EP-021 Canine Prions: A New Form of Prion Disease
Mourad Tayebi1, Monique A David2, Brian Summers3
1 University of Melbourne, Veterinary Sciences, Australia; 2Ausbiologics,
Sydney, Australia; 3Royal Veterinary College, London, UK
The origin of bovine spongiform encephalopathy (BSE), which rapidly evolved
into a major epidemic remains unresolved and was initially widely attributed to
transmission of sheep scrapie to cattle with contaminated feed prepared from
rendered sheep carcasses. Alternative transmission hypotheses also include feed
contaminated with unrecognized subclinical case(s) of bovine prion disease or
with prion-infected human remains. However, following the demonstration of a BSE
case exhibiting the novel mutation E211 K, similar to the E200K mutation
associated with most genetic CJD in humans, support for a genetic origin of
prion disease in cattle is gaining momentum. In contrast to other animal species
such as feline, the canine species seems to be resistant to prion disease as no
canine prion cases were previously reported.
We describe here three cases of Rottweiler puppy (called RWD cases) with
neurological deficits and spongiform change. We used animal bioassays and in
vitro studies to show efficient interspecies transmission of this novel canidae
prion isolate to other species.
Biochemical studies revealed the presence of partially proteinase K
(PK)-resistant fragment and immunohistochemistry displayed staining for PrPSc in
the cerebral cortex. Importantly, interspecies transmission of canine PrPSc
derived from RWD3 brain homogenates following inoculation of hamsters led to
signs of prion disease and replication of PrPSc in brains, spinal cords and
spleens of these animals.
These findings if confirmed by further cases of prion disease in canidae
and regardless of the origin of the disease would have a major impact on animal
and public health.
PRION 2016 TOKYO
*** DEFRA TO SINGELTARY ON HOUND STUDY AND BSE 2001 ***
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904
6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long
delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform
Encephalopathy Advisory Committee (SEAC), the UK Government's independent
Advisory Committee on all aspects related to BSE-like disease, gave the hound
study detailed consideration at their meeting in January 1994. As a summary of
this meeting published in the BSE inquiry noted, the Committee were clearly
concerned about the work that had been carried out, concluding that there had
clearly been problems with it, particularly the control on the histology, and
that it was more or less inconclusive. However was agreed that there should be a
re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound
study to see if any useful results could be gained from it. The Chairman
concluded that there were varying opinions within the Committee on further work.
It did not suggest any further transmission studies and thought that the lack of
clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as
conducted. As a result it is likely that the authors felt that it would not
stand up to r~eer review and hence it was never published. As noted above, and
in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether
additional work should be performed to examine dogs for evidence of TSE
infection. Although the Committee had mixed views about the merits of conducting
further work, the Chairman noted that when the Southwood Committee made their
recommendation to complete an assessment of possible spongiform disease in dogs,
no TSEs had been identified in other species and hence dogs were perceived as a
high risk population and worthy of study. However subsequent to the original
recommendation, made in 1990, a number of other species had been identified with
TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry,
gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership
of the data essentially remains with the original researchers. Thus
unfortunately, I am unable to help with your request to supply information on
the hound survey directly. My only suggestion is that you contact one of the
researchers originally involved in the project, such as Gerald Wells. He can be
contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases
of spongiform encephalopathy in animals and poultry were made notifiable. Hence
since that date there has been a requirement for vets to report any suspect SE
in dogs for further investigation. To date there has never been positive
identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's
minute.
I do NOT think that we can justify devoting any resources to this study,
especially as larger and more important projects such as the pathogenesis study
will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound
brains then it should be passed entirely to the VI Service.
J W WILESMITH Epidemiology Unit 18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would
by the end of the year, indentify the three brains that were from the
''POSITIVE'' end of the lesion spectrum.
TSE in dogs have not been documented simply because OF THE ONLY STUDY,
those brain tissue samples were screwed up too. see my investigation of this
here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS
BRAIN TISSUE SAF's. ...TSS
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to
other species will invariably present pathology typical of a scrapie-like
disease.
snip...
76 pages on hound study;
snip...
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).
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...
NEW URL ;
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an
unrecognized sporadic or genetic case of bovine prion disease incorporated into
cattle feed or even cattle feed contaminated with prion-infected human remains.1
However, strong support for a genetic origin of BSE has recently been
demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2
Furthermore, a specific prion protein strain causing BSE in cattle is believed
to be the etiological agent responsible for the novel human prion disease,
variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in
a number countries, including France, Italy, Ireland, the Netherlands, Canada,
Japan, US and the UK with the largest number of cases. Naturally occurring
feline spongiform encephalopathy of domestic cats4 and spongiform
encephalopathies of a number of zoo animals so-called exotic ungulate
encephalopathies5,6 are also recognized as animal prion diseases, and are
thought to have resulted from the same BSE-contaminated food given to cattle and
humans, although and at least in some of these cases, a sporadic and/or genetic
etiology cannot be ruled out. The canine species seems to display resistance to
prion disease and no single case has so far been reported.7,8 Here, we describe
a case of a 9 week old male Rottweiler puppy presenting neurological deficits;
and histological examination revealed spongiform vacuolation characteristic of
those associated with prion diseases.9 Initial biochemical studies using
anti-PrP antibodies revealed the presence of partially proteinase K-resistant
fragment by western blotting. Furthermore, immunohistochemistry revealed
spongiform degeneration consistent with those found in prion disease and
displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross
the species barrier transmitted to hamster in vitro with PMCA and in vivo (one
hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100%
attack rate (n = 4) and animals displayed untypical lesional profile and shorter
incubation period.
In this study, we show that the canine species might be sensitive to prion
disease and that PrPSc isolated from a dog can be transmitted to dogs and
hamsters in vitro using PMCA and in vivo to hamsters.
If our preliminary results are confirmed, the proposal will have a major
impact on animal and public health and would certainly lead to implementing new
control measures for ‘canine spongiform encephalopathy’ (CSE).
References 1. Colchester AC, Colchester NT. The origin of bovine spongiform
encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61;
PMID:16139661; http://
dx.doi.org/10.1016/S0140-6736(05)67218-2.
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation.
PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal.
ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy
(BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/
hmg/6.10.1699.
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith
JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic
cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus
angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI.
Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu
(Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink
encephalopathy species barrier effect between ferret and mink: PrP gene and
protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317-
75-11-2947.
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et
al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad
Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30;
PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.
=======================================
2013
Strain characteristics of the in vitro-adapted rabbit and dog BSE agent
remained invariable with respect to the original cattle BSE prion, suggesting
that the naturally low susceptibility of rabbits and dogs to prion infections
should not alter their zoonotic potential if these animals became infected with
BSE.
=======================================
Neurobiology of Disease
Bovine Spongiform Encephalopathy Induces Misfolding of Alleged
Prion-Resistant Species Cellular Prion Protein without Altering Its
Pathobiological Features
Enric Vidal3, Natalia Fernández-Borges1, Belén Pintado4, Montserrat
Ordóñez3, Mercedes Márquez6, Dolors Fondevila5,6, Juan María Torres7, Martí
Pumarola5,6, and Joaquín Castilla1,2 + Author Affiliations
1CIC bioGUNE, 48160 Derio, Bizkaia, Spain,
2IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Bizkaia, Spain,
3Centre de Recerca en Sanitat Animal, Campus de la Universitat Autònoma de
Barcelona (UAB)-IRTA, 08193 Bellaterra, Barcelona, Spain,
4Centro Nacional de Biotecnología, Campus de Cantoblanco, 28049
Cantoblanco, Madrid, Spain,
5Department of Animal Medicine and Surgery, Veterinary Faculty, UAB, 08193
Bellaterra (Cerdanyola del Vallès), Barcelona, Spain,
6Murine Pathology Unit, Centre de Biotecnologia Animal i Teràpia Gènica,
UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, and
7Centro de Investigación en Sanidad Animal-Instituto Nacional de
Investigación y Tecnología Agraria y Alimentaria, 28130 Valdeolmos, Madrid,
Spain
Author contributions: E.V., N.F.-B., and J.C. designed research; E.V.,
N.F.-B., B.P., M.O., M.M., D.F., and J.C. performed research; E.V., N.F.-B.,
B.P., and J.C. contributed unpublished reagents/analytic tools; E.V., N.F.-B.,
B.P., M.O., M.M., D.F., J.M.T., M.P., and J.C. analyzed data; E.V. and J.C.
wrote the paper.
Abstract
Bovine spongiform encephalopathy (BSE) prions were responsible for an
unforeseen epizootic in cattle which had a vast social, economic, and public
health impact. This was primarily because BSE prions were found to be
transmissible to humans. Other species were also susceptible to BSE either by
natural infection (e.g., felids, caprids) or in experimental settings (e.g.,
sheep, mice). However, certain species closely related to humans, such as canids
and leporids, were apparently resistant to BSE. In vitro prion amplification
techniques (saPMCA) were used to successfully misfold the cellular prion protein
(PrPc) of these allegedly resistant species into a BSE-type prion protein. The
biochemical and biological properties of the new prions generated in vitro after
seeding rabbit and dog brain homogenates with classical BSE were studied.
Pathobiological features of the resultant prion strains were determined after
their inoculation into transgenic mice expressing bovine and human PrPC. Strain
characteristics of the in vitro-adapted rabbit and dog BSE agent remained
invariable with respect to the original cattle BSE prion, suggesting that the
naturally low susceptibility of rabbits and dogs to prion infections should not
alter their zoonotic potential if these animals became infected with BSE. This
study provides a sound basis for risk assessment regarding prion diseases in
purportedly resistant species.
Received January 18, 2013. Revision received March 7, 2013. Accepted March
23, 2013. Copyright © 2013 the authors 0270-6474/13/337778-09$15.00/0
Friday, March 8, 2013
Dogs may have been used to make Petfood and animal feed
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND
NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease
Association 2011
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
*** Singeltary reply ; Molecular, Biochemical and Genetic
Characteristics of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
see page 17 6 of 201 pages...tss
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Freas, William
From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Monday, January 08,2001 3:03 PM
TO: freas@CBS5055530.CBER.FDA.GOV
Subject: CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To
Scientific Advisors and Consultants Staff January 2001 Meeting (short
version)
CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific
Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and
Consultants Staff 2001 Advisory Committee (short version).
I understand the reason of having to shorten my submission, but only hope
that you add it to a copy of the long version, for members to take and read at
their pleasure, (if cost is problem, bill me, address below). So when they
realize some time in the near future of the 'real' risks i speak of from
human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk
of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt
here:
remember AIDS/HIV, 'no problem to heterosexuals in the U.S.? no need to go
into that, you know of this blunder:
DO NOT make these same stupid mistakes again with human/animal TSE's aka
MADCOW DISEASE. I lost my Mom to hvCJD, and my neighbor lost his Mother to sCJD
as well (both cases confirmed). I have seen many deaths, from many diseases. I
have never seen anything as CJD, I still see my Mom laying helpless, jerking
tremendously, and screaming "God, what's wrong with me, why can't I stop this".
I still see this, and will never forget. Approximately 10 weeks from 1st of
symptoms to death. This is what drives me. I have learned more in 3 years about
not only human/animal TSE's but the cattle/rendering/feeding industry/government
than i ever wished to.
I think you are all aware of CJD vs vCJD, but i don't think you all know
the facts of human/animal TSE's as a whole, they are all very very similar, and
are all tied to the same thing, GREED and MAN.
I am beginning to think that the endless attempt to track down and ban,
potential victims from known BSE Countries from giving blood will be futile. You
would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT
SWIFTLY to find blood test for TSE's, whether it be blood test, urine test,
.eyelid test, anything at whatever cost, we need a test FAST.
DO NOT let the incubation time period of these TSEs fool you.
To think of Scrapie as the prime agent to compare CJD, but yet overlook the
Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by
scrapie from a vaccine made of scrapie infected sheep brains, would be foolish.
I acquired this full text version of the event which was recorded in the Annual
Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. from the
BVA and the URL is posted in my (long version).
U.S.A. should make all human/animal TSE's notifiable at all ages, with
requirements for a thorough surveillance and post-mortem examinations free of
charge, if you are serious about eradicating this horrible disease in man and
animal.
There is histopathology reports describing o florid plaques" in CJD victims
in the USA and some of these victims are getting younger. I have copies of such
autopsies, there has to be more. PLUS, sub-clinical human TSE's will most
definitely be a problem.
THEN think of vaccineCJD in children and the bovine tissues used in the
manufacturing process, think of the FACT that this agent surviving 6OO*C. PNAS
-- Brown et al. 97 (7): 3418 scrapie agent live at 600*C
Then think of the CONFIDENTIAL documents of what was known of human/animal
TSE and vaccines in the mid to late 80s, it was all about depletion of stock, to
hell with the kids, BUT yet they knew. To think of the recall and worry of TSE's
from the polio vaccine, (one taken orally i think?), but yet neglect to act on
the other potential TSE vaccines (inoculations, the most effective mode to
transmit TSEs) of which thousands of doses were kept and used, to deplete
stockpile, again would be foolish.
--Oral polio; up to 1988, foetal calf serum was used from UK and New
Zealand (pooled); since 1988 foetal calf serum only from New Zealand. Large
stocks are held.
--Rubella; bulk was made before 1979 from foetal calf serum from UK and New
Zealand. None has been made as there are some 15 years stock.
--Diphtheria; UK bovine beef muscle and ox heart is used but since the end
of 1988 this has been sourced from Eire. There are 1,250 litres of stock.
--Tetanus; this involves bovine material from the UK mainly Scottish. There
are 21,000 litres of stock.
--Pertussis; uses bovine material from the UK. There are 63,000 litres of
stock. --They consider that to switch to a non-UK source will take a minimum of
6-18 months and to switch to a non-bovine source will take a minimum of five
years.
3. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These are
sourced from the USA and the company believes that US material only is
used.
89/2.14/2.1
============
BSE3/1 0251
4. XXXXXXXXXXX have a measles vaccine using bovine serum from the UK. there
are 440,000 units of stock. They have also got MMR using bovine serum from the
UK.
5. XXXXXXXXXXX have influenza, rubella, measles,' MMR vaccines likely to be
used in children. Of those they think that only MMR contains bovine material
which is probably a French origin.
6. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial. hese
use veal material, some of which has come from the UK and has been ade by
XXXXXXXXXXX (see above).
I have documents of imports from known BSE Countries, of ferments, whole
blood, antiallergenic preparations,
2
human blood plasma, normal human blood sera, human immune blood sera, fetal
bovine serum, and other blood fractions not elsewhere specified or included,
imported glands, catgut, vaccines for both human/animal, as late as 1998. Let us
not forget about PITUITARY EXTRACT. This was used to help COWS super ovulate.
This tissue was considered to be of greatest risk of containing BSE and
consequently transmitting the disease.
ANNEX 6
MEETING HELD ON 8 JUNE 1988 TO DISCUSS THE IMPLICATIONS OF BSE TO
BIOLOGICAL PRODUCTS CONTAINING BOVINE - EXTRACTED MATERIAL
How much of this was used in the U.S.?
Please do not keep making the same mistakes; 'Absence of evidence is not
evidence of absence'.
What are the U.S. rules for importing and manufacturing vaccines, medicines
and medical devices?
Does the U.S.A. allow sourcing of raw material of ruminants from the
U.S.A.?
U.S. cattle, what kind of guarantee can you give for serum or tissue donor
herds? . The U.S. rendering system would easily amplify T.S.E.'s:
Have we increased the stability of the system (improved heat treatments)
since the EU SSC report on the U.S.A. was published in july 2000?
What is done to avoid cross-contaminations in the U.S.A.?
How can the U.S. control absence of cross-contaminations of animal TSE's
when pig and horse MBM and even deer and elk are allowed in ruminant feed, as
well as bovine blood? I sadly think of the rendering and feeding policy before
the Aug. 4, 1997 'partial' feed ban, where anything went, from the city police
horse, to the circus elephant, i will not mention all the scrapie infected
sheep. I am surprised that we have not included man 'aka soyent green'. It is a
disgusting industry and nothing more than greed fuels it.
When will the U.S.. start real surveillance of the U.S. bovine population
(not passive, this will not work)?
When will U.S. start removing SRMs?
Have they stopped the use of pneumatic stunners in the U.S.?
If so, will we stop it in all U.S. abattoirs or only in those abattoirs
exporting to Europe?
If not, WHY NOT?
same questions for removal of SRM in the U.S.A., or just for export?
If not, WHY NOT?
How do we now sterilize surgical/dental instruments in the U.S.A.?
Where have we been sourcing surgical catgut?
(i have copies of imports to U.S., and it would floor you) hen will
re-usable surgical instruments be banned?
'Unregulated "foods" such as 'nutritional supplements' containing various
extracts from ruminants, whether imported or derived from
3
US cattle/sheep/cervids ("antler velvet" extracts!) should be forbidden or
at least very seriously regulated. (neighbors Mom, whom also died from CJD, had
been taking bovine based supplement, which contained brain, eye, and many other
bovine/ovine tissues for years, 'IPLEX').
What is the use of banning blood or tissue donors from Germany, France,
etc... when the U.S.A. continues exposing cattle, sheep and people to SRM,
refuses to have a serious feed ban, refuses to do systematic
BSE-surveillance?
The FDA should feel responsible for the safety of what people eat, prohibit
the most dangerous foods, not only prohibit a few more donors - the FDA should
be responsible for the safe sourcing of medical devices, not only rely on
banning donors "from Europe", The 'real' risks are here in the U.S. as well, and
nave been for some time.
We must not forget the studies that have proven infectivity in blood from
TSE's.
The Lancet, November 9, 1985
Sir, --Professor Manuelidis and his colleagues (Oct 19, p896) report
transmission to animals of Creutzfeldt-Jakob disease (CJD) from the buffy coat
from two patients. We also transmitted the disease from, whole blood samples of
a patient (and of mice) infected with CJD.l Brain, Cornea, and urine from this
patient were also infectious, and the clinicopathological findings2 are
summarised as follows.
snip...
Samples,were taken aseptically at necropsy. 10% crude homogenates of brain
and cornea in saline, whole blood (after crushing a clot), and untreated CSF and
urine were innoculated intracerebrally into CFl strain mice (20 ul per animal).
Some mice showed emaciation, bradykinesia, rigidity of the body and tail, and
sometimes tremor after long incubation periods. Tissues obtained after the
animal died (or was killed) were studied histologically (table). Animals
infected by various inocula showed common pathological changes, consisting of
severe spongiform changes, glial proliferation, and a moderate loss of nerve
cells. A few mice inoculated with brain tissue or urine had the same amyloid
plaques found in patients and animals with CJD.3
snip...
Department of Neuropathology,. Neurological Institute, Faculty of Medicine,
Kyushu University, Fukuoka812, Japan JUN TATEISHI
(full text-long version)
and
CWD and transmission to man will be no different than other TSE's.
"Clearly, it is premature to draw firm conclusions about CWD passing
naturally into humans, cattle and sheep, but the present results suggest that
CWD transmissions to humans would be as limited by PrP incompatibility as
transmissions of BSE or sheep scrapie to humans. Although there is no evidence
that sheep scrapie has affected humans, it is likely that BSE has
4
caused variant CJD in 74 people (definite and probable variant CJD cases to
date according to the UK CJD Surveillance Unit). Given the presumably large
number of people exposed to BSE infectivity, the susceptibility of humans may
still be very low compared with cattle, which would be consistent with the
relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since
humans have apparently been infected by BSE, it would seem prudent to take
reasonable measures to limit exposure of humans (as well as sheep and cattle) to
CWD infectivity as has been recommended for other animal TSEs,"
G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O'Rourke3, L.E. McHolland4,
P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M. Smits2 and B.
Caughey1,7
or more recently transmission of BSE to sheep via whole blood Research
letters Volume 356, Number 9234 16 September 2000
Transmission of BSE by blood transfusion in sheep
Lancet 2000; 356: 999 – 1000
F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock
See Commentary
"We have shown that it is possible to transmit bovine spongiform
encephalopathy (BSE) to a sheep by transfusion with whole blood taken from
another sheep during the symptom-free phase of an experimental BSE infection.
BSE and variant Creutzfeldt-Jakob disease (vCJD) in human beings are caused by
the same infectious agent, and the sheep-BSE experimental model has a similar
pathogenesis to that of human vCJD. Although UK blood transfusions are
leucodepleted--a possible protective measure against any risk from blood
transmission-- this report suggests that blood donated by symptom-free
vCJD-infected human beings may represent a risk of spread of vCJD infection
among the human population of the UK."
"The demonstration that the new variant of Creutzfeldt-Jakob disease (vCJD)
is caused by the same agent that causes bovine spongiform encephalopathy (BSE)
in cattle1 has raised concerns that blood from human beings in the symptom-free
stages of vCJD could transmit infection to recipients of blood transfusions
(full text long version)"
and...
"The large number of cases (1040), temporal clustering of the outbreaks (15
in the first 6 months of 1997), the high in-flock incidence, and the exceptional
involvement of goats (390 cases), suggested an accidental infection. The source
of the epidemic might have been TSE-contaminated meat and bonemeal, but eight
flocks had never been fed any commercial feedstuff. Infection might have risen
from the use of a formol-inactivated vaccine against contagious agalactia
prepared by a single laboratory with brain and mammary gland homogenates of
sheep infected with Mycoplasma agalactiae. Although clinical signs of TSE in the
donor sheep have not been found, it is possible that one or more of them were
harbouring the
5
infectious agent. Between 1995 and 1996, this vaccine was given
subcutaneously to 15 of the affected flocks (to one flock in 1994) ; in these
animals the disease appeared between 23 and 35 months after vaccination. No
information is available for herd 13 because it was made up of stolen animals.
Sheep from the remaining three flocks (1-3, figure) did not receive the vaccine,
thus suggesting a naturally occurring disease.’’ (again, full text long
version).
IN SHORT, please do under estimate this data and or human/animal TSE's
including CWD in the U.S.A.
A few last words, please.
The cattle industry would love to have us turn our focus to CWD and forget
about our own home grown TSE in Bovines. This would be easy to do. Marsh's work
was from downer cattle feed, NOT downer deer/elk feed. This has been
proven.
DO NOT MAKE THAT MISTAKE.
There should be NO LESS THAN 1,000,000 tests for BSE/TSE ' in 2001 for
U.S.A. French are testing 20,000 a week. The tests are available. Why wait until
we stumble across a case from passive surveillance, by then it is to late. IF we
want the truth, this is a must???
United States Total ,Bovine Brain Submissions by State,
May 10 ,1990 thru October 31, 2000
Total 11,700
FROM 1.5 BILLION HEAD OF CATTLE since 1990 ???
with same feeding and rendering practices as that of U.K. for years and
years, same scrapie infected sheep used in feed, for years and years, 950
scrapie infect FLOCKS in the U.S. and over 20 different strains of scrapie known
to date. (hmmm, i am thinking why there is not a variant scrapie, that is
totally different than all the rest)? just being sarcastic.
with only PARTIAL FEED BAN implemented on Aug. 4, 1997??? (you really need
to reconsider that blood meal etc. 'TOTAL BAN')
AND PLEASE FOR GODS SAKE, STOP saying vCJD victims are the only ones tied
to this environmental death sentence. "PROVE IT". It's just not true. The
'CHOSEN ONES' are not the only ones dying because of this man-made death
sentence. When making regulations for human health from human/animal TSEs, you
had better include ALL human TSE's, not just vCJD. Do NOT underestimate sporadic
CJD with the 'prehistoric' testing available to date. This could be a deadly
mistake. Remember, sCJD kills much faster from 1st onset of symptoms to death,
and hvCJD is the fastest. Could it just be a higher titre of infectivity, or
route or source, or all three?
Last, but not least. The illegal/legal harvesting of body parts and tissues
will come back to haunt you. Maybe not morally, but due to NO background checks
and human TSEs, again it will continue to spread.
Stupidity, Ignorance and Greed is what fuels this disease. You must stop
all of this, and ACT AT ONCE...
Sent: Monday, January 08,2001 3:03 PM
TO: freas@CBS5055530.CBER.FDA.GOV
FDA CJD BSE TSE Prion Scientific Advisors and Consultants Staff January
2001 Meeting Singeltary Submission
2001 FDA CJD TSE Prion Singeltary Submission
Tuesday, August 4, 2015
FDA U.S. Measures to Protect Against BSE
Terry S. Singeltary Sr.
