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From: TSS ()
Subject: FSE: FIRST CONFIRMED CASE REPORTED IN PORTUGAL AND POTENTIAL MAD CAT ESCAPES LAB IN USA
Date: August 9, 2007 at 2:27 pm PST

DIA-45
FELINE SPONGIFORM ENCEPHALOPATHY: FIRST CONFIRMED CASE REPORTED IN PORTUGAL

J.F. Silva1, J.J. Correia, 1 J. Ribeiro2, S. Carmo2 and L.Orge3

1 Faculdade de Medicina Veterinária (UTL), Lisbon, Portugal
2 Clínica Veterinária Ani+, Queluz, Portugal
3 Laboratório Nacional de Investigação Veterinária, Unidade de BSE, Lisbon,
Portugal

Feline spongiform encephalopathy (FSE), affecting domestic and captive feline species, is a prion disease considered to be related to bovine spongiform encephalopathy (BSE). Here we report the first case diagnosed in Portugal, highlighting the neuroapthological findings. In 2004 a 9-year old intact female Siamese cat was referred with chronic progressive behavioural changes, polydipsia, gait abnormalities and episodes of hypersalivation. Clinical signs progressed to tetraparesis and dementia and euthanasia was performed. At necropsy, brain and spinal cord had no significative changes. Tissue samples from brain, cerebellum, brainstem and spinal cord were collected for histopathology and immunohistochemistry for detection of PrPres. Histology revealed neuropil and neuronal perikarion vacuolation in several areas of the central nervous system together with gliosis and cell rarefaction at the granular layer of the cerebellum. Immunohistochemical detection of PrPres showed a strong and widespread PrPres accumulation as granular and linear deposits as well as associated with some neurons. These findings are supportive of FSE. To the authors knowledge this is the first confirmed case of FSE reported in Portugal.


http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf

http://www.lniv.min-agricultura.pt/ResourcesUser/I_D/Feline%20Spongiform%20Encephalopathy.pdf

J Vet Diagn Invest 14:444–445 (2002)

Resistance of domestic cats to a US sheep scrapie agent by intracerebral
route

Amir N. Hamir, Wilber W. Clark, Diane L. Sutton, Janice M. Miller, Mick J.
Stack, Melanie J. Chaplin, Allen L. Jenny

Abstract.

Feline spongiform encephalopathy (FSE) is thought to have resulted from consumption of food
contaminated with bovine spongiform encephalopathy and the latter is believed to result from the consumption
of food contaminated with scrapie. However, no direct experimental documentation exists to indicate that the
scrapie agent is capable of amplifying in cats, and, therefore, crossing the species barrier. During 1979, 6 cats
ranging in age from 3.5 to 18 months were intracerebrally inoculated with sheep scrapie (inoculum G-639-PP)
and were observed for an extended period. Inoculated cats did not develop neurologic disease, and microscopic
lesions of spongiform encephalopathy were not evident. Immunohistochemistry and Western blot techniques
failed to detect the abnormal form of prion protein (PrPres). These results indicate that the sheep scrapie agent
(G-639-PP) used in this study was not capable of amplifying in cats and therefore was unable to cross the
species barrier to produce FSE.


snip...


Table 1. Experimental intracerebral inoculation of 6 cats with
the sheep scrapie (Suffolk G-639-PP) agent.


† NA  not applicable. Records indicate that this cat escaped at
24 mo after inoculation and was not recovered.


****************************************************
PLEASE NOTE. ...TSS

† NA  not applicable. Records indicate that this cat escaped at
24 mo after inoculation and was not recovered.

****************************************************


END...TSS

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


REMINDS me of ;


Another possible source of infection was discovered, however, not in
Wisconsin, but 800 miles away, in Colorado. Here another TSE, chronic
wasting disease (CWD) of deer, was identified, at an experimental centre,
now known as the “Fort Collins Wildlife Research Facility”, in the 1960’s.
Only mule- and black-tailed deer and elk were affected, and only animals in,
or near, the facility, which, prior to 1974, carried out extensive work on
sheep and goats for the purposes of disease-research and
antibody-production. CWD has not been recorded anywhere else on Earth,
excepting in, and around, another, similar research facility, in Wyoming.


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


In a 1992 paper, Williams warned that the advent of elk game ranching posed
a significant threat for the spread of the disease. Even so, during the
decade of the '90s, the state permitted wholesale expansion of elk ranches.

The game ranch risk is threefold. Regardless of which way the disease might
pass through the fence, free-ranging elk and deer have nose-to-nose contact
with captive animals. Animals escape from, or break into, the ranches.
Captive animals are transported in commerce around the state, across state
lines and to other countries.


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

Many elk and deer farmers and their lobbyists claim that CWD was introduced
into their industry by accident. In 1990, Colorado Division of Wildlife officials
confiscated a group of elk from a game farmer who had stolen them from the
wild. They then held them for several months in the CWD-infected Fort Collins
research pens. The wildlife officials then traded these wild elk to game farmers for red deer.
At the time, red deer were popular on elk farms for their ease of handling and the supposed
“hybrid vigor” they could offer domestic elk herds. But as biologists grew
increasingly concerned that these “reds” would escape and genetically contaminate wild elk herds,
Colorado joined many other states and provinces in banning them. Mike Miller
confirmed to the Rocky Mountain News that these trades did indeed occur in 1991, and said
they realized after the trades that “it wasn’t such a good idea,” and tried to buy the elk
back. They recovered and killed 13 of them, and all tested negative for CWD. But
several of the others disappeared into the elk industry.


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


How did CWD get started?

17 Mar 98 webmaster opinion
My best guess as to what really happened:


http://www.mad-cow.org/elk_cwd.html#ddd


Where all has CWD been found?
18 Mar 98 webmaster

http://www.mad-cow.org/elk_cwd.html#zzz

FRIENDLY FIRE CWD FENCE LINE FROM RESEARCH FACILITY WILD TO CAPTIVE CONTACT
...TSS

(page 28-31)

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf


Date: Wed, 6 Dec 2006 11:56:39 -0600
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Subject: FELINE ALZHEIMER'S OR MAD CAT DISEASE I.E. FSE ???


Subject: FELINE ALZHEIMER'S OR MAD CAT DISEASE I.E. FSE ???
Date: December 6, 2006 at 9:24 am PST
News & Events - 6 December 2006
Cats Can Succumb to Feline Alzheimer's
Ageing cats can develop a feline form of Alzheimer's disease, a new study
reveals.

Researchers at the Universities of Edinburgh, St Andrews, Bristol and
California have identified a key protein which can build up in the nerve
cells of a cat's brain and cause mental deterioration.

In humans with Alzheimer's disease, this protein creates ‘tangles’ inside
the nerve cells which inhibit messages being processed by the brain. The
team says that the presence of this protein in cats is proof that they too
can develop this type of disease.

By carrying out post-mortem examination of cats which have succumbed
naturally to the disease, scientists may now be able to uncover vital clues
about how the condition develops. This may eventually help scientists to
come up with possible treatments.

Researchers already thought cats were susceptible to dementia because
previous studies had identified thick, gritty plaques on the outside of
elderly cats' brain cells which are similar to those found in humans.

By pinpointing this second key marker, the Edinburgh-led team says we can be
sure that cats can suffer from a feline form of Alzheimer's.

Dr Danielle Gunn-Moore, at the University of Edinburgh's Royal (Dick) School
of Veterinary Studies, said:

“This newly discovered protein is crucial to our understanding of the ageing
process in cats. We've known for a long time that cats develop dementia, but
this study tells us that the cat's neural system is being compromised in a
similar fashion to that we see in human Alzheimer's sufferers. The gritty
plaques had only hinted that might be the case - now we know.

“The shorter life-span of a cat, compared to humans, allows researchers to
more rapidly assess the effects of diet, high blood pressure, and prescribed
drugs on the course of the disease. However, we also need to understand more
about our geriatric cats for their own benefit, so we can slow down the
degeneration the disease brings and keep them as happy cats for as long as
possible.”

The findings of the study are published in a recent edition of the Journal
of Feline Medicine.

http://www.ed.ac.uk/news/061206cats.html


Late onset cerebellar degeneration in a middle-aged cat

Arianna Negrin DVM1, , , Marco Bernardini DVM, Dipl ECVN2, Wolfgang
Baumgärtner Dr Med Vet, PhD, Dipl ECVP3 and Massimo Castagnaro DVM, PhD,
Dipl ECVP1

1Department of Public Health, Comparative Pathology and Veterinary Hygiene,
Faculty of Veterinary Medicine, Università degli Studi di Padova, Viale
dell'Università, 16, 35020 Legnaro, Padova, Italy
2Department of Veterinary Clinical Science, Faculty of Veterinary Medicine,
Università degli Studi di Padova, Viale dell'Università, 16, 35020 Legnaro,
Padova, Italy
3Department of Pathology, University of Veterinary Medicine Hannover,
Bünteweg 17, 30599 Hannover, Germany

Accepted 24 April 2006. Available online 15 June 2006.

Cerebellar degeneration (abiotrophy) (CD) is a spontaneous and accelerated
degeneration of one or several mature cerebellar neuronal cell populations
and has been described in many domestic animals, especially in dogs, with
numerous breed-related cases. In cats, CD is mentioned as a rare sporadic
entity. Late onset CDs are exceptionally uncommon and only two cases are
reported in young adults, both aged 18 months. This report describes
clinical and pathological findings of a late onset feline CD in a 9-year-old
male Persian cat. The cat was presented with a history of progressive ataxia
lasting 2 years. Neurological examination revealed severe neurological
deficits such as generalised and severe ataxia, hypermetria in all four
limbs, and bilateral absence of menace response. The lesion was diffusely
localised in cerebellum. On gross pathology, the cerebellum appeared of
normal size and shape and kidneys were characterised by mild hyperaemia.
Histologically, lesions were limited to the cerebellum and kidneys. In the
cerebellum, all cerebellar folia of both hemispheres and the vermis were
affected. Changes were characterised by severe and diffuse loss of Purkinje
cells, loss of cellularity in the granular layer, mild astrogliosis
associated with moderate hypertrophy of Bergmann's glia.
Immunohistochemistry for feline parvovirus antigen revealed a negative
result. Renal lesions consisted of chronic fibrosis associated with chronic
interstitial nephritis. CD is a rare disease and occurs commonly in puppies
or young animals, who are clinically normal at birth and usually develop
neurological signs within a few weeks or months after birth. This report
represents the first case of CD in a middle-aged cat.


http://www.sciencedirect.com/


Neuropathological study of cerebellar degeneration in prion disease


Qing Yang, Yoshio Hashizume, Mari Yoshida & Yin Wang
In order to clarify the relationship between cerebellar degeneration and
prion protein (PrP) accumulation, 17 cases of sporadic Creutzfeldt-Jakob
disease (CJD) and three cases of Gerstmann–Sträussler syndrome (GSS) were
analyzed neuropathologically. Immunohistochemical staining for PrP showed
synaptic-type deposits in all of the CJD cases. The punctate PrP stains in
CJD patients were almost identical with those of synaptophysin, suggesting
that PrP had accumulated in the synaptic structures. Synapses damage due to
PrP accumulation seemed to develop prior to granule cell loss. PrP
accumulation was inversely correlated with granule cell loss. The degree of
atrophy in the molecular layer was compatible with granule cell loss. The
nodulus showed severe PrP accumulation when compared with other sites in the
cerebellum. How-ever, in GSS cases, the loss of Purkinje cells and dentate
nucleus neurons was obvious. Further, immunohisto-chemical staining for PrP
demonstrated Kuru plaque-type and synaptic-type depositions in the molecular
layer, the granular cell layer, and the dentate nucleus, which was different
from CJD cases.

http://www.blackwell-synergy.com/links/doi/10.1046/j.1440-1789.1999.00212.x


Case Report

A 48-year-old woman was admitted to our hospital with

a 1-month history of lethargy, loss of appetite, and poor

mental performance. On admission, she exhibited inattentiveness,

lack of fluent speech, tremor, and dystonic

movement of the right hand. Her medical and family history

were unremarkable. Neurologic examination showed

her to be alert but with mutism. Her mental performance

was characterized by poor calculative abilities and sluggish

judgment as to person and place. Muscle strength was

normal, but with mild axial rigidity. The deep tendon reflexes

were increased, but the Babinski sign was not

present. A wide-based, shuffling gait was observed. Cerebrospinal

fluid analysis was normal. An electroencephalogram

(EEG) showed a generalized pattern of theta-delta

background slowing activity and periodic synchronized

sharp 1/s delta-wave discharge. Findings at cranial computed

tomography (CT) were unremarkable (Fig 1A). The

initial impression was dementia of unknown origin.

Two months later, the patient’s condition had deteriorated

to global aphasia and she was bedridden. Myoclonic

jerk was present and muscular rigidity developed in all

limbs. There was muscle wasting, followed by difficulty in

swallowing and incontinence of urination. Initial, noncontrast

MR images revealed a subtle increase in signal in the

heads of the caudate nuclei, putamina, and thalami on

T2-weighted images (Fig 1B–E). An open brain biopsy of

the right temporal lobe performed just after MR imaging

revealed severe loss of neurons, hypertrophic glial reaction,

and vacuolar-spongiform changes in the gray matter

(Fig 1F).

One year later, the patient was in a vegetative state with

poor respiratory control. Noncontrast T2-weighted MR images

obtained at this time revealed severe cerebral and

cerebellar atrophy, prominent dilatation of the ventricular

system, and a global increase in signal intensity in

the white matter with shrinkage of the basal ganglia

(Fig 1G–J).

One and a half years after admission, she was discharged

to a chronic-care unit, where she remained in a

vegetative state. She died 8 months later.


snip...


http://www.ajnr.org/cgi/reprint/18/3/583.pdf

PATHOLOGY OF PRION DISEASES
Pathology, in prion diseases, develops only in the brain. No other organ is
affected. Early on, neurons develop intracytoplasmic vacuoles. As the
disease progresses, vacuolization becomes more pronounced and the cortical
neuropil develops a spongy appearance, hence the term spongiform
encephalopathy.
Spongiform encephalopathy CJD: severe brain atrophy Cerebellar degeneration
Advanced cases show neuronal loss, gliosis, and brain atrophy. Cerebellar
atrophy is usually severe. Unlike most cerebellar degenerations, there is
more pronounced loss of granular neurons than Purkinje cells. There is no
inflammation. The CSF is normal. The changes are confined to the gray matter
(the primary pathology involves the neuronal body). In some cases, prion
proteins precipitate as amyloid plaques.

Creutzfeldt-Jakob disease (CJD) is the most common prion disease of humans,
but overall is a rare disease, affecting one in every million people. It
affects middle aged or old persons and causes dementia, myoclonus, ataxia
and other neurological abnormalities. This phenotype, also known as the
Heidenhain variant, is seen in 70% of sporadic CJD. The other 30% have less
typical features. The EEG shows perodic sharp wave complexes. CJD is
inexorably progressive and fatal within months up to 1 to 2 years. A
definitive diagnosis can only be made by microscopic examination of brain
tissue showing the characteristic spongy change. Abnormal prions can be
detected in brain tissue extracts by ELISA and in tissue sections by
immunohistochemistry. A protein called 14-3-3 is elevated in the CSF of
patients with CJD. Microtubule associated protein tau was also recently
shown to be elevated in the CSF, including in the new variant (see below)
and iatrogenic CJD cases in which 14-3-3 remains normal. Determination of
tau can be done in routine hospital laboratories. Detection of these
proteins provides much needed premortem diagnostic tests for CJD. Both, tau
and 14-3-3, are also elevated in other neurological diseases (tau most
notably in Alzheimer's disease) but these can be clinically distinguished
from CJD. For this reason they are helpful only when the differential
diagnosis has been narrowed down and more common neurological conditions
such as Alzheimer's disease, stroke, HIV encephalitis, etc, have been
excluded. Mutations of the PRNP gene and the codon 129 polymorphism can be
detected by DNA analysis of blood and tissues.


http://www.neuropathologyweb.org/chapter5/chapter5ePrions.html


more here;

http://www.google.com/search?num=30&hl=en&lr=&as_qdr=d&edition=us&q=cerebellar+degeneration+cjd&btnG=Search

X-Virus-Scanner: Found to be clean
Message-ID: <>
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
DATA
######## 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

Image] Research letters Volume 352, Number 9134 [Image] 3
October1998[Previous] [Next] [Image][Image]

Simultaneous occurrence of spongiform encephalopathy in a manand his cat in
Italy

[Image] Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi,
SergioFerrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto,
SalvatoreMonaco

Transmissible spongiform encephalopathies (TSE) encompass
inherited,acquired, and sporadic mammalian neurological disorders, and
arecharacterised by the conversion of the cellular prion protein (PrP) in
aninsoluble and protease-resistant isoform (PrPres). In human TSE, four
typesof PrPres have been identified according to size and glycoform ratios,
whichmay represent different prion strains. Type-1 and type-2 PrPres
areassociated with sporadic Creutzfeldt-Jakob disease (CJD), type 3
withiatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence
thatvariant CJD is caused by the bovine spongiform encephalopathy
(BSE)-prionstrain.2-4 The BSE strain has been identified in three cats with
felinespongiform encephalopathy (FSE), a prion disease which appeared in
1990 inthe UK.5 We report the simultaneous occurrence of sporadic CJD in a
man anda new variety of FSE in his cat. A 60-year-old man, with no unusual
dietary habits, was admitted in November,1993, because of dysarthria,
cerebellar ataxic gait, visual agnosia, andmyoclonus. An
electroencephalogram (EEG) showed diffuse theta-deltaactivity. A brain
magnetic resonance imaging scan was unremarkable. 10 dayslater, he was
speechless and able to follow only simple commands. RepeatEEGs showed
periodic triphasic complexes. 2 weeks after admission, he wasmute, 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. Nobites from the cat were
recalled. In the next few days, the cat becameataxic, with hindquarter
locomotor dysfunction; the ataxia got worse andthere was diffuse myoclonus.
The cat was killed in mid-January, 1994. No pathogenic mutations in the
patient's PrP gene were found. The patientand the cat were methionine
homozygous at codon 129. Histology of thepatient's brain showed neocortical
and cerebellar neuronal loss,astrocytosis, and spongiosis (figure A). PrP
immunoreactivity showed apunctate pattern and paralleled spongiform changes
(figure B). The cat'sbrain showed mild and focal spongiosis in deeper
cortical layers of all fourlobes (figure C), vacuolated cortical neurons
(figure D), and mildastrogliosis. The cerebellar cortex and the dentate
nucleus were gliosed.Immunoreactive PrP showed a punctate pattern in
neocortex, allocortex, andcaudate nucleus (figure E). Western blot analysis
of control and affectedhuman and cat brain homogenates showed 3 PrP bands of
27-35 kDa. Afterdigestion with proteinase K and deglycosylation, only
samples from theaffected patient and cat showed type-1 PrPres, with PrP
glycoform ratioscomparable to those observed in sporadic CJD1 (details
available fromauthor). [Image] Microscopic sections of patient and cat
brains A: Occipital cortex of the patient showing moderate
spongiformdegeneration and neuronal loss (haematoxylin and eosin) and B:
punctateperineuronal pattern of PrP immunoreactivity;
peroxidaseimmunohistochemistry with monoclonal antibody 3F4. C: cat parietal
cortexshowing mild spongiform degeneration (haematoxylin and
eosin).D:vacuolated neurons (arrow, haematoxylin and eosin), E:
peroxidaseimmunohistochemistry with antibody 3F4 shows punctate
perineuronaldeposition of PrP in temporal cortex. This study shows a
spatio-temporal association between human and felineprion diseases. The
clinical features of the cat were different frompreviously reported cases of
FSE which were characterised by gradual onsetof behavioural changes
preceding locomotor dysfunction and ataxia.5Neuropathological changes were
also at variance with the diffuse spongiosisand vacuolation of brainstem
neurons, seen in FSE.5 The synaptic pattern ofPrP deposition, similar in the
cat and in the patient, was atypical for aBSE-related condition. Evidence of
a new type of FSE was further provided bythe detection of a type-1 PrPres,
other than the BSE-associated type 4.2Taken together, our data suggest that
the same agent strain of sporadic CJDwas involved in the patient and in his
cat. It is unknown whether these TSE occurred as the result of
horizontaltransmission 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
phenotypicvariablity 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 ofprion 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 vCJDand BSE.
Nature 1997; 389: 448-50 [PubMed]. 5 Pearson GR, Wyatt JM, Henderson JP,
Gruffydd-Jones TJ. Feline spongiformencephalopathy: a review. Vet Annual
1993; 33: 1-10.

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

Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e
dellaVisione, Università di Verona, Policlinico Borgo Roma, 37134 Verona,
Italy(S Monaco; e mail [log in to unmask]); and Istituto
ZooprofilatticoSperimentale della Lombardia e dell' Emilia, Brescia

=========================================TSS

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: <[log in to unmask]>

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 [log in to unmask]

TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

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.

swissinfo

http://www.swissinfo.org/sen/Swissinfo.html

?siteSect=113&sid=41558971: Ann N Y Acad Sci. 1982;396:131-43.

Links Alzheimer's disease and transmissible virus dementia
(Creutzfeldt-Jakob disease).

Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.

Ample justification exists on clinical, pathologic, and biologic grounds for
considering a similar pathogenesis for AD and the spongiform virus
encephalopathies. However, the crux of the comparison rests squarely on
results of attempts to transmit AD to experimental animals, and these
results have not as yet validated a common etiology. Investigations of the
biologic similarities between AD and the spongiform virus encephalopathies
proceed in several laboratories, and our own observation of inoculated
animals will be continued in the hope that incubation periods for AD may be
even longer than those of CJD.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=6758661&query_hl=3&itool=pubmed_DocSum

1: Neurology. 1990 Feb;40(2):226-8.

Coexistence of Creutzfeldt-Jakob disease and Alzheimer's disease in the same
patient.

Brown P, Jannotta F, Gibbs CJ Jr, Baron H, Guiroy DC, Gajdusek DC.
Laboratory of CNS Studies, NINDS, National Institutes of Health, Bethesda,
MD 20892.

We report the case of a 73-year-old patient in whom a diagnosis of
Creutzfeldt-Jakob disease, suggested by the clinical course, was verified by
the neuropathologic finding of widespread spongiform change and
astrogliosis, the presence of proteinase-resistant protein in brain
extracts, and the experimental transmission of spongiform encephalopathy to
primates inoculated with brain tissue. However, neuropathologic examination
also revealed a profusion of senile and neuritic plaques and neurofibrillary
tangles that reacted with antibody to the amyloid beta-protein
characteristic of Alzheimer's disease, but not with antibody to the scrapie
amyloid protein characteristic of Creutzfeldt-Jakob disease.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=2405293&query_hl=9&itool=pubmed_DocSum

1: Prog Clin Biol Res. 1989;317:549-57. Links Neuroaxonal dystrophy: an
ultrastructural link between subacute spongiform virus encephalopathies and
Alzheimer's disease.Liberski PP, Yanagihara R, Gibbs CJ Jr, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, Bethesda, Maryland
20892.====================

Unconventional Viruses and the Origin and Disappearance of Kuru

333334 Physiology or Medicine 1976Table 12.

Creutzfeldt-Jakob disease in cats

Incubation period(months)Duration(months)Primary passageHuman brainSerial
passageCat brain (passage 1)Cat brain (passage 2)This geographic and
temporal clustering does not apply, however, to amajority of cases and is
unexplained by the 10% of the cases that are familial.Matthews has recently
made a similar observation in two clusters in England(50). There are two
reports of conjugal disease in which husband and wife died of CJD within a
few years of each other (30, 50).The prevalence of CJD has varied markedly
in time and place throughoutthe United States and Europe, but we have noted
a trend toward making thediagnosis more frequently in many neurological
clinics in recent years, sinceattention has been drawn to the syndrome by
its transmission to primates(3, 33). For many large population centers of
the United States, Europe,Australia, and Asia, we have found a prevalence
approaching one per millionwith an annual incidence and a mortality of about
the same magnitude, asthe average duration of the disease is 8 to 12 months.
Matthews (50) found anannual incidence of 1.3 per million in one of his
clusters, which was over 10times the overall annual incidence for the past
decade for England andWales (0.09 per million). Kahana et al. (40) reported
the annual incidence ofCJD ranging from 0.4 to 1.9 per million in various
ethnic groups in Israel. Theynoted, however, a 30-fold higher incidence of
CJD in Jews of Libyan originabove the incidence in Jews of European origin.
From recent discussions withour Scandinavian colleagues it is apparent that
an annual incidence of at leastone per million applies to Sweden and Finland
in recent years.Probable man-to-man transmission of CJD has been reported in
a recipientof a cornea1 graft, which was taken from a donor who was
diagnosed retrospectivelyto have had pathologically confirmed CJD ( 12). The
disease occurred18 months after the transplant, an incubation period just
the average forchimpanzees inoculated with human CJD brain tissue (32, 62).
From suspensionof brain of the cornea1 graft recipient we succeeded in
transmitting CJDto a chimpanzee although the brain had been at room
temperature in 10%formol-saline for seven months (26a). More recently we
learned that two of ourconfirmed cases of TVD were professional blood donors
until shortly beforethe onset of their symptoms. To date, there have been no
transmissions of CJDfrom blood of either human patients or animals affected
with the experimentallytransmitted disease. However, we have only transfused
two chimpanzees eachwith more than 300 ml of human whole blood from a
different CJD patientUnconventional Viruses and the origin and Disappearance
of KuruFigure 20. Six serial passages of CJD in chimpanzees, starting with
brain tissue from abiopsy of a patient (R. R.) with CJD in the United
Kingdom (U. K.). Also shown is transmissionof the disease directly from man
to the capuchin monkey and marmoset, and fromchimpanzee brain to three
species of New World monkeys (squirrel, capuchin, spidermonkeys), and to six
Old World species (rhesus, stumptailed, cynomolgus, African green,pigtailed,
and sooty mangabey). Incubation periods in the New World monkeys rangedfrom
19 to 47 months, and in the Old World monkeys from 43 to 60 months. The
pigtailedmacaque and the sooty mangabey showed positive CJD pathology when
sacrificed without336 Physiology or Medicine 1976within the past several
months. Finally, the recognition of TVD in a neurosurgeon(27), and more
recently in two physicians, has raised the question ofpossible occupational
infection, particularly in those exposed to infected humanbrain tissue
during surgery, or at postmortem examination (61, 63).The unexpectedly high
incidence of previous craniotomy in CJD patientsnoted first by Nevin et al.
(51) and more recently by Matthews (50) and byourselves (62), raises the
possibility of brain surgery either affording a mode ofentry for the agent
or of precipitating the disease in patients already carryinga latent
infection. The former unwelcome possibility now seems to be areality with
the probable transmission of CJD to two young patients withepilepsy from the
use of implanted silver electrodes sterilized with 70%ethanol and
formaldehyde vapor after contamination from their use on apatient who had
CJD. The patients had undergone such electrode implantationfor stereotactic
electroencephalographic localization of the epileptic focusat the time of
correctional neurosurgery (3a).Two patients with transmissible virus
dementias were not diagnosed clinicallyor neuropathologically as having CJD,
but rather as having Alzheimer’sdisease (62). In both cases the disease was
familial: in one (Fig. 21) therewere six close family members with the
disease in two generations; in the otherboth the patient’s father and sister
had died of presenile dementia. Thediseases as transmitted to primates were
clinically and pathologically typicalsubacute spongiform virus
encephalopathies, and did not have pathologicalfeatures of Alzheimer’s
disease in man. More than 30 additional specimens ofbrain tissue from
non-familial Alzheimer’s disease have been inoculated intoTVD-susceptible
primates without producing disease. Therefore, although weclinical disease.
A third passage to the chimpanzee was accomplished using frozen andthawed
explanted tissue culture of brain cells that had been growing in vitro for
36 days.Using 10-3, 10-4, and 10-4 dilutions of brain, respectively, the
4th, 5th, and 6th chimpanzeepassages were accomplished. This indicates that
the chimpanzee brain contains >50,000infectious doses per gram, and that
such infectivity is maintained in brain cells cultivatedin vitro at 37” C
for at least one month. The lower left shows transmission of CJD from
asecond human patient (J. T.) to a cat with a 30 month incubation and serial
passage in thecat with 19 to 24 month incubation.Unconventional Viruses and
the Origin and Disappearance of Kum 337Figure 21a. Y family. Brain tissue
obtained from patient A. Y. at biopsy induced subacutespongiform
encephalopathy in a squirrel monkey 24 months after intracerebral
inoculation.The patient, a 48-year old woman who died after a 68 month
course of progressive dementia,quite similar in clinical aspects to the
progressive dementia from which her fatherand brother had died at 54 and 56
years of age, respectively, was diagnosed clinically andneuropathologically
as suffering from Alzheimer’s disease. Her sister is at present
incapacitatedby a similar progressive dementia of 4 years’ duration.
Although the transmitteddisease in the squirrel monkey was characterized by
severe status spongiosis, none was seenin the patient. although amyloid
plaques and neurofibrillary tangles were frequent.21b. H family. Brain
tissue obtained from patient B. H. at surgical biopsy induced
subacutespongiform encephalopathy in a squirrel monkey and a capuchin monkey
29 1/2 monthsand 43 months, respectively, after intracerebral inoculations.
The patient, a 57 year oldwoman, has had slowly progressive dementia and
deterioration for the past 7 years. Neuropathologicalfindings revealed
abundant neurofibrillary tangles and senile plaques and noevidence of status
spongiosis. The patient’s father, A. S., had died at age 64 following
severalyears of progressive dementia, behavioral change and memory loss. B.
H. is presently aliveand institutionalized.338 Physiology or Medicine
1976cannot claim to have transmitted the classical sporadic Alzheimer’s
disease toprimates, we are confronted with the anomaly that the familial
form ofAlzheimer’s disease has, in these two instances, transmitted as
though it wereCJD.The above findings have added impetus to our already
extensive studies ofHuntington’s chorea, Alzheimer’s and Pick’s diseases,
parkinsonism-dementia,senile dementia, and even “dementia praecox", the
organic brain diseaseassociated with late uncontrolled schizophrenia. ......

http://nobelprize.org/nobel_prizes/medicine/laureates/1976/gajdusek-lecture.pdf

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

DEFRADepartment for Environment,Food & Rural Affairs

Area 307, London, SW1P 4PQTelephone: 0207 904 6000Direct line: 0207 904
6287E-mail: h.mcdonagh.defra.gsi.gov.uk

GTN:FAX:

Mr T S SingeltaryP.O. Box 42BacliffTexasUSA 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 MCDONAGHBSE CORRESPONDENCE SECTION

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

IN STRICT CONFIDENCE TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf

Regarding Alzheimer's disease (note the substantial increase on a yearly
basis)

http://www.bseinquiry.gov.uk/files/yb/1988/07/08014001.pdf

snip...

The pathogenesis of these diseases was compared to Alzheimer's disease at a
molecular level...

snip...

http://www.bseinquiry.gov.uk/files/yb/1990/03/12003001.pdf

And NONE of this is relevant to BSE? There is also the matter whether the
spectrum of ''prion disease'' is wider than that recognized at present.

http://www.bseinquiry.gov.uk/files/yb/1990/07/06005001.pdf

Human BSE snip...

These are not relevant to any possible human hazard from BSE nor to the much
more common dementia, Alzheimers.

snip...

http://www.bseinquiry.gov.uk/files/yb/1990/07/09001001.pdf

NOW, ASK yourself how many dogs and cats are ever examined and autopsied for
a TSE in the USA ???

HOW many are still rendered and fed to other animals for human and animal
consumption ???

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

********************************************************

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0612&L=sanet-mg&P=8385


tss




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