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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 & 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


76 pages on hound study;


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


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
P.O. Box 42
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


-------- 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 consumers 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

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

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

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

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

http://www.bseinquiry.gov.uk/files/yb/1989/04/25001001.pdf

some 100+ _documented_ TSE cats of all types later...tss

on occassions, materials obtained from slaughterhouses
will be derived from sheep affected with scrapie or
cattle that may be incubating BSE for use in petfood manufacture...

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

http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf

IN CONFIDENCE CJD TO CATS...

http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf

Confidential BSE and __________________

http://www.bseinquiry.gov.uk/files/yb/1989/05/22012001.pdf

1st case natural FSE

http://www.bseinquiry.gov.uk/files/yb/1990/05/09002001.pdf

FSE and pharmaceuticals

http://www.bseinquiry.gov.uk/files/yb/1990/05/10005001.pdf

confidential cats/dogs and unsatisfactory posture
MAFFs failure to assure key research

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

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

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

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

http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf

http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf

hope they did not go by the wayside as the hound study;

http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf

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

nothing to offer scientifically;

http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf

maddogs and Englishman

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

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

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

oral dose of BSE in primates--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.

Published online

January 27, 2005

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

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 ef.ciency 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 .ndings
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 (icip 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 .rst positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log.
icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula

snip...end

www.thelancet.com Published online January 27, 2005

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

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/


--------------------------------------------------------------------------------

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


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&

TSS




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