Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
I would kindly like to comment on ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
#158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
This version of the guidance replaces the version made available
September15, 2003.
This document has been revised to update the docket number, contact
information, and standard disclosures. Submit comments on this guidance at any
time.
Submit electronic comments to http://www.regulations.gov. Submit written
comments to the Division of Dockets Management (HFA-305), Food and Drug
Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852. All comments
should be identified with the Docket No. FDA-2003-D-0432 (formerly 03D-0186).
For further information regarding this guidance, contact Burt Pritchett,
Center for Veterinary Medicine (HFV-222), Food and Drug Administration, 7519
Standish Place, Rockville, MD 20855, 240-402-6276, E-mail:
burt.pritchett@fda.hhs.gov.
Additional copies of this guidance document may be requested from the
Policy and Regulations Staff (HFV-6), Center for Veterinary Medicine, Food and
Drug Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed
on the Internet at either http://www.fda.gov/AnimalVeterinary/default.htm
or http://www.regulations.gov.
U.S. Department of Health and Human Services Food and Drug Administration
Center for Veterinary Medicine March 2016
Contains Nonbinding Recommendations
2
Guidance for Industry Use of Material from Deer and Elk in Animal Feed
This guidance represents the current thinking of the Food and Drug
Administration (FDA or Agency) on this topic. It does not establish any rights
for any person and is not binding on FDA or the public. You can use an
alternative approach if it satisfies the requirements of the applicable statutes
and regulations. To discuss an alternative approach, contact the FDA office
responsible for this guidance as listed on the title page.
I. Introduction
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer
and elk is prohibited for use in feed for ruminant animals. This guidance
document describes FDA’s recommendations regarding the use in all animal feed of
all material from deer and elk that are positive for Chronic Wasting Disease
(CWD) or are considered at high risk for CWD. The potential risks from CWD to
humans or non-cervid animals such as poultry and swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer, and because CWD’s route of transmission is poorly understood,
FDA is making recommendations regarding the use in animal feed of rendered
materials from deer and elk that are CWD-positive or that are at high risk for
CWD.
In general, FDA’s guidance documents do not establish legally enforceable
responsibilities. Instead, guidances describe the Agency’s current thinking on a
topic and should be viewed only as recommendations, unless specific regulatory
or statutory requirements are cited. The use of the word should in Agency
guidances means that something is suggested or recommended, but not
required.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and in farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). These include bovine
spongiform encephalopathy (BSE or “mad cow” disease) in cattle; scrapie in sheep
and goats; and classical and variant Creutzfeldt-Jakob diseases (CJD and vCJD)
in humans. There is no known treatment for these diseases, and there is no
vaccine to prevent them. In addition, although validated postmortem diagnostic
tests are available, there are no validated diagnostic tests for CWD that can be
used to test for the disease in live animals.
Contains Nonbinding Recommendations
III. Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV. Use in animal feed of material from deer and elk considered at high
risk for CWD Deer and elk considered at high risk for CWD include: (1) animals
from areas declared by State officials 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 immediately before the time of slaughter were in a captive herd that
contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal.
V. Use in animal feed of material from deer and elk NOT considered at high
risk for CWD FDA continues to consider materials from deer and elk NOT
considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal
feeds in accordance with current agency regulations, 21 CFR 589.2000. Deer and
elk not considered at high risk include: (1) deer and elk from areas not
declared by State officials to be endemic for CWD and/or to be CWD eradication
zones; and (2) deer and elk that were not at some time during the 60-month
period immediately before the time of slaughter in a captive herd that contained
a CWD-positive animal.
3
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
MY comments and source reference of sound science on this very important
issue are as follows ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
I kindly wish to once again submit to Docket No. FDA-2003-D-0432 (formerly
03D-0186) Use of Material from Deer and Elk in Animal Feed.
Thank you kindly for allowing me to comment again, ...and again...and
again, on a topic so important, why it is ‘NON-BINDING’ is beyond me.
this should have been finalized and made ‘BINDING’ or MANDATORY OVER A
DECADE AGO.
but here lay the problem, once made ‘BINDING’ or ‘MANDATORY’, it is still
nothing but ink on paper.
we have had a mad cow feed ban in place since August 1997, and since then,
literally 100s of millions of pounds BANNED MAD COW FEED has been sent out to
commerce and fed out (see reference materials).
ENFORCEMENT OF SAID BINDING REGULATIONS HAS FAILED US TOO MANY TIMES.
so, in my opinion, any non-binding or voluntary regulations will not work,
and to state further, ‘BINDING’ or MANDATORY regulations will not work unless
enforced.
with that said, we know that Chronic Wasting Disease CWD TSE Prion easily
transmits to other cervid through the oral route.
the old transmission studies of BSE TSE floored scientist once they figured
out what they had, and please don’t forget about those mink that were fed 95%+
dead stock downer cow, that all came down with TME. please see ;
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.
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...
To further complicate things, we now know that science has shown that
plants and vegetables can uptake the TSE Prion, and that the Scrapie agent can
still be infectious from soil 16 years later. a frightening thought with the CWD
running rampant now in North America (please see source reference materials
below).
IF we don’t do this, we have failed, and the TSE Prion agent will
continue to spread, as it is doing as we speak.
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 well as non-ruminants such as cats and dogs as
well, as soon as possible for the following reasons...
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 ;
please see further ;
REFERENCE MATERIALS
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
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 long 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.
================
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures
ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
*** Title: Transmission of scrapie prions to primate after an extended
silent incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
***After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease.
***Upon postmortem examination and microscopic examination of tissues,
there was a widespread distribution of lesions consistent with a transmissible
spongiform encephalopathy.
***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.
Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion
disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the
past decades, c-BSE's zoonotic potential has been the driving force in
establishing extensive protective measures for animal and human health.
***In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period.
***Neuropathologic examination revealed all of the features of a prion
disease: spongiform change, neuronal loss, and accumulation of PrPres throughout
the CNS.
***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.
SPONTANEOUS TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW
TYPE DISEASE ???
*** We describe the transmission of spongiform encephalopathy in a
non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie.
Because of this extended incubation period in a facility in which other prion
diseases are under study, we are obliged to consider two alternative
possibilities that might explain its occurrence. We first considered the
possibility of a sporadic origin (like CJD in humans). Such an event is
extremely improbable because the inoculated animal was 14 years old when the
clinical signs appeared, i.e. about 40% through the expected natural lifetime of
this species, compared to a peak age incidence of 60–65 years in human sporadic
CJD, or about 80% through their expected lifetimes.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
>>> Moreover, sporadic disease has never been observed in breeding
colonies or primate research laboratories, most notably among hundreds of
animals over several decades of study at the National Institutes of Health25,
and in nearly twenty older animals continuously housed in our own facility.
<<<
Tuesday, December 16, 2014
*** Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. ***The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. ***These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
see more here ;
***The serial transmission of different scrapie isolates in these mice led
to the propagation of prions that are phenotypically identical to those causing
sporadic CJD (sCJD) in humans.***
***These results demonstrate that scrapie prions have a zoonotic potential
and raise new questions about the possible link between animal and human
prions.***
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral
Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6;
Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique,
France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious
Disease control, Sweden; 5Georg August University, Germany; 6German Primate
Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to
contract BSE through contaminated food. For this purpose, BSE brain was titrated
in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose
(MID50) for oral exposure to BSE in a simian model, and, by in doing this, to
assess the risk for humans. Secondly, we aimed at examining the course of the
disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE
brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals
were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the onset of
the clinical phase. However, there are differences in the clinical course
between orally and intracerebrally infected animals that may influence the
detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate. The difference in the incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years).
However, there are rapid progressors among orally dosed monkeys that develop
simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfillment of the study “BSE
in primates“ supported by the EU (QLK1-2002-01096).
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate.
look at the table and you'll see that as little as 1 mg (or 0.001 gm)
caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in
primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to non-human
primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months
after exposure, whereas the other remained free of disease at 76 months. On the
basis of these findings and data from other studies, we made a preliminary
estimate of the food exposure risk for man, which provides additional assurance
that existing public health measures can prevent transmission of BSE to
man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a similar
PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of disease in
the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula
Published online January 27, 2005
Calves were challenged by mouth with homogenised brain from confirmed cases
of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were
then left to develop BSE, but were not subjected to the normal stresses that
they might have encountered in a dairy herd. Animals in all four groups
developed BSE. There has been a considerable spread of incubation period in some
of the groups, but it appears as if those in the 1 and 10g challenge groups most
closely fit the picture of incubation periods seen in the epidemic. Experiments
in progress indicate that oral infection can occur in some animals with doses as
low as 0.01g and 0.001g. .........
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: 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=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 two 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, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry
R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1
Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road,
University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife,
Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097,
USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake
Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit,
Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall,
Washington State University, Pullman, WA 99164-7030, USA5
Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
ehoover@lamar.colostate.edu
Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain
homogenate prepared from mule deer with naturally occurring chronic wasting
disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns
were necropsied and examined for PrP res, the abnormal prion protein isoform, at
10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an
immunohistochemistry assay modified to enhance sensitivity. PrPres was detected
in alimentary-tract-associated lymphoid tissues (one or more of the following:
retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as
early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.).
No PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural tissue
of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue
treatment with formic acid, proteinase K and hydrated autoclaving prior to
immunohistochemical staining with monoclonal antibody F89/160.1.5. These results
indicate that CWD PrP res can be detected in lymphoid tissues draining the
alimentary tract within a few weeks after oral exposure to infectious prions and
may reflect the initial pathway of CWD infection in deer. The rapid infection of
deer fawns following exposure by the most plausible natural route is consistent
with the efficient horizontal transmission of CWD in nature and enables
accelerated studies of transmission and pathogenesis in the native
species.
snip...
These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the earliest
post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the
oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal
Peyer's patches and ileocaecal lymph nodes), which probably received the highest
initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and
spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of
nine sheep had infectivity in the retropharyngeal lymph node. He concluded that
the tissue distribution suggested primary infection via the gastrointestinal
tract. The tissue distribution of PrPres in the early stages of infection in the
fawns is strikingly similar to that seen in naturally infected sheep with
scrapie. These findings support oral exposure as a natural route of CWD
infection in deer and support oral inoculation as a reasonable exposure route
for experimental studies of CWD.
snip...
Journal of Wildlife Diseases, 42(3), 2006, pp. 640–645 # Wildlife Disease
Association 2006
Oral Transmission of Chronic Wasting Disease in Captive Shira’s Moose
Terry J. Kreeger,1,3 D. L. Montgomery,2 Jean E. Jewell,2 Will Schultz,1 and
Elizabeth S. Williams2 1 Wyoming Game and Fish Department, 2362 Highway 34,
Wheatland, Wyoming 82201, USA; 2 Department of Veterinary Sciences, University
of Wyoming, Laramie, Wyoming 82071, USA; 3 Corresponding author (email:
tkreeger@wildblue.net)
ABSTRACT: Three captive Shira’s moose (Alces alces shirasi) were orally
inoculated with a single dose (5 g) of whole-brain homogenate prepared from
chronic wasting disease (CWD)– affected mule deer (Odocoileus hemionus). All
moose died of causes thought to be other than CWD. Histologic examination of one
female moose dying 465 days postinoculation revealed spongiform change in the
neuropil, typical of transmissible spongiform encephalopathy.
Immunohistochemistry staining for the proteinase- resistant isoform of the prion
protein was observed in multiple lymphoid and nervous tissues. Western blot and
enzyme-linked immunosorbent assays provided additional confirmation of CWD.
These results represent the first report of experimental CWD in moose.
Key words: Alces alces shirasi, chronic wasting disease, enzyme-linked
immunosorbent assay, immunohistochemistry, moose, oral inoculation, prion,
PrPCWD.
Experimental Oral Transmission of Chronic Wasting Disease to Reindeer
(Rangifer tarandus tarandus)
Gordon B. Mitchell1, Christina J. Sigurdson2,3, Katherine I. O’Rourke4,
James Algire1, Noel P. Harrington1, Ines Walther1, Terry R. Spraker5, Aru
Balachandran1*
1 National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food
Inspection Agency, Ottawa Laboratory – Fallowfield, Ottawa, Ontario, Canada,
2 Departments of Pathology and Medicine, University of California, San
Diego, La Jolla, California, United States of America, 3 Department of
Pathology, Microbiology and Immunology, University of California, Davis,
California, United States of America, 4 Animal Disease Research Unit,
Agricultural Research Service, United States Department of Agriculture, Pullman,
Washington, United States of America, 5 Veterinary Diagnostic Laboratory,
Colorado State University, Fort Collins, Colorado, United States of America
Abstract
Chronic wasting disease (CWD), a transmissible spongiform encephalopathy of
cervids, remains prevalent in North American elk, white-tailed deer and mule
deer. A natural case of CWD in reindeer (Rangifer tarandus tarandus) has not
been reported despite potential habitat overlap with CWD-infected deer or elk
herds. This study investigates the experimental transmission of CWD from elk or
white-tailed deer to reindeer by the oral route of inoculation. Ante-mortem
testing of the three reindeer exposed to CWD from white-tailed deer identified
the accumulation of pathological PrP (PrPCWD) in the recto-anal mucosa
associated lymphoid tissue (RAMALT) of two reindeer at 13.4 months
post-inoculation. Terminal CWD occurred in the two RAMALT-positive reindeer at
18.5 and 20 months post-inoculation while one other reindeer in the white-tailed
deer CWD inoculum group and none of the 3 reindeer exposed to elk CWD developed
disease. Tissue distribution analysis of PrPCWD in CWD-affected reindeer
revealed widespread deposition in central and peripheral nervous systems,
lymphoreticular tissues, the gastrointestinal tract, neuroendocrine tissues and
cardiac muscle. Analysis of prion protein gene (PRNP) sequences in the 6
reindeer identified polymorphisms at residues 2 (V/M), 129 (G/S), 138 (S/N) and
169 (V/M). These findings demonstrate that (i) a sub-population of reindeer are
susceptible to CWD by oral inoculation implicating the potential for
transmission to other Rangifer species, and (ii) certain reindeer PRNP
polymorphisms may be protective against CWD infection.
This is the first evidence of CWD transmission to the sub-species Rangifer
tarandus tarandus, implicating the potential for transmission to others in this
genus. Current diagnostic tests, including antemortem RAMALT testing, appear
capable of detecting CWD in Rangifer species and increased surveillance would be
required to determine if natural transmission has indeed occurred. Additional
studies are ongoing to chart the distribution of infectivity during the course
of disease and determine the influence of PRNP polymorphisms in disease
susceptibility.
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
see Singeltary comment ;
EVEN MAFF UK SAYS THEY HAVE A HIGHER RISK FACTOR OF CWD FROM USA DUE TO
FEED ;
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...
SEE THE DRASTIC REDUCTION OF CONFIRMED BSE CASES IN THE UK ONCE THE FEED
BAN TOOK HOLD FROM THE TOP YEAR DOWN TO THE FIRST ZERO YEAR ;
1992 36680 SLAUGHTERED SUSPECTS IN WHICH BSE CONFIRMED
2013 0 0 0 0 0 0 0 0
*** 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
***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
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain
location and PrPsc by PMCA only, how many cases have we missed?
***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.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
***
Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT
Singeltary previous submission to DOCKET-- 03D-0186 -- FDA Issues Draft
Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability Fri, 16 May 2003 11:47:37 0500 EMC 1 Terry
S. Singeltary Sr. Vol #: 1
Date: Fri, 16 May 2003 11:47:37 0500 EMC 1 Terry S. Singeltary Sr. Vol #: 1
PLEASE SEE FULL TEXT SUBMISSION ;
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
From: "Terry S. Singeltary Sr." T
o: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability
Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials
being fed back to cattle is terribly flawed. without the _total_ and _mandatory_
ban of all ruminant materials being fed back to ruminants including cattle,
sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for
human/animal consumption), this half ass measure will fail terribly, as in the
past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of
deer fawns being infected with CWD, how many could possibly be sub-clinically
infected. until we have a rapid TSE test to assure us that all deer/elk are free
of disease (clinical and sub-clinical), we must ban not only documented CWD
infected deer/elk, but healthy ones as well. it this is not done, they system
will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL
tissues. recent new and old findings support infectivity in the rump or ass
muscle. wether it be low or high, accumulation will play a crucial role in
TSEs.
4. THERE are and have been for some time many TSEs in the USA. TME in mink,
Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has
been proven, but the TSE in USA cattle has been totally ignored for decades. i
will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL
ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient
numbers to find (1 million rapid TSE test in USA cattle annually for 5 years),
any partial measures such as the ones proposed while ignoring sub-clinical TSEs
and not rapid TSE testing cattle, not closing down feed mills that continue to
violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely
available those violations, will only continue to spread these TSE mad cow
agents in the USA. I am curious what we will call a phenotype in a species that
is mixed with who knows how many strains of scrapie, who knows what strain or
how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling
how many strains there), but all of this has been rendered for animal feeds in
the USA for decades. it will get interesting once someone starts looking in all
species, including humans here in the USA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially
''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family
of a victim of TSE. only checking death certificates will not be sufficient.
this has been proven as well (see below HISTORY OF CJD -- CJD
QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same
mistakes...
REFERENCES
Six white-tailed deer fawns test positive for CWD
MADISON -- Six fawns in the area of south central Wisconsin where chronic
wasting disease has been found in white-tailed deer have tested positive for the
disease, according to Department of Natural Resources wildlife health officials.
These are the youngest wild white-tailed deer detected with chronic wasting
disease (CWD) to date.
Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of fawns
sampled were between the ages of 5 to 9 months, though some were as young as 1
month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of
the positive fawns were taken from the core area of the CWD eradication zone
where the highest numbers of positive deer have been identified.
snip...
===================================================
Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS
RELEVANT TO CJD AND BSE
A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the National
Academy of Sciences, on new evidence for the existence of a 'sub-clinical' form
of BSE in mice which was unknown until now.
The scientists took a closer look at what is known as the 'species barrier'
- the main protective factor which limits the ability of prions2 to jump from
one species to infect another. They found the mice had a 'sub-clinical' form of
disease where they carried high levels of infectivity but did not develop the
clinical disease during their normal lifespan. The idea that individuals can
carry a disease and show no clinical symptoms is not new. It is commonly seen in
conventional infectious diseases.
Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease. However, on
closer inspection they found that the mice had high levels of mouse prions in
their brains. This was surprising because it has always been assumed that
hamster prions could not cause the disease in mice, even when injected directly
into the brain.
In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.
The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of prions. While
some barriers are quite small (for instance BSE easily infects mice), other
combinations of strain and species show a seemingly impenetrable barrier.
Traditionally, the particular barrier studied here was assumed to be
robust.
Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure species
barriers in the laboratory, and that we should not assume that just because one
species appears resistant to a strain of prions they have been exposed to, that
they do not silently carry the infection. This research raises the possibility,
which has been mentioned before, that apparently healthy cattle could harbour,
but never show signs of, BSE.
"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected material
getting into the food chain and for those considering how best to safeguard
health and reduce the risk that theoretically, prion disease could be contracted
through medical and surgical procedures."
ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET
BY THE JOURNAL.
FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR PROFESSOR
JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS
PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25 AUGUST AND
CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE MRC PRESS OFFICE. DR ANDREW HILL
(A CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF
MELBOURNE WILL BE AVAILABLE ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61
3 9443 0009 (OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD
OF UK TIME.
NOTES FOR EDITORS
Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine at St
Mary's Hospital. He is also a member of the UK Government's Spongiform
Encephalopathy Advisory Committee (SEAC). The MRC prion unit is was set up in
1999, and its work includes molecular genetic studies of human prion disease and
transgenic modelling of human prion diseases.
Prions are unique infectious agents that cause fatal brain diseases such as
Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad cow disease)
in animals. In some circumstances prions from one species of animals can infect
another and it is clear that BSE has done this to cause the disease variant CJD
in the UK and France. It remains unclear how large an epidemic of variant CJD
will occur over the years ahead.
The strain of prion used here to infect the mice is the Sc237 strain (also
known as 263K) which infects hamsters, and until now was assumed not to infect
mice.
This research was funded by the Medical Research Council and Wellcome
Trust.
The Medical Research Council (MRC) is a national organisation funded by the
UK tax-payer. Its business is medical research aimed at improving human health;
everyone stands to benefit from the outputs. The research it supports and the
scientists it trains meet the needs of the health services, the pharmaceutical
and other health-related industries and the academic world. MRC has funded work
which has led to some of the most significant discoveries and achievements in
medicine in the UK. About half of the MRC's expenditure of £345 million is
invested in over 50 of its Institutes and Units, where it employs its own
research staff. The remaining half goes in the form of grant support and
training awards to individuals and teams in universities and medical
schools.
The Wellcome Trust is the world's largest medical research charity with a
spend of some £600 million in the current financial year 1999/2000. The
Wellcome Trust supports more than 5,000 researchers, at 400 locations, in 42
different countries to promote and foster research with the aim of improving
human and animal health. As well as funding major initiatives in the public
understanding of science, the Wellcome Trust is the country's leading supporter
of research into the history of medicine.
©2002 Medical Research Council Data Protection policy Contact the
MRC
======================================
Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry
R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1
Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road,
University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife,
Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097,
USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake
Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit,
Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall,
Washington State University, Pullman, WA 99164-7030, USA5
Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
ehoover@lamar.colostate.edu
Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain
homogenate prepared from mule deer with naturally occurring chronic wasting
disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns
were necropsied and examined for PrP res, the abnormal prion protein isoform, at
10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an
immunohistochemistry assay modified to enhance sensitivity. PrPres was detected
in alimentary-tract-associated lymphoid tissues (one or more of the following:
retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as
early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.).
No PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural tissue
of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue
treatment with formic acid, proteinase K and hydrated autoclaving prior to
immunohistochemical staining with monoclonal antibody F89/160.1.5. These results
indicate that CWD PrP res can be detected in lymphoid tissues draining the
alimentary tract within a few weeks after oral exposure to infectious prions and
may reflect the initial pathway of CWD infection in deer. The rapid infection of
deer fawns following exposure by the most plausible natural route is consistent
with the efficient horizontal transmission of CWD in nature and enables
accelerated studies of transmission and pathogenesis in the native
species.
snip...
These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the earliest
post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the
oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal
Peyer's patches and ileocaecal lymph nodes), which probably received the highest
initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and
spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of
nine sheep had infectivity in the retropharyngeal lymph node. He concluded that
the tissue distribution suggested primary infection via the gastrointestinal
tract. The tissue distribution of PrPres in the early stages of infection in the
fawns is strikingly similar to that seen in naturally infected sheep with
scrapie. These findings support oral exposure as a natural route of CWD
infection in deer and support oral inoculation as a reasonable exposure route
for experimental studies of CWD.
snip...
===================================
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 –0700
From: "Terry S. Singeltary Sr." Reply-To: BSE-L To: BSE-L
8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed
Analysis Ingredients / Products Feeding Directions
snip...
_animal protein_
BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS
22.6 KG.
snip...
_animal protein_
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage
Products, Roughage Products 15%, Molasses Products, __Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Pyosphate, Salt, Calcium Carbonate, Vitamin A
Acetate with D-activated Animal Sterol (source of Vitamin D3), Vitamin E
Supplement, Vitamin B12 Supplement, Riboflavin Supplement, Niacin Supplement,
Calcium Panothenate, Choline Chloride, Folic Acid, Menadione Soduim Bisulfite
Complex, Pyridoxine Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous
Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum, Artificial
Flavors added.
===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER
Bode's #1 Game Pellets A RATION FOR DEER F3153
GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat (Min) 2.0% Crude
Fiber (Max) 19% Calcium (Ca) (Min) 1.25% Calcium (Ca) (Max) 1.75% Phosphorus (P)
(Min) 1.0% Salt (Min) .30% Salt (Max) .70%
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage
Products, Roughage Products, 15% Molasses Products, __Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt, Calcium Carbonate, Vitamin A
Acetate with D-activated Animal Sterol (source of Vitamin D3) Vitamin E
Supplement, Vitamin B12 Supplement, Roboflavin Supplement, Niacin Supplement,
Calcium Pantothenate, Choline Chloride, Folic Acid, Menadione Sodium Bisulfite
Complex, Pyridoxine Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous
Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum, Artificial
Flavors added.
FEEDING DIRECTIONS Feed as Creep Feed with Normal Diet
INGREDIENTS
Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products, __Animal Protein
Products__, L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium Phosphate,
Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic Copper Chloride,
Manganese Sulfate, Manganous Oxide, Sodium Selenite, Zinc Sulfate, Zinc Oxide,
Sodium Selenite, Potassium Iodide, Ethylenediamine Dihydriodide, Vitamin E
Supplement, Vitamin A Supplement, Vitamin D3 Supplement, Mineral Oil, Mold
Inhibitor, Calcium Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium
Bisulfite Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate
DIRECTIONS FOR USE
Deer Builder Pellets is designed to be fed to deer under range conditions
or deer that require higher levels of protein. Feed to deer during gestation,
fawning, lactation, antler growth and pre-rut, all phases which require a higher
level of nutrition. Provide adequate amounts of good quality roughage and fresh
water at all times.
===================================================
DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND
DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER
01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy
Lake, PA 16145 PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted an
inspection of your animal feed manufacturing operation, located in Sandy Lake,
Pennsylvania, on March 23, 2001, and determined that your firm manufactures
animal feeds including feeds containing prohibited materials. The inspection
found significant deviations from the requirements set forth in Title 21, code
of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant
Feed. The regulation is intended to prevent the establishment and amplification
of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being
manufactured at this facility to be misbranded within the meaning of Section
403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found failure to label your swine feed with the required
cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests
that the statement be distinguished by different type-size or color or other
means of highlighting the statement so that it is easily noticed by a
purchaser.
In addition, we note that you are using approximately 140 pounds of cracked
corn to flush your mixer used in the manufacture of animal feeds containing
prohibited material. This flushed material is fed to wild game including deer, a
ruminant animal. Feed material which may potentially contain prohibited material
should not be fed to ruminant animals which may become part of the food
chain.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal feed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law. We have enclosed
a copy of FDA's Small Entity Compliance Guide to assist you with complying with
the regulation... blah, blah, blah...
snip...end
Date: Thu, 15 May 2003 19:15:01 -0500
Subject: FDA ANNOUNCES USE OF MATERIAL FROM DEER AND ELK IN ANIMAL FEED ARE
AT HIGH RISK OF CWD
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Reply-To: Bovine Spongiform Encephalopathy <[log in to unmask]>
Date: Thu, 15 May 2003 19:15:01 -0500
Content-Type: text/plain
Parts/Attachments: Parts/Attachments text/plain (249 lines)
######## Bovine Spongiform Encephalopathy <[log in to unmask]>
#########
FDA Talk Paper
T03-34 May 15, 2003
Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed
The Food and Drug Administration (FDA) is announcing the availability of a
draft guidance for industry entitled "Use of Material From Deer and Elk in
Animal Feed." When finalized, this draft guidance will describe FDA’s
recommendations regarding the use in all animal feed of all material from deer
and elk that are positive, or at high risk, for Chronic Wasting Disease
(CWD).
The potential risks from CWD to humans or non-cervid animals such as
poultry and swine are not well understood. However, because of recent
recognition that CWD is spreading rapidly in white-tailed deer, and because
CWD’s route of transmission is poorly understood, FDA is recommending that any
material from CWD-positive animals, or deer and elk considered to be at high
risk for CWD, not be used in any animal feed or feed ingredients. High risk deer
and elk are those from 1) areas declared by state officials to be endemic for
CWD and/or to be CWD eradication zones and 2) those that at some time during the
60-month period before the time of slaughter were part of a captive herd with a
CWD-positive animal.
CWD is a neurological (brain) disease of farmed and wild deer and the elk
that belong in the cervidae animal family (cervids). Only deer and elk are known
to be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). These include bovine
spongiform encephalopathy (BSE or "mad cow" disease) in cattle; scrapie in sheep
and goats; and classical and variant Creutzfeldt-Jakob diseases (CJD and vCJD)
in humans. TSEs are very rare, but are always fatal.
There is no known treatment for these diseases, and there is no vaccine to
prevent them. In addition, although validated postmortem diagnostic tests are
available, there are no validated diagnostic tests for CWD that can be used to
test live animals for the disease.
FDA’s guidance documents are not regulations and are not mandatory. They
set forth voluntary recommendations from FDA. They do not create or confer any
rights for, or on, any person and do not operate to bind FDA or the public. An
alternate method may be used as long as it satisfies the requirements of
applicable statutes and regulations.
This draft guidance is being distributed for comment purposes only. Written
comments comments on the draft guidance may be submitted to the Dockets
Management Branch (HFA-305), Food and Drug Administration, 5630 Fishers Lane,
Room 1061, Rockville, MD 20852. Electronic comments may be submitted to http://www.accessdata.fda.gov/scripts/oc/dockets/comments/commentdocket.cfm.
Comments should be identified with the full title of the draft guidance and
Docket number 03D-0186. Written comments on the draft guidance may be submitted
at any time; however, comments should be submitted by June 16, 2003, to ensure
their adequate consideration in preparation of the final document.
Additional information on the draft guidance document may be found in the
May 16, 2003, Federal Register and from Dr. Burt Pritchett, Center for
Veterinary Medicine (HFV-222) Food and Drug Administration, 7500 Standish Place,
Rockville, MD 20855, 301-827-0177. E-mail: [log in to unmask] . The draft guidance is posted at
CONTAINS NON-BINDING RECOMMENDATIONS
158
Guidance for Industry Use of Material from Deer and Elk in Animal Feed
DRAFT GUIDANCE
This draft guidance is being distributed for comment purposes only.
Comments and suggestions regarding this draft guidance should be sent to the
Dockets Management Branch (HFA-305), Food and Drug Administration, 5630 Fishers
Lane, Room 1061, Rockville, MD 20852. Comments may also be submitted
electronically on the Internet at http://www.fda.gov/dockets/ecomments.
Once on this Internet site, select "[03D-0186][Use of Material from Deer and Elk
in Animal Feed]" and follow the directions. All written comments should be
identified with Docket No. 03D-0186. For questions regarding this draft
document, contact Burt Pritchett, Center for Veterinary Medicine (HFV- 222),
Food and Drug Administration, 7500 Standish Place, Rockville, MD 20855,
301-827-0177. E-mail: [log in to unmask] Additional copies of this draft
guidance document may be requested from the Communications Staff (HFV-12),
Center for Veterinary Medicine, Food and Drug Administration, 7500 Standish
Place, Rockville, MD 20855, and may be viewed on the Internet at http://www.fda.gov/cvm.
U.S. Department of Health and Human Services Food and Drug Administration
Center for Veterinary Medicine May 14, 2003 CONTAINS NON-BINDING RECOMMENDATIONS
1
158
Guidance for Industry1 Use of Material from Deer and Elk in Animal Feed I.
Introduction
FDA’s guidance documents, including this guidance, do not establish legally
enforceable responsibilities. Instead, guidances describe the Agency’s current
thinking on a topic and should be viewed only as recommendations, unless
specific regulatory or statutory requirements are cited. The use of the word
“should” in Agency guidances means that something is suggested or recommended,
but not required. Under FDA’s BSE feed regulation (21 CFR 589.2000) most
material from deer and elk is prohibited for use in feed for ruminant animals.
This draft guidance document describes FDA’s recommendations regarding the use
in all animal feed of all material from deer and elk that are positive for
Chronic Wasting Disease (CWD) or are considered at high risk for CWD. The
potential risks from CWD to humans or non-cervid animals such as poultry and
swine are not well understood. However, because of recent recognition that CWD
is spreading rapidly in white-tailed deer, and because CWD’s route of
transmission is poorly understood, FDA is making recommendations regarding the
use in animal feed of rendered materials from deer and elk that are CWD-positive
or that are at high risk for CWD. II. Background CWD is a neurological (brain)
disease of farmed and wild deer and elk that belong in the animal family
cervidae (cervids). Only deer and elk are known to be susceptible to CWD by
natural transmission. The disease has been found in farmed and wild mule deer,
white-tailed deer, North American elk, and in farmed black-tailed deer. CWD
belongs to a family of animal and human diseases called transmissible spongiform
encephalopathies 1 This draft guidance has been prepared by the Division of
Animal Feeds in the Center for Veterinary Medicine (CVM) at the Food and Drug
Administration. This draft guidance, when finalized, will represent the Food and
Drug Administration’s current thinking on the use of material from deer and elk
in animal feed. It does not create or confer any rights for or on any person and
does not operate to bind FDA or the public. You can use an alternative approach
if the approach satisfies the requirements of applicable statutes or
regulations. If you want to discuss an alternative approach, contact the FDA
staff responsible for implementing this guidance. If you cannot identify the
appropriate FDA staff, call the appropriate number listed on the title page of
this guidance.
CONTAINS NON-BINDING RECOMMENDATIONS
2
(TSEs). These include bovine spongiform encephalopathy (BSE or “mad cow”
disease) in cattle; scrapie in sheep and goats; and classical and variant
Creutzfeldt-Jakob diseases (CJD and vCJD) in humans. There is no known treatment
for these diseases, and there is no vaccine to prevent them. In addition,
although validated postmortem diagnostic tests are available, there are no
validated diagnostic tests for CWD that can be used to test for the disease in
live animals.
III. Use in animal feed of material from CWD-positive deer and elk Material
from CWD-positive animals may not be used in any animal feed or feed
ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and Cosmetic
Act, animal feed and feed ingredients containing material from a CWD-positive
animal would be considered adulterated. FDA recommends that any such adulterated
feed or feed ingredients be recalled or otherwise removed from the marketplace.
IV. Use in animal feed of material from deer and elk considered at high
risk for CWD Deer and elk considered at high risk for CWD include:
(1) animals from areas declared by State officials 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 immediately
before the time of slaughter were in a captive herd that contained a
CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal. V. Use in animal feed of material from deer
and elk NOT considered at high risk for CWD FDA continues to consider materials
from deer and elk NOT considered at high risk for CWD to be acceptable for use
in NON-RUMINANT animal feeds in accordance with current agency regulations, 21
CFR 589.2000. Deer and elk not considered at high risk include:
(1) deer and elk from areas not declared by State officials to be endemic
for CWD and/or to be CWD eradication zones; and
(2) deer and elk that were not at some time during the 60-month period
immediately before the time of slaughter in a captive herd that contained a
CWD-positive animal.
DAY LATE AND DOLLAR SHORT, they should have done this 30 years ago before
they fed all the cattle this recipe for TSEs. and what about those cattle, what
will we call this phenotype mixed up of scrapie, cwd and UTSEA in cattle
(uniditified TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY agent) in the USA?
i got a name for it, but cannot post to this list.
no wonder we don't test humans or cattle for tse's in the USA...
i just want to go out and slap some one, but i should ''DELAY'' myself. i
am in one of those moods. so i will not be posting for a short/long? period of
time, so i can get my diplomatic composure back, may wet a hook, or maybe
''DELAY'' that for a moment or two and just slap someone...
disgusted again in Bacliff, TEXAS USA...
Terry S. Singeltary Sr.
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############
Subject: MAD COW FEED BAN WARNING LETTER USA 2003
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Reply-To: Bovine Spongiform Encephalopathy <[log in to unmask]>
Date: Tue, 20 May 2003 08:39:31 -0500
Content-Type: text/plain
Parts/Attachments: Parts/Attachments text/plain (181 lines)
######## Bovine Spongiform Encephalopathy <[log in to unmask]>
#########
Public Health Service Food and Drug Administration
Minneapolis District Office Central Region 212 Third Avenue South
Minneapolis, MN 56401 Telephone: (612) 334-4100 FAX: (612) 334-4134
May 6, 2003
WARNING LETTER CERTIFIED MAIL RETURN RECEIPT REQUESTED Refer to MIN 03 -
20
Steve L. Denk President Barr Animal Foods A Division of Barr Enterprises,
Inc. W7276 Chickadee Road Greenwood, Wisconsin 54437
Dear Mr. Denk:
On April 8, 2003, an investigator from the Food and Drug Administration
(FDA) inspected your rendering and animal feed manufacturing operation located
at W7276 Chickadee Road, Greenwood, WI. This inspection found significant
deviations from the requirements set forth in Title 21, Code of Federal
Regulations, Part 589.2000, "Animal Proteins Prohibited in Ruminant Feed" (21
CFR 589.2000). The regulation is intended to prevent the establishment and
amplification of Bovine Spongiform Encephalopathy (BSE). Under 21 CFR
589.2000(g)(2), such deviations cause products being manufactured and/or
distributed by this facility to be deemed misbranded within the meaning of
Section 403(a)(1) of the Federal Food, Drug and Cosmetic Act (the Act), and
these products may not be lawfully introduced, or delivered for introduction,
into interstate commerce.
Products that contain or may contain protein derived from mammalian tissues
and are intended for use in animal feed must be labeled with the cautionary
statement, "Do not feed to cattle or other ruminants." This is required by 21
CFR 589.2000(c)(1)(i). The FDA suggests the statement be distinguished by
different type size or color, or other means of highlighting the statement so
that it is easily noticed by a purchaser. Our inspection found that you are not
labeling your 50-pound blocks of frozen beef and bulk loads of beef bone chips
and rendering waste, which are intended for animal feed, with that caution
statement. As a result, these products are misbranded within the meaning of
Section 403(a)(1) of the Act.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a renderer and manufacturer of materials intended for animal
feed use, you are responsible for ensuring that your overall operation and the
products you manufacture and distribute are in compliance with the law. We have
enclosed a copy of the FDA’s Small Entity Compliance Guide Nos. 67 and 68 to
assist you with complying with the regulation.
You should take prompt action to correct these violations and you should
establish a system whereby such violations do not recur. Failure to promptly
correct these violations may result in regulatory action without further notice.
These actions include, but are not limited to, seizure and/or injunction.
It is necessary for you to take action on this matter now. Please provide
this office a written response within 15 working days of receipt of this letter
with the steps you have taken to bring your firm into compliance with the law.
Your response should include an explanation of each step being taken to correct
the violations and prevent their recurrence. If corrective action cannot be
taken within 15 working days, state the reason for the delay and the date by
which the corrections will be completed. Please include copies of any available
documentation demonstrating that corrections have been made.
Your reply should be directed to Compliance Officer Timothy G. Philips at
the address indicated on the letterhead.
Sincerely,
/s/
David R. Yost for W. Charles Becoat
Minneapolis District
Greetings List Members,
what a surprise to see this posting of warning letter for feeding ruminants
to ruminants in the USA, simply astonishing. my question is, if they cannot stop
this practice of feeding cows to cows in the USA in 2003, after some 6 years
(since 8/4/97 partial and voluntary), how in the world do they plan on enforcing
a ban on deer/elk products from entering the feed market?
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed
TSS SUBMISSION TO FEDERAL DOCKET ON DRAFT GUIDANCE ON USE OF MATERIAL FROM
DEER AND ELK IN ANIMAL FEED
(if this url does not change again? it will be posted here for viewing for
those interested...TSS)
snip...end...TSS
Draft Guidance for Industry on Ensuring Safety of Animal Feed Maintained
and Fed On-Farm; Availability FDA-2014-D-1180-0001 Singeltary Submission Comment
Period Closed Jun 3 2015, at 11:59 PM ET
*** See attached file(s) No documents available. Attachments View All (1)
Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm
Terry Singeltary Comment View Attachment:
Sunday, April 5, 2015
*** Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed
On-Farm Draft Guidance FDA-2014-D-1180 ***
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Draft Guidance for Industry on Ensuring Safety of Animal Feed Maintained
and Fed On-Farm; Availability
# 203 entitled “Ensuring Safety of Animal Feed Maintained and Fed
On-Farm.”
Terry S. Singeltary Sr. submission ;
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
Posted: 12/30/2014 ID: APHIS-2014-0107-0001
Notice: Environmental Impact Statements; Availability, etc.: Animal Carcass
Management
Document ID: APHIS-2013-0044-0001 Docket ID: APHIS-2013-0044 Comment ID:
APHIS-2013-0044-0002
(APHIS) Notice: Agency Information Collection Activities; Proposals,
Submissions, and Approvals:
Chronic Wasting Disease Herd Certification Program Agency Information
Collection Activities; Proposals, Submissions, and Approvals:
Chronic Wasting Disease Herd Certification Program (Document ID
APHIS-2011-0032-0001)
Comment from Terry S Singletary Sr
Subject: BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM
BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01
Date: January 9, 2007 at 9:08 am PST [Federal...
Public Submission Posted:01/09/2007
ID:APHIS-2006-0041-0006 Agency: APHIS RIN:0579-AC01 Docket
ID:APHIS-2006-0041
Organization:na Submitter Name:Terry Singeltary Sr.
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE) Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
From:Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent:Thursday, September 08, 2005 6:17 PM
To:fsis.regulationscomments@fsis.usda.gov
Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified
Risk Materials for Human Food and Requirements for the Disposition of
Non-Ambulatory Disabled Cattle
APHIS-2006-0118-0096 CWD
Monday, January 08,2001
PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page 1.
J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr. [[log in to
unmask]] Monday, January 08,2001 3:03 PM freas ...
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
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
NEW URL LINK ;
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm120446.htm
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
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR
FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
2006 WAS A BANNER YEARS TOO FOR MAD COW PROTEIN IN COMMERCE IN USA.
a few examples below ;
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL,
TN, AND WV Date: September 6, 2006 at 7:58 am PST
PRODUCT a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick
Starter, Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d)
Performance Pheasant Finisher, Recall # V-133-6. CODE None RECALLING
FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc.,
Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006.
Firm initiated recall is complete.
REASON Dairy and poultry feeds were possibly contaminated with ruminant
based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons DISTRIBUTION AL
______________________________
PRODUCT a) Dairy feed, custom, Recall # V-134-6; b) Custom Dairy Feed with
Monensin, Recall # V-135-6. CODE None. Bulk product RECALLING FIRM/MANUFACTURER
Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June
28, 2006. Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm
initiated recall is complete.
REASON Possible contamination of dairy feeds with ruminant derived meat and
bone meal.
VOLUME OF PRODUCT IN COMMERCE 1,484 tons DISTRIBUTION TN and WV
http://www.fda.gov/bbs/topics/enforce/2
... 00968.html
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA,
MS, AL, GA, AND TN 11,000+ TONS Date: August 16, 2006 at 9:19 am PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________
PRODUCT Bulk custom made dairy feed, Recall # V-115-6 CODE None RECALLING
FIRM/MANUFACTURER Hiseville Feed & Seed Co., Hiseville, KY, by telephone and
letter on or about July 14, 2006. FDA initiated recall is ongoing.
REASON Custom made feeds contain ingredient called Pro-Lak which may
contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE Approximately 2,223 tons DISTRIBUTION KY
______________________________
PRODUCT Bulk custom made dairy feed, Recall # V-116-6 CODE None RECALLING
FIRM/MANUFACTURER Rips Farm Center, Tollesboro, KY, by telephone and letter on
July 14, 2006. FDA initiated recall is ongoing.
REASON Custom made feeds contain ingredient called Pro-Lak which may
contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 1,220 tons DISTRIBUTION KY
______________________________
PRODUCT Bulk custom made dairy feed, Recall # V-117-6 CODE None RECALLING
FIRM/MANUFACTURER Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006.
FDA initiated recall is completed.
REASON Possible contamination of animal feed ingredients, including
ingredients that are used in feed for dairy animals, with ruminant derived meat
and bone meal.
VOLUME OF PRODUCT IN COMMERCE 40 tons DISTRIBUTION LA and MS
______________________________
PRODUCT Bulk Dairy Feed, Recall V-118-6 CODE None RECALLING
FIRM/MANUFACTURER Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26,
2006. FDA initiated recall is complete.
REASON Possible contamination of animal feed ingredients, including
ingredients that are used in feed for dairy animals, with ruminant derived meat
and bone meal.
VOLUME OF PRODUCT IN COMMERCE 7,150 tons DISTRIBUTION MS
______________________________
PRODUCT Bulk custom dairy pre-mixes, Recall # V-119-6 CODE None RECALLING
FIRM/MANUFACTURER Walthall County Co-op, Tylertown, MS, by telephone on June 26,
2006. Firm initiated recall is complete.
REASON Possible contamination of dairy animal feeds with ruminant derived
meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 87 tons DISTRIBUTION MS
______________________________
PRODUCT Bulk custom dairy pre-mixes, Recall # V-120-6 CODE None RECALLING
FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006.
Firm initiated recall is complete.
REASON Possible contamination of dairy animal feeds with ruminant derived
meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons DISTRIBUTION AL and MS
______________________________
PRODUCT a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50
lb. bags, Recall # V-121-6; b) Tucker Milling, LLC #31120, Game Bird Breeder
Pellet, 50 lb. bags, Recall # V-122-6; c) Tucker Milling, LLC #31232 Game Bird
Grower, 50 lb. bags, Recall # V-123-6; d) Tucker Milling, LLC 31227-Crumble,
Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6; e) Tucker
Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6; f) Tucker
Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6; g)
Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING
FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by
telephone and visit on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall
is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with
ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags DISTRIBUTION AL, GA, MS, and
TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2
... 00964.html
Subject: MAD COW FEED RECALL MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN
COMMERCE 27,694,240 lbs
Date: August 6, 2006 at 6:14 pm PST PRODUCT Bulk custom dairy feds
manufactured from concentrates, Recall # V-113-6 CODE All dairy feeds produced
between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.
RECALLING FIRM/MANUFACTURER Vita Plus Corp., Gagetown, MI, by visit beginning on
June 21, 2006.
Firm initiated recall is complete. REASON The feed was manufactured from
materials that may have been contaminated with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs DISTRIBUTION MI
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2
... 00963.html
ENFORCEMENT REPORT FOR AUGUST 2, 2006 please note, considering .005 grams
is lethal, I do not know how much of this 125 TONS of banned mad cow protein was
part of the ;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
bbbut, this was about 10 years post mad cow feed ban from 1997. 10 years
later, and still feeding banned mad cow protein to cervids??? considering that
.005 gram is lethal to several bovines, and we know that the oral consumption of
CWD tainted products is very efficient mode of transmission of CWD.
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS
Products manufactured from 02/01/2005 until 06/06/2006 Date: August 6, 2006
at 6:16 pm PST PRODUCT a) CO-OP 32% Sinking Catfish, Recall # V-100-6; b)
Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking
Catfish Food Medicated, Recall # V-103-6; ***e) "Big Jim's" BBB Deer Ration, Big
Buck Blend, Recall # V-104-6; f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18%
W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP
STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks,
Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; j)
CO-OP LAYING CRUMBLES, Recall # V-109-6; k) CO-OP QUAIL FLIGHT CONDITIONER
MEDICATED, net wt 50 Lbs, Recall # V-110-6; l) CO-OP QUAIL STARTER MEDICATED,
Net Wt. 50 Lbs, Recall # V-111-6; m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6 CODE Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by
telephone, fax, email and visit on June 9, 2006. FDA initiated recall is
complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant
based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons DISTRIBUTION AL and FL END OF
ENFORCEMENT REPORT FOR AUGUST 2, 2006 ###
Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? Date:
August 6, 2006 at 6:19 pm PST PRODUCT Bulk custom made dairy feed, Recall #
V-114-6 CODE None RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY,
by letter on July 14, 2006. Firm initiated recall is ongoing.
REASON Custom made feeds contain ingredient called Pro-Lak, which may
contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE ?????
DISTRIBUTION KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2
... 00963.html
CJD WATCH MESSAGE BOARD TSS MAD COW FEED RECALL USA EQUALS 10,878.06 TONS
NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy
Animals, Recall # V-079-6; b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net
weight 50lb (22.6 kg), Recall # V-080-6; c) PRO-PAK, MARINE & ANIMAL PROTEIN
CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6; d) Feather Meal, Recall #
V-082-6 CODE a) Bulk b) None c) Bulk d) Bulk RECALLING FIRM/MANUFACTURER H. J.
Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by
press release on June 16, 2006. Firm initiated recall is ongoing.
REASON Possible contamination of animal feeds with ruminent derived meat
and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2
... 00960.html
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006 Date: June 27,
2006 at 7:42 am PST Public Health Service Food and Drug Administration
New Orleans District 297 Plus Park Blvd. Nashville, TN 37217
Telephone: 615-781-5380 Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO. 2006-NOL-06
FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State
Street Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration
(FDA) investigator inspected your rendering plant, located at 509 Fortson
Street, Shreveport, Louisiana. The inspection revealed significant deviations
from the requirements set forth in Title 21, Code of Federal Regulations, Part
589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This
regulation is intended to prevent the establishment and amplification of Bovine
Spongiform Encephalopathy (BSE). You failed to follow the requirements of this
regulation; products being manufactured and distributed by your facility are
misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the
Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found you failed to provide measures, including
sufficient written procedures, to prevent commingling or cross-contamination and
to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent
carryover of protein derived from mammalian tissues into animal protein or feeds
which may be used for ruminants. For example, your facility uses the same
equipment to process mammalian and poultry tissues. However, you use only hot
water to clean the cookers between processing tissues from each species. You do
not clean the auger, hammer mill, grinder, and spouts after processing mammalian
tissues.
You failed to maintain written procedures specifying the clean-out
procedures or other means to prevent carryover of protein derived from mammalian
tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived
from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR
589.2000(e)(1)(i), any products containing or may contain protein derived from
mammalian tissues must be labeled, "Do not feed to cattle or other ruminants."
Since you failed to label a product which may contain protein derived from
mammalian tissues with the required cautionary statement. the poultry meal is
misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your
facility. As a manufacturer of materials intended for animal feed use, you are
responsible for ensuring your overall operation and the products you manufacture
and distribute are in compliance with the law. You should take prompt action to
correct these violations, and you should establish a system whereby violations
do not recur. Failure to promptly correct these violations may result in
regulatory action, such as seizure and/or injunction, without further notice.
You should notify this office in writing within 15 working days of
receiving this letter, outlining the specific steps you have taken to bring your
firm into compliance with the law. Your response should include an explanation
of each step taken to correct the violations and prevent their recurrence. If
corrective action cannot be completed within 15 working days, state the reason
for the delay and the date by which the corrections will be completed. Include
copies of any available documentation demonstrating corrections have been made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S.
Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie,
Louisiana 70001. If you have questions regarding any issue in this letter,
please contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez Acting District Director New Orleans District
'ANIMAL PROTEIN' SEARCH 9/9/02
==============================
Darling International, Inc. 5/07/02 Seattle District Office Animal Proteins
Prohibited in Ruminant Feed/Misbranded [PDF] [HTML]
All American Feed & Tractor 4/01/02 Seattle District Office Animal
Proteins Prohibited in Ruminant Feed/Adulterated [PDF] [HTML]
Tyson Foods 2/12/02 Seattle District Office Animal Proteins Prohibited in
Ruminant Feed/Misbranded [PDF] [HTML]
The Feed Bucket 12/11/01 Atlanta District Office Animal Proteins Prohibited
in Ruminant Feed/Adulterated/Misbranded [PDF] [HTML]
Finlayson Ag Center 11/08/01 Minneapolis District Office Animal Proteins
Prohibited in Ruminant Feed/Adulterated [PDF] [HTML]
Dixon Feeds, Inc. 10/24/01 Seattle District Office Animal Proteins
Prohibited in Ruminant Feed/Adulterated [PDF] [HTML]
Buckeye Feed Mills, Inc. 9/20/01 Cincinnati District Office Animal Proteins
Prohibited in Ruminant Feed/Adulterated/Misbranded [PDF] [HTML]
Wilcox Farms, Inc. 9/14/01 Seattle District Office Animal Proteins
Prohibited in Ruminant Feed [PDF] [HTML]
now, compare search on 8/8/01...tss
===================================
'ANIMAL PROTEIN' SEARCH 8/8/01
==============================
Date: Tue, 28 Aug 2001 11:13:43 -0700 Reply-
To: BSE-L Sender: Bovine Spongiform Encephalopathy BSE-L
From: "Terry S. Singeltary Sr."
Subject: MAD COW FEED BAN WARNING LETTERS U.S.A. AUGUST 8, 2001
DEPARTMENT OF HEALTH AND HUMAN SERVICES
Food and Drug Administration
Seattle District Pacific Region 22201 23rd Drive SE Bothell, WA
98021-4421
Telephone: 426-486-8788 FAX: 426-483-4996
August 8, 2001
VIA CERTIFIED MAIL RETURN RECEIPT REQUESTED
In reply refer to Warning Letter SEA 01-75
William W. Himmelspach, Owner 22195 S.W. 78th Tualatin, Oregon 97062
WARNING LETTER
Dear Mr. Himmelspach:
An investigation at your animal feed manufacturing operation located at
22195 S.W. 78th Tualatin, Oregon 97062, conducted by a Food and Drug
Administration investigator on July 12, 2001, found significant deviations from
the requirements set forth in Title 21, Code of Federal Regulations, Part
589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is
intended to prevent the establishment and amplification of Bovine Spongiform
Encephalopathy (BSE). Such deviations cause products being manufactured at this
facility to be adulterated within the meaning of Section 402(a)(2)(C), and
402(a)(4) of the Federal Food, Drug and Cosmetic Act (the Act).
Our investigation found a failure to separate the receipt, processing, and
storage of the product containing prohibited material from non-prohibited
material; failure to establish a written system, including clean-out and
flushing procedures, to avoid commingling and cross-contamination of common
equipment; and failure to maintain records sufficient to track the materials
throughout the receipt, processing, and distribution of your products.
In addition, our investigation found a failure to label your products with
the required cautionary, statement "Do Not Feed to Cattle or Other Ruminants,"
Your pig feeds, containing prohibited materials, were not labeled with the
cautionary statement, and you reuse poly-tote bags for ruminant feed and pig
feed, where the bags could become contaminated with prohibited material. The FDA
suggests the statement be distinguished by different type size or color or other
means of highlighting the statement so that it is easily noticed by a
purchaser.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal feed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with
William W. Himmelspach Tualatin, Oregon Re: Warning Letter SEA 01-75 Page
2
your overall operation and the products you manufacture and distribute are
in compliance with the law. We have enclosed a copy of the FDA's Small Entity
Compliance Guide to assist you with complying with the regulation.
You should take prompt action to correct these violations, and you should
establish a system whereby such violations do not recur. Failure to promptly
correct these violations may result in regulatory action without further notice,
such as seizure and/or injunction.
You should notify this office in writing within 15 working days of receipt
of this letter, of the steps you have taken to bring your firm into compliance
with the law. Your response should include an explanation of each step being
taken to correct the violations, and prevent their recurrence. If corrective
action cannot be completed in 15 working days, state the reason for the delay
and the date by which the corrections will be completed. Include copies of any
available documentation demonstrating that corrections have been made.
Your reply should be directed to the Food and Drug Administration,
Attention: Bruce Williamson, Compliance Officer. If you have any questions
please contact Mr. Williamson at (425) 483-4976.
Sincerely,
Charles M. Breen District Director
Enclosure; Form FDA 483 Small Entity Compliance Guide
Warning Letters Index - Search Form Results Company Name Date Issued
Issuing Office
Subject
File Adrian Elevator, Inc. 5/03/01 Minneapolis District Office Animal
Proteins Prohibited in Ruminant Feed
View File Alaska Garden and Pet Supply, Inc. 4/27/01 Seattle District
Office Animal Proteins Prohibited in Ruminant Feed
View File Bryan Enterprises 2/20/01 Cincinnati District Office Feed
Mill/Animal Proteins Prohibited in Ruminant Feed/Adulterated
View File Carrollton Farmers Exchange 7/12/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed
View File Centerburg Mill and General Store, Inc 3/23/01 Cincinnati
District Office Animal Proteins Prohibited in Ruminant Feed
View File Centerburg Mill and General Store, Inc. 5/23/01 Cincinnati
District Office Animal Proteins Prohibited in Ruminant Feed
View File Central Ohio Farmers Cooperative, Inc. 5/24/01 Cincinnati
District Office Animal Protein Prohibited in Ruminant Feed
View File Champaign Landmark, Inc. 3/05/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed/Misbranded
View File Countryline Co-Op, Inc. 5/14/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed
View File Dorset Milling 4/16/01 Cincinnati District Office Animal Proteins
Prohibited in Ruminant Feed
View File Earl B. Olson Feed Mill 4/23/01 Minneapolis District Office
Animal Proteins Prohibited in Ruminant Feed
View File Faler Feed Store, Inc. 3/21/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed
View File Farmers Mill & Elevator Company 3/30/01 Atlanta District
Office Animal Proteins Prohibited in Ruminant Feed
View File Farnam Companies, Inc. 7/20/01 Kansas City District Office Animal
Proteins Prohibited in Ruminant Feed/Adulterated
View File Greeley Elevator Company 4/04/01 Denver District Office Animal
Proteins Prohibited in Ruminant Feed
View File Hartville Elevator Company, Inc. 2/22/01 Cincinnati District
Office Feed Mill/Animal Proteins Prohibited in Ruminant Feed/Adulterated
View File Himmelspach, William W. 8/08/01 Seattle District Office Animal
Proteins Prohibited in Ruminant Feed
View File Integral Fish Foods, Inc. 6/12/01 Denver District Office Animal
Proteins Prohibited in Ruminant Feed
View File Jefferson Milling Company 4/16/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed
View File Lime Creek Ag Services, Inc. 4/25/01 Minneapolis District Office
Animal Proteins Prohibited in Ruminant Feed
View File Material Resources LLC 5/04/01 Chicago District Office Animal
Proteins Prohibited in Ruminant Feed
View File Material Resources, LLC 5/04/01 Chicago District Office Animal
Protein Prohibited in Ruminant Feed
View File Medina Landmark, Inc. 3/23/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed
View File Minister Farmers Cooperative Exchange, Inc. 4/10/01 Cincinnati
District Office Animal Proteins Prohibited in Ruminant Feed/Feed Mill
View File Peco Foods, Inc. 2/23/01 New Orleans District Office CGMP
Requirements for Medicated Feeds/Animal Proteins Prohibited in Ruminant
Feed
View File Perry Coal and Feed Company 4/16/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed
View File Rietdyk's Milling Company 3/05/01 Seattle District Office Animal
Proteins Prohibited in Ruminant Feed
View File River Valley Co-Op 3/22/01 Cincinnati District Office Animal
Proteins Prohibeted in Ruminant Feed
View File River Valley Co-Op 5/22/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed
View File Round Lake Farmers Coop. 5/30/01 Minneapolis District Office
Animal Proteins Prohibited in Ruminant Feed
View File Rudy, Inc. 3/22/01 Cincinnati District Office Animal Proteins
Prohibited in Ruminant Feed
View File Rudy, Inc. 5/22/01 Cincinnati District Office Animal Proteins
Prohibited in Ruminant Feed
View File Sandy Lake Mills 4/09/01 Philadelphia District Office Animal
Proteins Prohibited in Ruminant Feed
View File Shields Feed and Supply Company 3/07/01 New Orleans District
Office Animal Proteins Prohibited in Ruminant Feed
View File Stewart's Farm Supply 3/21/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed
View File Superior Feeds 6/06/01 Seattle District Office Animal Proteins
Prohibited in Ruminant Feed
View File The Scoular Company 5/30/01 Minneapolis District Office Animal
Proteins Prohibited in Ruminant Feed
View File University of Minnesota 5/10/01 Minneapolis District Office
Animal Proteins Prohibited in Ruminant Feed
View File Valley Feed Mill, Inc. 5/22/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed
View File Wallowa County Grain Growers, Inc. 5/17/01 Seattle District
Office Animal Proteins Prohibited in Ruminant Feed
View File Wallowa County Grain Growers, Inc. 5/17/01 Seattle District
Office Animal Proteins Prohibited in Ruminant Feed
View File Western Reserve Farm Cooperative 3/21/01 Cincinnati District
Office Animal Protein Prohibited in Ruminant Feed
View File Yachere Feed, Inc. 4/09/01 Philadelphia District Office Animal
Proteins Prohibited in Ruminant Feed
View File Z & W Mill, Inc. 3/27/01 Denver District Office Animal
Proteins Prohibited in Ruminant Feed
View File
(TYPE IN 'ANIMAL PROTEIN')
we must not forget the ANIMAL PROTEIN FED TO DEER/ELK. those warning
letters were stopped long ago;
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002
18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-L To: BSE-L
8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed
Analysis Ingredients / Products Feeding Directions
snip...
_animal protein_
BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS
22.6 KG.
snip...
_animal protein_
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage
Products, Roughage Products 15%, Molasses Products, __Animal Protein Products__,
snip...
===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER
Bode's #1 Game Pellets A RATION FOR DEER F3153
GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat (Min) 2.0%
snip...
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage
Products, Roughage Products, 15% Molasses Products, __Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt, snip...
FEEDING DIRECTIONS Feed as Creep Feed with Normal Diet
INGREDIENTS
Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products, __Animal Protein
Products__, L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium
snip...
DIRECTIONS FOR USE
Deer Builder Pellets is designed to be fed to deer under range conditions
or deer that require higher levels of protein. Feed to deer during gestation,
fawning, lactation, antler growth and pre-rut, all phases which require a higher
level of nutrition. Provide adequate amounts of good quality roughage and fresh
water at all times.
DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND
DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER
01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy
Lake, PA 16145 PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted an
inspection of your animal feed manufacturing operation, located in Sandy Lake,
Pennsylvania, on March 23, 2001, and determined that your firm manufactures
animal feeds including feeds containing prohibited materials. The inspection
found significant deviations from the requirements set forth in Title 21, code
of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant
Feed. The regulation is intended to prevent the establishment and amplification
of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being
manufactured at this facility to be misbranded within the meaning of Section
403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found failure to label your swine feed with the required
cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests
that the statement be distinguished by different type-size or color or other
means of highlighting the statement so that it is easily noticed by a
purchaser.
In addition, we note that you are using approximately 140 pounds of cracked
corn to flush your mixer used in the manufacture of animal feeds containing
prohibited material. This flushed material is fed to wild game including deer, a
ruminant animal. Feed material which may potentially contain prohibited material
should not be fed to ruminant animals which may become part of the food
chain.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal feed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law. We have enclosed
a copy of FDA's Small Entity Compliance Guide to assist you with complying with
the regulation... blah, blah, blah...
=============================================
Subject: USA BSE/TSE RUMINANT-TO-RUMINANT FEED BAN VIOLATIONS ''cover-up''
From: "Terry S. Singeltary Sr."
Date: Mon, 2 Dec 2002 11:17:40 -0600 To: BSE-L
Greetings List members,
i have tried to inquire about the USA BSE/TSE feed ban violations with no
luck via USDA/APHIS. since about april or may of 2002, the warning letters have
ceased to be posted publicly, and at the site CVM and Ruminant feed inspections
site url, they have not been updated either. it seems to me the new
administration has taken away all rights for the public to view these
violations.
where are they now being posted ???
you can hide it, but it will not make it go away.
would/could the USDA/APHIS whom lurk on this list, please comment?
GBR risk assessment of BSE should be changed to all TSEs.
USA GBR II should be changed to GBR III immediately!
TSS
Terry S. Singeltary Sr. wrote:
> X-Virus-Scanner: Found to be clean > Message-ID: <[log in to
unmask]> > Date: Tue, 20 May 2003 08:39:31 -0500 > Reply-To: Bovine
Spongiform Encephalopathy Sender: Bovine Spongiform
Encephalopathy
> > From: "Terry S. Singeltary Sr." <[log in to unmask]> >
Subject: MAD COW FEED BAN WARNING LETTER USA 2003 > > ######## Bovine
Spongiform Encephalopathy > > Public Health Service Food and Drug
Administration > > Minneapolis District Office Central Region 212 Third
Avenue South > Minneapolis, MN 56401 Telephone: (612) 334-4100 FAX: (612)
334-4134 > > May 6, 2003 > > WARNING LETTER CERTIFIED MAIL RETURN
RECEIPT REQUESTED Refer to MIN 03 > - 20 > > Steve L. Denk President
Barr Animal Foods A Division of Barr > Enterprises, Inc. W7276 Chickadee Road
Greenwood, Wisconsin 54437 > > Dear Mr. Denk: > > On April 8, 2003,
an investigator from the Food and Drug > Administration (FDA) inspected your
rendering and animal feed > manufacturing operation located at W7276
Chickadee Road, Greenwood, > WI. This inspection found significant deviations
from the requirements > set forth in Title 21, Code of Federal Regulations,
Part 589.2000, > "Animal Proteins Prohibited in Ruminant Feed" (21 CFR
589.2000). The > regulation is intended to prevent the establishment and
amplification > of Bovine Spongiform Encephalopathy (BSE). Under 21 CFR >
589.2000(g)(2), such deviations cause products being manufactured > and/or
distributed by this facility to be deemed misbranded within the > meaning of
Section 403(a)(1) of the Federal Food, Drug and Cosmetic > Act (the Act), and
these products may not be lawfully introduced, or > delivered for
introduction, into interstate commerce. > > Products that contain or may
contain protein derived from mammalian > tissues and are intended for use in
animal feed must be labeled with > the cautionary statement, "Do not feed to
cattle or other ruminants." > This is required by 21 CFR 589.2000(c)(1)(i).
The FDA suggests the > statement be distinguished by different type size or
color, or other > means of highlighting the statement so that it is easily
noticed by a > purchaser. Our inspection found that you are not labeling your
> 50-pound blocks of frozen beef and bulk loads of beef bone chips and >
rendering waste, which are intended for animal feed, with that caution >
statement. As a result, these products are misbranded within the > meaning of
Section 403(a)(1) of the Act. > > The above is not intended to be an
all-inclusive list of deviations > from the regulations. As a renderer and
manufacturer of materials > intended for animal feed use, you are responsible
for ensuring that > your overall operation and the products you manufacture
and distribute > are in compliance with the law. We have enclosed a copy of
the FDA s > Small Entity Compliance Guide Nos. 67 and 68 to assist you with
> complying with the regulation. > > You should take prompt action to
correct these violations and you > should establish a system whereby such
violations do not recur. > Failure to promptly correct these violations may
result in regulatory > action without further notice. These actions include,
but are not > limited to, seizure and/or injunction. > > It is
necessary for you to take action on this matter now. Please > provide this
office a written response within 15 working days of > receipt of this letter
with the steps you have taken to bring your > firm into compliance with the
law. Your response should include an > explanation of each step being taken
to correct the violations and > prevent their recurrence. If corrective
action cannot be taken within > 15 working days, state the reason for the
delay and the date by which > the corrections will be completed. Please
include copies of any > available documentation demonstrating that
corrections have been made. > > Your reply should be directed to
Compliance Officer Timothy G. Philips > at the address indicated on the
letterhead. > > Sincerely, > > /s/ > > David R. Yost for W.
Charles Becoat > > Minneapolis District > > http://www.fda.gov/foi/warning_letters/g4000d.htm
> > Greetings List Members, > > what a surprise to see this posting
of warning letter for feeding > ruminants to ruminants in the USA, simply
astonishing. my question is, > if they cannot stop this practice of feeding
cows to cows in the USA > in 2003, after some 6 years (since 8/4/97 partial
and voluntary), how > in the world do they plan on enforcing a ban on
deer/elk products from > entering the feed market? > > FDA Issues Draft
Guidance on Use of Material From Deer and Elk in > Animal Feed > > http://www.fda.gov/bbs/topics/ANSWERS/2003/ANS01220.html
> > > TSS > > RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE
- CLASS II > ______________________________ > > PRODUCT > Unlabeled
bulk "Cattle Feed" sold by weight to user/farmers who pick it > up at the
firm. Product is a ruminant feed used to feed beef cattle. > Recall #
V-046-3. > CODE > Product is bulk and uncoded. > RECALLING
FIRM/MANUFACTURER > Zephyr Feed Company, Zephyrhills, FL., by letters on
March 19, 2003 and > March 26, 2003. FDA initiated recall is ongoing. >
REASON > Cattle feed was distributed to farmers that may contain prohibited
> protein for ruminants. > VOLUME OF PRODUCT IN COMMERCE > 517,990 lbs.
> DISTRIBUTION > FL. > > http://www.fda.gov/bbs/topics/enforce/2003/ENF00792.html
> > > RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE--CLASS II >
> _____________________________ > PRODUCT > Red Rooster Booster, Super
Gallo (brand), 60 capsules. Recall # V-011-3. > CODE > All codes. >
RECALLING FIRM/MANUFACTURER > Thomas Laboratories, Tolleson, AZ, by letters
on or about November 8, > 2002. State initiated recall is ongoing. >
REASON > Is not labeled "Do not feed to cattle or other ruminants" and
contains a > bovine tissue derivative. > VOLUME OF PRODUCT IN COMMERCE
> Unknown. > DISTRIBUTION > Nationwide. > >
_____________________________ > > PRODUCT > CATTLE FEED, Flock #999,
Date: 12/5/02, Quantity 8000, Load A, Feed > C205, Grower# Z001, Tag C100.
Recall # V-012-3. > CODE > C-205, C-210, C-220, C-302, C-406 and all other
codes manufactured and > distributed by Grove River Mills, Inc., >
RECALLING FIRM/MANUFACTURER > Grove River Mills Inc., Pendergrass, GA, by
telephone and letter on > December 9, 2002. Firm initiated recall is ongoing.
> REASON > Cattle Feed contaminated with prohibited materials. > VOLUME
OF PRODUCT IN COMMERCE > 235,668 lbs. > DISTRIBUTION > GA. > >
END OF ENFORCEMENT REPORT FOR FEBRUARY 5, 2003 > > http://www.fda.gov/bbs/topics/enforce/2003/ENF00781.html
> > another description here; > > > FEBRUARY 2003 > >
PRODUCT Red Rooster Booster, Super Gallo (brand), 60 capsules. > > CODE
All codes. > RECALLING FIRM/MANUFACTURER Thomas Laboratories, Tolleson, AZ,
> > REASON Is not labeled "Do not feed to cattle or other ruminants" and
> contains a bovine tissue derivative. > VOLUME OF PRODUCT IN COMMERCE
Unknown. > DISTRIBUTION Nationwide. > > > PRODUCT CATTLE FEED, Flock
#999, Date: 12/5/02, Quantity 8000, Load A, > Feed C205, Grower# Z001, Tag
C100. > > CODE C-205, C-210, C-220, C-302, C-406 and all other codes
manufactured > and distributed by Grove River Mills, Inc., > RECALLING
FIRM/MANUFACTURER Grove River Mills Inc., Pendergrass, GA, > > REASON
Cattle Feed contaminated with prohibited materials. > VOLUME OF PRODUCT IN
COMMERCE 235,668 lbs. > DISTRIBUTION GA. > > http://www.recalls.org/vet2003.html
> > Red Rooster Booster - 60 Capsules $7.95 > 210-4610-C03 > >
> > Concentrated nutritional supplement for body building gamebirds. >
> > http://www.thomasveterinarydrug.com/mailorder/catalog/product_info.php?manufacturers_id=11&products_id=65
> > > interesting; > Bone Meal with D3 - 25 lb. Powder $69.95 >
520-0210-P09 > > > http://www.thomasveterinarydrug.com/mailorder/catalog/product_info.php?manufacturers_id=11&products_id=651
> > > >
Subject: MAD COW FEED BAN WARNING LETTER USA (a real hum dinger) !
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Reply-To: Bovine Spongiform Encephalopathy <[log in to unmask]>
Date: Tue, 10 Jun 2003 07:43:21 -0500
######## Bovine Spongiform Encephalopathy <[log in to unmask]>
#########
Public Health Service Food and Drug Administration
New Orleano District Nashville Branch Office Plus Park Blvd. Nashville, TN
37217 Tel: 615-781-6388 FAX: 615-781-6383
May 22, 2003
VIA FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. John F. Turner, Owner, Manager Millstone Agri Distributors 3721 E.
Lamar Alexander Highway Maryville, TN 37804
Warning Letter No 03-NSV-16
Dear Mr. Turner:
An inspection of your animal feed manufacturing operation, located at
Maryville, Tennessee conducted by a U.S. Food and Drug Administration
investigator on February 13, 2003, found significant deviations from the
requirements set forth in Title 21, Code of Federal Regulations (21 CFR.), Part
589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is
intended to prevent the establishment and amplification of Bovine Spongiform
Encephalopathy (BSE). Because you failed to follow this rule, products you
manufactured and distributed are adulterated within the meaning of Sections
402(a)(2)(C) and 402(a)(4) of the Federal Food, Drug, and Cosmetic Act (the Act)
since they contain an unsafe food additive and were prepared, packed, or held
under insanitary conditions . . . whereby [they] may have been rendered
injurious to health. Feed you manuf~tured also was misbranded within the
meaning of Section 403(a)(1) of the Act because of your failure to follow this
rule.
Our investigation found the following violations of 21 C.F.R.
589.2000:
1. Failure to separate the receipt, processing, and storage of products
containing prohibited material from products not containing prohibited material
[21 C.F.R. 589.2000(e)(1)(iv)];
2. Failure to establish written procedures, including clean-out and
flushing procedures, to avoid commingling and cross-contamination of common
equipment [21 C.F.R. 589.2000(e)(1)(iii)(B)];
3. Failure to maintain records sufficient to track prohibited materials
throughout the receipt, processing, and distribution of your products [21 C.F.R.
589.2000(c)(1)(ii)];
4. Failure to provide for measures to avoid commingling or
cross-contamination of feeds intended for ruminants and feeds intended for
nonruminants that may contain prohibited materials [21 C.F.R.
589.2000(c)(1)(iii)]. Specifically, our investigation found that the ruminant
product 10% Beef Conditioned was formulated primarily with screenings and
fines derived from previously manufactured non-ruminant products, Premium
Rooster Kicker in particular, that contain or may contain prohibited material.
Such deviations cause the ruminant product 10% Beef Conditioner being
manufactured at this facility to be adulterated within the meaning of Sections
402(a)(2)(C) and 402(a)(4) of the Act;
5. Failure to label your non-ruminant products with the required cautionary
statement Do not Feed to Cattle or Other Ruminants [21 C.F.R.
589.2000(c)(1)(ii)]. Our investigation specifically found that dog food
containing prohibited material was added as an ingredient to your product
Premium Rooster Kicker. The failure of these feeds to bear the required BSE
warning statement causes them to be misbranded within the meaning of Section
403(f) of the Act.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal feed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law. We have enclosed
a copy of the FDA s Small Entity Compliance Guide to assist you with complying
with the regulations.
You should take prompt action to correct these violations, and you should
establish a system whereby such violations do not recur. Failure to promptly
correct these violations may result in regulatory action without further notice,
such as seizure and/or injunction. You should notify this office in writing
within 15 working days of receipt of this letter of the steps you have taken to
bring your iirm into compliance with the law. Your response should include an
explanation of each step being taken to correct the violations, and prevent
their recurrence. If corrective action cannot be completed in 15 working days,
state the reason for the delay and the date by which the corrections will be
completed. Include copies of any available documentation demonstrating that
corrections have been made.
Your reply should be directed to the attention of Joseph E. Hayes,
Compliance Officer, U.S. Food and Drug Administration, 297 Plus Park Boulevard,
Nashville, TN 37217.
Sincerely,
/s/ Carl E. Draper Director, New Orleans District Office
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE
sampling FROM HEALTHY USDA CATTLE)
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February
2007 to charges of theft of Government funds, mail fraud, and wire fraud. The
owner and his company defrauded the BSE Surveillance Program when they falsified
BSE Surveillance Data Collection Forms and then submitted payment requests to
USDA for the services.
In addition to the targeted sample population (those cattle that were more
than 30 months old or had other risk factors for BSE),
*** the owner submitted to USDA, or caused to be submitted, BSE obex (brain
stem) samples from healthy USDA-inspected cattle.
As a result, the owner fraudulently received approximately $390,000.
Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1
include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for
specified risk material (SRM) violations and improved inspection controls over
SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in
future semiannual reports as the relevant audits and investigations are
completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain
location and PrPsc by PMCA only, how many cases have we missed?
***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.
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Conclusions We demonstrated that the agent of L-BSE can be transmitted by
the oral route from cattle to mouse lemurs. As expected, orally inoculated
animals survived longer than IC-inoculated animals. Orally inoculated lemurs had
less severe clinical signs and symptoms, with no evidence of motor dysfunction.
It was previously suggested that the agent of L-BSE might be involved in the
foodborne transmission of a prion disease in mink (11,12), a species in which
several outbreaks of transmissible mink encephalopathy had been identified,
notably in the United States (13).
Our study clearly confirms, experimentally, the potential risk for
interspecies oral transmission of the agent of L-BSE. In our model, this risk
appears higher than that for the agent of classical BSE, which could only be
transmitted to mouse lemurs after a first passage in macaques (14). We report
oral transmission of the L-BSE agent in young and adult primates. Transmission
by the IC route has also been reported in young macaques (6,7). A previous study
of L-BSE in transgenic mice expressing human PrP suggested an absence of any
transmission barrier between cattle and humans for this particular strain of the
agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus,
it is imperative to maintain measures that prevent the entry of tissues from
cattle possibly infected with the agent of L-BSE into the food chain.
Dr Mestre-Francés is an assistant professor at the École Pratique des
Hautes Études. Her research focuses on neurodegenerative diseases (Alzheimer
disease, prion diseases) in the nonhuman primate model Microcebus murinus.
*** Needless conflict ***
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
Published online 16 May 2012
Terry S. Singeltary Sr. said:
I kindly wish to submit the following please ;
"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 they did before 2005
suspect," Brown said.
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened ***
Thursday, January 14, 2016
*** EMERGING ANIMAL DISEASES Actions Needed to Better Position USDA to
Address Future Risks Report to the Chairman, Committee on Energy and Commerce,
House of Representatives December 2015 GAO-16-132
GAO
Wednesday, March 2, 2016
*** RANCHO He did not know that they were placing healthy cow heads next to
suspect carcasses BSE TSE Prion ***
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials BSE TSE Prion
Thursday, June 12, 2014
Missouri Firm Recalls Ribeye and Carcass Products That May Contain
Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal
root ganglia may not have been completely removed
Saturday, November 10, 2012
Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk
Materials Nov 9, 2012 WI Firm Recalls Beef Tongues
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the
tongue and nasal mucosa of terminally diseased cattle
SPECIFIED RISK MATERIALS SRMs
seems USDA NSLP et al thought that it would be alright, to feed our
children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high
risk cattle for mad cow type disease, and other dangerous pathogens, and they
did this for 4 years, that was documented, then hid what they did by having a
recall, one of the largest recalls ever, and they made this recall and masked
the reason for the recall due to animal abuse (I do not condone animal abuse),
not for the reason of the potential for these animals to have mad cow BSE type
disease (or other dangerous and deadly pathogens). these TSE prion disease can
lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE
NEXT 5 DECADES FOR CJD ???
Saturday, September 21, 2013
Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry
Center January 2010 THE FLIM-FLAM REPORT
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH
RISK FOR MAD COW DISEASE ??? this recall was not for the welfare of the animals.
...tss you can check and see here ; (link now dead, does not work...tss)
see listings of schools from state to state, county to county, was your
child exposed ;
try this link ;
2015-2016
Friday, March 18, 2016
CFSAN Constituent Update: FDA Announces Final Rule on Bovine Spongiform
Encephalopathy BSE MAD COW TSE PRION
Center for Food Safety and Applied Nutrition - Constituent Update
Thursday, February 25, 2016
U.S. Food & Drug Administration (FDA) FDA/CFSAN Cosmetics Update:
Cosmetics Program; Import and Domestic and Transmissible Spongiform
Encephalopathy TSE Prion Disease Risk Factors
***WARNING TO ALL CONSUMERS AND COUNTRIES AROUND THE WORLD***
***Note: FDA labs do not conduct BSE analysis and thus no sampling guidance
is issued for BSE. ***
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
Friday, February 05, 2016
Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission ***
Sunday, January 17, 2016
Of Grave Concern Heidenhain Variant Creutzfeldt Jakob Disease
Saturday, February 13, 2016
The Risk of Prion Infection through Bovine Grafting Materials in dentistry
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. ...
CANINE AND FELINE TSE PRION AND PET FOOD
Assessing Transmissible Spongiform Encephalopathy Species Barriers with an
In Vitro Prion Protein Conversion Assay
Christopher J. Johnson1, Christina M. Carlson2, Aaron R. Morawski3, Alyson
Manthei4, Neil R. Cashman5
1USGS National Wildlife Health Center, 2Department of Soil Science,
University of Wisconsin–Madison, 3Laboratory of Immunology, National Institute
of Allergy and Infectious Diseases, National Institutes of Health, 4Merial
Veterinary Scholars Program, School of Veterinary Medicine, University of
Wisconsin–Madison, 5Department of Neurology, University of British Columbia
Summary
Measuring the barrier to the interspecies transmission of prion diseases is
challenging and typically involves animal challenges or biochemical assays.
Here, we present an in vitro prion protein conversion assay with the ability to
predict species barriers.
Date Published: 3/10/2015, Issue 97; doi: 10.3791/52522
Keywords: Medicine, Issue 97, Prion, species barrier, conversion,
immunoblotting, transmissible spongiform encephalopathy, interspecies
transmission Cite this Article
Johnson, C. J., Carlson, C. M., Morawski, A. R., Manthei, A., Cashman, N.
R. Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In
Vitro Prion Protein Conversion Assay. J. Vis. Exp. (97), e52522,
doi:10.3791/52522 (2015). Abstract
Studies to understanding interspecies transmission of transmissible
spongiform encephalopathies (TSEs, prion diseases) are challenging in that they
typically rely upon lengthy and costly in vivo animal challenge studies. A
number of in vitro assays have been developed to aid in measuring prion species
barriers, thereby reducing animal use and providing quicker results than animal
bioassays. Here, we present the protocol for a rapid in vitro prion conversion
assay called the conversion efficiency ratio (CER) assay. In this assay cellular
prion protein (PrPC) from an uninfected host brain is denatured at both pH 7.4
and 3.5 to produce two substrates. When the pH 7.4 substrate is incubated with
TSE agent, the amount of PrPC that converts to a proteinase K (PK)-resistant
state is modulated by the original host’s species barrier to the TSE agent. In
contrast, PrPC in the pH 3.5 substrate is misfolded by any TSE agent. By
comparing the amount of PK-resistant prion protein in the two substrates, an
assessment of the host’s species barrier can be made. We show that the CER assay
correctly predicts known prion species barriers of laboratory mice and, as an
example, show some preliminary results suggesting that bobcats (Lynx rufus) may
be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting
disease agent.
>>> show some preliminary results suggesting that bobcats (Lynx
rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic
wasting disease agent.
AD.63: Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1
1Colorado State University; Fort Collins, CO USA; 2University of Minnesota;
Saint Paul, MN USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD. These results demonstrate that
CWD can be transmitted and adapted to the domestic cat, thus raising the issue
of potential cervid-to- feline transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Monday, August 8, 2011
Susceptibility of Domestic Cats to CWD Infection
Sunday, August 25, 2013
Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats,
blood, and mother to offspring transmission
Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK
in 1990. Most cases have been reported in the UK, where the epidemic has been
consistent with that of the BSE epidemic. Some other countries (e.g. Norway,
Liechtenstein and France) have also reported cases.
Most cases have been reported in domestic cats but there have also been
cases in captive exotic cats (e.g. Cheetah, Lion, Asian leopard cat, Ocelot,
Puma and Tiger). The disease is characterised by progressive nervous signs,
including ataxia, hyper-reactivity and behavioural changes and is fatal.
The chemical and biological properties of the infectious agent are
identical to those of the BSE and vCJD agents. These findings support the
hypothesis that the FSE epidemic resulted from the consumption of food
contaminated with the BSE agent.
The FSE epidemic has declined as a result of tight controls on the disposal
of specified risk material and other animal by-products.
References: Leggett, M.M. et al.(1990) A spongiform encephalopathy in a
cat. Veterinary Record. 127. 586-588
Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat.
Veterinary Record. 129. 320
Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform
encephalopathy in five domestic cats. Veterinary Record. 129. 233.
Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J.
Small Animal Practice. 33. 471-476.
Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and
PrP studies. Veterinary Record. 131. 307-310.
Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma
(Felis concolor). Veterinary Record. 131. 431-434.
Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy
to mice. Veterinary Record 134. 449.
Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in
Norway. Veterinary Record 136. 444
Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in
France. Veterinary Record 141. 270-271
Zanusso, G et al. (1998) Simultaneous occurrence of spongiform
encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp
1116-1117.
Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural
tissues of cats with feline spongiform encephalopathy. Veterinary Record 146.
437-441
Kelly, D.F. et al. (2005) Neuropathological findings in cats with
clinically suspect but histologically unconfirmed feline spongiform
encephalopathy. Veterinary Record 156. 472-477.
3 further cheetah cases have occured, plus 1 lion, plus all the primates,
and 20 additional house cats. Nothing has been published on any of these UK
cases either. One supposes the problem here with publishing is that many
unpublished cases were _born_ long after the feed "ban". Caught between a rock
and a hard place: leaky ban or horizontal transmission (or both).
YOU explained that imported crushed heads were extensively used in the
petfood industry...
http://web.archive.org/web/20060303042720/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://web.archive.org/web/20040301231838/http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf
http://web.archive.org/web/20060303042732/http://www.bseinquiry.gov.uk/files/yb/1989/04/25001001.pdf
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://web.archive.org/web/20060303042739/http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf
*** Meldrum's notes on pet foods and materials used
http://web.archive.org/web/20060303042745/http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf
*** BSE & Pedigree Petfoods ***
http://web.archive.org/web/20060303042725/http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf
In 2003, Denver Post reporter Theo Stein interviewed scientists about CWD
spreading though deer and elk in Colorado. Dr. Valerius Geist, who paradoxically
has become a darling of anti-wolfers, made this assertion about the significance
of wolves in containing CWD spread via proteins called prions.
“Wolves will certainly bring the disease to a halt,” he said. “They will
remove infected individuals and clean up carcasses that could transmit the
disease.”
Stein added that “Geist and Princeton University biologist Andrew Dobson
theorize that killing off the wolf allowed CWD to take hold in the first
place.”
Wolves aren’t alone. In a 2009 study titled “Mountain lions prey
selectively on prion-infected mule deer,” researchers in Colorado discovered
that “adult mule deer killed by mountain lions were more likely to be
prion-infected than were deer killed more randomly … suggesting that mountain
lions were selecting for infected individuals when they targeted adult
deer.”
NO, NO, NOT NO, BUT HELL KNOW !!!
PLEASE be careful what you ask for.
recently, canine spongiform encephalopathy has been confirmed.
I proved this in 2005, with a letter from MAFF/DEFRA et al confirming my
suspicions of the ‘hound study’ way back. this was covered up. see documents
below.
also, recently, cwd to the domestic cat is a great concern.
even though to date, as far as I am aware of, the cwd study on the mountain
lion has not produced any confirmation yet, we already know that the feline
species is highly succeptible to the TSE prion. domestic cats and the exotic zoo
big cats.
so in my honest opinion, any program that would use wild animals to prey on
other wild animals, as a tool to help curb CWD TSE prion disease, would only
help enhance the spread of disease, and it would only help spread the disease to
other species. ...TSS
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
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.
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, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
=======================================
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
2005
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 ;
Friday, March 8, 2013
Dogs may have been used to make Petfood and animal feed
Tuesday, June 11, 2013
Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant
deviations from requirements in FDA regulations that are intended to reduce the
risk of bovine spongiform encephalopathy (BSE) within the United States
I lost my mother to the hvCJD and just made a promise, never forget, and
never let them forget, or we might all forget... Wednesday, January 06, 2016
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE U.K. 23rd ANNUAL REPORT 2014
(published 18th November 2015)
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Terry S. Singeltary Sr.
Evidence for human transmission of amyloid-β pathology and cerebral amyloid
angiopathy
07 02:27 AM
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-β pathology and cerebral
amyloid angiopathy
2015-12-07 02:27 AM
Terry S. Singeltary Sr. said: re-Evidence for human transmission of
amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
I would kindly like to comment on the Nature Paper, the Lancet reply, and
the newspaper articles.
First, I applaud Nature, the Scientist and Authors of the Nature paper, for
bringing this important finding to the attention of the public domain, and the
media for printing said findings.
Secondly, it seems once again, politics is getting in the way possibly of
more important Transmissible Spongiform Encephalopathy TSE Prion scientific
findings. findings that could have great implications for human health, and
great implications for the medical surgical arena. but apparently, the
government peer review process, of the peer review science, tries to intervene
again to water down said disturbing findings.
where have we all heard this before? it’s been well documented via the BSE
Inquiry. have they not learned a lesson from the last time?
we have seen this time and time again in England (and other Country’s) with
the BSE mad cow TSE Prion debacle.
That ‘anonymous' Lancet editorial was disgraceful. The editor, Dick Horton
is not a scientist.
The pituitary cadavers were very likely elderly and among them some were on
their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients who got
pooled extracts injected from thousands of cadavers were 100% certain to have
been injected with both seeds. No surprise that they got both diseases going
after thirty year incubations.
That the UK has a "system in place to assist science journalists" to squash
embargoed science reports they find ‘alarming’ is pathetic.
Sounds like the journalists had it right in the first place: ‘Alzheimer’s
may be a transmissible infection’ in The Independent to ’You can catch
Alzheimer’s’ in The Daily Mirror or ‘Alzheimer’s bombshell" in The Daily
Express.
if not for the journalist, the layperson would not know about these
important findings.
where would we be today with sound science, from where we were 30 years
ago, if not for the cloak of secrecy and save the industry at all cost
mentality?
when you have a peer review system for science, from which a government
constantly circumvents, then you have a problem with science, and humans die.
to date, as far as documented body bag count, with all TSE prion named to
date, that count is still relatively low (one was too many in my case, Mom
hvCJD), however that changes drastically once the TSE Prion link is made with
Alzheimer’s, the price of poker goes up drastically.
so, who makes that final decision, and how many more decades do we have to
wait?
the iatrogenic mode of transmission of TSE prion, the many routes there
from, load factor, threshold from said load factor to sub-clinical disease, to
clinical disease, to death, much time is there to spread a TSE Prion to
anywhere, but whom, by whom, and when, do we make that final decision to do
something about it globally? how many documented body bags does it take? how
many more decades do we wait? how many names can we make up for one disease, TSE
prion?
Professor Collinge et al, and others, have had troubles in the past with
the Government meddling in scientific findings, that might in some way involve
industry, never mind human and or animal health.
FOR any government to continue to circumvent science for monetary gain,
fear factor, or any reason, shame, shame on you.
in my opinion, it’s one of the reasons we are at where we are at to date,
with regards to the TSE Prion disease science i.e. money, industry, politics,
then comes science, in that order.
greed, corporate, lobbyist there from, and government, must be removed from
the peer review process of sound science, it’s bad enough having them in the
pharmaceutical aspect of healthcare policy making, in my opinion.
my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer’s
of some type (no autopsy?). just made a promise, never forget, and never let
them forget, before I do.
I kindly wish to remind the public of the past, and a possible future we
all hopes never happens again. ...
[9. Whilst this matter is not at the moment directly concerned with the
iatrogenic CJD cases from hgH, there remains a possibility of litigation here,
and this presents an added complication. There are also results to be made
available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on
the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention
of iatrogenic CJD transmission in neurosurgery, all of which will serve to
increase media interest.]
snip...see full Singeltary Nature comment here;
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the
intra- and cross-species transmission of AA amyloidosis Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by
extracellular deposition of AA fibrils. AA fibrils are found in several tissues
from food animals with AA amyloidosis. For hygienic purposes, heating is widely
used to inactivate microbes in food, but it is uncertain whether heating is
sufficient to inactivate AA fibrils and prevent intra- or cross-species
transmission. We examined the effect of heating (at 60 °C or 100 °C) and
autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western
blot analysis, transmission electron microscopy (TEM), and mouse model
transmission experiments. TEM revealed that a mixture of AA fibrils and
amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at
135 °C produced large amorphous aggregates. AA fibrils retained antigen
specificity in Western blot analysis when heated at 100 °C or autoclaved at 121
°C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and
bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly
stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA
fibrils at 121 °C or 135 °C significantly decreased amyloid deposition.
Moreover, amyloid deposition in mice injected with murine AA fibrils was more
severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils
autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These
results suggest that AA fibrils are relatively heat stable and that similar to
prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA
fibrils. These findings may contribute to the prevention of AA fibril
transmission through food materials to different animals and especially to
humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD
54.00
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
the warning shots fired over the bow of the boat that were never heard ;
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...
NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE
snip...
I was quite prepared to believe in unofficial pituitary hormones, also in
the 1970's, whether as described by Dr. Little, or in other circumstances, for
animal use.
snip...
The fact that there were jars of pituitaries (or extract) around on shelves
is attested by the still potent 1943 pituitaries, described in Stockell Hartree
et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the
trouble to collect them, they were not lightly thrown out...
3. The extraction is from a pool of pituitary glands collected from
abbatoirs and the process used is unlikely to have any effect on the BSE agent.
Hormones extracted from human pituitary glands have been responsible for a small
number of Creutzfeldt Jacob disease in man.
SEE LOOPHOLE ;
SEE LOOPHOLE SHOULD BE CLOSED ;
snip...see at bottom ;
Thursday, August 13, 2015
Iatrogenic CJD due to pituitary-derived growth hormone with genetically
determined incubation times of up to 40 years
*** PRION2015 Alzheimer’s disease ***
*** P.34: Preliminary study of Alzheimer’s disease transmission to bank
vole
Guido Di Donato1, Geraldina Riccardi1, Claudia D’Agostino1, Flavio
Torriani1, Maurizio Pocchiari2, Romolo Nonno1, Umberto Agrimi1, and Michele
Angelo Di Bari1
1Department of Food Safety and Veterinary Public Health Istituto Superiore
di Sanit a, Rome, Italy; 2Department of Cellular Biology and Neuroscience;
Istituto Superiore di Sanit a, Rome, Italy
Extensive experimental findings indicate that prion-like mechanisms underly
the pathogenesis of Alzheimer disease (AD). Transgenic mice have been pivotal
for investigating prionlike mechanisms in AD, still these models have not been
able so far to recapitulate the complex clinical-pathological features of AD.
Here we aimed at investigating the potential of bank vole, a wild-type rodent
highly susceptible to prions, in reproducing AD pathology upon experimental
inoculation.
Voles were intracerebrally inoculated with brain homogenate from a familial
AD patient. Animals were examined for the appearance of neurological signs until
the end of experiment (800 d post-inoculation, d.p.i.). Brains were studied by
immunohistochemistry for pTau Prion 2015 Poster Abstracts S29 (with AT180 and
PHF-1 antibodies) and b-amyloid (4G8).
Voles didn’t show an overt clinical signs, still most of them (11/16) were
found pTau positive when culled for intercurrent disease or at the end of
experiment. Interestingly, voles culled as early as 125 d.p.i. already showed
pTau aggregates. Deposition of pTau was similar in all voles and was
characterized by neuropil threads and coiled bodies in the alveus, and by rare
neurofibrillary tangles in gray matter. Conversely, b-amyloid deposition was
rather rare (2/16). Nonetheless, a single vole showed the contemporaneous
presence of pTau in the alveus and a few Ab plaque-like deposits in the
subiculum. Uninfected age-matched voles were negative for pTau and Ab.
*** These findings corroborate and extend previous evidences on the
transmissibility of pTau and Ab aggregation. Furthermore, the observation of a
vole with contemporaneous propagation of pTau and Ab is intriguing and deserves
further studies.
=================
P.155: Quantitative real-time analysis of disease specific tau amyloid
seeding activity
Davin Henderson and Edward Hoover Prion Research Center; College of
Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort
Collins, CO USA
A leading hypothesis for the cause of neurodegenerative diseases is the
templated misfolding of cellular proteins to an amyloid state. Spongiform
encephalopathies were the first diseases discovered to be caused by a misfolded
amyloid-rich protein. It is now recognized that the major human
neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s
disease (PD), and chronic traumatic encephalopathy (CTE), also are associated
with amyloid formation. Moreover, AD and PD amyloids have been shown competent
to transmit disease in experimental animal models, suggesting shared mechanisms
with traditional prion diseases. Sensitive detection of prion disease has been
advanced by in vitro amplification of low levels of disease specific amyloid
seeds, e.g. serial protein misfolding amplification (sPMCA), amyloid seeding
(ASA) and real-time quaking induced conversion (RT-QuIC), thereby replicating
the disease process in vitro. In addition, measurement of the amyloid formation
rate can estimate the level of disease-associated seed by using methods
analogous to quantitative polymerase chain reaction (qPCR). In the present work,
we apply these principles to show that seeding activity of in vitro generated
amyloid tau and AD brain amyloid tau can be readily detected and
quantitated.
=============
P.83: Gerstmann-Str€aussler-Scheinker disease with F198S mutation:
Selective propagation of PrPSc and pTau upon inoculation in bank vole
Michele Angelo Di Bari1, Romolo Nonno1, Laura Pirisinu1, Claudia
D’Agostino1, Geraldina Riccardi1, Guido Di Donato1, Paolo Frassanito1,
Bernardino Ghetti2, Pierluigi Gambetti3, and Umberto Agrimi1
1Department of Veterinary Public Health and Food Safety; Istituto Superiore
di Sanit a; Rome, Italy;
2Indiana University-Purdue University Indianapolis; Department of Pathology
and Laboratory Medicine; Indianapolis, IN USA; 3Case Western Reserve University;
Cleveland, OH USA
Gerstmann-Str€aussler-Scheinker disease with F198S mutation (GSS-F198S) is
characterized by the presence of PrP amyloid plaques as well as neurofibrillary
tangles with abnormally-phosphorylated tau protein (pTau) in the brain. The
relationship between tau protein and PrP in the pathogenesis of GSS-F198S is
unknown. In a previous study, we inoculated intracerebrally 2 GSS-F198S cases in
2 lines of voles carrying either methionine (Bv109M) or isoleucine (Bv109I) at
codon 109 of PrP. GSS-F198S transmitted rather efficiently to Bv109I, but not to
Bv109M.
Here we investigated the presence of pTau, as assessed by
immunohistochemistry with anti-pTau antibodies AT180 and PHF-1, in the same
voles previously inoculated with GSSF198S. Among these voles, most Bv109I showed
clinical signs after short survival times (»150 d.p.i.) and were positive for
PrPSc. The remaining Bv109I and all Bv109M survived for longer times without
showing prion-related pathology or detectable PrPSc. All Bv109I which were
previously found PrPSc-positive,
S54 Prion 2015 Poster Abstracts
were immunonegative for pTau deposition. In contrast, pTau deposition was
detected in 16/20 voles culled without clinical signs after long survival times
(225–804 d.p.i.). pTau deposition was characterized by neuropil threads and
coiled bodies in the alveus, and was similar in all voles analyzed.
These findings highlight that pTau from GSS-F198S can propagate in voles.
Importantly, pTau propagation was independent from PrPSc, as pTau was only found
in PrPSc-negative voles surviving longer than 225 d.p.i. Thus, selective
transmission of PrPSc and pTau proteinopathies from GSS-F198S can be
accomplished by experimental transmission in voles.
=========
=========
I3 Aβ Strains and Alzheimer’s Disease
Lary Walker Emory University, Atlanta, GA, USA
An essential early event in the development of Alzheimer’s disease is the
misfolding and aggregation of Aβ. Enigmatically, despite the extensive
deposition of human-sequence Aβ in the aging brain, nonhuman primates do not
develop the full pathologic or cognitive phenotype of Alzheimer’s disease, which
appears to be unique to humans. In addition, some humans with marked Aβ
accumulation in the brain retain their cognitive abilities, raising the question
of whether the pathogenicity of Aβ is linked to the molecular features of the
misfolded protein. I will present evidence for strain-like molecular differences
in aggregated Aβ between humans and nonhuman primates, and among end-stage
Alzheimer patients. I will also discuss a case of Alzheimer’s disease with
atypical Aβ deposition to illustrate heterogeneity in the molecular architecture
of Aβ assemblies, and how this variability might influence the nature of the
disease. As in the case of prion diseases, strain-like variations in the
molecular architecture of Aβ could help to explain the phenotypic variability in
Alzheimer’s disease, as well as the distinctively human susceptibility to the
disorder.
This research was conducted in collaboration with Harry LeVine, Rebecca
Rosen, Amarallys Cintron, David Lynn, Yury Chernoff, Anil Mehta and Mathias
Jucker and colleagues. Supported by AG040589, RR165/OD11132, AG005119, NS077049,
the CART Foundation and MetLife.
==========
I5 Pathogenic properties of synthetically generated prions
Jiyan Ma Van Andel Research Institute, Grand Rapids, Michigan, USA
Synthetically generating prions with bacterially expressed recombinant
prion protein (recPrP) strongly supports the prion hypothesis. Yet, it remains
unclear whether the pathogenic properties of synthetically generated prions
(rec-Prion) fully recapitulate those of naturally occurring prions. A series of
analyses including intracerebral and intraperitoneal transmissions of rec-Prion
in wild-type mice were performed to determine the characteristics of rec-Prion
induced diseases. Results from these analyses demonstrated that the rec-Prion
exhibits the same pathogenic properties with naturally occurring prions,
including a titratable infectivity that can be determined by endpoint titration
assays, capability of transmitting prion disease via routes other than the
direct intra-cerebral inoculation, causing ultra-structural lesions that are
specific to prion disease, and sharing a similar manner of visceral
dissemination and neuroinvasion with naturally occurring scrapie and chronic
wasting disease. These findings confirmed that the disease caused by rec-Prion
in wild-type mice is bona fide prion disease or transmissible spongiform
encephalopathiges, and the rec-Prion contains similar pathogenic properties as
naturally occurring prions.
I6 Transmissible protein toxins in neurodegenerative disease
Jacob Ayers, David Borchelt University of Florida, Gainesville, FL,
USA
Amyotrophic lateral sclerosis (ALS) is an obvious example of
neurodegenerative disease that seems to spread along anatomical pathways. The
spread of symptoms from the site of onset (e.g. limb) to the respiratory
musculature drives the rate of disease progression. In cognitive disorders, such
as Alzheimer’s disease, one can find similarly find evidence of spreading
dysfunction and pathology. One mechanism to account for this spread of disease
from one neural structure to another is by evoking prion-like propagation of a
toxic misfolded protein from cell to cell. Recent studies in animals that model
aspects of Alzheimer’s Disease, Parkinson’s Disease, and Tauopathy, have
bolstered the arguments in favor of prion-like, although in most of these models
the mice do not develop overt “clinical” symptoms. Recently, Jacob Ayers
demonstrated that the symptoms of ALS can be transmitted from a strain of mice
that expresses mutant SOD1-G93A at high levels to a second transgenic strain
that expresses mutant SOD1 at low, nontoxic, levels. This model showed many
prion-like features including evidence of host-adaptation (earlier and more
penetrant disease upon second passage). Interestingly, homogenates from
paralyzed mice expressing the G37R variant of SOD1 transmitted poorly, a finding
suggestive that different SOD1 variants may exhibit strain-like properties.
These “ i n d u c i b l e ” m o d e l s o f h u m a n neurodegenerative disease
enable the generation of models that do not require extraordinary levels of
transgene expression and provide a more precise means of initiating the disease
process, advances that may translate into more predictive pre-clinical
models.
=======
P188 Transmission of amyloid pathology by peripheral administration of
misfolded Aβ
Javiera Bravo-Alegria1 ,2, Rodrigo Morales2, Claudia Duran-Aniotz3, Claudio
Soto2 1University of Los Andes, Santiago, Chile, 2Mitchell Center for
Alzheimer’s Disease and Related Brain Disorders, Department of Neurology,
University of Texas Medical School, Houston, Texas, USA, 3University of Chile,
Santiago, Chile
Misfolding and aggregation of Amyloid-β (Aβ) is one of the primary events
involved in the pathogenesis of Alzheimer's disease (AD). Recently, it has been
proposed that Aβ aggregates can transmit and spread the pathology following a
prion-like mechanism. Prions can be exogenously transmitted by many different
routes of administration. In the case of Aβ, previous studies showed that
intraperitoneal (i.p.) injection of seeds can accelerate cerebral amyloidosis in
mouse models. However, other potential routes have not yet been studied. The
goal of this work was to assess whether Aβ amyloidosis can be seeded in the
brain of a transgenic mouse model of AD by peripheral administration of
misfolded particles.
Young tg2576 animals (50 days old) were inoculated with a pool of brain
extract coming from old Tg2576 animals (10%w/v) by different routes: i.p.
(100μL), eye drops (5μL each eye, 3 times), intramuscular (i.m., 50μL), and per
os (p.o., 1000μL). Animals were sacrificed at 300 days old, and brain samples
were analyzed for amyloid pathology by IHC and ELISA.
The i.p., i.m., and eye drops administration of Aβ seeds significantly
accelerated pathological features in tg2576. Regardless of the higher volume
administered, p.o. treated animals did not show any pathological changes when
compared to untreated controls. Differences in the proportion of diffuse, core
and vascular deposition was observed within experimental groups. Our data show
that peripheral administration of Aβ seeds could accelerate pathological changes
in the brain and suggest that an orchestrated cross-talk between the brain and
peripheral tissues occurs in AD.
==========
PLEASE REMEMBER, IN 55 YEARS AND OLDER, THE RATE OF DOCUMENTED CJD JUMPS TO
ONE IN 9,000. but officials don’t tell you that either. carry on...
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
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?
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America. Now scientists in France have stumbled across new
evidence that adds weight to the campaigners' fears. To their complete surprise,
the researchers found that one strain of scrapie causes the same brain damage in
mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb...
Terry S. Singeltary Sr.
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
posted by Terry S. Singeltary Sr. at
11:21 AM
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