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From: TSS (
Subject: FOOD SAFETY Mad cow madness
Date: December 13, 2004 at 10:24 am PST

FOOD SAFETY Mad cow madness

EVER SINCE MAD COW disease was discovered in a Washington state cow last month, U.S. officials and beef industry executives have tried to shift blame north of the border. This nonsense has fueled a misguided move in Congress to require country-of-origin labeling on meat.

The U.S. Department of Agriculture made much ado about the genetic tests showing that the Washington cow had been born in Alberta, Canada. So did Senate Minority Leader Tom Daschle, D-S.D., who vowed to block a $328 billion appropriations bill unless Congress moves quickly to require country-of-origin labeling.

But the labeling proposal is built on the faulty premise that there is a meaningful distinction between Canadian and American beef. In truth, it's one big market.

The world's largest supplier of premium beef and pork, Iowa Beef Packers, perfectly illustrates the new realities of meat packing. With a name like that, you might assume its products all come from Iowa, or at least the United States. But they don't. IBP has packing and processing facilities in two dozen states and several foreign countries. Some of the beef it sells in this country is processed in Alberta.

Cattle raised in Canada are routinely processed here, and vice versa. For example, the mother of the Alberta cow found with mad cow disease in May came from the United States and was pregnant when she crossed the border. In 2002, 1.2 million live cattle came into this country from Canada, 500,000 of them from Alberta.

Canadian standards are at least as tough as ours. The cow found with mad cow in Canada never got into the food supply, unlike the U.S. cow. Indeed, the diagnosis of the Alberta cow was done on a ranch; cattle in this country are tested only at the slaughterhouse.
The bogus focus on labeling could waste a golden opportunity to do something meaningful about food safety. Despite the announcement of somewhat tighter rules last month, there are still steps that must be taken to protect American consumers.

At the top of the list is a tightening of the so-called feed ban. Parts of the infected cow in Washington legally could be rendered into food for pigs and chickens. USDA officials insist that's safe because neither pigs or chickens can get mad cow disease. But pigs and chickens raised on beef protein can be ground up later and fed to cattle. Research suggests some animals that can't be infected with mad cow disease can harbor the prions believed to cause it. Material from those animals has been shown to cause mad cow disease when injected into beef. So feed made of pigs and chickens might spread the disease.

After years of dragging its feet on enacting tougher inspection standards for mad cow disease, the government has a responsibility to address the problem based on the facts rather than convenient fictions.

[[[At the top of the list is a tightening of the so-called feed ban. Parts of the infected cow in Washington legally could be rendered into food for pigs and chickens. USDA officials insist that's safe because neither pigs or chickens can get mad cow disease. But pigs and chickens raised on beef protein can be ground up later and fed to cattle. Research suggests some animals that can't be infected with mad cow disease can harbor the prions believed to cause it. Material from those animals has been shown to cause mad cow disease when injected into beef. So feed made of pigs and chickens might spread the disease.]]]



1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,


Click here to read

The neuropathology of experimental bovine spongiform encephalopathy
in the pig.

Ryder SJ, Hawkins SA, Dawson M, Wells GA.

Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw,
Addlestone, Surrey, KT15 3NB, UK.

In an experimental study of the transmissibility of BSE to the pig,
seven of 10 pigs, infected at 1-2 weeks of age by multiple-route
parenteral inoculation with a homogenate of bovine brain from
natural BSE cases developed lesions typical of spongiform
encephalopathy. The lesions consisted principally of severe neuropil
vacuolation affecting most areas of the brain, but mainly the
forebrain. In addition, some vacuolar change was identified in the
rostral colliculi and hypothalamic areas of normal control pigs. PrP
accumulations were detected immunocytochemically in the brains of
BSE-infected animals. PrP accumulation was sparse in many areas and
its density was not obviously related to the degree of vacuolation.
The patterns of PrP immunolabelling in control pigs differed
strikingly from those in the infected animals.

PMID: 10684682 [PubMed - indexed for MEDLINE]


In Reply to: Would chickens be safer to eat? posted by Robert on November 21, 2004 at 3:47 am:

GOOD question. they probably would not live long enough to
develop disease if fed ruminant/mammalian feed that was tainted
with the TSE agent. WITH that said, the agent would be in there
digestive track, therefore the potential to pass the agent via
feed made from poultry/turkey by-products to other species is there...

WE know that in the USA these products are still being fed to
not only cattle, but to deer, elk, chickens, pigs, sheep and goats.
THESE feed ban warnings letters are documented on this board.
The 8/4/97 R-T-R feed ban was merely words on a piece of
paper. still is...

ON the other hand, no one is really looking. IF we look at old
data when zoo animals such as the RED-NECKED OSTRICH which
i posted long ago on this board somewheres, here it is again;

The Red-Neck Ostrich 'THE AUTOPSY' & TSEs

ALSO; in Harash Narang's book THE LINK (i believe he went to work
for NIH on TSEs, not sure if he is still there) there is a part about
BSE IN HENS (page 135), that a farmer in kent in Nov. 1996 noticed
that one of his 20 free range hens the oldest, aged about 30 months,
was having difficulty entering its den and appeared frightened and
tended to lose its balance when excited. Having previously experiencing
BSE cattle on his farm, he took particular notice of the bird and
continued to observe it over the following weeks. It lost weight, its
balance deteriorated and characteristic tremors developed which were
closely associated with the muscles required for standing (Fig. 15).
In its attempts to maintain its balance it would claw the ground more
than usual and the ataxia progressively developed in the wings and legs,
later taking a typical form of paralysis with a clumsy involuntary jerky motion.
Violent tremors of the entire body, particularly the legs, similar to those
seen in BSE, became common sparked off by the slightest provocation.
Three other farmers from the UK are known to have reported
having hens with similar symptoms...

with this agent, i would not rule out anything or any species...TSS

* The Red-Neck Ostrich 'THE AUTOPSY' & TSEs


ate: Mon, 11 Jun 2001 16:24:51 -0700
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr."
Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY'

######## BSE #########




H A Schoon, Doris Brunckhorst and J Pohienz Institute of Pathology,
Veterinary University of Hannover


Since the first appearance of BSE in Great Britain in l985 {review in
TRUYEN & KAADEN, l990), research into the incidence, diagnosis,
differential diagnosis and epidemiology of spongiform encephalopathies
in humans and animals has been a focus of medical and public interest.
In view of the growing number of reports of "new" spontaneously or
experimentally susceptible species (cats: WYATT et al, l990; pigs:
DAWSON et al, 1990), and of the associated questions with regard to the
causal agent and in particular its transmissibility, it seems essential
that agnopathogenetic individual cases should also be described. We
therefore report below the preliminary findings of morphological
examinations of three red-necked ostriches in 1986, 1988 and 1989,
taking account of differential diagnostic factors.


The three ostriches (Flock A: Ostrich 1, female, adult, 150 kg; Flock B:
Ostrich 2, female, adult, 80 kg; Ostrich 3: male, juvenile, 60 kg) came
from two zoos in North West Germany and were euthenised because of their
hopeless prognosis. Preliminary reports indicated that all three birds
had presented protracted central nervous symptoms with ataxia,
disturbance of balance and discoordinated feeding behaviour. Ostrich 2
had also exhibited pronounced lameness of the left lower limbs and the
juvenile bird was suffering from perosis. The birds were fed on
vegetable material, supplemented by commercial compound poultry feed and
''raw meat'', some of which was ''obtained from local small emergency
slaughterers''. Comparable clinical pictures with fatal outcome in
individual birds had occurred in both flocks: in a male bird at the same
time (Flock A) and in several ostriches over recent years (Flock B).


Autopsy was followed in all three cases by histopathological examination
of the following tissues: heart (several locations including coronary
arteries and aorta), right and left pulmonary lobes, liver, kidneys,
limb musculature, peripheral nerves (brachial plexus, sciatic nerve, in
each case both left and right) and brain (left and right cerebral
hemispheres, two samples each from the cranial/caudal third, two
sagittal sections of the cerebellum, two cross-sections of the brain
stem at the level of the optical lobes, four cross-sections from the
medulla oblongata). The tissue material was fixed in formalin and
embedded in Paraplast by the conventional method and the sections were
evaluated using the following staining techniques and histochemical
reactions: all organs: haematoxylin eosin staining; brain: PAS reaction
(McManus), Ziehl/Neelsen staining (mod. Pearse), iron method (Lillie)
for detection of neuromelanin, Turnbull's reaction (Bancroft & Stevens),
alkaline Congo red method (Puchtler) (of SCOON & SCHINKEL, 1986), myelin
sheath staining (Spielmeyer) (ROMEIS, 1968). In addition, unstained
sections were examined by fluorescence microscopy (to detect
autofluorescing lipofuscin granula) and the following lipid stains were
applied to cryostat sections of liver, and of heart and skeletal
musculature: Sudan III, Sudan black, oil red.


Ostrich 1

Brain: whilst only middle grade oedematisation of the neuropil was noted
in the cerebral and cerebellar region, major changes were detected in
the brain stem and medulla oblongata (Figures 1-3): in addition to
pronounced vacuolation of the grey matter, optically vacant, ovoid to
spherical vacuoles of differing sizes occurred bilaterally symmetrically
in numerous neurons of the brain centres nucleus ruber, vestibular
nucleus and reticular formation, in certain cases compressing the Nissl
substance into a narrow fringe. In addition, fine granular pigments were
found in the perikaryon of the neurons (with and without vacuoles),
which showed a golden brown coloration in the haematoxylin eosin
specimen, gave positive reactions to both PAS and Ziehl-Neelsen and also
exhibited a yellowish-green spontaneous autofluorescence. Lillie
staining to detect neuromelanin gave a negative result. The pigments
thus exhibited the characteristics of lipofuscin (SCHOON & SCHINKEL,
1986). Ferruginous pigments and histochemically detectable amyloids were
absent. Mild gliosis, isolated necrotic neurons and neuronophagia were
observed only in the cranial locations of the brain stem.

Other findinqs: The ostrich exhibited marked adiposity and multiple
pressure sores of both lower limbs. Moderate steatosis was found in the
heart and skeletal musculature and in the liver. Multifocal
arteriosclerotic plaques were also noted in the coronary and limb arteries.

Ostrich 2

Brain: Histopathological changes in the brain of this ostrich were
limited to the medulla oblongata and were qualitatively consistent with
those found in Ostrich 1, although confined, bilaterally symmetrically,
to small localised areas and affecting only individual neurons. Gliosis
reaction was almost entirely absent.

Other findinqs: The carcase was moderately well nourished and exhibited
multifocal dermal and muscular necroses on both lower limbs in
conjunction with lateral chronically destructive tarsitis and coxitis.
In the internal organs, parenchymatous degeneration of the liver and
kidneys and multifocal arteriosclerotic plaques in the coronary arteries
were noted.

Ostrich 3

Brain: Whilst no histopathological changes were found in the cerebrum
and cerebellum of this ostrich, a high grade spongious dispersion of the
neuropil existed in all locations examined in the brain stem and medulla
oblongata (status spongiosus, Figure 4). Individual neurons contained
optically vacant vacuoles of varying size, whilst numerous nerve cells
exhibited clear signs of nuclear degeneration, in particular in the form
of nuclear pyknosis. Low grade gliosis was also noted in all locations.

Other findinqs: The left lower limb of this bird exhibited defective
positioning of the tarsal joint resulting from axial distortion of the
long bones with applanation of the lateral [Rollkamm - word not found]
and resultant instability of the tendons and inward turning of the tarsus.


Although ostriches are widely kept in zoos, there are virtually no
detailed descriptions of central nervous disorders with associated
locomotor disfunction in this species. Neurological symptoms have been
reported in connection with an outbreak of Newcastle Disease (KLOPPEL,
1969) and bacterial meningitis has been described (GRZIMEK, 1953),
whilst other, sporadic cases have remained etiologically unexplained
(ZUKOWSKY, 1959; LANDOWSKI, 1965). Disfunctions of the locomotor system
of extracerebral origin occur predominantly in juvenile ostriches, emus
and rheas in connection with muscular disease, perosis and trauma
(FROIKA, 1982, 1983; MIHALIK & SRANK, 1982; SCHRODER & SEIDEL0 1989).
One of the ostriches we examined was suffering from perosis, another
from unilateral tarsitis and coxitis. All three, however, exhibited
neuropathological findings consisting of a gradual, bilaterally
symmetrical, spongiform encephalopathy of varying degree in the brain
stem and medulla oblongata. No descriptions of such findings in this
species appear in any of the literature we have been able to obtain.

These histopathologically confirmed brain changes are not consistent
either with those caused by the classic viral infections in domesticated
and wild birds or with those described by GRATZL & KOHLER (1957) and
CHEVILLE (1966) as typical of Vitamin E deficiency-related
encephalopathy in chicks. Instead, at the light microscopy level, both
in qualitative terms and in the pattern of distribution in the central
nervous system, there is a high degree of coincidence with findings
which occur in transmissible spongiform encephalopathies in mammals
(scrapie, BSE, transmissible mink encephalopathy, chronic wasting
disease of captive mule deer and elk) (HADLOW, 1961; BURGER & HARTSOUGH,
1965; HARTSOUGH & BURGER, 1965; WILLIAMS & YOUNG, 1980; WELLS et al,
1987, 1989).

The sporadic occurrence of vacuoles in individual neurons of the nucleus
ruber in cattle was interpreted species-specifically as an artefact by
FRANKHAUSER et al (1972). We are unable to judge whether a similar
conclusion is also appropriate in the case of the ostrich, since our
experience is based on only a small number of neuropathologically
investigated cases. However, examination of the brains of twelve other
ostriches which came to autopsy after death from extracerebral causes
did not reveal any such findings. FRANKENHAUSER et al (1972) also
emphasise that none were observed by them either in small ruminants or
in the horse or the dog.

It is not possible at this time to determine whether and to what extent
our neuropathological findings in an omnivorous bird, the ostrich, are
etiopathogenetically consistent with those of the spongiform
encephatopathies of mammals. There are no indications whatever in the
relevant literature of even a hypothetical susceptibility in birds,
although it must be said by way of qualification that clinical
manifestations would be most unlikely in short-lived farm poultry, given
the long incubation period. Moreover, Germany was officially free of
scrapie and BSE at the time the condition appeared in the ostriches. The
question of possible contamination of carcase meal is discussed in the
work of TRUYEN & KAADEN (1990).

Conclusive diagnosis, especially in these cases, and in spite of the
certainty ascribed by WELLS et al (1989) to histopathological diagnosis
in cattle, also requires electron microscopic detection of so-called
scrapie-associated fibrils (SCOTT et al, 1987; HOPE et al, 1988) and
attempts, by inoculation of suspect brain material, to transmit the
disease to the mouse (TRUYEN & KAADEN, 1990). Both of these procedures
are normally carried out using fresh material, whereas we now have only
tissue fixed in formalin and embedded in Paraplast.

Etiological consideration must also be given retrospectively to
unidentified toxic influences, unknown species-specific deficiency
diseases and unexplained predisposing metabolic conditions.

The etiologically unexplained neuropathological findings reported here,
together with the multitude of unanswered questions in this connection,
underline the need for further, systematic, standardised studies in this
species, based on a larger sample of birds.

Summary and Literature

[Not translated]


Figure 1: Spongiform encephalopathy with oedematisation and vacuolation
of the neuropil and "ballooning" degeneration of virtually all neurons
in this area of the brain - brain stem. (H,-E.-Frgb., magnification x 120)

Figure 2: Detail of Figure 1. In 'addition to oedematisation of the
neuropil, numerous, optically vacant vacuoles in the neurons, with
partial displacement of the Nissl substance - brain stem. (H.-E.-Frgb.,
magnification x 480)

Figure 3: Medulla oblongara with high grade spongiform dissociation of
the neuropil. (H.-E.-Frgb., magnification x 300)

Figure 4: Medulla oblongata. Status spongiosus with neuron degeneration.
(H.-E.-Frgb., magnification x 300).


even the late great Dr. Gibbs once told me personally
that even if the Chicken did not contract a TSE,
IF the chicken had been fed the TSE tainted feed and
then slaughtered, the agent survives the digestinal tract
to pass on to other species through feed...


Date: Tue, 27 May 2003 08:07:58 -0500
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr."
Subject: FDA BSE Update - Pet Food from Canadian Manufacturer & MAD DOG

######## Bovine Spongiform Encephalopathy #########


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.

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.


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.


worse still, there is serious risk the media could get to hear of such a meeting...


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...

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...


YOU explained that imported crushed heads were extensively used in the petfood industry...

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...

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...

Meldrum's notes on pet foods and materials used


Confidential BSE and __________________

1st case natural FSE

FSE and pharmaceuticals

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

can't forget about the mad man and his mad cat;

Deaths of CJD man and cat linked

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.

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.)

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;



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).

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


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

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).

nothing to offer scientifically;

maddogs and Englishman

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: <>

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


########### ############

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -10 Accepted - Volume 2 [PART 1]

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -11 Accepted - Volume 2 [PART 2]

FDA BSE Update - Pet Food from Canadian Manufacturer & MAD DOG DATA



August 22, 2003 5:11 PM

Mad cat disease

A second case of feline spongiform encephalopathy (FSE), a disease affecting the brain tissue of cats, has been recorded in Switzerland. The veterinary authorities said the likely cause of the infection, which is similar to mad cow disease, was contaminated pet food. A first case of FSE was reported two years ago. Experts say the disease poses no health risk for people.




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