STRICTLY IN CONFIDENCE
EXTRACT FROM MINUTES OF SCIENTIFIC COMMITTEE MEETING HELD ON 29 SEPTEMBER
1994
BSE: S33/94
a) Sampling of Ruminant Feeding stuffs for Ruminant Protein:
The voluntary sampling‘ on farms with suspected cases of BSE had commenced
on 1 July 1994. The ELISA technique detected the presence of ruminant meat and
bone meal to a level of 0.25% in finished feeding stuffs. MAFF had released a
pre-publication copy of a paper discussing this technique which had been
developed at the VI Centre Luddington. It provided detail of the use of the
technique in meat and bone meal. It did not, however, discuss the extension of
the assay for use in compound feeding stuffs. At the request of UKASTA, MAFF was
looking at making the service commercially available in order for individual
compounders to do their own testing. MAFF estimated that the charge for such
testing would be £35 per sample (plus VAT).
It was reported that Luddington was carrying out further work in
identifying potential sources of interference, from individual raw materials,
which might produce a false positive result It was understood that glutens were
considered to present a particular problem. During a discussion the Committee
suggested that the conditioning temperatures, in different mills, might have
varying effects on the breakdown of proteins in animal feeding stuffs.
A number of sites where cross contamination between animal proteins and
other types of raw materials might occur were identified. These included not
only on-farm but in-store, in the country of origin, in boats, in transport as
well as different points within the feed mill. It was noted, however, that it
might be counter productive to stress these varying numbers and sites.
Concern was expressed that the MAFF had commenced on-farm testing without
necessarily thinking through the consequences for the whole of the agricultural
industry. Officials were aware that one course of action open to feed
compounders was to stop using meat and bone meal in the manufacture of any
feeding stuff. An alternative for the industry was the establishment of ruminant
feed only Such a step would only be open to those companies with more than one
manufacturing site.
Cont'd/...2
94/9.29/3.1
b)
-2-
A decision by the industry as a whole to stop using meat and bone meal
would have cost implications for the whole livestock industry. Not only would
there be poorer returns to beef producers but also higher raw material costs for
compounders when producing pig and poultry feeding stuffs. There would also be
the problem of disposing of the unwanted animal by-products. Thus, it was agreed
that whatever the actual consequences the effect o:n the livestock industry as a
whole would be very damaging.
Proposed Survey of Past a.nd Present Practices in Members Feed Mills:
A copy of the draft questionnaire was circulated to Committee members
“Strictly in Confidence". This was designed to investigate the likelihood that
feed produced after the introduction of the ruminant feed ban could have become
contaminated with ruminant derived protein and whether the likelihood of
contamination had changed over time. In discussing the contents, UKASTA had not
given any indication, on behalf of members, that they wanted them to complete
the questionnaire when finalised. MAFF had also been made fully aware of
UKASTA's concern that information submitted in response to the questionnaire by
individual companies might, at some future time, be subpoenaed by a Court. This
would be in any case taken against the company by a farmer seeking compensation
for BSE in his herd.
The Committee was advised that a member company was still in debate over a
case concerning the Fowl Pest outbreak in 1984. Lawyers acting for poultry
producers had. submitted subpoenas for relevant Ministry documents. MAFF Legal
Department was looking at the papers and aimed to resist the subpoena. However,
the outcome of this action would not be known until March 1995. At the very
least, it was considered that compounders should not: complete the questionnaire
until the outcome of the Fowl Pest discussions were known. It was also reported
that another company had been recommended, by its legal advisors, not to
complete the questionnaire.
At a scientific level, it was noted that the aim of the CVL was to explain
why BABs had occurred. Unfortunately, in the investigations it was necessary to
identify the name and address of individual mills on the questionnaire in order
to reconcile information on BABs regarding feeding practices on farm. It would
not be possible for questionnaires to be sent to the CVL via UKASTA on an
anonymous basis. UKASTA was seeking guidance from the Association's solicitors
on what powers MAFF might have to require completion of the questionnaire.
It was suggested that whilst the CVL was finalising details of the
questionnaire UKASTA should co-operate. Thus members were asked to send to the
Secretariat their comments on the contents of the questionnaire by mid-November.
Views were particularly required on which questions were difficult and/ or
impossible to answer both because they were
Cont'd/...3 94/9.29/3.2
-3-
impractical as well as being able to put individual companies in a
vulnerable position. These were to be passed on to the CVL with a request for
amendments and/ or detailed responses in time for the Committee to discuss at
the December meeting. Members were asked to discuss the questionnaire with as
few people as possible because of the sensitive nature of this subject.
Members were also asked to keep the Secretariat informed of the nature of
any enquiries which MAFF officials might address to them. It was also noted, by
one member company who no longer used meat and bone meal, that since taking such
action they had not received any queries from MAFF.
C) Recent Legislation:
The MAFF was implementing the two EU Decisions agreed in May. The ban on
the use of mammalian meat and bone meal in ruminant feedingstuffs was to be
incorporated into the BSE Order. At the same time the SBO ban was to be extended
to cover the thymus and intestines of calves less than six months of age.
The European legislation on the rendering industry introduced a processing
time/ temperature combination based on the results of rendering trials which had
achieved an 80-fold diminution of the BSE agent. The legislation was not due to
be brought into operation until the end of 1994. It was, however, hoped that UK
rendering plants could have their processes validated and thus be in compliance
with the new legislation by the end of October. Although it was not possible to
prove zero infectivity, MAFF considered that adherence to the new standards
would be a huge step forward in the control of BSE.
The Ministry was also reviewing the SBO legislation in order to make it
more straightforward an.d simple to operate. The Committee also noted that,
because of the nature of the material concerned, it would be extremely difficult
to enforce the legislation. Concern was expressed, therefore, that the Ministry
might just be introducing controls on paper. Effective auditing of the
legislation should be introduced; for example by weighing the amount of SBO's
collected and comparing this against the number of animals slaughtered.
In the light of all these concerns, the Committee considered that an easy
reaction would be for the feed industry to stop using meat and bone meal in the
manufacture of any animal feeding stuff. However, whereas this would be
relatively painless, if somewhat expensive, for the feed industry, it would have
serious repercussions throughout the whole of the livestock industry. It would
also beg the question as to why it was safe for humans to eat meat whilst the
by-products of the butchery trade that we use to produce meat and bone meal were
unsatisfactory for animals.
Cont'd/...4
94/9.29/3.3
-4-
d) Origins of BSE:
A transcript of the Radio 4 interview with Mr. Keith Meldrum, Chief
Veterinary Officer, held on 22 September was circulated. This raised the
possibility of BSE being of bovine as opposed to ovine origin. Clarification
had, therefore, been sought from the CVL. The response was that it was not
possible to dismiss the possibility that BSE was bovine in origin. However, it
was more difficult to support such a theory given current knowledge whereby the
BSE epidemic had seen a sudden increase in numbers in the mid 1980's. It was
thus still considered that the epidemic was explained by :-
- High level of sheep numbers in the UK;
- A change in the rendering practices in the late 1970's which permitted
infected ovine material to survive the production process;
- The recycling of bovine material in the cattle population.
For BSE to be solely of bovine origin there would have had to have been a
high prevalence of infected animals prior to the mid—1980‘s and this was not
seen. It was thus possible that there was an element of politics in the comments
made by Mr. Meldrum and it was probably no coincidence that a report of possible
BSE cases in northern Germany had emerged at about the same time.
Meeting with Minister:
The Committee was advised that if necessary the Association would
request
a meeting with the Minister to outline members‘ concerns regarding BSE and
associated matters.
94/9.29/3.4
TEXAS One sorghum DDGS sample out of 168 DG samples was contaminated with
bovine spongiform encephalopathy, but the transmission route of the bovine
spongiform encephalopathy agent could not be clearly defined.
J Food Prot. 2015 Oct;78(10):1861-9. doi: 10.4315/0362-028X.JFP-15-157.
Evaluation of Selected Nutrients and Contaminants in Distillers Grains from
Ethanol Production in Texas.
Lee KM1, Herrman TJ2. Author information 1Office of the Texas State
Chemist, Texas A&M AgriLife Research, Texas A&M University System,
College Station, Texas 77841, USA. kml@otsc.tamu.edu. 2Office of the Texas State
Chemist, Texas A&M AgriLife Research, Texas A&M University System,
College Station, Texas 77841, USA.
Abstract
This study evaluated distillers grain (DG) by-products produced in
different ethanol plants and supplemented in animal diets in Texas, based on
samples analyzed from 2008 to 2014. The samples were assessed for concentration,
occurrence, and prevalence of selected nutrients and contaminants. Protein and
sulfur contents of DG were largely different between corn and sorghum
by-products as well as wet distillers grain with solubles and dry distillers
grain with solubles (DDGS), indicating a significant effect of grain feedstock
and dry-grind process stream on DG composition and quality. Salmonella was
isolated in 4 DDGS samples out of a total of 157 DG samples, a percentage (2.5%)
that is much lower than the percentage of Salmonella-positive samples found in
other feed samples analyzed during the same period. A small amount of
virginiamycin residue was found in 24 corn DDGS, 1 corn wet distillers grain
with solubles, and 2 sorghum DDGS samples out of 242 samples in total. One
sorghum DDGS sample out of 168 DG samples was contaminated with bovine
spongiform encephalopathy, but the transmission route of the bovine spongiform
encephalopathy agent could not be clearly defined. The concentrations of
aflatoxin and fumonisin DG by-products averaged 3.4 μg/kg and 0.7 mg/kg,
respectively. Among contaminated corn DG samples, five DDGS samples for
aflatoxin contained a higher concentration than the U.S. Food and Drug
Administration action level for use in animal feed, whereas no sample for
fumonisin was found above the action level. The study results raised some
important issues associated with the quality and use of DG by-products,
suggesting several approaches and strategies for their effective and safe use as
a feed ingredient to promote animal and human health and welfare.
PMID: 26408135 [PubMed - in process]
Sunday, September 27, 2015
TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE
SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
please note, the author of this study contacted me ;
corrected to
"One sorghum DDGS out of 168 DG samples was contaminated with animal
protein prohibited for use in ruminant feed and was channeled to poultry feed."
We requested the journal editor to correct some errors and the relevant
statements, or to withdraw the article from the journal.
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
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
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s 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.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
*** 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 176 of 201 pages...tss
P.97: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and
Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State
University; Ames, IA USA
The purpose of this work was to determine susceptibility of white-tailed
deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to
that of the original inoculum and chronic wasting disease (CWD). We inoculated
WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5)
with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues at preclinical time points,
and deer necropsied after 28 months post-inoculation had clinical signs,
spongiform encephalopathy, and widespread distribution of PrPSc in neural and
lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular
profiles. WB on cerebral cortex had a profile similar to the original scrapie
inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc
with a higher profile resembling CWD. Homogenates with the 2 distinct profiles
from WTD with clinical scrapie were further passaged to mice expressing cervid
prion protein and intranasally to sheep and WTD. In cervidized mice, the 2
inocula have distinct incubation times. Sheep inoculated intranasally with WTD
derived scrapie developed disease, but only after inoculation with the inoculum
that had a scrapie-like profile. The WTD study is ongoing, but deer in both
inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary,
this work demonstrates that WTD are susceptible to the agent of scrapie, 2
distinct molecular profiles of PrPSc are present in the tissues of affected
deer, and inoculum of either profile readily passes to deer.
From: Terry S. Singeltary Sr.
Sent: Tuesday, December 01, 2015 5:05 PM
To: Terry Singeltary Sr.
Subject: Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry
Singeltary Sr. Submission
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
SUMMARY: We are reopening the comment period for our proposed rule that
would revise completely the scrapie regulations, which concern the risk groups
and categories established for individual animals and for flocks, the use of
genetic testing as a means of assigning risk levels to animals, movement
restrictions for animals found to be genetically less susceptible or resistant
to scrapie, and recordkeeping requirements. This action will allow interested
persons additional time to prepare and submit comments.DATES: The comment period
for the proposed rule published on September 10, 2015 (80 FR 54660-54692) is
reopened. We will consider all comments that we receive on or before December 9,
2015. ...
Comment from Terry Singeltary This is a Comment on the Animal and Plant
Health Inspection Service (APHIS) Proposed Rule: Scrapie in Sheep and
Goats
For related information, Open Docket Folder Docket folder icon
--------------------------------------------------------------------------------
Show agency attachment(s) AttachmentsView All (0)
--------------------------------------------------------------------------------
Comment View document:Indeed, much science has changed about the Scrapie
TSE prion, including more science linking Scrapie to humans. sadly, politics,
industry, and trade, have not changed, and those usually trump sound science, as
is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease
in livestock producing animals and the OIE. we can look no further at the legal
trading of the Scrapie TSE prion both typical and atypical of all strains, and
CWD all stains. With as much science of old, and now more new science to back
this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and
CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge
APHIS et al and the OIE, and all trading partners to take heed to the latest
science on the TSE prion disease, all of them, and seriously reconsider the
blatant disregards for human and animal health, all in the name of trade, with
the continued relaxing of TSE Prion trade regulations through the 'NEGLIGIBLE
BSE RISK' PROGRAM, which was set up to fail in the first place. If the world
does not go back to the 'BSE RISK ASSESSMENTS', enhance, and or change that
assessment process to include all TSE prion disease, i.e. 'TSE RISK ASSESSMENT',
if we do not do this and if we continue this farce with OIE and the USDA et al,
and the 'NEGLIGIBLE BSE RISK' PROGRAM, we will never eradicate the TSE prion aka
mad cow type disease, they will continue to mutate and spread among species of
human and animal origin, and they will continue to kill. ...
please see ;
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
please see file attachment for full submission and recent science and my
deep concerns on the TSE Prion disease... No documents available.
AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:
***********OCTOBER 2015*************
*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***
THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and
Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and
Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.
P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine
Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge;
Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology
Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and
food-borne fatal neurological disease which can be orally transmitted to cattle
and humans. Due to the presence of contaminated milk replacer, it is generally
assumed that cattle become infected early in life as calves and then succumb to
disease as adults. Here we challenged three 14 months old cattle per-orally with
100 grams of C-type BSE brain to investigate age-related susceptibility or
resistance. During incubation, the animals were sampled monthly for blood and
feces and subjected to standardized testing to identify changes related to
neurological disease. At 53 months post exposure, progressive signs of central
nervous system disease were observed in these 3 animals, and they were
euthanized. Two of the C-BSE animals tested strongly positive using standard BSE
rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts
S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing
resulted in the detection of pathologic lesion in unusual brain location and
PrPsc detection by PMCA only. Our study demonstrates susceptibility of adult
cattle to oral transmission of classical BSE. We are further examining
explanations for the unusual disease presentation in the third challenged
animal.
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
***We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period, with
features similar to some reported for human cases of sporadic CJD, albeit
requiring fourfold longe incubation than BSE.
***Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the
third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases...
===============
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, ***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
================
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
It also appears to Mr MacLean that Mr Bradley’s answer (that it would take
less than say 100 grams) was probably given with the benefit of hindsight:
particularly if one considers that later in the same answer Mr Bradley expresses
his surprise that it could take as little of 1 gram of brain to cause BSE by the
oral route within the same species. This information did not become available
until the “attack rate” experiment had been completed in 1995/96. This was a
titration experiment designed to ascertain the infective
2
dose. A range of dosages was used to ensure that the actual result was
within both a lower and an upper limit within the study and the designing
scientists would not have expected all the dose levels to trigger infection. The
dose ranges chosen by the most informed scientists at that time ranged from 1
gram to three times one hundred grams. It is clear that the designing scientists
must also have shared Mr Bradley’s surprise at the results because all the dose
levels right down to 1 gram triggered infection.
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
Saturday, September 12, 2015
The Canadian Management of Bovine Spongiform Encephalopathy in Historical
and Scientific Perspective, 1990-2014
>>>We propose that Canadian policies largely ignored the implicit
medical nature of BSE, treating it as a purely agricultural and veterinary
issue. In this way, policies to protect Canadians were often delayed and
incomplete, in a manner disturbingly reminiscent of Britain’s failed management
of BSE. Despite assurances to the contrary, it is premature to conclude that BSE
(and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of
Canada’s past: BSE remains very much an issue in Canada’s present.
<<<
small amount of leftover contaminated feed’ ...LOL...maybe large amount in
USA. see ;
Monday, November 30, 2015
*** Report on the Investigation of the Nineteenth Case of Bovine Spongiform
Encephalopathy (BSE) in Canada November 2015 ***
Wednesday, September 23, 2015
NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15;
8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE
Strains by RT-QuIC
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED 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
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials BSE TSE Prion
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
spontaneous atypical BSE ???
don’t let anyone fool you. spontaneous TSE prion disease is a hoax in
natural cases, never proven.
all one has to do is look at France. France is having one hell of an
epidemic of atypical BSE, probably why they stopped testing for BSE, problem
solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow
disease in numbers they could find any with, after those atypical BSE cases
started showing up. shut down the testing to numbers set up by OIE that are so
low, you could only by accident find a case of BSE aka mad cow disease. and this
brilliant idea by the WHO et al, to change the name of mad cow disease, thinking
that might change things is preposterous. it’s all about money now folks, when
the OIE, USDA and everyone else went along and made the TSE prion disease aka
mad cow type disease a legal trading commodity by the BSE MRR policy, I would
say everyone bit off more then they can chew, and they will just have to digest
those TSE Prions coming from North America, and like it, and just prey you don’t
get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE
prion disease in the decades to come, and or pass it to some other poor soul via
the iatrogenic medical surgical tissue friendly fire mode of transmission i.e.
second hand transmission. it’s real folks, just not documented much, due to lack
of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the
iatrogenic event is tracked down and documented, and put into the academic and
public domain, which very seldom happens. ...
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
***so 20 cases of atypical BSE in France, compared to the remaining 40
cases in the remaining 12 Countries, divided by the remaining 12 Countries,
about 3+ cases per country, besides Frances 20 cases. you cannot explain this
away with any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Sunday, October 18, 2015
World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
Terry S. Singeltary Sr.
No comments:
Post a Comment