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From: TSS ()
Subject: Cognitive Dysfunction Syndrome (CDS) or MAD DOG DISEASE
Date: April 4, 2005 at 1:33 pm PST

-------- 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 WHERE we know that
.1 gram is lethal and the 8/4/97 partial and voluntary ruminant feed ban
was nothing more than ink on paper, nobody adhered to it, others did not
even know about it for pete's sake. YOU know, we now have some 4.5
MILLION people in the USA with alzheimers, i read some other 19 million
taking care of them, and by 2050 there will be a projected 14 MILLION
with Alzheimer's in the USA. Mad cows, mad sheep, mad goats, mad deer,
mad elk, mad mink, mad cats, mad people, NO mad dogs? DEER, CAT and DOG
SPONGIFORM ENCEPHALOPATHY SURVEY

http://www.priondata.org/data/A_deerdog.html

Why did the appearance of new TSEs in animals matter so much? It has
always been known that TSEs will transfer across species boundaries. The
reason for this was never known until the genetic nature of the prion
gene was fully investigated and found to be involved. The gene is found
to have well preserved sites and as such there is a similar gene
throughout the animal kingdom...and indeed a similar gene is found in
insects! It is NOT clear that the precise close nature of the PrP gene
structure is essention for low species barriers. Indeed it is probably
easier to infect cats with BSE than it is to infect sheep. As such it is
not clear that simply because it is possible to infect BSE from cattle
into certain monkeys then other apes will necessarily be infectable with
the disease. One factor has stood out, however, and that is that BSE,
when inoculated into mice would retain its apparent nature of disease
strain, and hence when it was inoculated back into cattle, then the same
disease was produced. Similarly if the TSE from kudu was inoculated into
mice then a similar distribution of disease in the brain of the mouse is
seen as if BSE had been inoculated into the mouse. This phenomenon was
not true with scrapie, in which the transmission across a species
barrier was known to lose many of the scrapie strain phenomena in terms
of incubation period or disease histopathology. This also suggested that
BSE was not derived from scrapie originally but we probably will never
know.
------------------------------------------------------------------------
TSE in wild UK deer? The first case of BSE (as we now realise) was in a
nyala in London zoo and the further zoo cases in ungulates were simply
thought of as being interesting transmissions of scrapie initially. The
big problem started to appear with animals in 1993-5 when it became
clear that there was an increase in the CJD cases in people that had
eaten deer although the statistics involved must have been questionable.
The reason for this was that the CJD Surveillance was well funded to
look into the diet of people dying of CJD. This effect is not clear with
vCJD...if only because the numbers involved are much smaller and hence
it is difficult to gain enough statistics. They found that many other
foods did not appear to have much association at all but that deer
certainly did and as years went by the association actually became
clearer. The appearance of vCJD in 1996 made all this much more
difficult in that it was suddenly clearer that the cases of sporadic CJD
that they had been checking up until then probably had nothing to do
with beef...and the study decreased. During the period there was an
increasing worry that deer were involved with CJD..see references:
http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf It is not
clear that deer may well become infected with BSE although the rate at
which this is taking place is unclear. DEFRA issued a document
specifically to tell farmers what to do if they found a deer with
potential symptoms:
http://www.defra.gov.uk/animalh/bse/bse-publications/adv-TSEs-deer.pdf
------------------------------------------------------------------------
TSE in zoo ungulates (hoofed animals) In parallel to the first BSE
cases, sporadic cases of spongiform encephalopathy in hoofed zoo species
were diagnosed in British zoos. Strain typing indicates that all these
TSEs are caused by the same strain that had caused cttle BSE. Until
April 2002, 6 kudus, 5 elands, 2 Arabian orynx, 2 ankole cows and one
nyala, Gemsbock and bison were affected (DEFRA). The animals showed a
range of clinical symptoms that, depending on the species, were
distinctly different from those of cattle BSE or sheep scrapie.
Incubation time and duration of clinical disease seemed to be shorter in
the zoo ungulates, which could be a reflection of the generally shorter
lifespan of those species in comparison to that of domestic cattle. In
the majority of those TSE cases in zoos, exposure to animal feed
produced with animal protein (and therefore potentially containing BSE
infectivity) was either documented, or at least could not be excluded.
The fact that the nyala case was so early was simply showing just how
quickly an animal that was exposed early in life could incubate the
disease. Also the suggestion has always been that BSE had been in small
quantities in bovine feed early in the 1970s. Kirkwood JK, Cunningham AA
. Epidemiological observations on spongiform encephalopathies in captive
wild animals in the British Isles. Vet Rec. 1994 Sep 24;135(13):296-303.
Since 1986, scrapie-like spongiform encephalopathy has been diagnosed in
19 captive wild animals of eight species at or from eight zoological
collections in the British Isles. The affected animals have comprised
members of the family Bovidae: one nyala (Tragelaphus angasi), four
eland (Taurotragus oryx), and six greater kudu (Tragelaphus
strepsiceros), one gemsbok (Oryx gazella), one Arabian oryx (Oryx
leucoryx), and one scimitar-horned oryx (Oryx dammah), and members of
the family Felidae: four cheetah (Acinonyx jubatus) and one puma (Felis
concolor). In addition, three cases of a spongiform encephalopathy of
unknown aetiology have been reported in ostriches (Struthio camellus)
from two zoos in north west Germany. Three features suggest that some of
these cases may have been caused by the agent of bovine spongiform
encephalopathy (BSE). First, they have been temporally and
geographically coincident with the BSE epidemic. Secondly, in all the
ungulates for which details are available, it is possible that either
the affected animal itself, or the herd into which it was born or moved,
had been exposed to proprietary feeds containing ruminant-derived
protein or other potentially contaminated material, and all the
carnivores had been fed parts of cattle carcases judged unfit for human
consumption. Thirdly, the pathological results of inoculating mice with
a homogenate of fixed brain tissue from the nyala and from one greater
kudu were similar to the results of inoculating mice with BSE brain
tissue. (notably a few cases of this type of disease are still appearing
in UK zoos)
------------------------------------------------------------------------
TSE in cervidae (deer and elk) A chronic wasting condition (Chronic
Wasting Disease, CWD) in captive and free-roaming North-American deer
and elk has been described since approx. 1980. Initially, cases were
only reported from captive cervidae in Colorado, but now also from both
captive and free roaming animals in Colorado, Wyoming, Wisconsin, South
Dakota and Nebraska. In addition, several captive herds in Canada that
had imported animals from affected farms in the USA have diagnosed CWD
cases. In an increased surveillance (screening) of hunted deer and elk
and animals killed in car accidents, in some regions in Northern
Colorado (Larimer County) and Southern Wyoming 8% (hunted animals) and
11% (car accidents) of the tested brains were CWD-positive in histology
and/or immunhistochemistry (IHC). Recent reports of 50% CWD prevalence
in hunted cervidae in one geographically defined region in the USA still
need to be validated. Until now cervidae are the only known free-roaming
species with a spontaneous (naturally transmitted?) TSE. The origin of
CWD is still unknown. There was some contact to sheep reported. However,
sheep scrapie was not observed in the sheep flocks in the regions where
CWD was initially observed, and in general is a rarely observed
condition in Colorado and Wyoming. Close contact to cattle did not
occur. One hypothesis is that the disease was introduced into the
captive herds with subclinically infected captured wildlife, and that it
spread in the captive population due to higher animal density. However,
even recent studies were not able to answer the question whether CWD
started in the captive or the free-roaming deer and elk population, and
they also were not able to determine the mode of transmission among
free-roaming cervidae. The clinical picture of the disease is
characterized by a chronic wasting with loss of condition and untidy
coat, behavioural disorders, polydipsia and polyuria, lowered head and
hanging ears. Feed intake is reduced, and affected animals loose weight
and die within a few months after the onset of clinical symptoms. In
Switzerland, until April 2002 approx. 80 brain samples of captive elk
have been examined for CWD, all with a negative result. The full list
details are on
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html
(by rights this is up to date) also see the internal reference on this
site and http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf
------------------------------------------------------------------------
Hound studies This largely started after it was found that dogs were
being reported with a spongiform encephalopathy and ataxia. The
condition seemed to take place in older dogs and was being reported from
various parts of the UK. There was never any proof that it was caused by
a TSE. One of the most difficult prblems to get around in all this was
the outbreak of the disease that was seen in a large pack of game dogs.
It was as if all the animals developed the disease concurrently..as
would be expected if an infection was involved. The animals were not
very young and no specific infective cause or toxic cause was found. The
documents below became clear during the Phillips Inquiry and represent
documents passed around in the UK Ministry of Agriculture and Central
Veterinary Laboratory:
http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf From these
various documents: 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. Terry Singletary 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/files/ws/s067.pdf 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
Editorial: Things are really not as clear with dogs and TSE as you might
think. The first thing was that the MAFF in the UK decided to do no
scientific work investigating the cases (e.g. by inoculating them into
animals), and that they were really not happy about discussing this with
the public. I was contacted by an Member of the UK Parliament in 1994
concerning the possibility that a series of dogs near Doncaster had gone
down with a similar condition that sounded very similar to BSE. The
animals were roughly the same age, and had been fed collectively by the
owner. The other main possibility was that the condition was due to a
poisoning element present in the food. A second group was in contact in
around 1995 in which the animals were considered to have been poisoned
with heavy metals but no proof (or even investigation) seems to have
taken place. This determination by MAFF not to carry out any studies of
inoculating BSE into dogs was indeed strange at the time. The reason for
this being so odd is that dogs are commonly available for experimental
animals and it would be looked on as being a low cost experiment.
However politically it is always extremely bad to do experiments with
loveable domestic dogs by inoculating them with a disease that could, to
some degree be blamed on the incompitence of the government of the time.
------------------------------------------------------------------------
Cats Only four years after initial BSE cases had been diagnosed in
cattle in the UK, first reports of a new spontaneous spongiform
encephalopathy in domestic cats were published. Epidemiological research
and strain typing indicated that cattle BSE and this new disease in
domestic cats, called Feline Spongiform Encephalopathy (FSE), are
linked. All but four of the approx. 100 FSE cases diagnosed worldwide
until April 2002 have been seen in the UK (DEFRA). One of the four
non-UK cases was diagnosed in Northern Ireland, one in Norway, one in
Liechtenstein, and one in 2001 in Switzerland. The most widely accepted
hypothesis, although not proven, is that the affected domestic cats were
exposed to BSE infectivity through contaminated commercial cat feed or
fresh slaughter offal that contained brain or spinal cord from cattle
BSE cases. An interesting observation is that in addition to domestic
cats, several large cats kept in zoos were diagnosed with FSE. Based on
data provided by the British ministry (DEFRA) until April 2002 5
cheetahs, 4 lions and 3 ocelots, pumas and tigers were affected. The
large cats that were diagnosed with FSE outside of the UK all originated
from UK zoos. It is suspected that these large cats acquired the
infection by being fed meat and bones of BSE-infected cattle. There is a
parallel development in the significant reduction in clinical BSE cases
in the UK (peak in 1992) and the course of the FSE epidemic. This can be
seen as additional evidence for the feed-related association between
cattle BSE and FSE. Until April 2002, only adult cats around 4-6 years
of age have been diagnosed with clinical FSE. 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 Various things
appeared in the Phillips Inquiry: * imported crushed heads were
extensively used in the petfood
industry...http://www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf *
it was clear that vets in the MAFF did 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 and
http://www.bseinquiry.gov.uk/files/yb/1989/04/25001001.pdf * some 100+
_documented_ TSE cats of all types later. .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 and
http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf and
http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf * In
confidence concerning passing CJD to
cats....http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf * BSE
and cats....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 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
Editorial: At the time of BSE first being isolated and identified at the
CVL in Weybridge it was realised quite quickly by the staff that the
disease was probably the case of the illness in the zoo animals, and
that it may well represent a risk to domestic cats and dogs. At that
point Richard Kimberlin was both sitting on the committee that advised
the Government and also advised the manufacturers of pet food in the UK.
As you will realise if you read the (many volumes!) Phillips Inquiry,
you will realise that on the Government Committee they were only really
listened to their advice when the Government had asked for it, and any
other advice could be simply ignored. As it was all being done in
private and no information could be released to the public, it was
possible for the MAFF to simply decide that there was no risk to
humans....whereas Kimberlin had already told the pet food manufacturers
association in the UK to stop all bovine offal in pet food. They did
this immediately as far as I can tell. One company (this must be looked
on as simply heresay), however decided to check up whether BSE was a
risk to cats at all. They fed a large number (?80) of cats with infected
bovine brain and when cats started to produce the symptoms and it seemed
that all of them were likely to die of the disease, the experiment was
stopped and the as yet asymptomatic cats were slaughtered! The reason
for the simultaneous appearance of the FSE in the cat and the CJD in the
Italian man....has not come to light.
------------------------------------------------------------------------
Zoo Cats Only four years after initial BSE cases had been diagnosed in
cattle in the UK, first reports of a new spontaneous spongiform
encephalopathy in domestic cats were published. Epidemiological research
and strain typing indicated that cattle BSE and this new disease in
domestic cats, called Feline Spongiform Encephalopathy (FSE), are
linked. All but four of the approx. 100 FSE cases diagnosed worldwide
until April 2002 have been seen in the UK (DEFRA). One of the four
non-UK cases was diagnosed in Northern Ireland, one in Norway, one in
Liechtenstein, and one in 2001 in Switzerland. The most widely accepted
hypothesis, although not proven, is that the affected domestic cats were
exposed to BSE infectivity through contaminated commercial cat feed or
fresh slaughter offal that contained brain or spinal cord from cattle
BSE cases. An interesting observation is that in addition to domestic
cats, several large cats kept in zoos were diagnosed with FSE. Based on
data provided by the British ministry (DEFRA) until April 2002 5
cheetahs, 4 lions and 3 ocelots, pumas and tigers were affected. The
large cats that were diagnosed with FSE outside of the UK all originated
from UK zoos. It is suspected that these large cats acquired the
infection by being fed meat and bones of BSE-infected cattle. 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,restlessnessand 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). see: http://www.neurocenter-bern.ch/tse_e.shtml
There is a lot more information about each individual case of disease.
For example 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 and
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html
and http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf It now
seems clear that all of the cases of zoo cats (as felidiae) that have
been reported either were directly found in the UK or were exported from
the UK to the country in which the disease was reported. It is not so
much an export of animal food, but more of the animal exported itself.
The age of infection is not clear but seems to have been relatively
young because of this i.e. they could be exported when less than a year
old.
------------------------------------------------------------------------
References Br Med Bull. 2003;66:199-212. Other animal prion diseases.
Sigurdson CJ, Miller MW. Department of Microbiology, Immunology, and
Pathology, Colorado State University, Fort Collins, Colorado, USA. In
addition to bovine spongiform encephalopathy (BSE) of cattle and scrapie
of sheep and goats, a few other animal prion diseases have been
reported. These include feline spongiform encephalopathy of zoological
and domestic cats (FSE) and transmissible spongiform encephalopathy
(TSE) of zoological ruminants and non-human primates, as well as chronic
wasting disease of deer and elk (CWD) and transmissible mink
encephalopathy of farmed mink (TME). The origins of TSE in cats, zoo
bovids, and non-human primates are clearly linked to the BSE epidemic;
however, the origins of CWD and TME are less clear, but are not
epidemiologically linked to the BSE epidemic. Here we review the
epidemiology, transmission, clinical features and pathology of these
other animal prion diseases. Schweiz Arch Tierheilkd. 2002
Dec;144(12):664-73. [Beyond BSE: Transmissible spongiform
encephalopathies in other animal species] Heim D, Geiser F, Perler L,
Wyss R. Bundesamt fur Veterinarwesen, Bern-Liebefeld.
dagmar.heim@bvet.admin.ch There are several other diseases besides BSE
which belong to the group of transmissible spongiform encephalopathies
(TSE). Although most mammals can be experimentally infected with the
agent of these diseases, generally only single representatives of the
orders Artiodactyla (cloven-hoofed animals), Carnivora (carnivores) and
Primates (humans and monkeys) are naturally infected in the field. An
overview of the current state of knowledge on TSE in several species
like exotic ruminants, deer, mink and cats is presented. Etiological,
clinical, anatomic-pathological and epidemiological aspects are
described. Gene. 1997 Oct 15;199(1-2):283-6. Sequencing analysis of
prion genes from red deer and camel. Kaluz S, Kaluzova M, Flint
AP.University of Nottingham, Sutton Bonington Campus, Loughborough, UK.
virukalu@savba.sk An abnormal isoform of the prion protein (PrP) appears
to be the agent responsible for transmissible spongiform
encephalopathies (TSE). The normal isoform of PrP is host-encoded and
expressed in the central nervous system. The recent bovine spongiform
encephalopathy (BSE) epidemic in the UK and the incidence of
prion-related diseases in other animals could indicate that ruminants
are highly susceptible to infection via ingestion of prion-contaminated
food. Sequence analysis of PrP gene open reading frames from red deer
and camel was carried out to investigate sequence variability of these
genes among ruminants. (this article merely shows that the PrP gene of
the deer and camel are similar to those of sheep, cattle and
humans...but this is not surprising!)
------------------------------------------------------------------------
This an excellent review by Terry Singletary: see message on 1.3.5
concerning pet food manufacture and rulings.
http://www.priondata.org/data/A_deerdog.html


Pet Food


EU Pet food Legislation

http://www.useu.be/agri/petfood.html I just wonder with these new more
sensitive TSE testing coming out, what they might find, IF a real study
was funded and undertaken for TSEs in dogs? WELL heck, we can't even get
an honest TSE study in cattle in the USA, so i guess one in dogs or cats
would be way out of the question ... TSS

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