ 589.1001 Propylene glycol in or on cat food.
§ 589.2000 Animal proteins prohibited in ruminant feed.
http://ecfr.gpoaccess.gov/cgi/t/text/text-idx?c=ecfr&sid=8f6d4f71330c3337921d820e1854476e&rgn=div5&view=text&node=21:6.0.1.1.26&idno=21
archived url link;
NOT KNOWING EXACTLY what this recall is about, we must assume it is just more mad cow feed in commerce, but they refuse to tell us exactly what it is.
ruminant animals may have been contaminated with prohibited material
exactly what was it ???
under regs just previously posted, if i understand this right, you now have 3
Subpart B-Listing of Specific Substances Prohibited From Use in Animal Food or Feed ;
§ 589.1000 Gentian violet.
§ 589.1001 Propylene glycol in or on cat food.
§ 589.2000 Animal proteins prohibited in ruminant feed.
http://ecfr.gpoaccess.gov/cgi/t/text/text-idx?c=ecfr&sid=8f6d4f71330c3337921d820e1854476e&rgn=div5&view=text&node=21:6.0.1.1.26&idno=21
archived url link;
http://web.archive.org/web/20100608070225/http://ecfr.gpoaccess.gov/cgi/t/text/text-idx?c=ecfr&sid=8f6d4f71330c3337921d820e1854476e&rgn=div5&view=text&node=21:6.0.1.1.26&idno=21
SO, which one is it ???
THIS recall is not confusing ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
archived url link;
SO, which one is it ???
THIS recall is not confusing ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
archived url link;
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
How to Make a FOIA Request All FOIA requests must be in writing and should include the following information:
A. Requestor's name, address, and telephone number.
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
281-xxx-xxxx
B. A description of the records being sought. The records should be identified as specifically as possible. A request for specific records that are releasable to the public can be processed much more quickly than a request for "all information" on a particular subject. Also fees for a more specific and limited request will generally be less.
SEE ABOVE FOIA SPECIFIC REQUEST OF RECORDS. ...TSS
C. Separate requests should be submitted for each firm or product involved.
DUE TO THE LACK OF INFORMATION IN THE ORIGINAL WARNING LETTER, THIS IS NOT POSSIBLE. ...TSS
D. A statement concerning willingness to pay fees, including any limitations.
I CANNOT PAY ANYTHING. I AM DISABLED AND ON FIXED INCOME. THIS INFORMATION I REQUEST IS FOR ME AND THE PUBLIC. ...TSS
Questions relating to FOI requests may be addressed to the Division of the Freedom of Information Offices at 301-827-6567.
All FOIA requests must be in writing. At this time, FDA does not accept FOIA requests sent via e-mail. Requests should be mailed to the following address:
Food and Drug Administration
Division of Freedom of Information (HFI-35)
Office of Shared Services
Office of Public Information and Library Services
5600 Fishers Lane
Rockville, MD 20857
Or requests may be sent via fax to: fax number 301-443-1726 or 301-443-1719. If experience difficulty sending a fax, please call (301) 443-2414.
FAXED AND RECIEVED TO THE ABOVE NUMBER SEPTEMBER 4, 2009...TSS
Subject: FDA BSE MAD COW and the safety of your pet, the rest of the story
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Mon, 7 Nov 2005 09:28:23 -0600
Content-Type: text/plain
Parts/Attachments: text/plain (1529 lines)
Reply
##################### Bovine Spongiform Encephalopathy #####################
From: TSS
Subject: FDA BSE MAD COW and the safety of your pet, the rest of the story
Date: November 5, 2005 at 8:09 am PST
BSE and the safety of pets
With the exception of cats, no pets (companion animals) are known to be susceptible to the infectious agent that causes BSE in cattle. No evidence of BSE has ever been found in dogs, horses, birds, or reptiles.
However, cats are susceptible. Approximately 90 cats in the UK and several cats in other European countries have been diagnosed with the feline version of BSE, or FSE. Before it was recognized that they were susceptible to the BSE agent, cats were exposed to the infectious agent through commercial cat food or through meat scraps provided by butchers. The number of reported cases of FSE in the UK and Europe has been declining annually since 1994 after implementation of feed bans in those countries.
Currently in the U.S. , animal products that are prohibited from cattle feed are acceptable for use in pet food. Such products include meat and bone meal, for example. However, FDA believes that the safeguards it has put into place (i.e. ruminant feed rule) to prevent BSE in the U.S. have also protected cats. To date, no case of FSE has been found in the U.S. FDA continues to review these safeguards to be sure they are adequate, especially in light of the BSE case found in Washington State in December, 2003.
Material from the BSE positive cow in Washington State did not pose a risk to cats in the U.S. because none of it was released into distribution. All firms involved with the incident in Washington State were found to be in compliance with the BSE rules.
In addition, when the BSE positive cow was found in Canada in May 2003, the FDA stopped imports of all pet foods made from material derived from mammalian sources, and the pet food manufacturer recalled the food it had manufactured that was thought to contain material from the infected cow.
In an Advance Notice of Proposed Rulemaking published in the Federal Register on July 14, 2004, the FDA announced that the agency intends to further strengthen the ruminant feed rule (or BSE feed regulation) by prohibiting the use of high-risk tissues, often referred to as specified risk material or SRM, in any animal feed including pet food.
CVM DOES NOT recommend one product over another or offer guidance on individual pet health issues that are normally provided by the pet’s veterinarian. Questions regarding your pets' health and/or the specific use of any veterinary drug, pet food, or other product should always be referred to your veterinarian.
The following documents contain information on the regulation, marketing and labeling of pet foods in the United States.
News Releases
http://www.fda.gov/cvm/petfoods.htm
TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS
http://www.mad-cow.org/00/aug00_late_news.html#ggg
archived url link;
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
HOUND STUDY
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.
snip...
http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
NEW URL ;
http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
76 pages on hound study;
http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf
NEW URL ;
http://web.archive.org/web/20030327022236/http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf
I thought that in Britain dogs had contracted BSE, but perhaps not.
not so fast here;
The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.
41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).
http://www.bseinquiry.gov.uk/witness/htm/stat067.htm
It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
snip...
http://www.bseinquiry.gov.uk/files/ws/s324.pdf
archived url link ;
http://web.archive.org/web/20090506004016/http://www.bseinquiry.gov.uk/files/ws/s324.pdf
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
The signs of canine cognitive dysfunction syndrome or "old dog syndrome" commonly seen in dogs are: lose of house training increased barking or whining increased anxiety or fear signs disorientation-appearing lost or confused,getting stuck behind furniture or in corners, walking in circles, becoming forgetful,walking aimlessly,staring into space, repetitious or compulsive behavior change in sleep patterns-up at night, sleep all day
lack of responsiveness other changes,may not recognize you, their name,may become more docile, more aggressive.. You can liken it to human senility. An article at the petcenter says "CDS is not "normal aging". A number of pathophysiological changes are suspected to play a role in its development. These include: * deposition of amyloid plaques in the cerebral cortex and hippocampal part of the brain * alterations in neurotransmitters, including dopamine * increased levels of monoamine oxidase B (MAOB) in the brain * increased levels of free radicals L-DEPRENYL HYDROCHLORIDE SELEGILINE HYDROCHLORIDE,BRAND NAME: ANIPRYL OR ELDEPRYL is used to help treat canine cognitive dysfunction by increasing brain concentrations of the neurotransmitter dopamine. Hopefully you can see a difference in a month or so. If you don't see a difference in the first month, your vet might tell you to try two pills a day for the next month. ANIPRYL doesn't work for all dogs. A great writeup on L-DEPRENYL can be found at
http://www.petsinfo.org/elderlydogs1.html.
"One third of canine CD patients respond extremely well to treatment with deprenyl by regaining their youthful vigor; another one third respond reasonably well; and one third do not respond at all (perhaps there is a variant of CD with different neuropathology). The bottom line is that for any dog that is slowing down to the point that problems become apparent, treatment with deprenyl is the logical route once other organic causes for reduced mental function have been ruled out. Here is a write up on selegline " Selegiline has immune-system-boosting and anti-neurodegenerative effects. ....
Taken consistently in low doses, selegiline tends to extend the life-expectancy of rats by some 20%; enhances drive, libido and endurance; and independently improves cognitive performance in Alzheimer's patients and in some healthy normals. It is used successfully to treat canine cognitive dysfunction syndrome (CDS) in dogs...Selegiline protects the brain's dopamine cells from oxidative stress. " Some also use alpha lipoic acid and r-lipoic acid. powerful antioxidants to help slow down canine cognitive dysfunction. There is a dog food that is rich in antioxidants for CDS but I am assuming if you supplement with your own antioxidants you don't have to worry if your dog likes the food or not. I know my dog Hammy has become very picky and at least if I pill him, I know he is getting his antioxidants.
http://www.thensome.com/cds.htm
Doggie Dementia
Does 14-year-old Fido get lost in his own back yard?
Does he not respond when you call his name?
Does he generally seem confused?
According to Pulse, the official magazine of the Southern California Veterinary Medical Association, just as humans in the 21st Century are living longer, so is man’s best friends—more than 7.3 million dogs in the United States are age 10 or older. And with age dogs become prone to the same age-related diseases as their human companions, including dementia.
A disease of old age affects dogs and humans alike
Kazzy, a 17-year-old Lhasa Apso, is one of the 60 percent of dogs aged 11 to 15 who suffer from one or more symptoms of canine cognitive dysfunction syndrome (CDS), also known to veterinarians as doggie dementia. "He used to be the most incredible watchdog," says his owner, Olivia Feldman-Rich. "But he’s not like that anymore. He’s quite bewildered."
Experts like Dr. Maritza Perez, a veterinarian at West Orange (NJ) Animal Hospital, say that confusion is one of the four major signs of CDS (see sidebar). Dr. Perez says dogs may "pace around in circles, get stuck behind furniture, or they don’t know where the back door is anymore."
Often the most distressing sign of CDS is that, like human patients with Alzheimer’s disease, your pet seems to forget you and your family. "A lot of people notice that when you walk in the door, and this dog that was happy to see you doesn’t get up off the couch or off the floor to greet you," says Dr. Perez. "And he doesn’t come anymore when you call him."
These symptoms, coupled with others debilitating diseases affecting older dogs, such as arthritis, all add up to a serious loss in quality of life for your canine friend. The American Veterinary Medical Association reports that some 500,000 dogs are put to sleep each year because of CDS.
Researchers say that deposits of beta-amyloid plaques in brain tissues are likely to play a role in CDS. These plaques build up and eventually inhibit transmission of the brain’s neural signals. Still, the recognized symptoms of CDS are behavioral, so a diagnosis is exclusionary, meaning it is arrived at only after all other physical and neurological causes are ruled out.
No cure yet, but relief for some dogs
Dr. Perez with a 14 year-old beagle who is on Anipryl.
While scientists search for a permanent cure for CDS, there is one treatment currently FDA-approved for CDS. Selegiline hydrochloride, whose brand name is Anipryl, may give some dogs relief from its symptoms. Researchers speculate that Anipryl works by increasing levels of dopamine, a neurotransmitter. Other treatments are currently being investigated, including diets high in anti-oxidants as well as a new drug, Adrafinil, in one Canadian study.
Dr. Perez says that Anipryl does cause an improvement in many dogs with CDS, meaning relief from at least one of the common symptoms. "We have lots of animals on it and it does work," she says. But it’s not a sure thing—Dr. Perez tried it on her own dog with no effect.
Feldman-Rich is debating putting Kazzy on Anipryl. "I’m hoping that it will give a little more balance to his life and make him a little more aware that he’s still here and we’re still here for him," she says. "I always told him that he couldn’t leave me too soon, and he’s definitely kept up his end of it, but I’d definitely like for him to feel a little more like he’s part of the family."
by Debra Utacia Krol
http://www.sciencentral.com/articles/view.php3?article_id=218391360&cat=1_6
[Image] Research letters Volume 352, Number 9134 [Image] 3 October 1998 [Previous] [Next]
[Image][Image]
Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy
[Image]
Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, Sergio Ferrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, Salvatore Monaco
Transmissible spongiform encephalopathies (TSE) encompass inherited, acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four types of PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 in the UK.5 We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.
A 60-year-old man, with no unusual dietary habits, was admitted in November, 1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, and myoclonus. An electroencephalogram (EEG) showed diffuse theta-delta activity. A brain magnetic resonance imaging scan was unremarkable. 10 days later, he was speechless and able to follow only simple commands. Repeat EEGs showed periodic triphasic complexes. 2 weeks after admission, he was mute, akinetic, and unable to swallow. He died in early January, 1994.
His 7-year-old, neutered, female shorthaired cat presented in November, 1993, with episodes of frenzy, twitching of its body, and hyperaesthesia. The cat was usually fed on canned food and slept on its owner's bed. No bites from the cat were recalled. In the next few days, the cat became ataxic, with hindquarter locomotor dysfunction; the ataxia got worse and there was diffuse myoclonus. The cat was killed in mid-January, 1994.
No pathogenic mutations in the patient's PrP gene were found. The patient and the cat were methionine homozygous at codon 129. Histology of the patient's brain showed neocortical and cerebellar neuronal loss, astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a punctate pattern and paralleled spongiform changes (figure B). The cat's brain showed mild and focal spongiosis in deeper cortical layers of all four lobes (figure C), vacuolated cortical neurons (figure D), and mild astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed. Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and caudate nucleus (figure E). Western blot analysis of control and affected human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After digestion with proteinase K and deglycosylation, only samples from the affected patient and cat showed type-1 PrPres, with PrP glycoform ratios comparable to those observed in sporadic CJD1 (details available from author).
[Image]
Microscopic sections of patient and cat brains
A: Occipital cortex of the patient showing moderate spongiform degeneration and neuronal loss (haematoxylin and eosin) and B: punctate perineuronal pattern of PrP immunoreactivity; peroxidase immunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortex showing mild spongiform degeneration (haematoxylin and eosin).D: vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase immunohistochemistry with antibody 3F4 shows punctate perineuronal deposition of PrP in temporal cortex.
This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2 Taken together, our data suggest that the same agent strain of sporadic CJD was involved in the patient and in his cat.
It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source, or the chance occurrence of two sporadic forms.
1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypic variablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39: 767-78 [PubMed].
2 Collinge J, Sidle KCL, Meads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996; 383: 685-90 [PubMed].
3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501 [PubMed].
4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJD and BSE. Nature 1997; 389: 448-50 [PubMed].
5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiform encephalopathy: a review. Vet Annual 1993; 33: 1-10.
------------------------------------------------------------------------ Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e della Visione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy (S Monaco; e mail rizzuto@Gorgorna.univr.it); and Istituto Zooprofilattico Sperimentale della Lombardia e dell' Emilia, Brescia
=======================================
Terry S. Singeltary Sr. wrote:
######## Bovine Spongiform Encephalopathy #########
Greetings list members,
ODD that some FELINE in Italy seem to have this same or maybe very similar phenotype of TSE;
In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html
archived url link;
-------- Original Message --------
Subject: FDA BSE Update - Pet Food from Canadian Manufacturer & MAD DOG DATA
Date: Tue, 27 May 2003 08:07:58 -0500
From: "Terry S. Singeltary Sr." To: Bovine Spongiform Encephalopathy
Statement
FOR IMMEDIATE RELEASE Statement May 26, 2003
Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
FDA BSE Update - Pet Food from Canadian Manufacturer
The Food and Drug Administration (FDA) has learned from the government of Canada that rendered material from a Canadian cow that last week tested positive for bovine spongiform encephalopathy (BSE, also known as mad cow disease ) may have been used to manufacture pet food, specifically dry dog food, some of which was reported to have been shipped to the United States. The Canadian government prevented the BSE positive cow from being processed for human food. Therefore, consumers can be assured that their food does not contain any remnants of the BSE positive cow.
It is also important to stress that there is no scientific evidence to date that dogs can contract BSE or any similar disease. In addition there is no evidence that dogs can transmit the disease to humans.
FDA notified the U.S. pet food firm, The Pet Pantry International, of Carson City, Nevada, when FDA learned that the pet food that the firm received may have included rendered material from the BSE positive cow. The manufacturer of the pet food is Champion Pet Food, Morinville, Alberta. Even though there is no known risk to dogs from eating this dog food, as a prudent measure to help assure that the U.S. stays BSE free The Pet Pantry International is asking its customers who may have purchased the suspect product to hold it for pickup by the distributor so that the dog food will not mistakenly be mixed into cattle or other feeds if any of the dog food is discarded or otherwise not used to feed dogs. The suspect dog food was produced by Champion Pet Food between February 4, 2003, and March 12, 2003.
The Pet Pantry products were packaged in 50 lb bags, distributed to franchises around the country, and sold by home delivery only. There was no retail distribution of the product. Consumers purchase Pet Pantry products by phone or email orders. The product is then delivered by the nearest franchisee directly to the consumer s home.
The product subject to this notification includes Maintenance Diet labeled with a use by date of 17FEB04 and Beef with Barley with a use by date of 05MAR04 . Consumers who have purchased dog food from The Pet Pantry since February of this year are asked to check their present supplies and see if any match the description of the product being removed. If so, consumers are asked to contact The Pet Pantry at 1-800-381-7387 for further information on how to return the product to The Pet Pantry for proper disposal. Consumers are asked not to destroy or discard the product themselves. The Pet Pantry will also use its sales records to contact consumers who purchased the affected product.
FDA is working closely with the Pet Pantry International to assure for proper disposal of the recovered product.
FDA will continue to provide updates on this case of BSE in Canada as additional information becomes available.
http://www.fda.gov/bbs/topics/NEWS/2003/NEW0910.html
archived url link;
It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994)
Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier.
Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
snip...
http://www.bseinquiry.gov.uk/files/ws/s324.pdf
archived url link;
cases have been reported in domestic cats), are characterised by long asymptomatic incubation periods followed by progressive symptoms and signs of degeneration of the brain, leading eventually to death.
http://www.bsereview.org.uk/download/draft_2.pdf
PET FOODS MAD CATS AND MAD DOGS BSE/TSEs
worse still, there is serious risk the media could get to hear of such a meeting...
snip...
Crushed heads (which inevitably involve brain and spinal cord material) are used to a limited extent but will also form one of the constituent raw materials of meat and bone meal, which is used extensively in pet food manufacturer...
http://www.bseinquiry.gov.uk/files/yb/1989/03/17004001.pdf
ARCHIVED URL LINK ;
http://web.archive.org/web/20090505225022/http://www.bseinquiry.gov.uk/files/yb/1989/03/17004001.pdf
2. The Parliamentary Secretary said that he was concerned about the possibility that countries in which BSE had not yet been detected could be exporting raw meat materials (in particular crushed heads) contaminated with the disease to the UK for use in petfood manufacture...
snip...
YOU explained that imported crushed heads were extensively used in the petfood industry...
http://www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf
ARCHIVED URL LINK ;
http://web.archive.org/web/20090505233039/http://www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf
In particular I do not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed...
http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf
ARCHIVED URL LINK ;
http://web.archive.org/web/20090505233046/http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf
BSE IN PETFOOD
1. The Secretary asked on 19 April whether I was content with the advice in para 3 of the record of the meeting on 17 March with the Parliamentary Secretary (Mr Thompson). The simple answer is ''not entirely''.
2. On occasions, material obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in petfood manufacture. Some of this material must be classified as high risk since it contains brain, spinal cord, spleen or lymphatic glands.
http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf
ARCHIVED URL LINK;
Meldrum's notes on pet foods and materials used
http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090505233041/http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf
http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf
ARCHIVED URL LINK;
IN CONFIDENCE CJD TO CATS...
It should be noted that under experimental conditions cats succumb to an encephalopathy after intracerebral inoculation of material derived from patients affected with Creutzfeldt-Jakob Disease.
http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506055329/http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf
Confidential BSE and __________________
3. I have thought very hard about whether the Branch should carry out a similar exercise with meat and meat products for human foods. On balance I do NOT think we should undertake it, but a final decision has not been taken and you may wish to discuss this further. ...
http://www.bseinquiry.gov.uk/files/yb/1989/05/22012001.pdf
ARCHIVED URL LINK;
1st case natural FSE
NATURAL SPONGIFORM ENCEPHALOPATHY IN A DOMESTIC CAT
1. We have heard from MAFF that a domestic Siamese cat from the Bristol area has had spongiform encephalopathy confirmed. Although there are previous instances of experimental infection in cats, there have been no previous natural infections reported. The assumption must be the cat became infected by scrapie/BSE agent in it's food. ...
http://www.bseinquiry.gov.uk/files/yb/1990/05/09002001.pdf
ARCHIVED URL LINK;
FSE and pharmaceuticals
1. An analysis by MCA Professional staff of the results to the questionnaire sent out to industry to obtain additional data about the use of animal materials of any origin in the manufacture of pharmaceutical products for human use, reveals that material of feline or canine origin is used in only two licensed products. In both instances the material is sourced from outside the U.K. and from areas currently believed to be free from B.S.E.
ARCHIVED URL LINK;
http://web.archive.org/web/20090506041332/http://www.bseinquiry.gov.uk/files/yb/1990/05/10005001.pdf
CONFIDENTIAL
Confidential cats/dogs and unsatisfactory posture MAFFs failure to assure key research
3. First, I am very uneasy about the relative lack of urgency and interest that MAFF appear to hold for getting the necessary research programme on BSE and related encephalopathies started, and getting it going fast. FOR EXAMPLE, MR BRADLEY of CVL said that there were difficulties in organizing transmission experiments from the brain of the cat which died of an encephalopathy in Bristol. There were arguments going on about who should pay for this work. Should it be MAFF, the Bristol Veterinary School or someone else? Dr. Tyrrell was clearly exasperated.
snip...
11. The Committee were even LESS FORTHCOMING on what their reaction might be if an encephalopathy is found in another species, perhaps in DOGS. Their first reaction was that, as with the cats, the first step could be to investigate whether this was really a new disease, or simply one that had not previously been recognized and to see whether it has any links to BSE, scrapie or other transmissible encephalopathies. Indeed, some members of the Committee seem to regard the whole question of another species as a hypothetical question to be addressed only when it happened. A rather UNSATISFACTORY POSTURE.
12. In advance of your meeting with Dr Tyrrell on Monday morning, I have not voiced my ANXIETIES about the support the Committee is receiving from MAFF to anyone OTHER THAN DR PICKLES. ...
http://www.bseinquiry.gov.uk/files/yb/1990/06/14006001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20030605151602/http://www.bseinquiry.gov.uk/files/yb/1990/06/14006001.pdf
can't forget about the mad man and his mad cat;
Deaths of CJD man and cat linked
http://news.bbc.co.uk/1/hi/health/184558.stm
In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html
Image] Research letters Volume 352, Number 9134 [Image] 3 October1998[Previous] [Next] [Image][Image]
Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy
[Image] Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, SergioFerrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, SalvatoreMonaco
Transmissible spongiform encephalopathies (TSE) encompass inherited,acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four typesof PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 inthe UK.5 We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat. A 60-year-old man, with no unusual dietary habits, was admitted in November,1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, andmyoclonus. An electroencephalogram (EEG) showed diffuse theta-deltaactivity. A brain magnetic resonance imaging scan was unremarkable. 10 days later, he was speechless and able to follow only simple commands. Repeat EEGs showed periodic triphasic complexes. 2 weeks after admission, he was mute, akinetic, and unable to swallow. He died in early January, 1994. His 7-year-old, neutered, female short haired cat presented in November,1993, with episodes of frenzy, twitching of its body, and hyperaesthesia.The cat was usually fed on canned food and slept on its owner's bed. No bites from the cat were recalled. In the next few days, the cat became ataxic, with hind quarter locomotor dysfunction; the ataxia got worse and there was diffuse myoclonus. The cat was killed in mid-January, 1994. No pathogenic mutations in the patient's PrP gene were found. The patientand the cat were methionine homozygous at codon 129. Histology of thepatient's brain showed neocortical and cerebellar neuronal loss,astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a punctate pattern and paralleled spongiform changes (figure B). The cat's brain showed mild and focal spongiosis in deeper cortical layers of all four lobes (figure C), vacuolated cortical neurons (figure D), and mild astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed. Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and caudate nucleus (figure E). Western blot analysis of control and affected human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After digestion with proteinase K and deglycosylation, only samples from the affected patient and cat showed type-1 PrPres, with PrP glycoform ratios comparable to those observed in sporadic CJD1 (details available fromauthor).
[Image] Microscopic sections of patient and cat brains
A: Occipital cortex of the patient showing moderate spongiformde generation and neuronal loss (haematoxylin and eosin) and
B: punctate perineuronal pattern of PrP immunoreactivity; peroxidase immunohistochemistry with monoclonal antibody 3F4.
C: cat parietal cortex showing mild spongiform degeneration (haematoxylin and eosin).
D: vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase immunohistochemistry with antibody 3F4 shows punctate perineuronalde position of PrP in temporal cortex. This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2
Taken together, our data suggest that the same agent strain of sporadic CJDs involved in the patient and in his cat. It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source,or the chance occurrence of two sporadic forms.
http://www.ncbi.nlm.nih.gov/pubmed/9798590
http://www.lancet.com/journals/lancet/article/PIIS0140-6736(05)79756-7/fulltext
Monday, May 12, 2008
Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease
http://betaamyloidcjd.blogspot.com/2008/05/fecal-transmission-of-aa-amyloidosis-in.html
indeed there have been 4 documented cases of TSE in Lions to date.
Lion 32 December 98 Born November 86
Lion 33 May 1999 (euthanased) Born November 81.
Lion 36 Euthanased August 2000 Born July 87. Deteriorating hind limb ataxia.
Lion 37 Euthanased November 2001 Male, 14 years. Deteriorating hind limb ataxia since September 2001. (Litter mate to Ref. 36.)
http://www.defra.gov.uk/animalh/bse/index.html
ARCHIVED URL LINK;
go to the url above, on the bar at the top, click on _statistics_, then in middle of next page, click on _other TSEs_.
or go here;
http://www.defra.gov.uk/animalh/bse/bse-statistics/level-3-tsestat.html
and
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html
SPONGIFORM ENCEPHALOPATHY IN A CAPTIVE PUMA
an article in yesterday's Times (attached) which suggested that the puma concerned had never ''eaten any part of a cow or sheep which, in the opinion of Government Scientists, could transmit the species to a different species''.
3. You explained to me that this was INCORRECT. The position was as set out in the briefing for Prime Minister's questions attached to Mr Taylor's note. The puma had probably been fed low quality beef meat in the form of split carcasses. ...
http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf
ARCHIVED URL LINK;
also;
Reports on the clinical symptoms presented by these cats give a relatively homogeneous picture: Affected cats show a lack of coordination with an ataxia mainly of the hind limbs, they often fall and miss their target when jumping. Fear and increased aggressiveness against the owner and also other animals is often seen. They do not longer tolerate to be touched (stroked) and start hiding. These behavioural chances might be the result of a hypersensibility to touch and noise, but also to increased fear. Excessive salivation is another more frequently seen symptom. Cats with FSE in general show severe behavioural disturbances, restlessness and depression, and a lack of coat cleaning. Symptoms in large cats in general are comparable to those in domestic cats. A report on FSE (in german) has been presented in 2001 in the Swiss FVO Magazin. A paper on the first FSE case in a domestic cat in Switzerland is currently in press in the Journal Schweizer Archiv für Tierheilkunde (SAT).
http://www.neurocenter-bern.ch/tse_e.shtml
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Thu, 17 Oct 2002 17:04:51 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L
Greetings BSE-L,
is there any other CWD surveys/testing in the UK on their deer? what sort of testing has been done to date on UK/EU deer? any input would be helpful... thank you
DEER SPONGIFORM ENCEPHALOPATHY SURVEY
3. This will be a low key study with no publicity to avoid unnecessary media interest. It will be carried out in two stages ;
(I) A small scale examination of around 30 deer brains to establish the normal histology of the healthy brain; and
(II) A larger scale random examination of 300 or more adult deer brains drawn from both deer farms and parks to establish whether there is any evidence of a cervine spongiform encephalopathy. ...
http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
ARCHIVED URL LINK;
Ministry of Agriculture Fisheries and Food
Veterinary Investigation Centre
West House. Station Road. Thirsk Y07 IPZ
Telephone: 0845·522065 Fax: 0845·525224
Your reference
Our reference RJH/ASB
Date 4 November 1992
DEER SPONGIFORM ENCEPHALOPATHY SURVEY
Dear Paul
I have now found time to review the 10 deer- brains collected from Mr Walker farm··via Winchester Via Winchester
VIC. In answer to your specific question was there sufficient difference in preservation of brain tissue to warrant the extra effort involved in rapid brain removal on the farm, the answer is definitely "Yes." The original five brains (Winchester ref M487/11) showed varying degrees of autolytic vacuolation affecting both white and grey matter throughout the brain. vacuolation and separation of Purkinje cells and marked perivascular spaces. These artifacts made interpretation of subtle, specific pathological vacuolation more difficult. By contrast the second submission (Winchester reference N736/2) showed excellent preservation of white and grey matter. Any vacuolar Change present could be confidently interpreted as pathological albeit of unknown pathogenesis.
I can only reiterate the comments made by Gerald Wells and myself at the preliminary discussion at Weybridge in Autumn 1991. If the survey's purpose is an accurate histopathological interpretation of brain tissue. the material must be collected in a pristine state. This is particularly valid when looking for ar unrecognised and undefined spongiform encephalopathy in a new species. Deer brains are very large structures which take a lot of fixation and therefore must be handled sympathetically from the start. We have already seen the problems encountered in comparatively smaller hound brains where delayed fixation was a major limitation on interpretation of true pathological change.
The bottom line must be that if a pathologist's expertise is to be used, it is critical to collect artefact free brain material. If the politics or economics do not allow this, then I would suggest that an electron microscopy survey involving detection of scrapie associated fibrils would be much more appropriate.
Best wishes
Yours sincerely
R J HIGGINS VIO 92/11.4/2.1
http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506032702/http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's minute.
I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.
J W WILESMITH
Epidemiology Unit
18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20030910030852/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.
http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506043913/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf
37. Putative TSE in hounds - work started 1990 -(see para 41)
Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) dated November 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.
41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).
http://www.bseinquiry.gov.uk/witness/htm/stat067.htm
1. I have had no further submission of material or communication regarding this survey since January 1991.
http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf
ARCHIVED URL LINK;
http://web.archive.org/web/20090506031340/http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf
HOUND SURVEY PATHOLOGICAL REPORT (see positive results)
http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf
ARCHIVED ULR LINK;
http://web.archive.org/web/20090506035936/http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf
kind regards, terry
###########bse-l ############
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" wt.net="">
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
Incubation periods for BSE are proportional to the life expectancy of the animal affected. The disease's incubation period is 18% of a cow's life expectancy and would be expected to about double when crossing to another species [---] that is, to 36% of 70 years in humans.
Steve Dealler, consultant in medical microbiology. Burnley General Hospital, Burnley BB10 2PQ deal@airtime.co.uk
=======================================
-------- Original Message --------
Subject: Cognitive Dysfunction Syndrome (CDS) or MAD DOG DISEASE
Date: Mon, 4 Apr 2005 13:14:12 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@KALIV.UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy #####################
Greetings,
THIS is a hoot from purina, as to why your dog might be acting a bit strangely. nothing mentioned about the decades of feeding those dogs the same thing we been feeding humans, potentially tainted feed, tainted with TSEs. dog food (like cat food) is loaded with SRMs. new regulations are suppose to go into effect, but that will not help all the animals exposed over the decades. some data on dogs, cats and TSE. THE reason of bringing this up again, there was a small write-UP in question to a Dr. Michael Fox about this in the Houston Chronicle 'Easing Life of older dogs' ; 'My black Lab is 12 years old and has entered his ''Alzheimer's'' phase ... 'it's called canine cognitive dysfunction disorder ... snip... end SO, went to see what the feed sellers say about this ; Does your dog suffer from Cognitive Dysfunction Syndrome? Find out how to cope with dog dementia. Typically, an elderly dog tends to sleep longer hours and slow down in comparison to his or her younger or middle-aged years. But some older dogs exhibit behaviour changes that appear abnormal. Until recently, such changes had been attributed to normal aging, for which little could be done. However, behaviour changes in elderly dogs may be due to a disorder called Cognitive Dysfunction Syndrome. Cognitive Dysfunction Syndrome (CDS) is associated with a number of clinical signs. The diagnosis is made when dogs exhibit multiple signs which develop in old age, and which are not completely due to other medical or physical problems. Dogs with CDS may appear disoriented in familiar surroundings such as their own homes, wandering aimlessly and perhaps appearing to 'forget' to back out of corners. Those that were flawlessly housetrained throughout their lives may start to have 'accidents'. They may no longer greet their owners at the door, bring them balls to throw, or appear to care about being petted. And while they may sleep throughout the day, the night may bring restlessness and increased wandering, as though their biological clocks were reversed. Because aging dogs are increasingly susceptible to medical problems (see 'The Elderly Dog'), regular examinations by a vet are important. Only a veterinary surgeon can determine whether your dog's behaviour changes are due to CDS (rather than, for example, liver, heart, or kidney disease). If a diagnosis of CDS is made, your vet may recommend treatment. Behaviour changes in aging dogs may be responsive to treatment. Whatever, happens, after a lifetime of unconditional love and companionship, our older dogs deserve every consideration we can give them.
http://www.purina.co.uk/index.asp?frame=/dog/article.asp&id=71
ARCHIVED URL LINK;
Is your dog elderly? If so, you'll have to ease their way. Here's how... Often dogs are older than we think they are. It's hard to guess-timate how old a dog is as there are considerable breed differences between dogs. Generally speaking, small dogs live the longest (a Yorkshire Terrier is considered 'old' at 10 years), while large breeds have relatively short lifespans (a Great Dane is considered 'old' at six years). Here we help you tell if your dog is old and then advise you on how to make your elderly dog's life easier& The physical signs: Physical inactivity- Difficulty getting up after lying down for a while or after a long walk can be a sign of deteriorating joints due to wear and tear through life. Some dogs may be less keen to go for walks and prefer to curl up in a warm bed. Others may be initially keen to go out but as the joints ease with gentle exercise may be tempted to do a little too much with dire consequences later in the day as joints stiffen up and become even worse. Hair loss- The skin may appear dry and scaly while the coat texture may be harsher, thinner with bald patches or white hairs. Often the coat is dull and the colour may be less vivid. Dog breath- Bad teeth or gum infections may cause bad breath or inability to eat. A common sign is of food being dropped or excessive salivation and pawing at the mouth. Swellings appearing below the eye may be signs of tooth root abscesses and need veterinary attention. Lumps and bumps- Warts, fatty lumps and even tumours may appear in old age. Check these out with your vet as early detection may save your dog's life. Loss of bladder control- Incontinence: this is sometimes associated with changes in thirst but sometimes it's associated with sore joints, which make posturing difficult. Mental alertness- Many older dogs become confused and fail to recognise their surroundings, their name or their owner! They may become less interested in food or what is happening around them. Some dogs appear dull and depressed while others become disobedient or destructive. Many older dogs get anxious if left alone for any length of time. Sleep- Many older dogs sleep more during the day but sleep less at night. Some may prowl around the house at night because of sore joints, senility or even loneliness. Ways to make your dog's life easier If your dog shows these signs, consider the following to make your dog's life easier: * Install ramps to allow your dog to get back into the house from the garden. * Dry your dog well if you've been walking in the rain. * Arthritic dogs may have trouble standing up after lying down for a period of time so gently rub the muscles to warm them up and relieve some of the stiffness. * Understand that changes in oxygen flow to the brain in old age mean dogs are likely to remember events from the past much better than if they happened yesterday. They get confused. Another change experienced by some dogs, cognitive dysfunction syndrome, may affect behaviour in more general ways, similar to the changes caused by senile dementia in humans. * Some retraining may be necessary. Often using treats is a particularly good way to retrain the older dog. Food is a great motivator but beware of obesity in a less active older dog. * Perhaps amounts at mealtimes need adjusting as elderly dogs usually become less active and require fewer calories. But conversely in some dogs, particularly the very old, more calories are needed. The main thing is to keep an eye on the dog's weight, however. * Deteriorating vision and hearing may reduce a dog's ability to respond to his environment. He/she may not greet you immediately only because he/she isn't aware that you've arrived. Take a look at how to cope with blindness and deafness. * Older dogs may also develop a fear of thunderstorms. The booming sounds of thunder may be exaggerated because of a loss of high-frequency hearing. * Ensure their bed is in a warm draught-free place to make sleep time that bit more comfortable.
http://www.purina.co.uk/index.asp?frame=/dog/article.asp&id=69
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FOR IMMEDIATE RELEASE P01-05 January 30, 2001
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
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PRION 2009 CONGRESS BOOK OF ABSTRACTS
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Prion Infectivity and PrPBSE in the Peripheral and Central Nervous System of Cattle 8 Months Post Oral BSE Challenge
Ivett Ackermann 1 , Reiner Ulrich 2 , Kerstin Tauscher 3 , Olanrewaju I. Fatola 1,4 , Markus Keller 1 , James C. Shawulu 1,5, Mark Arnold 6 , Stefanie Czub 7 , Martin H. Groschup 1 and Anne Balkema-Buschmann 1,*
1 Institute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institute, 17493 Greifswald-Insel Riems, Germany; Ivett.Ackermann@fli.de (I.A.); fatolan@yahoo.com (O.I.F.); Markus.Keller@fli.de (M.K.); james.shawulu@ymail.com (J.C.S.); Martin.Groschup@fli.de (M.H.G.) 2 Institute of Veterinary Pathology, Faculty of Veterinary Medicine, Leipzig University, 04103 Leipzig, Germany; reiner.ulrich@vetmed.uni-leipzig.de 3 Department of Experimental Animal Facilities and Biorisk Management, Friedrich-Loeffler-Institute, 17493 Greifswald-Insel Riems, Germany; Kerstin_Tauscher@gmx.de 4 Neuroscience Unit, Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Ibadan, Ibadan 200284, Nigeria 5 Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Abuja, Abuja 900105, Nigeria 6 Animal and Plant Health Agency Sutton Bonington, Sutton Bonington, Leicestershire LE12 5RB, UK; Mark.Arnold@apha.gov.uk 7 Canadian Food Inspection Agency, Lethbridge Laboratory, Lethbridge, AB T1J 3Z4, Canada; stefanie.czub37@gmail.com * Correspondence: anne.buschmann@fli.de
Abstract: After oral exposure of cattle with classical bovine spongiform encephalopathy (C-BSE), the infectious agent ascends from the gut to the central nervous system (CNS) primarily via the autonomic nervous system. However, the timeline of this progression has thus far remained widely undetermined. Previous studies were focused on later time points after oral exposure of animals that were already 4 to 6 months old when challenged. In contrast, in this present study, we have orally inoculated 4 to 6 weeks old unweaned calves with high doses of BSE to identify any possible BSE infectivity and/or PrPBSE in peripheral nervous tissues during the first eight months postinoculation (mpi). For the detection of BSE infectivity, we used a bovine PrP transgenic mouse bioassay, while PrPBSE depositions were analyzed by immunohistochemistry (IHC) and by protein misfolding cyclic amplification (PMCA). We were able to show that as early as 8 mpi the thoracic spinal cord as well as the parasympathetic nodal ganglion of these animals contained PrPBSE and BSE infectivity. This shows that the centripetal prion spread starts early after challenge at least in this age group, which represents an essential piece of information for the risk assessments for food, feed, and pharmaceutical products produced from young calves.
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5. Conclusions
In summary, we detected PrPBSE and BSE infectivity as early as 8 mpi in the nodal ganglion as well as in the thoracic spinal cord from one calf challenged before weaning in this study and also at eight mpi in the thoracic spinal cord sampled from cattle challenged at 4 to 6 months of age during an earlier pathogenesis study [5,20]. This current study considerably expands the existing data on the early C-BSE pathogenesis by demonstrating that after challenge with an unnaturally high dose of 100 g BSE-positive brainstem tissue, parts of the peripheral and central nervous system from cattle may already contain PrPBSE and BSE infectivity after short time periods up to 8 months after oral infection, which should be considered relevant information for risk assessments for food and pharmaceutical products.
Supplementary Materials: The following are available online at https://www.mdpi.com/article/10 .3390/ijms222111310/s1 .
Keywords: prion protein; BSE; infectivity; PrPBSE; cattle; peripheral and central nervous system; protein misfolding cyclic amplification (PMCA)
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.
P.4.23
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.
Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice.
BSE-H is also transmissible in our humanized Tg mice.
The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
P03.137
Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan
Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf
Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle
G. A. H. Wells,1 T. Konold,1 M. E. Arnold,1 A. R. Austin,1 3 S. A. C. Hawkins,1 M. Stack,1 M. M. Simmons,1 Y. H. Lee,2 D. Gavier-Wide´n,3 M. Dawson1 4 and J. W. Wilesmith1 1 Correspondence G. A. H. Wells
1 Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK
2 National Veterinary Research and Quarantine Service, Anyang, Republic of Korea
3 National Veterinary Institute (SVA), SE-75189 Uppsala, Sweden
Received 27 July 2006
Accepted 18 November 2006
The dose–response of cattle exposed to the bovine spongiform encephalopathy (BSE) agent is an important component of modelling exposure risks for animals and humans and thereby, the modulation of surveillance and control strategies for BSE. In two experiments calves were dosed orally with a range of amounts of a pool of brainstems from BSE-affected cattle. Infectivity in the pool was determined by end-point titration in mice. Recipient cattle were monitored for clinical disease and, from the incidence of pathologically confirmed cases and their incubation periods (IPs), the attack rate and IP distribution according to dose were estimated. The dose at which 50 % of cattle would be clinically affected was estimated at 0.20 g brain material used in the experiment, with 95 % confidence intervals of 0.04–1.00 g. The IP was highly variable across all dose groups and followed a log-normal distribution, with decreasing mean as dose increased. There was no evidence of a threshold dose at which the probability of infection became vanishingly small, with 1/15 (7 %) of animals affected at the lowest dose (1 mg).
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DISCUSSION
The study has demonstrated that disease in cattle can be produced by oral exposure to as little as 1 mg brain homogenate (¡100.4 RIII mouse i.c./i.p. ID50 units) from clinically affected field cases of BSE and that the limiting dose for infection of calves is lower than this exposure...
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P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasm�zas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; L�wer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat � l�Energie Atomique, France; 3Instituto Superiore di Sanit�, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study �BSE in primates� supported by the EU (QLK1-2002-01096).
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
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BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
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Chow Down Fido - Dog Food is Safe
FDA report shows no risk from low levels of pentobarbital in dog food.
The low levels of exposure to sodium pentobarbital (pentobarbital) that dogs might receive through food is unlikely to cause them any adverse health effects, Food and Drug Administration (FDA) scientists concluded after conducting a risk assessment.
During the 1990s, FDA’s Center for Veterinary Medicine (CVM) received reports from veterinarians that pentobarbital, an anesthetizing agent used for dogs and other animals, seemed to be losing its effectiveness in dogs. Based on these reports, CVM officials decided to investigate a plausible theory that the dogs were exposed to pentobarbital through dog food, and that this exposure was making them less responsive to pentobarbital when used as a drug.
The investigation consisted of two parts. First, CVM had to determine if dog food could contain residues of the drug. Second, if residues were found, the Center had to determine what risk, if any, the residues posed to dogs. In conjunction with the investigation, the Center wanted to determine if pet food contained rendered remains of dogs and cats.
How Pentobarbital Can Get into Dog Food
Because in addition to producing anesthesia, pentobarbital is routinely used to euthanize animals, the most likely way it could get into dog food would be in rendered animal products.
Pentobarbital seems to be able to survive the rendering process. If animals are euthanized with pentobarbital and subsequently rendered, pentobarbital could be present in the rendered feed ingredients.
In order to determine if pentobarbital residues were present in animal feeds, CVM developed a sophisticated process to detect and quantify minute levels – down to two parts per billion of pentobarbital in dry dog food. To confirm that the methods they developed worked properly, CVM scientists used the methods to analyze dry commercial dog foods purchased from retail outlets near to their Laurel, MD, laboratories. The scientists purchased dog food as part of two surveys, one in 1998 and the second in 2000. They found some samples contained pentobarbital.
Dogs, Cats Not Found
Because pentobarbital is used to euthanize dogs and cats at animal shelters, finding pentobarbital in rendered feed ingredients could suggest that the pets were rendered and used in pet food.
CVM scientists, as part of their investigation, developed a test to detect dog and cat DNA in the protein of the dog food. All samples from the most recent dog food survey (2000) that tested positive for pentobarbital, as well as a subset of samples that tested negative, were examined for the presence of remains derived from dogs or cats.
The results demonstrated a complete absence of material that would have been derived from euthanized dogs or cats. The sensitivity of this method is 0.005 percent on a weight/weight basis; that is, the method can detect a minimum of five pounds of rendered remains in 50 tons of finished feed. Presently, it is assumed that the pentobarbital residues are entering pet foods from euthanized, rendered cattle or even horses.
Finding Levels of Pentobarbital Residues
Upon finding pentobarbital residues in dog food, the researchers undertook an assessment of the risk dogs might face. Dogs were given known quantities of pentobarbital for eight weeks to determine if consumption of small amounts of pentobarbital resulted in any physiological changes that could indicate potential effects on health. In short, the scientists wanted to find the level of pentobarbital dogs could be exposed to that would show no biological effects. The most sensitive indicator that pentobarbital had an effect is an increase in the production of certain enzymes collectively called cytochrome P450.
Virtually all animals produce enzymes as a normal response to metabolize naturally occurring and man-made chemicals in their environment. Barbituates, such as pentobarbital, are especially efficient at causing the liver to produce these enzymes. In dogs, the most sensitive biological response to pentobarbital is an increase in the production of cytochrome P450 enzymes, which is why the scientists chose that as the best indicator of biological effect. If a low level of pentobarbital did not cause a dog to produce additional cytochrome P450 enzymes, then scientists could assume that the pentobarbital at that low level had no significant effect on the dog.
In CVM’s study, experimental animals were each dosed orally with either 50, 150, or 500 micrograms pentobarbital/day for eight weeks. The results were compared with control animals, which were not exposed to pentobarbital.
Several significant pentobarbital-associated effects were identified in this study.
1. Dogs that received 150 and 500 micrograms pentobarbital once daily for eight weeks had statistically higher liver weights (relative to their bodyweights) than the animals in the control groups. Increased liver weights are associated with the increased production by the liver of cytochrome P450 enzymes.
2. An analysis showed that the activity of at least three liver enzymes was statistically greater than that of the controls at doses of approximately 200 micrograms pentobarbital per day or greater.
But researchers found no statistical differences in relative liver weight or liver enzyme activity between the group receiving 50 micrograms pentobarbital per day and the controls. Based on the data from this study, CVM scientists were able to determine that the no-observable-effect level – which is the highest dose at which no effects of treatment were found – for pentobarbital was 50 micrograms of pentobarbital per day.
Adverse Health Effects Unlikely
For the purposes of CVM’s assessment, the scientists assumed that at most, dogs would be exposed to no more than four micrograms/kilogram body weight/day based on the highest level of pentobarbital found in the survey of dog foods. In reality, dogs are not likely to consume that much. The high number was based on the assumption that the smallest dogs would eat dog food containing the greatest amount of pentobarbital detected in the survey of commercial pet foods – 32 parts per billion.
However, to get to the exposure level of 50 micrograms of pentobarbital per day, which is the highest level at which no biological response was seen, a dog would have to consume between 5 to 10 micrograms of pentobarbital per kilogram of body weight. But the most any dog would consume, based on the survey results, was four micrograms pentobarbital per kilogram of body weight per day.
It should be emphasized that induction of cytochrome P450 enzymes is a normal response to many substances that are naturally found in foods. It is not an indication of harm, but was selected as the most sensitive indicator to detect any biological effect due to pentobarbital.
Thus, the results of the assessment led CVM to conclude that it is highly unlikely a dog consuming dry dog food will experience any adverse effects from exposures to the low levels of pentobarbital found in CVM’s dog food surveys.
Additional information, including the survey results, can be found on CVM’s Web site at www.fda.cvm.gov under “Freedom of Information.”
April 2002 Render
http://www.rendermagazine.com/April2002/ChowDownFido.html
Reprinted with permission from Earth Island Journal (vol. 11, no. 3, Summer 1996) (vol. 5, no. 4, Fall 1990) 300 Broadway, Suite 28 San Francisco, CA 94133, USA Phone: +1 (415) 788 3666 Fax: +1 (415) 788 7324 E-mail: earthisland@igc.apc.org Web page: http://www.earthisland.org/ei/
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1. THE TRUTH ABOUT CATS AND DOGS by Ann Martin
The pet food industry, a billion-dollar, unregulated operation, feeds on the garbage that otherwise would wind up in landfills or be transformed into fertiliser. The hidden ingredients in a can of commercial pet food may include roadkill and the rendered remains of cats and dogs. The pet food industry claims that its products constitute a "complete and balanced diet" but, in reality, commercial pet food is unfit for human or animal consumption.
"Vegetable protein", the mainstay of dry dog foods, includes ground yellow corn, wheat shorts and middlings, soybean meal, rice husks, peanut meal and peanut shells (identified as "cellulose" on pet food labels). These often are little more than the sweepings from milling room floors. Stripped of their oil, germ and bran, these "proteins" are deficient in essential fatty acids, fat-soluble vitamins and antioxidants. "Animal protein" in commercial pet foods can include diseased meat, roadkill, contaminated material from slaughterhouses, faecal matter, rendered cats and dogs and poultry feathers. The major source of animal protein comes from dead-stock removal operations that supply so-called "4-D" animals - dead, diseased, dying or disabled - to "receiving plants" for hide, fat and meat removal. The meat (after being doused with charcoal and marked "unfit for human consumption") may then be sold for pet food.
Rendering plants process decomposing animal carcasses, large roadkill and euthanised dogs and cats into a dry protein product that is sold to the pet food industry. One small plant in Quebec, Ontario, renders 10 tons (22,000 pounds) of dogs and cats per week. The Quebec Ministry of Agriculture states that "the fur is not removed from dogs and cats" and that "dead animals are cooked together with viscera, bones and fat at 115° C (235° F) for 20 minutes".
The US Food and Drug Administration's Center for Veterinary Medicine (CVM) is aware of the use of rendered dogs and cats in pet foods, but has stated: "CVM has not acted to specifically prohibit the rendering of pets. However, that is not to say that the practise of using this material in pet food is condoned by the CVM."
In both the US and Canada, the pet food industry is virtually self-regulated. In the US, the Association of American Feed Control Officials (AAFCO) sets guidelines and definitions for animal feed, including pet foods. In Canada, the most prominent control is the "Labeling Act", simply requiring product labels to state the name and address of the manufacturer, the weight of the product and whether it is dog or cat food. The Canadian Veterinary Medical Association (CVMA) and the Pet Food Association of Canada (PFAC) are voluntary organisations that, for the most part, rely on the integrity of the companies they certify to assure that product ingredients do not fall below minimum standards.
The majority - 85 to 90 per cent - of the pet food sold in Canada is manufactured by US-based multinationals. Under the terms of the US-Canada Free Trade Agreement, neither the CVMA nor PFAC exercises any control over the ingredients in cans of US pet food.
Pet food industry advertising promotes the idea that, to keep pets healthy, one must feed them commercially formulated pet foods. But such a diet contributes to cancer, skin problems, allergies, hypertension, kidney and liver failure, heart disease and dental problems. One more item should be added to pet food labels: a skull-and-crossbones insignia!
(Ann Martin is an animal rights activist and leading critic of the commercial pet food industry. She lives in London, Ontario, Canada.)
2. FOOD NOT FIT FOR A PET
by Dr Wendell O. Belfield, D.V.M. The most frequently asked question in my practice is, "Which commercial pet food do you recommend?" My standard answer is "None." I am certain that pet-owners notice changes in their animals after using different batches of the same brand of pet food. Their pets may have diarrhoea, increased flatulence, a dull hair coat, intermittent vomiting or prolonged scratching. These are common symptoms associated with commercial pet foods.
In 1981, as Martin Zucker and I wrote How to Have a Healthier Dog, we discovered the full extent of negative effects that commercial pet food has on animals. In February 1990, San Francisco Chronicle staff writer John Eckhouse went even further with an exposé entitled "How Dogs and Cats Get Recycled into Pet Food".
Eckhouse wrote: "Each year, millions of dead American dogs and cats are processed along with billions of pounds of other animal materials by companies known as renderers. The finished product...tallow and meat meal...serve as raw materials for thousands of items that include cosmetics and pet food."
Pet food company executives made the usual denials. But federal and state agencies, including the Food and Drug Administration, and medical groups, such as the American Veterinary Medical Association and the California Veterinary Medical Association (CVMA), confirm that pets, on a routine basis, are rendered after they die in animal shelters or are disposed of by health authorities - and the end product frequently finds its way into pet food.
Government health officials, scientists and pet food executives argue that such open criticism of commercial pet food is unfounded. James Morris, a professor at the School of Veterinary Medicine at Davis, California, has said, "Any products not fit for human consumption are very well sterilised, so nothing can be transmitted to the animal." Individuals who make such statements know nothing of the meat and rendering business.
For seven years I was a veterinary meat inspector for the US Department of Agriculture and the State of California. I waded through blood, water, pus and faecal material, inhaled the fetid stench from the killing floor and listened to the death cries of slaughtered animals.
Prior to World War II, most slaughterhouses were all-inclusive; that is, livestock was slaughtered and processed in one location. There was a section for smoking meats, a section for processing meats into sausages, and a section for rendering. After World War II, the meat industry became more specialised. A slaughterhouse dressed the carcasses, while a separate facility made the sausages. The rendering of slaughter waste also became a separate speciality - no longer within the jurisdiction of federal meat inspectors and out of the public eye.
To prevent condemned meat from being rerouted and used for human consumption, government regulations require that meat be "denatured" before removal from the slaughterhouse and shipment to rendering facilities. In my time as a veterinary meat inspector, we denatured with carbolic acid (a potentially corrosive disinfectant) and/or creosote (used for wood-preservation or as a disinfectant). Both substances are highly toxic. According to federal meat inspection regulations, fuel oil, kerosene, crude carbolic acid and citronella (an insect repellent made from lemon grass) are all approved denaturing materials.
Condemned livestock carcasses treated with these chemicals can become meat and bone meal for the pet food industry. Because rendering facilities are not government-controlled, any animal carcasses can be rendered - even dogs and cats. As Eileen Layne of the CVMA told the Chronicle, "When you read pet food labels, and it says "meat and bone meal", that's what it is: cooked and converted animals, including some dogs and cats."
Some of these dead pets - those euthanised by veterinarians - already contain pentobarbital before treatment with the denaturing process. According to University of Minnesota researchers, the sodium pentobarbital used to euthanise pets "survives rendering without undergoing degradation". Fat stabilisers are introduced into the finished rendered product to prevent rancidity. Common chemical stabilisers include BHA (butylated hydroxyanisole) and BHT (butylated hydroxytoluene) - both known to cause liver and kidney dysfunction - and ethoxyquin, a suspected carcinogen. Many semi-moist dog foods contain propylene glycol - first cousin to the anti-freeze agent, ethylene glycol, that destroys red blood-cells. Lead frequently shows up in pet foods, even those made from livestock meat and bone meal. A Massachusetts Institute of Technology study, titled "Lead in Animal Foods", found that a nine-pound cat fed on commercial pet food ingests more lead than the amount considered potentially toxic for children.
I have been practising small-animal medicine for more than 25 years. Every day I see the casualties of pet industry propaganda. But the professors in the teaching institutions of veterinary medicine generally support an industry that has little regard for the quality of health in our companion animals.
One last word of caution: meat and bone meal from sources not fit for human consumption have found their way into poultry feed. This means that animal products rendered under questionable conditions are fed to birds that may wind up on your table. Remember this when you are eating your next piece of chicken or turkey.
(Dr Belfield is a graduate of Tuskegee Institute of Veterinary Medicine and is now in private practice in San Jose, California. Dr Belfield established the first orthomolecular veterinary hospital in the US. He is co-author of The Very Healthy Cat Book and How to Have a Healthier Dog. This article first appeared in Let's Live Magazine, May 1992.)
3. A LOOK INSIDE A RENDERING PLANT
by Gar Smith Rendering has been called "the silent industry". Each year in the US, 286 rendering plants quietly dispose of more than 12.5 million tons of dead animals, fat and meat wastes. As the public relations watchdog newsletter PR Watch observes, renderers "are thankful that most people remain blissfully unaware of their existence".
When City Paper reporter Van Smith visited Baltimore's Valley Proteins rendering plant last summer, he found that the "hoggers" (the large vats used to grind and filter animal tissues prior to deep-fat-frying) held an eclectic mix of body parts ranging from "dead dogs, cats, raccoons, possums, deer, foxes [and] snakes" to a "baby circus elephant" and the remains of Bozeman, a Police Department quarterhorse that "died in the line of duty".
In an average month, Baltimore's pound hands over 1,824 dead animals to Valley Proteins. Last year, the plant transformed 150 millions pounds of decaying flesh and kitchen grease into 80 million pounds of commercial meat and bone meal, tallow and yellow grease. Thirty years ago, most of the renderer's wastes came from small markets and slaughterhouses. Today, thanks to the proliferation of fast-food restaurants, nearly half the raw material is kitchen grease and frying oil.
Recycling dead pets and wildlife into animal food is "a very small part of the business that we don't like to advertise," Valley Proteins' President, J. J. Smith, told City Paper. The plant processes these animals as a "public service, not for profit," Smith said, since "there is not a lot of protein and fat [on pets]..., just a lot of hair you have to deal with somehow."
According to City Paper, Valley Proteins "sells inedible animal parts and rendered material to Alpo, Heinz and Ralston-Purina". Valley Proteins insists that it does not sell "dead pet by-products" to pet food firms since "they are all very sensitive to the recycled pet potential". Valley Proteins maintains two production lines - one for clean meat and bones and a second line for dead pets and wildlife. However, Van Smith reported, "the protein material is a mix from both production lines. Thus the meat and bone meal made at the plant includes materials from pets and wildlife, and about five per cent of that product goes to dry-pet-food manufacturers..."
A 1991 USDA report states that "approximately 7.9 billion pounds of meat and bone meal, blood meal and feather meal [were] produced in 1983". Of that amount, 34 per cent was used in pet food, 34 per cent in poultry feed, 20 per cent in pig food and 10 per cent in beef and dairy cattle feed.
Transmissible spongiform encephalopathy (TSE) carried in pig- and chicken-laden foods may eventually eclipse the threat of "mad cow disease". The risk of household pet exposure to TSE from contaminated pet food is more than three times greater than the risk for hamburger-eating humans.
(Gar Smith is Editor of Earth Island Journal.)
4. THE DARK SIDE OF RECYCLING [Author's name withheld]
[In February 1990, the San Francisco Chronicle carried a macabre two-part story detailing how stray dogs, cats and pound animals are routinely rounded up by meat renderers and ground up into - of all things - pet food. According to the researcher who brought the information to the Chronicle, the paper buried the story and deleted many of the charges he had documented. A report he worked on for ABC television's 20-20 was similarly watered down. In exasperation, he sent the story to Earth Island Journal. NEXUS has been asked to withhold the name of the author/researcher, who has been forced to flee San Francisco with his wife and go into hiding as a result of the threats made against his well-being. Ed.]
The rendering plant floor is piled high with "raw product": thousands of dead dogs and cats; heads and hooves from cattle, sheep, pigs and horses; whole skunks; rats and raccoons - all waiting to be processed. In the 90-degree heat, the piles of dead animals seem to have a life of their own as millions of maggots swarm over the carcasses.
Two bandana-masked men begin operating Bobcat mini-dozers, loading the "raw" into a 10-foot- deep stainless-steel pit. They are undocumented workers from Mexico, doing a dirty job. A giant auger-grinder at the bottom of the pit begins to turn. Popping bones and squeezing flesh are sounds from a nightmare you will never forget.
Rendering is the process of cooking raw animal material to remove the moisture and fat. The rendering plant works like a giant kitchen. The cooker, or "chef", blends the raw product in order to maintain a certain ratio between the carcasses of pets, livestock, poultry waste and supermarket rejects.
Once the mass is cut into small pieces, it is transported to another auger for fine shredding. It is then cooked at 280 degrees for one hour. The continuous batch cooking process goes on non-stop, 24 hours a day, seven days a week as meat is melted away from bones in the hot 'soup'. During this cooking process, the 'soup' produces a fat of yellow grease or tallow that rises to the top and is skimmed off. The cooked meat and bone are sent to a hammermill press, which squeezes out the remaining moisture and pulverises the product into a gritty powder. Shaker screens sift out excess hair and large bone chips. Once the batch is finished, all that is left is yellow grease, meat and bone meal.
A Meaty Menu As the American Journal of Veterinary Research explains, this recycled meat and bone meal is used as "a source of protein and other nutrients in the diets of poultry and swine and in pet foods, with lesser amounts used in the feed of cattle and sheep. Animal fat is also used in animal feeds as an energy source." Every day, hundreds of rendering plants across the United States truck millions of tons of this "food enhancer" to poultry ranches, cattle feed-lots, dairy and hog farms, fish-feed plants and pet-food manufacturers where it is mixed with other ingredients to feed the billions of animals that meat-eating humans, in turn, will eat.
Rendering plants have different specialities. The labelling designation of a particular "run" of product is defined by the predominance of a specific animal. Some product-label names are: meat meal, meat by-products, poultry meal, poultry by-products, fish meal, fish oil, yellow grease, tallow, beef fat and chicken fat.
Rendering plants perform one of the most valuable functions on Earth: they recycle used animals. Without rendering, our cities would run the risk of becoming filled with diseased and rotting carcasses. Fatal viruses and bacteria would spread uncontrolled through the population.
The Dark Side Death is the number one commodity in a business where the demand for feed ingredients far exceeds the supply of raw product. But this elaborate system of food production through waste management has evolved into a recycling nightmare. Rendering plants are unavoidably processing toxic waste.
The dead animals (the "raw") are accompanied by a whole menu of unwanted ingredients. Pesticides enter the rendering process via poisoned livestock, and fish oil laced with bootleg DDT and other organophosphates that have accumulated in the bodies of West Coast mackerel and tuna.
Because animals are frequently shoved into the pit with flea collars still attached, organophosphate-containing insecticides get into the mix as well. The insecticide Dursban arrives in the form of cattle insecticide patches. Pharmaceuticals leak from antibiotics in livestock, and euthanasia drugs given to pets are also included. Heavy metals accumulate from a variety of sources: pet ID tags, surgical pins and needles.
Even plastic winds up going into the pit. Unsold supermarket meats, chicken and fish arrive in styrofoam trays and shrink wrap. No one has time for the tedious chore of unwrapping thousands of rejected meat-packs. More plastic is added to the pits with the arrival of cattle ID tags, plastic insecticide patches and the green plastic bags containing pets from veterinarians.
Rendering Judgements Skyrocketing labour costs are one of the economic factors forcing the corporate flesh-peddlers to cheat. It is far too costly for plant personnel to cut off flea collars or unwrap spoiled T-bone steaks. Every week, millions of packages of plastic-wrapped meat go through the rendering process and become one of the unwanted ingredients in animal feed.
The most environmentally conscious state in the nation is California, where spot checks and testing of animal-feed ingredients happen at the wobbly rate of once every two-and-a-half months. The supervising state agency is the Department of Agriculture's Feed and Fertilizer Division of Compliance. Its main objective is to test for truth in labelling: does the percentage of protein, phosphorous and calcium match the rendering plant's claims; do the percentages meet state requirements? However, testing for pesticides and other toxins in animal feeds is incomplete.
In California, eight field inspectors regulate a rendering industry that feeds the animals that the state's 30 million people eat. When it comes to rendering plants, however, state and federal agencies have maintained a hands-off policy, allowing the industry to become largely self-regulating. An article in the February 1990 issue of Render, the industry's national magazine, suggests that the self-regulation of certain contamination problems is not working.
One policing program that is already off to a shaky start is the Salmonella Education/Reduction Program, formed under the auspices of the National Renderers Association. The magazine states that "...unless US and Canadian renderers get their heads out of the ground and demonstrate that they are serious about reducing the incidence of salmonella contamination in their animal protein meals, they are going to be faced with...new and overly stringent government regulations."
So far, the voluntary self-testing program is not working. According to the magazine, "...only about 20 per cent of the total number of companies producing or blending animal protein meal have signed up for the program..." Far fewer have done the actual testing.
The American Journal of Veterinary Research conducted an investigation into the persistence of sodium phenobarbital in the carcasses of euthanised animals at a typical rendering plant in 1985 and found "...virtually no degradation of the drug occurred during this conventional rendering processŠ" and that "...the potential of other chemical contaminants (e.g., heavy metals, pesticides and environmental toxicants, which may cause massive herd mortalities) to degrade during conventional rendering needs further evaluation."
Renderers are the silent partners in our food chain. But worried insiders are beginning to talk, and one word that continues to come up in conversation is "pesticides". The possibility of petrochemically poisoning our food has become a reality. Government agencies and the industry itself are allowing toxins to be inadvertently recycled from the streets and supermarket shelves into the food chain. As we break into a new decade of increasingly complex pollution problems, we must rethink our place in the environment. No longer hunters, we are becoming the victims of our technologically altered food chain.
The possibility of petrochemically poisoning our food has become a reality.
(First published in Earth Island Journal, Fall 1990.)
Mad cow outbreak may have been caused by animal rendering plants N.Y. Times News Service Mar 11, 1997
When cows in Britain began staggering around and dying, their brains eaten away by a mysterious disease, officials in the United States were reassuring. The disease would not be a problem here, they said. Later, when it appeared that a few people in Britain had contracted a similar lethal condition from eating affected meat, experts at the Department of Agriculture said there was no reason for Americans to worry.
Now, though, the Food and Drug Administration is starting to talk about new regulations in the aftermath of disturbing hints that something similar conceivably could appear in American animals. So far, the only affected animals are a few hundred mink in Wisconsin. Nevertheless, the agency wants to restrict the little-known agricultural practice that lies behind the problem in Britain: the use of rendered animal tissue in animal feed. In the process, they are drawing new attention to rendering -- the ancient but seldom-discussed practice of boiling down and making feed meal and other products out of slaughterhouse and restaurant scraps, dead farm animals, road kill and -- distasteful as it may seem -- cats and dogs euthanized in some animal shelters.
This quasi-cannibalism lies behind the outbreak in Britain and regulators want to be sure it will not cause problems in the United States. The disease that struck the British cows, bovine spongiform encephalopathy, may have originated as scrapie, a mysterious condition limited to sheep. Scientists believe the so-called mad cow disease results when cattle eat feed made from the brains or spinal cords of sheep suffering from scrapie. They believe the people who died were infected when they ate beef or other products from these cows, a theory that remains controversial, though evidence is accumulating.
Public health officials and agricultural experts say there are good reasons to believe that mad cow disease will not become a problem in the United States. Scrapie is less common in this country than in Britain. More importantly, the Food and Drug Administration is moving to ban the use of certain animal tissues in cattle feed. The agency recently held hearings on the effects that such a ban might have on the billion-dollar industry and hopes to decide this year whether to impose a ban.
Rendering, which dates to the early Egyptians, operates in the shadows of polite society, persisting because it provides an essential service: disposing of millions of pounds of dead animals every day.
"If you burned all the carcasses, you'd get a terrible air pollution problem," said Dr. William Heuston, associate dean of the Virginia-Maryland College of Veterinary Medicine at College Park, Md. "If you put it all into landfills, you'd have a colossal public health problem, not to mention stench. Dead animals are an ideal medium for bacterial growth."
Renderers in the United States pick up 100 million pounds of waste material every day -- a witch's brew of feet, heads, stomachs, intestines, hooves, spinal cords, tails, grease, feathers and bones. Half of every butchered cow and a third of every pig is not consumed by humans. An estimated six million to seven million dogs and cats are killed in animal shelters each year, said Jeff Frace, a spokesman for the American Society for the Prevention of Cruelty to Animals in New York City.
For example, the city of Los Angeles sends 200 tons of euthanized cats and dogs to West Coast Rendering, in Los Angeles, every month, according to Chuck Ellis, a spokesman for the city's Sanitation Department. Pet food companies try not to buy meat and bone meal from renderers who grind up cats and dogs, said Doug Anderson, president of Darling International Inc., a large rendering company in Dallas. "We do not accept companion animals," he said. "But there are still a number of small plants that will render anything."
At least 250 rendering plants operate in the United States, said Bruce Blanton, executive director of the 130-member National Renderers Association in Alexandria, Va. While there are still a few small operations on the outskirts of some cities, he said, modern rendering plants are large and centralized, and the industry's revenues amount to $2.4 billion a year.
After trucks deliver the wastes to the plants, the material is minced and fed into a vessel where it is steam-cooked to 250 degrees or more, and then the stew is cooked for 20 to 90 minutes, Blanton said. In the resulting mash, heavier material drops to the bottom and the lighter stuff floats to the top. Fat is siphoned off the top, filtered and sent through centrifuges to further refine it, Blanton said. Chemical manufacturers turn much of it into fatty acids for lubricants, lipstick, cement, polish, inks and waxes. Other fractions, including gelatinous layers, tallow and grease, go into thousands of products, including soaps, candles, pharmaceuticals, homeopathic medicines and gummy candies.
The heavier protein material on the bottom goes through a separate process, Blanton said. It is dried, squeezed to remove more fat and dried again. The resulting powder is the major ingredient in pet and animal feed. It is a cannibalistic practice that has proved highly profitable.
"We are the original recyclers," said Dr. Don A. Franco, a veterinarian and director of scientific services for the Animal Protein Producers' Industry, another trade group representing rendering firms. "We recycle 40 billion pounds of material a year."
Mad cow disease erupted in Britain because of a number of factors there, said Dr. Linda Detweiler, a veterinarian with the United States Agriculture Department's Animal and Plant Health Inspection Service in Trenton. Unlike the United States, Britain has a large sheep population relative to cows and a serious problem with scrapie, a transmissible, slowly progressive degenerative brain disease of sheep.
Many scientists who have studied the problem now believe that scrapie somehow crossed a species barrier to infect cows, possibly when the cows ate feed composed in part of brain tissue from infected sheep. The disease presumably jumped to people who ate infected cow brains. Current theory holds that some people may have genes that make them particularly susceptible.
Mad cow disease was first recognized as a cattle disorder in November 1986. Since then more than 165,000 cows have been affected. Heuston said renderers were shocked to learn that an agent like scrapie might survive the rendering process.
But British rendering practices may have helped spread the disease, said David Evans, president of Carolina Byproducts, a rendering company in Greensboro, N.C. There are people in Britain, called knackers, who make a living going around the countryside picking up dead animals and rendering them in their backyards. The fat they obtain brings good money from chemical firms, he said.
These knackers simply grind up and partly cook their daily haul to break fat cells and collect the gunk from the top of their vats. The remaining material, called greaves or crackling, was sold to farmers who then mixed it with grain and fed it to their animals. This material, some derived from sheep with scrapie or cattle with mad cow disease, was fed in large amounts to dairy herds in the late 1980s, Detweiler said.
Yet another factor lay in the way greaves were processed in conventional rendering plants, Anderson said. Until the early 1980s, many renderers had used flammable solvents to dissolve fats and the solvents may have deactivated the agent that causes mad cow disease and scrapie. But after several plant explosions, the companies switched to other methods that appear not to deactivate the agent -- a mysterious particle called a prion.
Since 1989, British renderers have tried to keep infected meat out of their products, many knackers have gone out of business and brains are no longer put into hamburger. But the incubation for the human disease is 7 to 30 years, Evans said. While only 15 cases of human disease have been confirmed, many experts fear a latent epidemic.
In 1989, the American rendering industry initiated a voluntary program under which, for example, no sheep heads were to be accepted at rendering plants. An Agriculture Department survey three years later found that 6 of 11 plants inspected still did accept sheep heads. Nevertheless, many experts feel that American shores are safe from mad cow disease, especially if scrapie is the underlying vector. In Britain, sheep account for 14 percent of raw rendering material. Here it is 0.6 percent and most of that material is free from scrapie.
The reason is that scrapie is closely monitored by United States Agriculture Department veterinarians under a federal program. There are no knackers in this country and no greaves to infect cattle, Detweiler said. Few ranchers here feed meat and bone meal to young cows and American renderers usually treat the raw material at higher temperatures.
But the key element in efforts to prevent the cow disease is a newly proposed Agriculture Department ban on feeding protein derived from ruminant animals to other ruminants. Ruminants are animals that chew cuds, including cows, sheep, goats, deer and elk. Mink are included in the ban because they can be affected by a disorder similar to mad cow disease.
If the Agriculture Department rules are adopted, cow protein might still be fed to fish, chicken or pigs in hope that if mad cow disease were to appear, a species barrier would stop it from spreading. At the same time, the Agriculture Department continues to monitor American cows for signs of mad cow disease. Scientists have examined the brains of 5,342 cows that displayed symptoms of central nervous system disease; no cases have been discovered.
But a major reason to worry is that the cow epidemic may have nothing to do with scrapie or the processing techniques used by renderers, said Dr. Richard F. Marsh, a veterinarian at the University of Wisconsin in Madison. There are reasons to believe that mad cow disease has already risen spontaneously in American cattle, he said. But it apparently has not jumped into the animal feed supply at this point.
The strongest evidence is an outbreak of mink encephalopathy (a disorder similar to mad cow disease) that occurred in 1985 in Stetsonville, Wis. The mink farmer did not feed commercial meal to his animals, Marsh said. Rather he fed them the meat from a downer cow, a cow that is down and cannot get up. It is possible that the cow had a spontaneous case of mad cow disease and passed it into mink, Marsh said.
Spontaneous cases of mad cow disease may well occur in one cow out of every million cows each year, said Dr. Joseph Gibbs, a leading expert on mad cow disease at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. There are 150 million cows in this country, which means that each year 150 of them might develop mad cow disease -- all on their own, without any exposure to tainted feed.
Renderers pick up the carcasses of 100,000 downer cows every year and mix them in with other animals, Marsh said. Although the Agriculture Department tries to test downer cows for signs of mad cow disease, it can only sample a small percentage. Moreover, animals can be quite sick and not show signs of it before they are sent to slaughter, Marsh said. Thus, try as they might to avoid the problem, renderers could unknowingly introduce infected animals into animal feed and start an epidemic.
Deer and elk also have a spontaneous mad-cow-like disease, Gibbs said. If they die in the woods, the disease would not be transmitted. But if they are killed on the road, they are sent to zoos or greyhound tracks or, more often, go straight to the rendering plant to end up as cattle feed or pet food.
http://www.mad-cow.org/~tom/render_ed.html
Recycled pets and potential for TSE amplification Assuming that a tiny fraction of cats with BSE-FSE ever get diagnosed as such (vestibular disorder more likely, no diagnosis at all likliest), there would be a potential for re-cycling the disease should these infected cats be non-discriminately rendered for pet food:
From Summer 1996 Earth Island Journal v11, #3 pg 27-31:
"The rendering plant floor is piled high with raw product. Thousands of dead dogs and cats; head and hooves from cattle, sheep, pigs and horses; whole skunks; rats and raccoons -- all waiting to be processed. In the 90-degree heat, the piles of dead animals seem to have a life of their own as millions of maggots swarm over the carcassess." "Rendering plants process decomposing animal carcasses, large roadkill and euthanized dogs and cats into a dry protein product that is sold in the pet food industry. One small plant in Quebec renders 22,000 pounds of dogs and cats per week... The fur is not removed and dead animals are cooked together with viscera, bones and fat at 115 C for 20 minutes."
"Each year in the US, 286 rendering plants quietly dispose of more than 12,500,000 tons of dead animals, fat and meat wasts. ... Baltimore's Valley Proteins "hogger" vat contained an eclectic mix of body parts ranging from dead dogs, cats, raccoons, possums, deer, foxes, snakes, a baby circus elephant, and a police quarterhorse.... In an average year, Baltimore's pound hands over 21,888 dead animals to Valley Proteins [which] sells inedible animal parts and rendered material to Alpo, Heinz, and Ralston-Purina [US pet food manufactureres]"
"Valley Protein maintains two production lines -- one for clean meat and bons and a second line for dead pets and wildlife. However, VP President Smith reported, that the [final] protein material is a mix from both production lines. Thus the meat and bone meal made at the plant includes materials from pets and wildlife, and are about five percent of that product goes to dry-pet-food manufacturers."
--------------------------------------------------------------------------------
Valley Protein responds Gerald F. Smith, Jr., President of Valley Proteins, Inc. responds to your Wednesday, October 23, 1996 transmission at 10:45 a.m. as follows:
"I was misquoted in the article you referenced. Our plant in Baltimore, MD does indeed process dead domestic house pets which have been euthanized by veterinarians, animal control officials, humane societies and other animal protection organizations. This represents less than one-half of 1% of our Baltimore plant's business on an annual basis. Valley Proteins has a total of nine rendering plants in five states. Except for one pet food producer which purchased approximately 10 tons from our Baltimore plant on three different occasions during the last 12 months, we only sell animal proteins to pet food manufacturers from our facilities which are capable of recycling poultry by-products from poultry slaughter facilities. This pet food producer purchased less than one -half of 1% of our total Baltimore Meat Meal production. Therefore, during the last 12 months approximately 300 pounds of our animal protein containing by-products from dead domestic house pets entered the pet food market."
http://www.mad-cow.org/~tom/cats_bse_rend.html
ARCHIVED URL LINK;
http://web.archive.org/web/20070122180434/http://www.earthisland.org/eijournal/fall97/fe_fall97petfood.html
Defense opens case Cattlemen vs. Oprah Winfrey
By CHIP CHANDLER Globe-News Staff Writer
snip...
Van Smith, a reporter with City Paper in Baltimore, testified about an article he wrote on rendering plants. Smith said he saw sheep taken to a plant despite a voluntary ban on using processed sheep in protein-enhanced feed, backing up a statement Lyman made on Winfrey's show.
Under cross-examination, Smith said he was not sure whether the sheep were used for feed or other animal-derived products.
snip...
Van Smith, a reporter with City Paper in Baltimore, testified about an article he wrote on rendering plants. Smith said he saw sheep taken to a plant despite a voluntary ban on using processed sheep in protein-enhanced feed, backing up a statement Lyman made on Winfrey's show.
Under cross-examination, Smith said he was not sure whether the sheep were used for feed or other animal-derived products.
http://www.amarillonet.com/ns-search/stories/021998/036-3052.001.shtml?NS-search-set=/3704d/aaaa2813004db0d&NS-doc-offset=5&
Web posted Wednesday, February 18, 1998 2:02 p.m. CT
Graphic pictures greet Winfrey jury
By KAY LEDBETTER Globe-News Farm and Ranch Editor
Pictures of sheep heads, euthanized pets and roadkill greeted jurors this morning as they returned to the continuation of the cattlemen vs. Oprah Winfrey lawsuit.
The lawsuit continues today in U.S. District Mary Lou Robinson's court, but in a much diminished state.
snip...
Defense lawyer Charles Babcock called Van Smith, a City Paper reporter from Baltimore who had written an article on rendering plants in September 1995.
Smith and Babcock went through more than 50 pictures taken as the reporter toured the Valley Proteins plant in Baltimore and followed a rendering truck to the local animal shelter, a sausage plant and a slaughterhouse.
The pictures showed offal being emptied from the slaughterhouses. They showed animal shelter workers in the euthanasia room; barrels of dead animals in a refrigerated room at the animal shelter; waste meat from the sausage plant; and dead sheep from the slaughterhouse.
http://www.amarillonet.com/stories/021898/graphic.shtml
Web posted Friday, January 23, 1998 5:49 a.m. CT
TSS
Witness testifies some ill cattle sent to rendering plant
By CHIP CHANDLER Globe-News Staff Writer
snip...
Mike Engler -- son of Paul Engler, the original plaintiff and owner of Cactus Feeders Inc. -- agreed that more than 10 cows with some sort of central nervous system disorder were sent to Hereford By-Products.
The younger Engler, who has a doctorate in biochemistry from Johns Hopkins University, was the only witness jurors heard Thursday in the Oprah Winfrey defamation trial. His testimony will resume this morning.
According to a U.S. Department of Agriculture report from which Winfrey attorney Charles Babcock quoted, encephalitis caused by unknown reasons could be a warning sign for bovine spongiform encephalopathy, or mad cow disease.
Encephalitis was indicated on the death certificates -- or ``dead slips'' -- of three Cactus Feeders cows discussed in court. The slips then were stamped, ``Picked up by your local used cattle dealer'' before the carcasses were taken to the rendering plant.
snip...
http://www.amarillonet.com/ns-search/stories/012398/cattle.shtml?NS-search-set=/3704d/aaaa2813004db0d&NS-doc-offset=93&
Date: Fri, 09 Jan 2004 03:12:18 -0000
Man learns he ate beef linked to Holstein with mad cow disease 01/08/2004 Associated Press
A man says it was "like getting hit by lightning" to learn that he and his family ate hamburger linked to a Holstein that was found to have mad cow disease.
Brian Weinstein, 49, a lawyer who lives in this Seattle suburb, told the Seattle Post-Intelligencer that at his request, the meat was traced by the supermarket chain where he bought it.
"I know the odds that any of us will get sick are slim," Weinstein said, "but my family's risk is greater than anyone else's in the U.S. because we actually ate it."
The trace showed the meat was among 10,410 pound of recalled beef from the Holstein and 19 other animals that were slaughtered Dec. 9 -- but not whether it came from the deceased animal or from the other cattle.
In an interview Wednesday, Weinstein said he knows there is little chance that he, his wife, their two daughters, 9 and 12, or their 14-year-old son will contract variant Cruetzfeldt-Jakob disease, which has been linked to eating brain or spinal matter from animals with bovine spongiform encephalopathy, the scientific name for mad cow disease.
The U.S. Agriculture Department has said that about 100 people, mostly from Oregon and Washington, had reported they had consumed recalled meat and were worried. The USDA said they were told the meat was safe because it was muscle meat and not affected.
Still, Weinstein said, it was a jolt to learn that the recall, issued Dec. 23, covered the meat he mixed into a ragu sauce and served his family in a spaghetti dinner Dec. 21.
"It's bad luck, really," Weinstein said. "It's like getting hit by lightning. There's one cow in the U.S. with mad cow, and my family probably ate it."
As of Wednesday, officials knew of no recalled meat still "in circulation," said Dan Puzo, a spokesman for the Agriculture Department's Food Inspection and Safety Service.
Meat that was returned, including 102 cases of beef recalled by QFC, probably will be dumped in landfills or incinerated, but non will be tested for mad cow disease because "there are no tests for BSE muscle flesh," Puzo said.
Agriculture Secretary Ann Veneman has repeatedly said there is an extremely low risk from eating muscle cuts from an infected cow.
About 150 people worldwide have been diagnosed with vCJD, a fatal brain-wasting disease.
Infected cattle have been found to harbor prions, deformed proteins that are believed to cause mad cow disease, mainly in the brain and central nervous system. Scientists believe cattle contract the disease from eating feed that contains material from infected animals.
Authorities have said the Holstein, a 6 1/2-year-old dairy cow, was born in Alberta, imported into the United States from Canada about two years ago and lived on the Sunny Dene Ranch near Mabton.
The cow became ill after delivering a calf, couldn't walk and was slaughtered at Vern's Moses Lake Meat Co. on Dec. 9.
Carcasses from that cow and 19 others that were slaughtered the same day were sent to Midway Meats in Centralia for deboning, and the processed meat -- mostly ground beef -- was then sent to two distributors in Oregon that shipped it to groceries in seven states.
Meanwhile, because the cow was ailing before slaughter, samples of its brain were sent to a laboratory in Ames, Iowa, and tested positive for BSE on Dec. 23.
That night, seeing television news reports on the discovery, "I started getting sick," Weinstein said. "I started thinking about all the times we'd eaten ground beef recently."
He dismissed the matter as the family left the next day for Hawaii, but upon returning after New Year's he learned of the recall on another trip to the store.
"Lo and behold, there was a very inconspicuous one-sheet paper posted by the meat counter that explained the recall," Weinstein said.
Soon afterward he contacted the headquarters of QFC, a division of Kroger Co., and had the meat traced through purchase records showing product codes on his frequent shopper card.
Dean Olson, a spokesman at QFC headquarters in Bellevue, said Weinstein was among a "very few customers' who had inquired and for whom the company determined whether they had bought meat subject to the recall.
Information from: Seattle Post-Intelligencer
http://www.kgw.com/sharedcontent/APStories/stories/D7VUR2483.html
AN endless cycle of greed and TSEs...TSS
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NO mad dogs? DEER, CAT and DOG SPONGIFORM ENCEPHALOPATHY SURVEY
http://www.priondata.org/data/A_deerdog.html
Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.
------------------------------------------------------------------------
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
ARCHIVED URL LINK;
http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf
ARCHIVED URL LINK ;
http://web.archive.org/web/20090506032702/http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf
It is not clear that deer may well become infected with BSE although the rate at which this is taking place is unclear. DEFRA issued a document specifically to tell farmers what to do if they found a deer with potential symptoms:
http://www.defra.gov.uk/animalh/bse/bse-publications/adv-TSEs-deer.pdf
ARCHIVED URL LINK;
------------------------------------------------------------------------
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
Subject: Alert in Latest Mad-Cow Case Was Delayed by a Misdiagnosis (came from pet food plant in TEXAS) WSJ
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Mon, 27 Jun 2005 10:38:51 -0500
Content-Type: text/plain
Parts/Attachments: text/plain (58 lines)
Reply
##################### Bovine Spongiform Encephalopathy #####################
From: TSS
Subject: Alert in Latest Mad-Cow Case Was Delayed by a Misdiagnosis (came from pet food plant in TEXAS) WSJ
Date: June 27, 2005 at 8:33 am PST
Alert in Latest Mad-Cow Case Was Delayed by a Misdiagnosis
By SCOTT KILMAN Staff Reporter of THE WALL STREET JOURNAL June 27, 2005; Page A2
A misdiagnosis by U.S. Department of Agriculture scientists caused a seven-month delay in alerting consumers to the U.S.'s second case of mad-cow disease.
Because of the error, uncovered only at the prodding of the department's Inspector General Phyllis K. Fong and confirmed by British scientists Friday, Agriculture Secretary Mike Johanns unveiled several changes in the government's mad-cow testing program, some long sought by consumer advocates.
"Science is ever evolving.... And as we learn more, we apply the knowledge," said Mr. Johanns. He also highlighted some instances of human error in the case, including missing paperwork and sloppy handling of the beef cow's brain sample.
TALLYING MAD-COW
See a graphic that tallies world-wide cattle and human cases of mad-cow disease.
Probably no other American cow's brain has been tested so extensively as this one, which was collected at a pet-food-related plant in Texas. The female, which was at least eight years old, came to the attention of regulators in November when it was flagged by a preliminary rapid-screening test. The carcass was incinerated. After announcing a possible case of mad-cow disease, scientists at a USDA laboratory in Ames, Iowa, cleared the animal using a brain-tissue test called immunohistochemistry.
But questions persisted about the cow. Mr. Johanns, who was confirmed as agriculture secretary in January, disclosed Friday that the public wasn't told in November that an experimental test on the brain sample had detected abnormalities. "Obviously, it should have been reported," said John Clifford, the USDA's chief veterinary officer, who added that he wasn't aware until recently of the experimental work, which was designed to speed up the immunohistochemistry method, which normally takes days.
The inspector general's office, a watchdog agency within USDA that has highlighted problems in the department's testing program, learned of the conflicting test results and quietly enlisted a different group of USDA scientists to test the sample using a more-sensitive method, called Western blot, routinely employed in Europe.
When the Western blot test came up positive two weeks ago, Mr. Johanns ordered the matter settled by the world's premier mad-cow testing laboratory in Weybridge, England. The British laboratory managed to detect the abnormal prions that cause mad-cow disease using the immunohistochemistry technique, raising questions about the USDA's laboratory prowess.
Cattle prices are widely expected to drop at the start of trading today on fears that the new discovery will discourage countries such as Japan and South Korea from reopening borders they closed to American beef in December 2003. Those actions were taken after U.S. authorities found the brain-wasting disease in a Washington state dairy cow imported from Canada. So far, the U.S. has regained only one-third of that $3 billion export business.
"This case, I'm afraid, has to be taken into consideration," said Akira Chiba, spokesman for Japan's Foreign Ministry. An agreement by Japan in October to accept meat from U.S. cattle younger than 21 months has been mired in red tape there ever since. Taiwan closed its border again to U.S. beef immediately after the USDA's announcement Friday.
Mad-cow disease, or bovine spongiform encephalopathy, can trigger a rare but always-fatal brain disorder in people who eat infected meat. The USDA hasn't found any evidence that the infected cow was imported; if it is confirmed that the animal was born in the U.S., it would make the U.S. the 24th nation to find an indigenous case of mad-cow disease since the malady was discovered in Britain in the 1980s.
Cattle contract BSE by eating feed contaminated with remains of other infected animals, so it is possible other U.S. cattle were exposed. (The U.S. and Canadian governments largely banned the use of rendered cattle material in cattle rations in August 1997, although there are some loopholes.) Regulators are now trying to find and test offspring, siblings and companions that might have shared the infected cow's rations.
Beef industry officials believe the vast majority of consumers still trust the USDA's declaration that the U.S. beef supply is safe. Over the past 12 months, the department has screened 388,000 of the 455,000 cattle it deemed most likely to have the disease, and the cow that died in Texas is the only new confirmed case. But NPD Group, a consumer research firm based in Port Washington, N.Y., said that 19% of the 500 consumers it surveyed in mid-May were extremely or very concerned about mad-cow disease.
---- Janet Adamy and Andrew Morse contributed to this article.
Write to Scott Kilman at scott.kilman@wsj.com
http://online.wsj.com/article/0,,SB111963867150169044,00.html?mod=djemHL
TSS
#################### https://lists.aegee.org/bse-l.html ####################
Subject: Canine spongiform encephalopathy?
From: J Ralph Blanchfield
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 29 Apr 1997 06:51:38 GMT
Content-Type: text/plain
Parts/Attachments: text/plain (83 lines)
Reply
Hello Everyone,
Report in Daily Telegraph, 29 April.
Tests on labrador could prove BSE has spread to dogs
By Roger Highfield, Science Editor
BRAIN sections from a dog have been sent to Britain by Norwegian pathologists to confirm that it is the first example of canine spongiform disease, akin to BSE.
The move came as Labour accused the Government of excessive secrecy for not publishing results of a 1991 study to investigate the possibility of BSE being transferred to dogs.
The 11-year-old labrador suffered nervous symptoms, lack of muscle co-ordination and seizures. A post mortem examination showed that its brain had a spongiform appearance, said Prof Jon Teige, a pathologist at the Norwegian College of Veterinary Medicine in Oslo.
"To our surprise, we saw these lesions in the brain similar to those observed in scrapie in sheep and mad cow disease," said Prof Teige. If confirmed, it would mark the first example of the disease in a dog.
Samples have had been sent to the Institute of Animal Health's neuropathogenesis unit in Edinburgh for a second opinion. "Although there are some features of the pathology in common with spongiform encephalopathies, a number of other conditions have similar aspects," said Dr Chris Bostock, of the institute.
If confirmed, it is also important to determine if it is the spontaneous form of BSE or if the dog had been infected in its diet and had a transmissible disease. About 95 per cent of Norway's dog and cat food is imported, mainly from Britain. Parts of bovine material, which could contain BSE, were removed from the animal food chain in 1990.
Scientists are interested in whether dogs are susceptible but confirmation would not change the big picture of BSE, Dr Bostock said. Dr Gavin Strang, shadow food minister, yesterday accused Douglas Hogg, the Agriculture Minister, of secrecy over BSE research. "This work on possible BSE in dogs was funded by the public," he said. "Results should have been made public."
The Government ruled out further research on dogs yesterday despite disclosures in a report six years ago that there was a possibility that they could catch a form of mad cow disease from contaminated food. "It is unnecessary," said a spokesman. "There is no threat to human or animal health."
Tests six years ago by ministry experts on the brains of 444 hunting hounds found some abnormalities called fibrils. However, some brains had started to degenerate, making the results ambiguous.
The results were passed to the Spongiform Encephalopathy Advisory Committee, which agreed that they were inconclusive and ruled out further research because there was no public health issue. "We don't eat dogs in Britain," the spokesman said.
Mr Hogg said that the research on dogs and BSE "adds nothing to human knowledge" during a tour of the North-East which included a visit to a sausage factory in marginal Stockton South.
End of Telegraph Report.
Regards
Ralph
****************************************************************** J Ralph Blanchfield Food Science, Food Technology & Food Law Consultant Chair, IFST External Affairs Web Editor, Institute of Food Science & Technology IFST Web address:
Subject: Re: Canine spongiform encephalopathy?
From: "Hans G. Andersson"
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 29 Apr 1997 06:02:33 -0700
Content-Type: text/plain
Parts/Attachments: text/plain (38 lines)
Reply
Hello Ralph and everybody,
Excerpt from the article you forwarded:
"The Government ruled out further research on dogs yesterday despite disclosures in a report six years ago that there was a possibility that they could catch a form of mad cow disease from contaminated food. "It is unnecessary," said a spokesman. "There is no threat to human or animal health."
Tests six years ago by ministry experts on the brains of 444 hunting hounds found some abnormalities called fibrils. However, some brains had started to degenerate, making the results ambiguous.
The results were passed to the Spongiform Encephalopathy Advisory Committee, which agreed that they were inconclusive and ruled out further research because there was no public health issue. "We don't eat dogs in Britain," the spokesman said.
Mr Hogg said that the research on dogs and BSE "adds nothing to human knowledge" during a tour of the North-East which included a visit to a sausage factory in marginal Stockton South."
I got two dogs myself, both 13 years old and fed British pet food during the period 1984-89.
The statement from the British government is tasteless!
Best regards,
Hans
Hans G. Andersson, NYC -- hasse@sprynet.com Editor, Ebola section of OUTBREAK http://www.outbreak.org/
"There is a crack in everything. That's how the light gets in." Leonard Cohen
BSE-LIST
Subject: Re: Canine Spongiform Encephalopathy?
From: Olav Hungnes
Reply-To: Bovine Spongiform Encephalopathy
Date: Wed, 23 Apr 1997 10:19:14 +0200
Content-Type: text/plain
Parts/Attachments: text/plain (47 lines)
Reply
Date: Mon, 21 Apr 1997 20:59:16 +0200 From: Torsten Brinch
Hello everyone,
I wondered if we have a Norwegian subscriber, who could brief the list on the suspected case of spongiform encephalopathy in a Norwegian dog?
Best regards,
Torsten Brinch
Torsten Brinch - Risboege, 6640, Denmark - e-mail: iaotb@inet.uni-c.dk http://inet.uni-c.dk/~iaotb/ IAO Agrochemical Pages Denmark
The story, first brought by Norwegian TV2, is that an 11 year old golden retriever was brought to the Norwegian College of Veterinary Medicine for an autopsy. The dog had shown neurological symptoms over a longer period. Microscopy of brain tissue showed spongiform encephalopathy.
Samples have been sent to another pathological laboratory in Oslo (probably at Rikshospitalet (The National Hospital)), as well as to Weybridge Central Veterinary Institute, London, for further investigation.
This is said to be the first reported case of spongiform encephalopathy in dogs.
Media focus has been on BSE-contaminated dog food as a possible cause. 95 % of dog food in this country is imported, and speculation goes that the dog could have got its disease from eating feed prepared from British meat-and-bone meal during the eighties. The possibility of genetic factors should, however, not be ignored. I would guess that investigation of the dog's PrP genotype is underway. Is anything known about polymorphism in dogs?
Source(in Norwegian, for the benefit of Torsten): Articles from NTB, appearing in the newspaper Aftenposten Saturday and Tuesday
BSE-LIST
Subject: Re: Canine Spongiform Encephalopathy
From: "Hans G. Andersson"
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 22 Apr 1997 00:15:18 -0700
Content-Type: text/plain
Parts/Attachments: text/plain (41 lines)
Reply
Hi Torsten and everybody,
Here's some additional information from media in Norway:
A Norwegian golden retriever may have died of Canine Spongiform Encephalopathy, possibly linked to BSE.
Most pet food in Norway is imported, mainly from the UK, and before 1994 there was no quality-control inspection:
"If the dog contracted the brain ailment, it probably was through dog food in the late 1980s", said Eivind Liven, Director of the National Animal Health Board.
The 11-year-old dog showed symptoms of psychiatric and neurological illness a couple of months ago, and died around Easter. An autopsy at Norway's Veterinary School showed changes in the brain consistent with those seen in the brains of cattle with late stage BSE.
Tissue samples from the brain of the dog will be studied by researchers at MAFF's Central Veterinary Laboratory, Weybridge, UK.
Source: Dagbladet in Oslo, Norway. April 20 and 21, 1997
Best regards,
Hans
Hans G. Andersson, NYC -- hasse@sprynet.com Editor, Ebola section of OUTBREAK http://www.outbreak.org/
"There is a crack in everything. That's how the light gets in." Leonard Cohen
BSE-LIST
GREETINGS AGAIN,
IT SEEMS THE USDA ET AL have taken a page, or two, from the U.K. et al on screwing up brains for the testing of Transmissible Spongiform Encephalopathy BSE i.e. mad cow disease (all strains), when they do not want to document it.
From: TSS Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE) Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf
ARCHIVED URL LINK;
-MORE Office of the United States Attorney District of Arizona FOR IMMEDIATE RELEASE For Information Contact Public Affairs February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681
CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD COW DISEASE SURVEILLANCE PROGRAM
PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, “The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA’s Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law.” Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the “USDA Agreement”) to collect obex samples from cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.
Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.
Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA’s ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:
(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;
(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;
(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s testing laboratory that were false and misleading;
(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;
(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and
(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.
Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #
http://www.usdoj.gov/usao/az/press_releases/2007/2007-051(Farabee).pdf
WE can only hope that this is a single incident. BUT i have my doubts. I remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5 grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and the FDA was bragging at the time that the amount of potentially BANNED product was so little and the cattle were so big ;
"It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated."
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed. ... FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
WE now know all that was a lie. WE know that literally Thousands of TONS of BANNED and most likely tainted product is still going out to commerce. WE know now and we knew then that .005 to a gram was lethal. WE know that CWD infected deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been rendered and fed back to livestock (including cattle) for human and animal consumption.
Paul Brown, known and respected TSE scientist, former TSE expert for the CDC said he had ''absolutely no confidence in USDA tests before one year ago'', and this was on March 15, 2006 ;
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
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, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"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."
OR, what the Honorable Phyllis Fong of the OIG found ;
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
"These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS
USDA 2003
We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
snip...
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
USDA: In 9,200 cases only one type of test could be used
WASHINGTON (AP)--The U.S. Department of Agriculture acknowledged Aug. 17 that its testing options for bovine spongiform encephalopathy were limited in 9,200 cases despite its effort to expand surveillance throughout the U.S. herd.
In those cases, only one type of test was used--one that failed to detect the disease in an infected Texas cow.
The department posted the information on its website because of an inquiry from The Associated Press.
Conducted over the past 14 months, the tests have not been included in the department's running tally of BSE tests since last summer. That total reached 439,126 on Aug. 17.
"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."
Officials intended to report the tests later in an annual report, Clifford said.
These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC.
In the Texas case, officials had declared the cow free of disease in November after an IHC test came back negative. The department's inspector general ordered an additional kind of test, which confirmed the animal was infected.
Veterinarians in remote locations have used the preservative on tissue to keep it from degrading on its way to the department's laboratory in Ames, Iowa. Officials this year asked veterinarians to stop using preservative and send fresh or chilled samples within 48 hours.
The department recently investigated a possible case of BSE that turned up in a preserved sample. Further testing ruled out the disease two weeks ago.
Scientists used two additional tests--rapid screening and Western blot--to help detect BSE in the country's second confirmed case, in a Texas cow in June. They used IHC and Western blot to confirm the first case, in a Washington state cow in December 2003.
"The IHC test is still an excellent test," Clifford said. "These are not simple tests, either."
Clifford pointed out that scientists reran the IHC several times and got conflicting results. That happened, too, with the Western blot test. Both tests are accepted by international animal health officials.
Date: 8/25/05
http://www.hpj.com/archives/2005/aug05/aug29/BSEtestoptionswerelimited.cfm
""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
As for lowering standards, R-CALF has referenced the OIE (World Organization for Animal Health) as the authority on animal health issues. That's fine, as far as it goes. Trouble is, the OIE does not set standards, as R-CALF has claimed. Further, the OIE does not recommend countries ban meat imported - with SRMs removed - from countries with low or high BSE risk, contrary to R-CALF's implication.
In addition, there are no standards recognized for importing meat from minimal- or low-risk BSE countries. The U.S. is trying to set standards as precedent for trade, based on nearly 20 years of science. R-CALF wants trade only with countries who have never had a BSE case. They have not explained how many years they want the rest of the world to sit around and wait until it's okay to trust science and begin trading. Or how they would justify keeping imports out if ever a BSE case was discovered in the U.S. or export again ever.
http://www.mad-cow-facts.com/News-Commentary/r-calf-bullard-4-4-05.htm
JUST ABOUT EVERY COUNTRY THAT WENT BY THOSE FAILED OIE BSE GUIDELINES WENT DOWN WITH BSE. ...TSS
http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
see full text ;
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the USA Question number: EFSA-Q-2003-083
Adopted: 1 July 2004 Summary (0.1Mb)
Report (0.2Mb)
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594180.htm
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Canada Question number: EFSA-Q-2003-083
Adopted: 1 July 2004 Summary (0.1Mb)
Report (0.2Mb)
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked to provide an up-to-date scientific report on the GBR in Canada, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Canada. This scientific report addresses the GBR of Canada as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into the country middle of the eighties and could have reached domestic cattle in the early nineties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early 90s. It is possible that imported meat and bone meal (MBM) into Canada reached domestic cattle and led to an internal challenge in the early 90s.
A certain risk that BSE-infected cattle entered processing in Canada, and were at least partly rendered for feed, occurred in the early 1990s when cattle imported from UK in the mid 80s could have been slaughtered. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of Canada is III, i.e. it is confirmed at a lower level that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as the system remains unstable, it is expected that the GBR continues to grow, even if no additional external challenges occur.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594094.htm
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Mexico Question number: EFSA-Q-2003-083
Adopted: 1 July 2004 Summary (108 KB)
Report (168 KB)
Annex (251 KB)
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993.
It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system.
EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.
Further information
Overview of GBR assessments covering 2000-2006: list of countries and their GBR level of risk (64 KB)
Published: 20 August 2004 Last updated: 8 September 2004
http://www.efsa.europa.eu/en/scdocs/scdoc/4r.htm
Wednesday, April 16, 2008
MBM, greaves, meat offal, live cattle, imports from UK to USA vs Canada
http://madcowtesting.blogspot.com/2008/04/mbm-greaves-meat-offal-live-cattle.html
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.
http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html
MY comments/questions are as follows ;
1. SINCE the first Harvard BSE Risk Assessment was so flawed and fraught with error after the PEER REVIEW assessment assessed this fact, how do you plan on stopping this from happening again, will there be another peer review with top TSE Scientist, an impartial jury so-to-speak, to assess this new and updated Harvard BSE/TSE risk assessment and will this assessment include the Atypical TSE and SRM issues ?
*** Suppressed peer review of Harvard study October 31, 2002 ***
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
***
http://www.scribd.com/doc/1490709/USDA-200600111
***
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
***
http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
***
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
***
Response to Public Comments on the Harvard Risk Assessment of BSE USA
RESPONSE TO COMMENTS FROM TERRY S. SINGELTARY SR. Comment #1: SINCE the first Harvard BSE Risk Assessment was so flawed and fraught ...
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
IT ALL STARTED, LEGALLY, RIGHT HERE ;
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
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1
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
Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY
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.
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 ???
go figure. ...
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8151
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
January 28, 2007
Greetings APHIS,
I would kindly like to submit the following to ;
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8
Monday, October 26, 2009
MAD COW DISEASE, AND U.S. BEEF TRADE
MAD COW DISEASE, CJD, TSE, SOUND SCIENCE, COMMERCE, AND SELLING YOUR SOUL TO THE DEVIL
http://usdameatexport.blogspot.com/2009/10/mad-cow-disease-and-us-beef-trade.html
Greetings USDA/APHIS et al,
I would kindly like to comment on OIE proposed guidelines.
AS I said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. THE reason most every country around the globe came down with BSE/TSE in their cattle, were due to the failed and flawed BSE/TSE testing and surveillance policy of the O.I.E. NOW, they don't even acknowledge atypical scrapie it seems, as one for concern $
SO, chew on that !
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.
http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html
Wednesday, February 10, 2010
NAIS MAD COW TRACEABILITY DUMPED BY USDA APHIS 2010
http://naiscoolyes.blogspot.com/2010/02/nais-mad-cow-traceability-dumped-by.html
Thursday, January 07, 2010
Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008
http://scrapie-usa.blogspot.com/2010/01/scrapie-and-nor-98-scrapie-november.html
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html
Wednesday, March 3, 2010
NOR-98 ATYPICAL SCRAPIE USA 4 CASES DETECTED JANUARY 2010
http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-usa-4-cases.html
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
snip...
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.
Thanks for your interest.''
Best regards,
Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
END...TSS
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
International Society for Infectious Diseases Web: http://www.isid.org/
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Friday, February 05, 2010
New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review
http://vcjd.blogspot.com/2010/02/new-variant-creutzfelt-jakob-disease.html
Sunday, February 14, 2010
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th
ICID International Scientific Exchange Brochure -
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
TSE
http://transmissiblespongiformencephalopathy.blogspot.com/
WHO WILL WATCH THE CHILDREN FOR CJD OVER THE NEXT 5 + DECADES ???
Do you actually believe that the USDA et al jumped in on the law suit against Westland/Hallmark, at the time the largest beef recall in USA history, just because a few animals were abused on a video, or to cover their ass, for letting our children, from school district to school district, from state to state, be fed dead stock downer cows.
>>>In the papers, the government alleges the meatpacking plant slaughtered and processed downer cows for nearly four years — from January 2004 to September 2007 — at the average rate of one every six weeks... <<<>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
and there from, what will friendly fire, i.e. pass it forward, i.e. iCJD, the pathology, what will that look like pathologically?
sporadic CJD does not mean one strain of CJD. it is multiple strains, and they are growing in number ;
CJD USA RISING, with UNKNOWN PHENOTYPE ;
5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Terry S. Singeltary Sr. Bacliff, Texas USA 77518
