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From: TSS ()
Subject: FELINE AND CANINE ALZHEIMER'S OR MAD CAT and MAD DOG DISEASE FROM PET FOOD ???
Date: April 13, 2007 at 9:43 am PST

FELINE AND CANINE ALZHEIMER'S OR MAD CAT and MAD DOG DISEASE FROM PET FOOD ???

1ST AND FOREMOST, WE HAVE BEEN LIED TO ABOUT THE RISK FACTORS, SURVEILLANCE, AND ERADICATION OF TSE IN THE USA, ESPECIALLY, MAD COW DISEASE'S IN THE USA BOVINE. but this is only part of the problem. the USA has the most documented TSE i.e. mad cow disease's i.e. prion disease, in more species than any other country in the world. then we wonder why the elder are demented. that's another story too. i am here to talk about our feline and canine friends that we have all come to love as if they were part of the family, and mine are. but you must remember, all these species i speak of that have TSE in the USA have all been rendered and fed back to animals for human and animal consumption. and to take it a step further, from a very old investigative report from a van smith from the baltimore sun years ago; everything including a city police horse and a circus elephant went to the render. yes, and even your feline and canine friends are rendered and fed back to other animals, some of which you consume in some instances. are you disgusted yet? if not now, you will be. i will first document the truth about mad cow disease's in the USA as short as i can, then to follow will be more than you ever wanted to know about mad cow disease, including the story about the man and his cat with cjd i.e. mad cow disease in humans, nvcjd or one of 6 phenotypes of sporadic CJD, it really makes no difference, both are 100% fatal, and sporadic CJD is now tied to BSE and mad cow disease. ...TSS


USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...

64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.


snip...

http://www.seac.gov.uk/minutes/95.pdf


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***


6:30 Close of Day One


http://www.healthtech.com/2007/tse/day1.asp


SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resources-casereport.html

There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf

MADCOW Postcard from … Seoul
(READ AND SKROLL ALL THE WAY TO BOTTOM OF PAGE. ...TSS



Name: Terry S. Singeltary Sr. Date: Jan 26, 2007
Dear Terry S. Singeltary Sr.
My name in Seoungwon Lee and I work for National Assemblywoman (MP) Sang-Jeong Sim, in South Korea. Below is a message from Mr. Kwon. Please get back to us regarding the letter.
Thank you.
Seoungwon Lee
Legislative Assistant
National Assembly
Republic of Korea
Dear Terry S. Singeltary Sr.
Greetings from Korea.
I have learned about what you and your family have been through a internet. Being the father of a small family, I can only imagine the sense of loss that you and your family still must feel regarding your mother.


SNIP...FULL TEXT ;

http://www.fpif.org/fpiftxt/3940



10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007



Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI

___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007


http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html

the FDA ruminant to ruminant mad cow feed ban was nothing more than a piece of paper as you can see from the latest mad cow mbm feed ban above.


THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;


CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006


The U.S. Department of Agriculture was quick to assure the public earlier
this week that the third case of mad cow disease did not pose a risk to
them, but what federal officials have not acknowledged is that this latest
case indicates the deadly disease has been circulating in U.S. herds for at
least a decade.

The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is
thought that cows usually contract the disease from contaminated feed they
consume as calves. The concern is that humans can contract a fatal,
incurable, brain-wasting illness from consuming beef products contaminated
with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the
National Institutes of Health's Laboratory for Central Nervous System
Studies and an expert on mad cow-like diseases, told United Press
International. "The question was, 'How many?' and we still can't answer
that."

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before
one year ago" because of the agency's reluctance to retest the Texas cow
that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end


http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r


CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ...
Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central
Nervous System ... Address for correspondence: Paul Brown, Building 36, Room
4A-05, ...


http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm

PAUL BROWN COMMENT TO ME ON THIS ISSUE

Tuesday, September 12, 2006 11:10 AM


"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."


OR, what the Honorable Phyllis Fong of the OIG found ;


Audit Report

Animal and Plant Health Inspection Service

Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II

and

Food Safety and Inspection Service

Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III

Report No. 50601-10-KC January 2006

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain


http://www.usda.gov/oig/webdocs/50601-10-KC.pdf


EXPORTATION AND IMPORTATION OF ANIMALS AND ANIMAL PRODUCTS:
BSE; MRR AND IMPORTATION OF COMMODITIES, 65758-65759 [E6-19042]

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=3854


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&T=0&P=3381


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=498


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&T=0&P=10277


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=9972


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=4492


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2583


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2470




FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP
Re: FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP (4843 lines)
From: Terry S. Singeltary Sr. <[log in to unmask]>
Date: Mon, 2 Apr 2007 14:43:32 -0500

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=816




Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/

JOURNAL OF NEUROLOGY

MARCH 26, 2003


RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States


Email Terry S. Singeltary:


flounder@wt.net


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


http://www.neurology.org/cgi/eletters/60/2/176#535


BRITISH MEDICAL JOURNAL

SOMETHING TO CHEW ON

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2

BMJ

http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1

CJD WATCH

http://disc.server.com/Indices/236650.html

NOW, WHAT YOU NEVER WANTED TO HEAR ABOUT YOUR PET FOOD ;


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/science?_ob=ArticleURL&_udi=B6WJC-4K66F8J-2&_user=10&_handle=V-WA-A-W-AC-MsSAYZW-UUA-U-AAZDEDCEDY-AAZCCCZDDY-AWYBZZADA-AC-U&_fmt=summary&_coverDate=12%2F31%2F2006&_rdoc=10&_orig=browse&_srch=%23toc%236875%232006%23999919993%23636973!&_cdi=6875&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=9cb579124f38fbfaa6dd03422d3bd9ac


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 CJD was 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 rizzuto@Gorgorna.univr.it); 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: <3DAF5023.4080804@wt.net>

Dear Terry,
An excellent piece of review as this literature is desparately difficult
to get back from Government sites.

What happened with the deer was that an association between deer meat
eating and sporadic CJD was found in about 1993. The evidence was not great but did not
disappear after several years of asking CJD cases what they had eaten.
I think that the work into deer disease largely stopped because it was
not helpful to the UK industry...and no specific cases were reported.
Well, if you dont look adequately like they are in USA currenly then you
wont find any!

Steve Dealler
===============

Incubation periods for BSE are proportional to the life expectancy of
the animal affected. The disease's incubation period is 18% of a cow's
life expectancy and would be expected to about double when crossing to
another species [---] that is, to 36% of 70 years in humans.

Steve Dealler, consultant in medical microbiology.
Burnley General Hospital, Burnley BB10 2PQ deal@airtime.co.uk

TSS

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

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

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html


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

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.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_DocSum1:

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_DocSum1:


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 passage Human 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 diedof 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

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

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

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

SAME AS HUMANS, OR EVEN LESS, VERY VERY FEW............


i apologize for the length of this post. but it needed to be said.


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




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