Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers
Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
Greetings Texas,
I got this email from an individual the other day, and thought I would
follow up with it here. This Gentleman brought up some valid points.
any comments?
From: xxxx xxx
Sent: Sunday, July 17, 2016 12:23 AM
To: flounder9@verizon.net
Subject: Texas Parks Dept HIDING TSE (CWD) in Deer Herds
You want a story? Here’s some background and information that should
provide for the start of a very interesting piece of investigative
journalism....
Texas State regulatory agencies conspired with industry organizations to
HIDE and AVOID detecting a fatal neurological disease in farmed animals – a
disease that’s the same for deer as Mad Cow Disease is for beef ... and one that
poses just as much risk to HUMANS.
· Texas Parks and Wildlife pushed through a new set of rules to “regulate”
the movement of farmed deer, supposedly to control the spread of Chronic Wasting
Disease (CWD) in deer
· The rules are designed to use a “rectal test” the find CWD in deer as
young as 16 months old
· The “rectal test” uses rectal tissue – which has been shown
scientifically to NOT reflect CWD until 3 years after the animal is infected
with CWD.
· By using this rectal test on animals under 3 years old, there is no way
that CWD can be detected – because even if these animals are infected, the
rectal test won’t show CWD in an infected animal until 3 years – and the animals
that are being tested aren’t old enough to show CWD in a rectal test – EVEN IF
THE ANIMAL IS INFECTED.
· This means that TPWD has passed rules that are designed to NOT find CWD,
while claiming they do.
· The rules ONLY require 50% of a herd to be tested to achieve a
certification (TC-1 status) that requires NO follow-on testing, and allows
unrestricted movement of deer in Texas.
· This allows Deer Breeders to test the 50% of their herd that is under 3
years old and achieve a TC-1 status
· This means that a herd can have every animal infected with CWD – and with
the blessing of TPWD, Deer Breeders will be able to legally ship deer infected
with a deadly, always fatal neurological disease to any location in the State –
and under the new “rules”, there will be no follow-on testing or any basic
scientific or medical monitoring of these animals – less than a truly WILD DEER
would get anywhere in Texas.
These “rules” allow a breeder to achieve a TC-1 status (transfer category
one) by testing 50% of the herd for CWD. Once they test to TC-1, any deer they
sell to a hunting ranch don’t have to be tested when they are shot. Think about
that. If you hunt a wild deer, you have to go thru a game check station where
TPWD will take a certain number of samples for CWD testing from hunted animals.
This is on top of testing road kill and other deaths of wild deer.
The “Deer Industry” has been able to get TPWD to EXEMPT these packaged
hunts from ANY testing. So CWD could be rampant in these hunt ranches, and the
State of Texas would NEVER KNOW. The venison from these “trophy” bucks? Often
given away to local people or ranch staff – people who are just making ends meet
and use the meat to supplement their meals. So Joe-Learjet from some foreign
country gets his trophy head, and a local Texan is exposed to a deadly
neurological disease with no cure.
It gets even better.
So the “deer industry” has gone out and gotten as many local Vets as
possible ‘trained’ in doing these rectal tests, co-opting Texas’ Vets to
unknowingly further their agenda. Vet license at risk because of this? Not my
problem, my Learjet’s waiting and I have to go poach more deer out-of-state.
The deer breeders are starting to test animals UNDER 3 years old, with this
rectal test, which – by science and definition – CAN’T FIND CWD, EVEN IF IT WAS
THERE in animals under 3 years old – because they couldn’t have had 3 years
since being exposed.
OH – and the “rules”? Very cleverly, there’s a “transition” period. After
the transition period, no more live testing required. No more testing of any
animals that are hunted.
What’s that time period? TWO YEARS – which is EXACTLY when CWD WOULD be
able to be detected in young 16 month old animals that were tested.
But don’t worry – that’s covered too.
The “rules” say that no animal can be used for more than one test. That
way, some unscrupulous breeder can’t just keep submitting the same animal for
testing, right?
The problem with this is that this rectal test is DESIGNED to be used more
than once on the same animal!
The Texas Animal Health Commission allows this rectal test to be used to
find out if CWD is in a herd of animals during their CWD investigations. Because
of the test and the SCIENCE, TAHC ONLY allows the test to be used 3 years after
any possible exposure to CWD, the test has to be done twice over 6 months, and
it has to be done on the entire herd – while it’s quarantined with no movement –
because the test has an accuracy around 50%.
Parks? No time considerations, use it once-and-done, and only test 50% of
the herd...OH, and if you test 25% of the herd you can start moving them around
as long as you test the other 25% within a year.
--
xxxx xxx
Overview of 2016 CWD Rules with Amendments
June 21, 2016
The following summarizes the chronic wasting disease rules (CWD) adopted by
the TPW Commission on June 20, 2016.
Deer Breeder CWD Rules
Period 1 (effective date of rule thru 3/31/2019)
1. From the effective date of the rule until March 31, 2017, a facility
will be movement qualified (MQ) if 20% of eligible mortalities have been tested
since May 23, 2006, or if fewer than five eligible mortalities have occurred in
the facility.
2. Beginning April 1, 2017, a deer breeding facility must have tested 80%
of the eligible mortalities occurring in the previous report year to be
MQ.
3. In order to qualify for no release site testing (TC1), a facility
must:
a. Have Certified or “5th-Year” status in TAHC Herd Certification Program;
or
b. Have tested an average of at least 80% of eligible mortalities over the
previous five years, and satisfied the minimum testing requirement (sufficient
tests on file to equal or exceed 3.6% of the sum of the eligible-age deer
reported in the facility inventory on the March 31 of each of the most recently
completed 5 report years plus the eligible mortalities during the same period);
or
c. Have ante-mortem tested 50% of herd. Note: By ante-mortem testing a
minimum of 25%, a facility may temporarily attain TC1 status prior to May 15,
2017. In order to maintain TC1 status after May 15, 2017, the facility must
supply the remainder of ante-mortem samples to reach the 50% testing level by no
later than May 15, 2017. A facility will be able to test up to TC1 via 50%
ante-mortem testing after May 15, 2017 as well, but the full 50% must be
provided for the facility to be upgraded.
4. Facilities that are not TC3 (CWD trace herds), and not TC1, will be
classified as TC2 and release site testing will be required at associated (Class
II) release sites.
5. All TC2 release sites (Class II) must CWD-test the first 15 deer
harvested per season through the end of the 2018/2019 hunting season.
Period 2 (04/01/2019 and on)
1. All deer breeding facilities are either MQ, not movement qualified (NMQ)
or TC3.
2. Facilities must test 80% of eligible mortalities that occur each report
year to be MQ.
3. Facilities that have not tested 80% of eligible mortalities annually
will be NMQ.
4. There will be no release site testing for any facilities, except for
non-compliant sites as indicated below under Release Site Provisions.
TC3 or CWD Trace Facilities
1. Irrespective of the time periods described above, CWD positive and trace
facilities (TC3) will be required to test 100% of eligible mortalities in the
pen, and 100% of hunter harvested deer at Class III release sites.
2. All deer released on Class III release sites must be tagged with an RFID
or NUES tag.
Transition Provisions
1. 2015/2016 Class II Release Sites will be reset back to Class I if they
complied with all interim release site requirements.
2. 2016/2017 Class II Release Sites that are in compliance with all release
site requirements will be reset back to Class I if all TC2 facilities that
contributed deer during 2016/2017 “test up” to TC1 status by ante-mortem testing
50% of the herd by May 15, 2017.
3. 2016/2017 Class II Release Sites will be reset back to Class I if all
the breeder deer liberated after the effective date of the rule (approximately
August 15, 2016) and prior to October 1, 2016 are harvested and CWD-tested
during the 2016-2017 hunting season, and no additional deer are released from a
TC2 or TC3 facility after October 1, 2016.
Release Site Provisions
1. A harvest log must be maintained on site and each deer harvested must be
entered in the log the day of harvest – Applies to Class II and Class III
release sites, and DMP sites that receive TC2 deer.
2. All breeder deer release sites must be high-fenced (7 ft.) and the
landowner must ensure all deer remain on the release site.
3. Failure to comply with release site testing requirements will result in
release site testing requirements carrying forward until testing requirements
are fulfilled.
4. Failure to comply with release site testing requirements will make the
release site ineligible to receive a DMP permit or additional breeder deer for
release until testing requirements are fulfilled.
5. Liberated deer must have access to the entire acreage listed on the
release site registration form, except that deer may be excluded from areas for
safety reasons (i.e., airstrips) or for the purpose of protecting crops,
orchards, ornamental plants, lawns, etc.
6. A release site owner may notify the department to modify the acreage of
a registered release site and the release site requirements will expand to the
new acreage.
Other Breeder Deer Provisions
1. Each breeding facility herd that has been permitted for at least 6
months on March 31 must provide a minimum number of CWD test results annually,
irrespective of whether there are mortalities. The minimum number of post-mortem
tests required is equal to 3.6% of the eligible-aged inventory on March 31 of a
given report year plus the eligible mortalities that occurred during that report
year. Ante-mortem tests may be substituted as provided for in #2 below.
2. A deer breeder may substitute ante-mortem tests for required post-mortem
tests on a 3:1 basis to meet testing requirements.
3. Ante-mortem tests must be conducted on animals at least 16 months of
age.
4. An individual deer may be the source of a valid ante-mortem test result
no more frequently than every two years. A deer may be re-tested within the
2-year period if the initial sample produced an invalid test result (i.e.,
“insufficient follicles”).
5. There is no residency requirement for an animal to qualify for
ante-mortem testing.
6. Ante-mortem tests may be conducted on retropharyngeal lymph node, rectal
mucosa or tonsillar tissue collected by or under the supervision of a qualified
licensed veterinarian.
7. After May 15, 2017, ante-mortem test results provided to upgrade to TC1
status must have been collected within the 6-month period prior to the status
upgrade being sought.
8. A facility will be disqualified from being upgraded to TC1 if deer from
a TC2 or TC3 facility are introduced into that facility after ante-mortem
testing has begun.
9. If a facility receives deer from a facility of lower status, the
receiving facility must stay down-graded for 2 years. TC1 is the highest status
and TC3 is the lowest status.
10. If a TC1 facility fails to test 80% of eligible mortalities in a report
year, the facility will become NMQ and be will be downgraded. The facility will
have 60 days to provide substitution tests as described in #2 above to regain MQ
and TC1 status, otherwise the facility will remain downgraded for 2 years. MQ
status may be regained at any time.
11. A new facility will “inherit” the lowest status level from among all
facilities contributing deer to that facility. Example: if a new facility
receives deer from TC1 facilities, the new facility will be classified as a
TC1.
DMP
1. If a DMP breeding pen receives deer from a TC2 facility or Class II
Release Site, the DMP release site must CWD test the first 15 hunter harvested
deer each season through the 2018/2019 hunting season, beginning the season
following the release of deer from the DMP pen.
2. TC3 deer may not be transferred to a DMP facility.
3. Class 3 release sites may not conduct DMP activities.
4. If a breeder buck is commingled with does from a lower status herd in a
DMP facility, and that breeder buck is returned to the breeding facility, the
breeding facility status will be down-graded.
TTT
1. Prior to issuance of a TTT permit, all TTT trap sites must provide 15
valid post-mortem CWD samples collected after the Saturday nearest September 30.
Exception: TTT trap sites in urban areas may utilize samples collected and
tested between April 1 and the time of application.
2. All TTT deer must be tagged with an RFID button tag in addition to the
existing tattoo requirement.
3. RFID numbers must be reported to TPWD.
4. No TTT trapping from any breeder deer release sites.
TTP
1. TTP Permittees must supply 15 CWD samples at the end of the
season.
2. CWD samples must be provided on 100% of deer taken by TTP on Class III
release sites.
Greetings again Texas,
now, let’s look over some history of the cwd tse prion diagnostic testing
shall we...
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Antemortem detection of chronic wasting disease prions in nasal
brush collections and rectal biopsies from white-tailed deer by real time
quaking-induced conversion
Authors
item Haley, Nicholas - item Siepker, Chris - item Walter, W. David - item
Thomsen, Bruce - item Greenlee, Justin item Lehmkuhl, Aaron - item Richt, Jürgen
-
Submitted to: Journal of Clinical Microbiology Publication Type: Peer
Reviewed Journal Publication Acceptance Date: November 27, 2015 Publication
Date: February 10, 2016 Citation: Haley, N.J., Siepker, C., Walter, W.D.,
Thomsen, B.V., Greenlee, J.J., Lehmkuhl, A.D., Richt, J.A. 2016. Antemortem
detection of chronic wasting disease prions in nasal brush collections and
rectal biopsy specimens from white-tailed deer by real time quaking-induced
conversion. Journal of Clinical Microbiology. 54(4):1108-1116.
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal
neurodegenerative disease that occurs in farmed and wild cervids (deer and elk)
of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are
caused by infectious proteins called prions that are resistant to various
methods of decontamination and environmental degradation. Early diagnosis of CWD
in wild and captive herds would be very helpful to controlling the spread of
CWD, for which there are not yet any preventative or treatment measures
available. The purpose of this study was to test a laboratory method of prion
detection (real-time Quaking Induced Conversion; RT-QuIC) that has the potential
to detect very low levels of infectious prions in samples collected from live
animals against the gold standard diagnostic where abnormal prion in tissues is
stained on a microscope slide. This study reports that RT-QuIC detects more
cases of CWD than standard methods, but also can identify a small number of
animals without CWD as being positive. In the case of CWD, where it is likely
that large numbers of animals within a herd may be positive, misidentifying a
negative as a positive may have less of an impact than in the case of other
prion diseases such as bovine spongiform encephalopathy considering that this
test allows testing much larger numbers of samples with a faster turn around
time than traditional methods. This information could have an impact on
regulatory and wildlife officials developing plans to reduce or eliminate CWD
and cervid farmers that want to ensure that their herd remains CWD-free.
Technical Abstract: Chronic wasting disease (CWD), a transmissible
spongiform encephalopathy of cervids, was first documented nearly fifty years
ago in Colorado and Wyoming and has since spread to cervids in 23 states, 2
Canadian provinces, and the Republic of Korea. The increasing expansion of this
disease makes the development of sensitive diagnostic assays and antemortem
sampling techniques crucial for the mitigation of spread; this is especially
true in cases of relocation/reintroduction of farmed or free-ranging deer and
elk, or surveillance studies in private or protected herds where depopulation
may be contraindicated. This study sought to evaluate the sensitivity of the
real-time quaking-induced conversion (RT-QuIC) assay in samples collected
antemortem. Antemortem findings were then compared to results from ante- and
postmortem samples evaluated using the current gold standard diagnostic assay,
immunohistochemistry (IHC). Recto-anal mucosal associated lymphoid tissue
(RAMALT) biopsies and nasal brush collections from three separate herds of
farmed white-tailed deer (n=409) were evaluated, along with standard postmortem
microscopic analysis of brainstem at the level of the obex and retropharyngeal
lymph nodes. We hypothesized the sensitivity of RT-QuIC would be comparable to
IHC in antemortem tissues, and would correlate with both genotype and stage of
clinical disease. Our results showed that RAMALT testing by RT-QuIC had the
highest sensitivity (69.8%) when compared to postmortem testing. This data
suggests that RT-QuIC, like IHC, is a fairly sensitive assay for detection of
CWD prions in rectal biopsies and other antemortem samples, and with further
investigation has potential for large scale and rapid automated testing for CWD
diagnosis.
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=320291
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=320291
DOI: 10.7589/2014-12-284 Journal of Wildlife Diseases, 51(4), 2015, pp.
801–810 # Wildlife Disease Association 2015 801
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA
Chris Geremia,1,6,7 Jennifer A. Hoeting,2 Lisa L. Wolfe,3 Nathan L.
Galloway,4 Michael F. Antolin,4 Terry R. Spraker,5 Michael W. Miller,3 and N.
Thompson Hobbs1
1 Natural Resource Ecology Laboratory, Graduate Degree Program in Ecology,
1499 Campus Delivery, Colorado State University, Fort Collins, Colorado, 80523,
USA
2 Department of Statistics, 1877 Campus Delivery, Colorado State
University, Fort Collins, Colorado 80523, USA
3 Colorado Division of Parks andWildlife,Wildlife Health Program, 4330
Laporte Avenue, Fort Collins, Colorado 80521,USA
4 Department of Biology, 1878 Campus Delivery, Colorado State University,
Fort Collins, Colorado 80523, USA
5 Colorado State Diagnostics Laboratory, College of Veterinary Medicine,
Colorado State University, Fort Collins, Colorado 80523, USA
6 Current address: Yellowstone Center for Resources, P.O. Box 168,
Yellowstone National Park, Mammoth Hot Springs, Wyoming 82190, USA
7 Corresponding author (email: chris_geremia@nps.gov)
ABSTRACT: Biopsy of rectal mucosa–associated lymphoid tissue provides a
useful, but imperfect, live-animal test for chronic wasting disease (CWD) in
mule deer (Odocoileus hemionus). It is difficult and expensive to complete these
tests on free-ranging animals, and wildlife health managers will benefit from
methods that can accommodate test results of varying quality. To this end, we
developed a hierarchical Bayesian model to estimate the probability that an
individual is infected based on test results. Our model was estimated with the
use of data on 210 adult female mule deer repeatedly tested during 2010214. The
ability to identify infected individuals correctly declined with age and may
have been influenced by repeated biopsy. Fewer isolated lymphoid follicles
(where PrPCWD accumulates) were obtained in biopsies of older deer and the
proportion of follicles showing PrPCWD was reduced. A deer’s genotype in the
prion gene (PRNP) also influenced detection. At least five follicles were needed
in a biopsy to assure a 95%accurate test in PRNP genotype 225SS deer.
snip...
DISCUSSION
Reliably detecting prion infection in mule deer requires some consideration
of sample quality. Our findings resemble earlier work suggesting examination of
at least nine lymphoid follicles in a tonsil biopsy might be necessary to
determine CWD status in mule deer accurately (Wolfe et al. 2002).We found that
examining five follicles in a rectal biopsy of 225SS mule deer, regardless of
age, should ensure 95% probability of an accurate test; negative results were
less conclusive for deer genotypes including phenylalanine (225SF, 225FF).
Importantly, examining fewer follicles provided meaningful, but less certain
information about the disease status of the individual. For example, fewer than
five follicles were observed in 13 of 31 (42%) tests on animals that were
confirmed PrPCWD negative postmortem. These less-conclusive live tests ensured
61% probability of the correct result when one follicle was obtained, and
increased to 82% with two follicles, 91% with three, and 94% with four.
Likewise, we encountered four apparent false-negative results in 225SS deer. In
each case, we could not ensure a 95% accurate test based on deer age and numbers
of follicles in biopsies.
Rarely have individual animals infected with prion disease been repeatedly
tested after a positive test. Instead, infected animals have generally been
presumed to remain positive if retested because postmortem exams have confirmed
their infection status (e.g.,Wolfe et al. 2007; Gona´ lez et al. 2008). This
belief appears well-founded based on evidence that prion diseases are
progressive and that the proportion of positive lymphoid follicles increases
over the course of infection (e.g., Fox et al. 2006). Given this
well-established pattern, we were surprised that nearly half of the follow-up
biopsies collected from deer that had already yielded a positive biopsy were
negative.
Repeated biopsy of the rectal mucosa may have given rise to these
false-negative tests. Isolated lymphoid follicles show dynamic properties,
including de novo formation in adult animals (Lorenz et al. 2003).
Gut-associated lymphoid tissue serves a variety of mucosal barrier defense
functions, and isolated lymphoid follicles have been suggested to play a role in
mucosal repair (Sipos et al. 2010). If the damage resulting from a biopsy
stimulated new isolated lymphoid follicles to form in adjacent rectal mucosa,
then the follicles available for subsequent sampling would be a mix of newer and
older follicles. Because new follicles (#12 mo old) would not have the same
opportunity for prion accumulation as older follicles, their presence in nearby
spans of mucosa could dilute or supplant the IHC-positive follicle pool in
subsequent samples even as PrPCWD accumulation progressed unabated in static
lymphoid structures that remain undisturbed. This phenomenon could explain the
static or declining proportion of positive follicles observed in biopsies from
some infected individuals that were repeatedly sampled (Fig. 4) as well as the
pattern of increasing follicle counts in repeatedly sampled individuals in the
face of aging (Fig. 3). If isolated lymphoid follicle formation occurs in
response to rectal mucosa biopsy, then repeated sampling could lower the
likelihood of detecting infected animals, particularly in individuals
genetically inclined toward more gradual disease progression. Alternatively, we
implicitly assumed no laboratory errors occurred in the processing of biopsy
samples. However, because three of the four false-negative cases came from the
same year’s IHC accession, we cannot preclude the possibility of a systematic
error somewhere in the course of testing.
The decline in the proportion of isolated lymphoid follicles showing PrPCWD
in older deer did not appear to be solely the result of repeated testing and
associated disruption of tissue structure. Among eight deer that were biopsy
positive on first testing, the proportion of follicles showing PrPCWD in
122-yr-old deer was 100% (n52), whereas proportions ranged from 27% to 100%
(mean of proportions 63%) in $3-yr-old deer (n56). We speculate that the higher
proportion of positive follicles in young mule deer may result from greater
activity in the immature lymphatic system or greater exposure because of close
association with an infected dam or contaminated environment. Regardless of
whether the foregoing observations were an artifact of small sample size, in the
absence of repeated biopsy, age appeared to decrease ability to detect infection
because fewer isolated lymphoid follicles were obtained in biopsies of older
deer.
Every test sample is not the same; each individual exhibits unique
variation, and the technique for estimating CWD infection that we developed here
can account for some of these complications. Disease status becomes a
probabilistic statement conditioned on the current test result, previous disease
status, and infection and test sensitivity probabilities. Therefore, uncertainty
in sampling becomes incorporated into the placement of individuals into discrete
disease categories. This step forward allows us to make explicit probabilistic
statements about whether an individual is infected and the chance that a test
result is correct. With CWD, rather than conclude that an individual is not
infected based on a test with few follicles or decide that the test was
inconclusive, we can now state the probability that an individual is truly
infected. Consequently, we can make conclusions that “a 90% chance exists that
this deer is not infected, based on the results.”
Surveillance and containment programs for CWD benefit from an ability to
diagnose animals correctly with the use of antemortem tests. Our model can
easily be applied to surveillance on mule deer, facilitating use of all
available samples regardless of total follicle counts. Probabilistic estimates
of the infection status of each tested individual could then be used to provide
95% credible intervals of population prevalence that account for differences in
test quality. Our model is robust to differences in population prevalence except
when prevalence is low (e.g., ,0.02%), because the detection and infection
parameters become inestimable. When planning surveillance in areas where disease
may not occur, we recommend assuming values for the test detection parameters to
allow for estimation of population prevalence. Our approach also has application
to CWD screening for transport of wild or captive deer or targeted culling
efforts. Individuals could be identified that require additional testing to
confirm disease status with desired levels of certainty, although our approach
cannot account for misdiagnosing deer in early stages of infection when PrPCWD
is undetectable (Wolfe et al. 2002, 2007). In light of our findings, further
attention to the potential for repeated sampling to lower the probability of
detecting infection via rectal mucosa biopsy appears warranted before such
approaches are substituted for more conventional surveillance that relies on
samples collected postmortem.
Key words: Bayesian, capture–mark–recapture, chronic wasting disease, mule
deer, prion, test sensitivity.
Article Citation: (2015)
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA.
Journal of Wildlife Diseases In-Press. doi: http://dx.doi.org/10.7589/2014-12-284
Ahead of Print
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA
Chris Geremia1,6,7 Jennifer A. Hoeting2, Lisa L. Wolfe3, Nathan L.
Galloway4, Michael F. Antolin4, Terry R. Spraker5, Michael W. Miller3, and N.
Thompson Hobbs1
1 Natural Resource Ecology Laboratory, Graduate Degree Program in Ecology,
Colorado State University, Fort Collins, Colorado, 80523-1499, USA
2 Department of Statistics, Colorado State University, Fort Collins,
Colorado 80523, USA
3 Colorado Division of Parks and Wildlife, Wildlife Health Program, 4330
Laporte Avenue, Fort Collins, Colorado 80521, USA
4 Department of Biology, Colorado State University, Fort Collins, Colorado
80523-1878, USA
5 Colorado State University Diagnostics Laboratory, Colorado State
University, Fort Collins, Colorado 80523, USA
Key words: Bayesian, capture–mark–recapture, chronic wasting disease, mule
deer, prion, test sensitivity
Abstract
Biopsy of rectal-mucosa associated lymphoid tissue provides a useful, but
imperfect, live-animal test for chronic wasting disease (CWD) in mule deer
(Odocoileus hemionus). It is difficult and expensive to complete these tests on
free-ranging animals, and wildlife health managers will benefit from methods
that can accommodate test results of varying quality. To this end, we developed
a hierarchical Bayesian model to estimate the probability that an individual is
infected based on test results. Our model was estimated with the use of data on
210 adult female mule deer repeatedly tested during 2010−2014. The ability to
identify infected individuals correctly declined with age and may have been
influenced by repeated biopsy. Fewer isolated lymphoid follicles (where PrPCWD
accumulates) were obtained in biopsies of older deer and the proportion of
follicles showing PrPCWD was reduced. A deer’s genotype in the prion gene (PRNP)
also influenced detection. At least five follicles were needed in a biopsy to
assure a 95% accurate test in PRNP genotype 225SS deer.
snip...
DISCUSSION
Reliably detecting prion infection in mule deer requires some consideration
of sample quality. Our findings resemble earlier work suggesting examination of
at least nine lymphoid follicles in a tonsil biopsy might be necessary to
determine CWD status in mule deer accurately (Wolfe et al. 2002). We found that
examining five follicles in a rectal biopsy of 225SS mule deer, regardless of
age, should ensure 95% probability of an accurate test; negative results were
less conclusive for deer genotypes including phenylalanine (225SF, 225FF).
Importantly, examining fewer follicles provided meaningful, but less certain
information about the disease status of the individual. For example, fewer than
five follicles were observed in 13 of 31 (42%) tests on animals that were
confirmed PrPCWD negative postmortem. These less-conclusive live tests ensured
61% probability of the correct result when one follicle was obtained, and
increased to 82% with two follicles, 91% with three, and 94% with four.
Likewise, we encountered four apparent false-negative results in 225SS deer. In
each case, we could not ensure a 95% accurate test based on deer age and numbers
of follicles in biopsies.
Rarely have individual animals infected with prion disease been repeatedly
tested after a positive test. Instead, infected animals have generally been
presumed to remain positive if retested because postmortem exams have confirmed
their infection status (e.g., Wolfe et al. 2007; Gonález et al. 2008). This
belief appears well-founded based on evidence that prion diseases are
progressive and that the proportion of positive lymphoid follicles increases
over the course of infection (e.g., Fox et al. 2006). Given this
well-established pattern, we were surprised that nearly half of the follow-up
biopsies collected from deer that had already yielded a positive biopsy were
negative.
Repeated biopsy of the rectal mucosa may have given rise to these
false-negative tests. Isolated lymphoid follicles show dynamic properties,
including de novo formation in adult animals (Lorenz et al. 2003).
Gut-associated lymphoid tissue serves a variety of mucosal barrier defense
functions, and isolated lymphoid follicles have been suggested to play a role in
mucosal repair (Sipos et al. 2010). If the damage resulting from a biopsy
stimulated new isolated lymphoid follicles to form in adjacent rectal mucosa,
then the follicles available for subsequent sampling would be a mix of newer and
older follicles. Because new follicles (≤12 mo old) would not have the same
opportunity for prion accumulation as older follicles, their presence in nearby
spans of mucosa could dilute or supplant the IHC-positive follicle pool in
subsequent samples even as PrPCWD accumulation progressed unabated in static
lymphoid structures that remain undisturbed. This phenomenon could explain the
static or declining proportion of positive follicles observed in biopsies from
some infected individuals that were repeatedly sampled (Fig. 4) as well as the
pattern of increasing follicle counts in repeatedly sampled individuals in the
face of aging (Fig. 3). If isolated lymphoid follicle formation occurs in
response to rectal mucosa biopsy, then repeated sampling could lower the
likelihood of detecting infected animals, particularly in individuals
genetically inclined toward more gradual disease progression. Alternatively, we
implicitly assumed no laboratory errors occurred in the processing of biopsy
samples. However, because three of the four false-negative cases came from the
same year's IHC accession, we cannot preclude the possibility of a systematic
error somewhere in the course of testing.
The decline in the proportion of isolated lymphoid follicles showing PrPCWD
in older deer did not appear to be solely the result of repeated testing and
associated disruption of tissue structure. Among eight deer that were biopsy
positive on first testing, the proportion of follicles showing PrPCWD in
1−2-yr-old deer was 100% (n = 2), whereas proportions ranged from 27% to 100%
(mean of proportions 63%) in ≥3-yr-old deer (n = 6). We speculate that the
higher proportion of positive follicles in young mule deer may result from
greater activity in the immature lymphatic system or greater exposure because of
close association with an infected dam or contaminated environment. Regardless
of whether the foregoing observations were an artifact of small sample size, in
the absence of repeated biopsy, age appeared to decrease ability to detect
infection because fewer isolated lymphoid follicles were obtained in biopsies of
older deer.
Every test sample is not the same; each individual exhibits unique
variation, and the technique for estimating CWD infection that we developed here
can account for some of these complications. Disease status becomes a
probabilistic statement conditioned on the current test result, previous disease
status, and infection and test sensitivity probabilities. Therefore, uncertainty
in sampling becomes incorporated into the placement of individuals into discrete
disease categories. This step forward allows us to make explicit probabilistic
statements about whether an individual is infected and the chance that a test
result is correct. With CWD, rather than conclude that an individual is not
infected based on a test with few follicles or decide that the test was
inconclusive, we can now state the probability that an individual is truly
infected. Consequently, we can make conclusions that “a 90% chance exists that
this deer is not infected, based on the results.”
Surveillance and containment programs for CWD benefit from an ability to
diagnose animals correctly with the use of antemortem tests. Our model can
easily be applied to surveillance on mule deer, facilitating use of all
available samples regardless of total follicle counts. Probabilistic estimates
of the infection status of each tested individual could then be used to provide
95% credible intervals of population prevalence that account for differences in
test quality. Our model is robust to differences in population prevalence except
when prevalence is low (e.g., <0 .02="" 2002="" 2007="" account="" additional="" al.="" allow="" also="" although="" and="" appears="" application="" approach="" approaches="" are="" areas="" assuming="" attention="" be="" because="" become="" before="" biopsy="" cannot="" captive="" certainty="" collected="" confirm="" conventional="" could="" culling="" cwd="" deer="" desired="" detecting="" detection="" disease="" div="" early="" efforts.="" estimation="" et="" findings="" for="" further="" has="" identified="" in="" individuals="" inestimable.="" infection="" is="" levels="" light="" lower="" may="" misdiagnosing="" more="" mucosa="" not="" occur="" of="" olfe="" on="" or="" our="" parameters="" planning="" population="" postmortem.="" potential="" prevalence.="" probability="" prpcwd="" recommend="" rectal="" relies="" repeated="" require="" samples="" sampling="" screening="" stages="" status="" substituted="" such="" surveillance="" targeted="" test="" testing="" that="" the="" to="" transport="" undetectable="" values="" via="" warranted="" we="" when="" where="" wild="" with="">
Received: December 15, 2014; Accepted: April 23, 2015
6 Current address: Yellowstone Center for Resources, P.O. Box 168,
Yellowstone National Park, Mammoth Hot Springs, Wyoming 82190, USA
7 Corresponding author (email: chris_geremia@nps.gov)
Journal of Wildlife Diseases 49(2):270-278. 2013 doi: http://dx.doi.org/10.7589/2011-12-362
EFFICACY OF ANTEMORTEM RECTAL BIOPSIES TO DIAGNOSE AND ESTIMATE PREVALENCE
OF CHRONIC WASTING DISEASE IN FREE-RANGING COW ELK (CERVUS ELAPHUS NELSONI)
Ryan J. Monello1,6, Jenny G. Powers1, N. Thompson Hobbs2, Terry R.
Spraker3, Katherine I. O’Rourke4,5, and Margaret A. Wild1
1 National Park Service, Biological Resource Management Division, 1201 Oak
Ridge Drive, Suite 200, Fort Collins, Colorado 80525, USA
2 Natural Resource Ecology Laboratory and Graduate Degree Program in
Ecology, Colorado State University, Fort Collins, Colorado 80523, USA
3 Colorado State Diagnostic Laboratory, College of Veterinary Medicine,
Colorado State University, Fort Collins, Colorado 80523, USA
4 United States Department of Agriculture, Agricultural Research Service,
Animal Disease Research Unit, 3003 Animal Disease Biotechnology Facility,
Washington State University, Pullman, Washington 99164, USA
5 Current address: Department of Veterinary Microbiology and Pathology,
School of Veterinary Medicine, Washington State University, Pullman, Washington
99164, USA
6 Corresponding author (email: Ryan_Monello@nps.gov)
A reliable antemortem test is needed to understand the ecology of chronic
wasting disease (CWD) in elk (Cervus elaphus nelsoni). We measured the ability
of antemortem biopsy samples from the rectal mucosa to detect the abnormal prion
protein associated with CWD (PrPCWD), the relationship between test results from
the obex and rectal biopsies at varying stages of CWD progression, and the
prevalence of CWD in free-ranging elk from Rocky Mountain National Park,
Colorado, USA. We sampled and placed radio collars on 136 adult female elk in
the winter of 2007–08. Elk with biopsy samples found positive for PrPCWD by
immunohistochemistry (IHC) were euthanized and the obex and retropharyngeal
lymph nodes were examined with IHC. We resampled, euthanized, and necropsied 20,
25, and 34 of the remaining study elk in each of the three following winters,
respectively. Sensitivity of rectal biopsy samples increased in an asymptotic
fashion with follicle count and was maximized at 85% (95% credible limits
[CL]=60, 98) in the beginning of the study, when a greater proportion of elk
were in a detectable stage of prion infection. However, maximum sensitivity was
reduced to 72% (CL=46, 94) when we included resampled elk, which included
recently infected elk that were initially negative using rectal biopsies and
IHC. Test results were similar between rectal biopsies and the obex, but the
earliest stages of prion infection were only detected by using retropharyngeal
lymph nodes. Minimum CWD prevalence was estimated to be 9.9% (CL=5.7, 15.7)
using rectal biopsies, but this rose to 12.9% (CL=8.0, 19.1) when we included
four elk that were likely misdiagnosed at initial capture. Our results indicate
rectal biopsies can provide a useful research tool for CWD in elk populations,
but should be used with caution because they can miss individuals in early
stages of infection and underestimate prevalence. Prevalence estimates from this
population are the highest reported to date in elk and indicate that under
appropriate conditions, CWD may be able to affect the dynamics of high-density
elk populations.
Received: December 22, 2011; Accepted: October 9, 2012
Keywords: Biopsy, Cervus elaphus, chronic wasting disease, Colorado, CWD,
elk, prion, rectal mucosa
***but should be used with caution because they can miss individuals in
early stages of infection and underestimate prevalence.
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
Effects of age, sex, polymorphism at PRNP codon 96, and disease progression
Bruce V. Thomsen1 David A. Schneider Katherine I. O’Rourke Thomas Gidlewski
James McLane Robert W. Allen Alex A. McIsaac Gordon B. Mitchell Delwyn P. Keane
Terry R. Spraker Aru Balachandran
U.S. Department of Agriculture, National Veterinary Services Laboratories,
Ames, IA (Thomsen)
U.S. Department of Agriculture, Agricultural Research Service, Pullman, WA
(Schneider, O’Rourke)
U.S. Department of Agriculture, Animal and Plant Health Inspection Service,
Wildlife Services, Fort Collins, CO (Gidlewski)
Canadian Food Inspection Agency, Battleford, Saskatchewan, Canada (McLane)
Canadian Food Inspection Agency, Prince Albert, Saskatchewan, Canada
(Allen)
Canadian Food Inspection Agency, Saskatoon, Saskatchewan, Canada (McIsaac)
National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food
Inspection Agency, Ottawa Laboratory–Fallowfield, Ottawa, Ontario, Canada
(Mitchell, Balachandran)
University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory,
Madison, WI (Keane)
Colorado State University Diagnostic Laboratory, Fort Collins, CO
(Spraker)
↵1 Bruce V. Thomsen, National Veterinary Services Laboratories, 1920 Dayton
Avenue, Ames, IA 50010. bruce.v.thomsen@aphis.usda.gov
Abstract
An effective live animal diagnostic test is needed to assist in the control
of chronic wasting disease (CWD), which has spread through captive and wild
herds of white-tailed deer (Odocoileus virginianus) in Canada and the United
States. In the present study, the diagnostic accuracy of rectal mucosa biopsy
sample testing was determined in white-tailed deer from 4 CWD-infected captive
herds. Specifically, the current study compared the immunohistochemical
detection of disease-associated prion protein in postmortem rectal mucosa biopsy
samples to the CWD status of each deer as determined by immunodiagnostic
evaluations of the brainstem at the obex, the medial retropharyngeal lymph node,
and the palatine tonsil. The effects of age, sex, genotype, and disease
progression were also evaluated. Diagnostic sensitivity on rectal biopsy samples
for CWD in white-tailed deer ranged from 63% to 100%; the pooled estimate of
sensitivity was 68% with 95% confidence limits (95% CLs) of 49% and 82%.
However, diagnostic sensitivity was dependent on genotype at prion protein gene
(PRNP) codon 96 and on disease progression as assessed by obex grade. Diagnostic
sensitivity was 76% (95% CLs: 49%, 91%) for 96GG deer but only 42% (95% CLs:
13%, 79%) for 96GS deer. Furthermore, diagnostic sensitivity was only 36% for
deer in the earliest stage of disease (obex grade 0) but was 100% for deer in
the last 2 stages of preclinical disease (obex grades 3 and 4). The overall
diagnostic specificity was 99.8%. Selective use of antemortem rectal biopsy
sample testing would provide valuable information during disease investigations
of CWD-suspect deer herds.
Development of an antemortem test for detecting the misfolded prion protein
associated with CWD (PrPCWD) in nonclinical animals would be useful for wildlife
and captive population management strategies. To date, preclinical testing for
PrPCWD utilizes immunohistochemistry (IHC) of the palatine tonsils or rectal
lymphoid tissues in cervids.18,21,24 However, IHC does not routinely detect very
early cases of CWD in these tissues.17,20
USDA APHIS Veterinary Services Chronic Wasting Disease Program – Sample
Collection Guidance Procedure for Removal of Obex & Retropharyngeal Lymph
Nodes (RPLN)
From: Will Laegreid
Sent: Monday, May 05, 2014 4:45 PM
To: Terry S. Singeltary Sr.
Subject: RE: cwd testing with immunohistochemistry (IHC) of the palatine
tonsils
Dear Mr. Singletary,
Thank you for your inquiry about CWD testing. If I understand your question
correctly, you are asking about the accuracy of IHC for early preclinical
diagnosis of CWD. The quote you included in your message is spot on, IHC will
not reliably detected very early cases of CWD. The differences between samples,
tonsil versus rectal lymphoid biopsies, is largely affected by two factors, the
relative number of lymphoid follicles in each tissue (tonsil > rectal) and
the skill of the person taking the biopsy. It is my opinion that both samples
can work, but that tonsil biopsies are more sensitive (probably due to the
greater number of follicles for examination). It also appears that disease
progression, affected by prion genotype of the individual animal, influences
sensitivity. I hope this addresses your questions.
Best regards,
William W. Laegreid, DVM, PhD
Director, Wyoming State Veterinary Laboratory
Head, Department of Veterinary Sciences
University of Wyoming
1174 Snowy Range Road
Laramie, WY 82070
(307) 766-9929
(307) 721-2051 Fax
wlaegrei@uwyo.edu
snip...
more test in the pipeline, too long to post, for anyone interested see
references ;
Monday, May 05, 2014
cwd tse prion testing PMCA , IHC, tonsil, rectal, biopsy ???
Antemortem detection of chronic wasting disease prions in nasal brush
collections and rectal biopsies from white-tailed deer by real time
quaking-induced conversion
Nicholas J. Haleya#, Chris Siepkera, W. David Walterb, Bruce V. Thomsenc,
Justin J. Greenleed, Aaron D. Lehmkuhlc and Jürgen A. Richta
+ Author Affiliations Department of Diagnostic Medicine and Pathobiology,
College of Veterinary Medicine, Kansas State University, Manhattan, Kansas, USAa
U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research
Unit, Pennsylvania State University, University Park, Pennsylvania, USAb 3USDA,
APHIS, VS, STAS, National Veterinary Service Laboratories, Ames, Iowa, USAc
Virus and Prion Research Unit, National Animal Disease Center, ARS, USDA, Ames,
Iowa, USAd
ABSTRACT
Chronic wasting disease (CWD), a transmissible spongiform encephalopathy of
cervids, was first documented nearly fifty years ago in Colorado and Wyoming,
and has since spread to cervids in 23 states, two Canadian provinces, and the
Republic of Korea. The expansion of this disease makes the development of
sensitive diagnostic assays and antemortem sampling techniques crucial for the
mitigation of spread; this is especially true in cases of
relocation/reintroduction of farmed or free-ranging deer and elk, or
surveillance studies in private or protected herds where depopulation is
contraindicated. This study sought to evaluate the sensitivity of the real-time
quaking-induced conversion (RT-QuIC) assay using recto-anal mucosa associated
lymphoid tissue (RAMALT) biopsies and nasal brush samples collected antemortem
from farmed white-tailed deer (n=409). Antemortem findings were then compared to
results from ante- and postmortem samples (RAMALT, brainstem and medial
retropharyngeal lymph nodes) evaluated using the current gold standard in vitro
assay, immunohistochemistry (IHC). We hypothesized the sensitivity of RT-QuIC
would be comparable to IHC in antemortem tissues, and would correlate with both
genotype and stage of clinical disease. Our results showed that RAMALT testing
by RT-QuIC had the highest sensitivity (69.8%) when compared to postmortem
testing, with a specificity of >93.9%. These data suggest that RT-QuIC, like
IHC, is an effective assay for detection of PrPCWD in rectal biopsies and other
antemortem samples, and with further research to identify more sensitive
tissues, bodily fluids, or experimental conditions, has potential for large
scale and rapid automated testing for CWD diagnosis.
FOOTNOTES
↵#Address correspondence to Nicholas J. Haley, nicholas.j.haley@gmail.com.
Copyright © 2016, American Society for Microbiology. All Rights Reserved.
Tuesday, September 22, 2015
*** Host Determinants of Prion Strain Diversity Independent of Prion
Protein Genotype
Friday, August 28, 2015
*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical
infection
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING
‘’The differences between samples, tonsil versus rectal lymphoid biopsies,
is largely affected by two factors, the relative number of lymphoid follicles in
each tissue (tonsil > rectal) ***and the skill of the person taking the
biopsy.’’
Wednesday, July 22, 2015
Texas Certified Chronic Wasting Disease CWD Sample Collector, like the Wolf
Guarding the Henhouse
Just got off the phone with TAHC, and I wanted to confirm this. but it
seems true, that in the state of Texas, even if you are a Captive game farmer,
breeder, part of the captive industry at all, if you want to sample your own
cervid for cwd, instead of the TAHC, TPWD, or Doctor, all you have to do is pass
the Certified CWD Sample Collector course, and bingo, you sample your own herd.
...tss
Friday, August 14, 2015
Carcass Management During a Mass Animal Health Emergency Draft Programmatic
Environmental Impact Statement—August 2015
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie TSE Prion Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Tuesday, June 21, 2016
TPW Commission Adopts Amended Deer Movement Rules and Some Deer breeders
walk out of hearing on chronic wasting disease CWD TSE Prion
Thursday, June 16, 2016
Help fight this fatal disease CWD TSE PRION threat to Texas wild deer herd
Tuesday, June 07, 2016
*** Comparison of two US sheep scrapie isolates supports identification as
separate strains ***
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Friday, June 03, 2016
Chronic Wasting Disease CWD TSE Prion Surveillance and Testing in Texas, a
very concerning situation
Saturday, May 28, 2016
TPWD gives in to Breeders again and postponed their decision regarding
proposed changes to state regulations for managing CWD allowing the TSE Prion to
spread further
Sunday, May 22, 2016
TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND
SCIENCE TO LET DISEASE SPREAD
Sunday, June 12, 2016
TPWD Special Meeting Chronic Wasting Disease Response Rules June 20, 2016
Wednesday, May 04, 2016
TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99
Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment
Submission
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer
Monday, April 25, 2016
TEXAS Nilgai Exotic Antelope Let Loose for Trophy Hunts Blamed for
Spreading Cattle Tick Fever, and what about CWD TSE Prion Disease ?
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Saturday, January 23, 2016
Texas new interim rule governing Deer Management Permit (DMP) activities as
part of the state’s response to the detection of chronic wasting disease (CWD)
in captive deer populations
Sunday, January 17, 2016
Texas 10,000 deer in Texas tested for deadly disease CWD TSE, but not
tested much in the most logical place, the five-mile radius around the Medina
County captive-deer facility where it was discovered
Friday, January 15, 2016
TEXAS PARKS & WILDLIFE CWD Ante-Mortem Testing Symposium Texas Disposal
Systems Events Pavilion January 12, 2016
Sunday, January 10, 2016
TEXAS MEDIA REPORTING A BIT OF GOOD NEWS ON CWD TESTING SO FAR INSTEAD OF
TAHC which is still mum, still refusing timely updates to the public TSE PRION
DISEASE
Tuesday, December 29, 2015
*** TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS
STILL DON'T GET IT $
Chronic Wasting Unease
*** The emergence of a deadly disease has wildlife officials and deer
breeders eyeing each other suspiciously. ***
Monday, November 16, 2015
*** TEXAS PARKS AND WILDLIFE DEPARTMENT EXECUTIVE DIRECTOR ORDER NO.
015-006
*** Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer
and mule deer resources of Texas
Saturday, November 14, 2015
TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DECTECTED
BRINGING NUMBER TO 7 DETECTED IN CAPTIVE BREEDER (if/when the last two are
confirmed).
Thursday, November 05, 2015
*** TPW Commission Adopts Interim Deer Breeder Movement Rules
Friday, October 09, 2015
Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October
2015
Saturday, October 03, 2015
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO
2015
Thursday, September 24, 2015
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE
Prion Testing
*** I cannot stress enough to all of you, for the sake of your family and
mine, before putting anything in the freezer, have those deer tested for CWD.
...terry
***raw and uncut
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig
and take her to the dance in Texas
Friday, August 07, 2015
*** Texas CWD Captive, and then there were 4 ?
Thursday, August 06, 2015
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
I understand that the 84th Legislation might have made some terrible
mistakes with regards to Chronic Wasting Disease CWD TSE Prion aka mad cow type
disease, by weakening CWD rules for breeders.
Sunday, December 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected
to advocate for bills that will seek to further deregulate their industry
Tuesday, December 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry
TAHC TPWD CWD TSE PRION
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
2011 – 2012
Friday, October 28, 2011
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
I kindly submit the following ;
***for anyone interested, here is some history of CWD along the Texas, New
Mexico border, and my attempt to keep up with it...terry
snip...
see history CWD Texas, New Mexico Border ;
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
Sunday, October 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic
Wasting Disease in New Mexico New Mexico Department of Game and Fish
Thursday, August 20, 2015
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks
and CWD
a review of sorts ;
Sunday, July 17, 2016
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
Thursday, April 07, 2016
*** What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016 ***
Sheep and cattle may be exposed to CWD via common grazing areas with
affected deer but so far, appear to be poorly susceptible to mule deer CWD
(Sigurdson, 2008).
***In contrast, cattle are highly susceptible to white-tailed deer CWD and
mule deer CWD in experimental conditions but no natural CWD infections in cattle
have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how
susceptible humans are to CWD but given that the prion can be present in muscle,
it is likely that humans have been exposed to the agent via consumption of
venison (Sigurdson, 2008). Initial experimental research, however, suggests that
human susceptibility to CWD is low and there may be a robust species barrier for
CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD
is affecting wild and farmed cervid populations in endemic areas with some deer
populations decreasing as a result.
snip...
For the purpose of the qualitative risk assessment developed here it is
necessary to estimate the probability that a 30-ml bottle of lure contains urine
from an infected deer. This requires an estimate of the proportion of deer herds
in the USA which are infected with CWD together with the within herd prevalence.
The distribution map of CWD in US shows it is present mainly in central
states (Figure 1). However, Virginia in the east of the country has recorded
seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take
steps to prevent urine being taken from infected animals eg by sourcing from
farms where the deer are randomly tested for CWD (Anon 2015a). However, if
disease is already present and testing is not carried out regularly, captive
populations are not necessarily disease free (Strausser 2014). Urine-based deer
lures have been known to be collected from domestic white-tailed deer herds and
therefore there is a recognised risk. This is reflected by 6 US States which
have
14
banned the use of natural deer urine for lures, as the deer urine may be
sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For
example, the US State of Virginia is banning the use of urine-based deer lures
on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska
banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned
urine-based deer lures and acknowledged that there is no way to detect their use
(Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it
appears that up to 50% of deer herds can be infected with 80-90% of animals
infected within some herds.
*** It is therefore assumed that probability that a 30-ml bottle of deer
urine lure imported from the USA is sources from an infected deer is medium.
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 cannot be determined, however, as it is not specified in TRACES. It may
constitute a small percentage of the very low tonnage of non-fish origin
processed animal proteins that were imported from US into GB.
*** Overall, therefore, it is considered there is a greater than negligible
risk that (non-ruminant) 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...
Summary and MORE HERE ;
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
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 THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
*** 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: 12/30/2014ID: 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
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*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
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 ;
with CWD TSE Prions, I am not sure there is any absolute yet, other than
what we know with transmission studies, and we know tse prion kill, and tse
prion are bad. science shows to date, that indeed soil, dirt, some better than
others, can act as a carrier. same with objects, farm furniture. take it with
how ever many grains of salt you wish, or not. if load factor plays a role in
the end formula, then everything should be on the table, in my opinion. see
;
***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 ;
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable
neurological diseases likely caused by a misfolded form of the prion protein.
TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’
disease) in cattle, chronic wasting disease in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are
unique among TSEs because they can be transmitted between animals, and the
disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations
of deposition via transport processes affecting soil particles, including
entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several
years. Significant interest remains in developing methods that could be applied
to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests
that serine proteases and the microbial consortia in stimulated soils and
compost may partially degrade PrPTSE. Transition metal oxides in soil (viz.
manganese oxide) may also mediate prion inactivation. Overall, the effect of
prion attachment to soil particles on its persistence in the environment is not
well understood, and additional study is needed to determine its implications on
the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding,
inferring a durable environmental reservoir, and an efficient mechanism for
indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
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
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
CHRONIC WASTING DISEASE TSE PRION
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting
disease (CWD) is the prion disease affecting deer, elk and moose, and it is a
widespread and expanding epidemic affecting 22 US States and 2 Canadian
provinces so far. CWD poses the most serious zoonotic prion transmission risks
in North America because of huge venison consumption (>6 million deer/elk
hunted and consumed annually in the USA alone), significant prion infectivity in
muscles and other tissues/fluids from CWD-affected cervids, and usually high
levels of individual exposure to CWD resulting from consumption of the affected
animal among often just family and friends. However, we still do not know
whether CWD prions can infect humans in the brain or peripheral tissues or
whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no
essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) CWD transmission to humans has already occurred. We will test these
hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in
vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain
or peripheral lymphoid tissues at low levels by conducting systemic bioassays in
a set of "humanized" Tg mouse lines expressing common human PrP variants using a
number of CWD isolates at varying doses and routes. Experimental "human CWD"
samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission
barrier is dependent on prion strain and influenced by the host (human) PrP
sequence by examining and comparing the transmission efficiency and phenotypes
of several atypical/unusual CWD isolates/strains as well as a few prion strains
from other species that have adapted to cervid PrP sequence, utilizing the same
panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD
infection in humans by examining in details the clinical, pathological,
biochemical and in vitro seeding properties of existing and future experimental
"human CWD" samples generated from Aims 1-2 and compare them with those of
common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining
a significant number of brain samples from prion-affected human subjects in the
USA and Canada who have consumed venison from CWD-endemic areas utilizing the
criteria and essays established in Aim 3. The findings from this proposal will
greatly advance our understandings on the potential and characteristics of
cervid prion transmission in humans, establish reliable essays for CWD zoonosis
and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure
to cervid prions because chronic wasting disease (CWD, a widespread and highly
infectious prion disease among deer and elk in North America) continues
spreading and consumption of venison remains popular, but our understanding on
cervid-to-human prion transmission is still very limited, raising public health
concerns. This proposal aims to define the zoonotic risks of cervid prions and
set up and apply essays to detect CWD zoonosis using mouse models and in vitro
methods. The findings will greatly expand our knowledge on the potentials and
characteristics of cervid prion transmission in humans, establish reliable
essays for such infections and may discover the first case(s) of CWD infection
in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
===========================================================
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) *** CWD transmission to humans has already occurred. *** We will test
these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary
in vitro approaches.
============================================================
Key Molecular Mechanisms of TSEs
Zabel, Mark D.
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs),
are fatal neurodegenerative diseases affecting humans, cervids, bovids, and
ovids. The absolute requirement of PrPC expression to generate prion diseases
and the lack of instructional nucleic acid define prions as unique infectious
agents. Prions exhibit species-specific tropism, inferring that unique prion
strains exist that preferentially infct certain host species and confront
transmission barriers to heterologous host species. However, transmission
barriers are not absolute. Scientific consensus agrees that the sheep TSE
scrapie probably breached the transmission barrier to cattle causing bovine
spongiform encephalopathy that subsequently breached the human transmission
barrier and likely caused several hundred deaths by a new-variant form of the
human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human
health, emotion and economies can still be felt in areas like farming, blood and
organ donations and the threat of a latent TSE epidemic. This precedent raises
the real possibility of other TSEs, like chronic wasting disease of cervids,
overcoming similar human transmission barriers. A groundbreaking discovery made
last year revealed that mice infected with heterologous prion strains facing
significant transmission barriers replicated prions far more readily in spleens
than brains6. Furthermore, these splenic prions exhibited weakened transmission
barriers and expanded host ranges compared to neurogenic prions. These data
question conventional wisdom of avoiding neural tissue to avoid prion
xenotransmission, when more promiscuous prions may lurk in extraneural tissues.
Data derived from work previously funded by NIH demonstrate that Complement
receptors CD21/35 bind prions and high density PrPC and differentially impact
prion disease depending on the prion isolate or strain used. Recent advances in
live animal and whole organ imaging have led us to generate preliminary data to
support novel, innovative approaches to assessing prion capture and transport.
We plan to test our unifying hypothesis for this proposal that CD21/35 control
the processes of peripheral prion capture, transport, strain selection and
xenotransmission in the following specific aims.
1. Assess the role of CD21/35 in splenic prion strain selection and host
range expansion.
2. Determine whether CD21/35 and C1q differentially bind distinct prion
strains
3. Monitor the effects of CD21/35 on prion trafficking in real time and
space
4. Assess the role of CD21/35 in incunabular prion trafficking
Public Health Relevance Transmissible spongiform encephalopathies, or prion
diseases, are devastating illnesses that greatly impact public health,
agriculture and wildlife in North America and around the world. The impact to
human health, emotion and economies can still be felt in areas like farming,
blood and organ donations and the threat of a latent TSE epidemic. This
precedent raises the real possibility of other TSEs, like chronic wasting
disease (CWD) of cervids, overcoming similar human transmission barriers. Early
this year Canada reported its first case of BSE in over a decade audits first
case of CWD in farmed elk in three years, underscoring the need for continued
vigilance and research. Identifying mechanisms of transmission and zoonoses
remains an extremely important and intense area of research that will benefit
human and other animal populations.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Allergy and Infectious Diseases (NIAID)
Type High Priority, Short Term Project Award (R56)
Project # 1R56AI122273-01A1
Application # 9211114
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Beisel, Christopher E
Project Start 2016-02-16
Project End 2017-01-31
Budget Start 2016-02-16
Budget End 2017-01-31
Support Year 1
Fiscal Year 2016
Total Cost
Indirect Cost Institution Name Colorado State University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
Hoover, Edward Arthur
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly
transmissible prion disease now recognized in 18 States, 2 Canadian provinces,
and Korea. We have shown that Infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces, and in the tissues
generating those body fluids and excreta, thereby leading to facile transmission
by direct contact and environmental contamination. We have also shown that CWD
can infect some non-cervid species, thus the potential risk CWD represents to
domestic animal species and to humans remains unknown. Whether prions borne in
blood, saliva, nasal fluids, milk, or excreta are generated or modified in the
proximate peripheral tissue sites, may differ in subtle ways from those
generated in brain, or may be adapted for mucosal infection remain open
questions. The increasing parallels in the pathogenesis between prion diseases
and human neurodegenerative conditions, such as Alzheimer's and Parkinson's
diseases, add relevance to CWD as a transmissible protein misfolding disease.
The overall goal of this work is to elucidate the process of CWD prion
transmission from mucosal secretory and excretory tissue sites by addressing
these questions: (a) What are the kinetics and magnitude of CWD prion shedding
post-exposure? (b) Are excreted prions biochemically distinct, or not, from
those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the
source of excreted prions? and (d) Are excreted prions adapted for horizontal
transmission via natural/trans-mucosal routes? The specific aims of this
proposal are: (1) To determine the onset and consistency of CWD prion shedding
in deer and cervidized mice; (2); To compare the biochemical and biophysical
properties of excretory vs. CNS prions; (3) To determine the capacity of
peripheral tissues to support replication of CWD prions; (4) To determine the
protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To
compare the mucosal infectivity of excretory vs. CNS prions. Understanding the
mechanisms that enable efficient prion dissemination and shedding will help
elucidate how horizontally transmissible prions evolve and succeed, and is the
basis of this proposal. Understanding how infectious misfolded proteins (prions)
are generated, trafficked, shed, and transmitted will aid in preventing,
treating, and managing the risks associated with these agents and the diseases
they cause.
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an
emergent highly transmissible prion disease now recognized throughout the USA as
well as in Canada and Korea. We have shown that infected deer harbor and shed
high levels of infectious prions in saliva, blood, urine, and feces thereby
leading to transmission by direct contact and environmental contamination. In
that our studies have also shown that CWD can infect some non-cervid species,
the potential risk CWD may represents to domestic animal species and humans
remains unknown. The increasing parallels in the development of major human
neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and
prion diseases add relevance to CWD as a model of a transmissible protein
misfolding disease. Understanding how infectious misfolded proteins (prions) are
generated and transmitted will aid in interrupting, treating, and managing the
risks associated with these agents and the diseases they cause.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 4R01NS061902-07
Application # 9010980
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May Project Start 2009-09-30
Project End 2018-02-28
Budget Start 2016-03-01
Budget End 2017-02-28
Support Year 7
Fiscal Year 2016
Total Cost $409,868
Indirect Cost $134,234 Institution Name Colorado State University-Fort
Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** 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).***
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.
***********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
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
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.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** 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.
*** now, let’s see what the authors said about this casual link, personal
communications years ago, and then the latest on the zoonotic potential from CWD
to humans from the TOKYO PRION 2016 CONFERENCE.
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 ;
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
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 ***
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
SCRAPIE AND CWD ZOONOSIS
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Transmission of scrapie prions to primate after an extended silent
incubation period
***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.***
Wednesday, June 29, 2016
CWD, SCRAPIE, ZOONOSIS, it’s for real folks, the risk factors have
increased greatly, and science has spoken, cwd and scrapie to humans as sporadic
cjd may have already happened.
Transmission of scrapie prions to primate after an extended silent
incubation period
Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne
Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen ,
Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee
, Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion
disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD)
in humans and having guided protective measures for animal and human health
against animal prion diseases. Recently, partial transmissions to humanized mice
showed that the zoonotic potential of scrapie might be similar to c-BSE. We here
report the direct transmission of a natural classical scrapie isolate to
cynomolgus macaque, a highly relevant model for human prion diseases, after a
10-year silent incubation period, with features similar to those reported for
human cases of sporadic CJD. Scrapie is thus actually transmissible to primates
with incubation periods compatible with their life expectancy, although fourfold
longer than BSE. Long-term experimental transmission studies are necessary to
better assess the zoonotic potential of other prion diseases with high
prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98
scrapie.
snip...
In addition to previous studies on scrapie transmission to primate1,8,9 and
the recently published study on transgenic humanized mice13, our results
constitute new evidence for recommending that the potential risk of scrapie for
human health should not be dismissed. Indeed, human PrP transgenic mice and
primates are the most relevant models for investigating the human transmission
barrier. To what extent such models are informative for measuring the zoonotic
potential of an animal TSE under field exposure conditions is unknown. During
the past decades, many protective measures have been successfully implemented to
protect cattle from the spread of c-BSE, and some of these measures have been
extended to sheep and goats to protect from scrapie according to the principle
of precaution. Since cases of c-BSE have greatly reduced in number, those
protective measures are currently being challenged and relaxed in the absence of
other known zoonotic animal prion disease. We recommend that risk managers
should be aware of the long term potential risk to human health of at least
certain scrapie isolates, notably for lymphotropic strains like the classical
scrapie strain used in the current study. Relatively high amounts of infectivity
in peripheral lymphoid organs in animals infected with these strains could lead
to contamination of food products produced for human consumption. Efforts should
also be maintained to further assess the zoonotic potential of other animal
prion strains in long-term studies, notably lymphotropic strains with high
prevalence like CWD, which is spreading across North America, and atypical/Nor98
scrapie (Nor98)50 that was first detected in the past two decades and now
represents approximately half of all reported cases of prion diseases in small
ruminants worldwide, including territories previously considered as scrapie
free. Even if the prevailing view is that sporadic CJD is due to the spontaneous
formation of CJD prions, it remains possible that its apparent sporadic nature
may, at least in part, result from our limited capacity to identify an
environmental origin.
***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.***
2015
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 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.
==============
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
***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.***
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”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.
Texas has been covering up mad cow disease for decades. on the second
attempt at covering up a second mad cow in Texas, myself and others wrote to the
Honorable Phyllis Fong of the OIG and asked for a second test be done in
Weybridge, this after I wrote ever scientist around the globe. finally, this 2nd
attempt at covering up mad cow disease in Texas failed, the Texas BSE madcow was
finally confirmed, 7 months after a supposedly 48 hour turnaround on testing per
their own BSE RED BOOK. this is why I have absolutely no faith in what’s going
on now in Texas. it’s just another dog pony show imo...
Gov. Perry Responds to Mad Cow Confirmation
AUSTIN – Gov. Rick Perry issued the following statement concerning
confirmation from the USDA that a single cow in Texas has tested positive for
BSE or Mad Cow:
“I want to urge calm and reassure the public that they can have the highest
confidence in our beef supply, and the safeguards we have in place to protect
the public from the spread of BSE. I, for one, will continue to eat red meat,
and intend to do so later tonight with complete confidence it is safe to do
so.”
“We have had plans in place for more than a decade to address a confirmed
case of Mad Cow disease to ensure it is contained and kept out of the food
supply. Working with federal officials, all precautions are being taken to
protect the public.”
“We have been given no specific information from USDA on the origin of the
cow that tested positive for BSE other than it came from a Texas herd.”
Statement of Gov. Rick Perry on BSE Announcement
Thursday, June 30, 2005 • Press Release
AUSTIN – Gov. Rick Perry issued the following statement today on the
announcement by the U.S. Department of Agriculture that a cow recently tested
for Bovine Spongiform Encephalopathy – commonly known as mad cow disease – is
from a Texas herd.
“I want to urge calm and reassure the public that they can have the highest
confidence in our beef supply, and the safeguards we have in place to protect
the public from the spread of BSE. There is not, nor has there ever been, a
known instance of BSE contaminating the food supply in Texas or anywhere else in
the United States.
The animal in question was not processed into food or any other product.
Texans can be sure that the beef they buy at their local supermarkets or
restaurants is as safe today as it was yesterday, and I encourage Texans to
continue to enjoy Texas beef products.”
Section 2. Testing Protocols and Quality Assurance Controls
In November 2004, USDA announced that its rapid screening test, Bio-Rad
Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test
result as part of its enhanced BSE surveillance program. The ELISA rapid
screening test performed at a BSE contract laboratory produced three high
positive reactive results.40 As required,41 the contract laboratory forwarded
the inconclusive sample to the APHIS National Veterinary Services Laboratories
(NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again
produced three high positive reactive results.42 In accordance with its
established protocol, NVSL ran its confirmatory test, an immunohistochemistry
(IHC) test, which was interpreted as negative for BSE. In addition, NVSL
performed a histological43 examination of the tissue and did not detect
lesions44 consistent with BSE.
Faced with conflicting results, NVSL scientists recommended additional
testing to resolve the discrepancy but APHIS headquarters officials concluded no
further testing was necessary because testing protocols were followed. In our
discussions with APHIS officials, they justified their decision not to do
additional testing because the IHC is internationally recognized as the "gold
standard." Also, they believed that conducting additional tests would undermine
confidence in USDA’s established testing protocols.
USDA orders silence on mad cow in Texas
Susan Combs by no means has public and consumer health at heart while she
is protecting the cattle industry. She is oblivious to mad cow disease. Her soul
purpose is to protect the cattle industry at all cost, including my mothers life
(DOD 12/14/97), or maybe one of your family members from any strain of mad cow
disease in TEXAS. SHE helped cover-up mad cow disease in TEXAS both on that
inconclusive that was positive so many times it will make your head spin. PLUS,
the other mad cow in TEXAS they rendered without testing at all, that came from
the top out of Austin. THEY should be tried for murder. corporate homicide is
what i call it. they knew for years, but kept on keeping on.
Faced with conflicting results between the rapid screening and IHC tests,
NVSL scientists recommended additional testing to resolve the discrepancy but
APHIS headquarters officials concluded that no further testing was necessary
since testing protocols were followed and the confirmatory test was negative. In
our discussions with APHIS officials, they justified their decision to not do
additional testing because the IHC test is internationally recognized as the
“gold standard” of testing. Also, they believed that
USDA/OIG-A/50601-10-KC/ Page iv
conducting additional tests would undermine confidence in USDA’s testing
protocols.
OIG obtained evidence that indicated additional testing was prudent. We
came to this conclusion because the rapid screening tests produced six high
positive reactive results, the IHC tests conflicted, and various standard
operating procedures were not followed. Also, our review of the relevant
scientific literature, other countries’ protocols, and discussions with experts
led us to conclude that additional confirmatory testing should be considered in
the event of conflicting test results.
To maintain objectivity and independence, we requested that USDA’s
Agricultural Research Service (ARS) perform the Office International des
Epizooties (OIE) Scrapie-Associated Fibrils (SAF) immunoblot test. The
additional testing produced positive results. To confirm, the Secretary of
Agriculture requested that an internationally recognized BSE laboratory in
Weybridge, England (Weybridge) perform additional testing. Weybridge conducted
various tests, including their own IHC tests and three Western blot tests. The
tests confirmed that the cow was infected with BSE. The Secretary immediately
directed USDA scientists to work with international experts to develop new
protocols that include performing dual confirmatory tests in the event of an
inconclusive BSE screening test.
We attribute the failure to identify the BSE positive sample to rigid
protocols, as well as the lack of adequate quality assurance controls over its
testing program. Details of our concerns are discussed in Findings 3 and 4.
Texas BSE Investigation Final Epidemiology Report August 2005
Executive Summary
In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample
from November 2004, that had originally been classified as negative on the
immunohistochemistry test, was confirmed positive on SAF immunoblot (Western
blot). The U.S. Department of Agriculture (USDA) identified the herd of origin
for the index cow in Texas; that identification was confirmed by DNA analysis.
USDA, in close cooperation with the Texas Animal Health Commission (TAHC),
established an incident command post (ICP) and began response activities
according to USDA’s BSE Response Plan of September 2004. Response personnel
removed at-risk cattle and cattle of interest (COI) from the index herd,
euthanized them, and tested them for BSE; all were negative. USDA and the State
extensively traced all at-risk cattle and COI that left the index herd. The
majority of these animals entered rendering and/or slaughter channels well
before the investigation began. USDA’s response to the Texas finding was
thorough and effective.
Background of the Investigation
On June 10, 2005, USDA announced that the November 2004 inconclusive BSE
sample tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s
National Animal Disease Center (NADC) upon the recommendation of USDA’s Office
of the Inspector General. Samples were sent to a World Organization for Animal
Health (OIE) reference laboratory for BSE in Weybridge, England, for
confirmatory tests. Farm A, located in Texas, was the suspected farm of origin
for the index cow and was placed under hold order on June 20, 2005 pending
confirmation of the positive results and DNA analysis of the herd. Weybridge
confirmed the BSE positive on June 24, 2005. The carcass of the index cow had
been disposed of by incineration in November 2004.
News Release
Texas Animal Health Commission
Box l2966 * Austin, Texas 78711 * (800) 550-8242 * FAX (512) 719-0719
Bob Hillman, DVM * Executive Director
For info, contact Carla Everett, information officer, at 1-800-550-8242,
ext. 710, or
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:mailto:ceverett@tahc.state.tx.us
For immediate release---
State-Federal Team Responds to Texas BSE Case
The US Department of Agriculture announced June 29 that genetic testing has
verified that an aged cow that tested positive for Bovine Spongiform
Encephalopathy or BSE originated from a Texas beef cattle herd. Tissues for
laboratory testing were initially collected from the animal in November 2004,
and the carcass was incinerated and did not enter the human food, animal feed or
fertilizer supply system. While tests in November indicated the animal did not
have BSE, retesting in England in June confirmed the animal had the disease. The
Texas Animal Health Commission (TAHC), the state’s livestock and poultry health
regulatory agency, and USDA have jointly assigned a state-federal team to
conduct the epidemiological investigation and response.
“The TAHC and US Department of Agriculture’s Veterinary Services are
working with a complement of experts from federal and state animal health, food
safety, public health and feed regulatory agencies to ensure the continued
safety and wholesomeness of our meat supply,” said Dr. Bob Hillman, Texas state
veterinarian and executive director of the TAHC, the state’s livestock and
poultry health regulatory agency. “Epidemiological investigations are thorough
and focus on verifying the herd of origin, and when, where and how the animal
and potentially, any herd mates, were exposed to the abnormal prion, or disease
agent, that causes BSE. Additionally, epidemiology investigations trace the
infected animal’s movement and herd mates. Animals potentially exposed to the
disease will be depopulated, with proper disposal. The animals will not be
introduced into the human or animal food chain.”
The USDA’s BSE testing protocol requires testing of emaciated or injured
cattle, cattle that exhibit central nervous system disorder, cattle unable to
rise or to walk normally, and cattle that die of unknown causes. Since June 1,
2004, brain tissue samples from more than 394,000 cattle have been tested in the
U.S. and were negative for BSE. Of those, 38,320 were tested in Texas, Dr.
Hillman noted. BSE surveillance has been conducted in the U.S. since l990.
The U.S. has taken preventive measures against the introduction of BSE
since l989, when prohibitions were placed on cattle and other ruminants from
BSE-affected countries, noted Dr. Hillman. In 1997, the importation ban was
extended to all of Europe.
Dr. Hillman said the U.S. Food and Drug Administration (FDA) in 1997 banned
the use of ruminant-derived protein (from animals such as cattle and sheep) in
feed for cattle and other ruminants. There is no evidence that BSE spreads from
live animal to animal in the herd, but cattle can be exposed by eating feed that
contains rendered protein from infected animals. “These measures taken by the
USDA and the FDA are safeguards that work to protect livestock, and ultimately,
our meat supply,” he said.
--30--
Second BSE case occurred in Texas, USDA says Jun 30, 2005 (CIDRAP News) –
The United States' second case of bovine spongiform encephalopathy (BSE) was in
a 12-year-old cow that came from a Texas herd and would have been made into pet
food if it hadn't been flagged for BSE testing, federal officials announced
yesterday evening.
US Department of Agriculture (USDA) officials said the cow was to be
processed at a pet food plant in Waco, Tex., when it was diverted for testing
because it couldn't walk. Officials didn't name the plant or say exactly where
the cow came from. But an Associated Press (AP) report today identified the
plant as Champion Pet Food in Waco and said the cow was already dead when
brought there last November.
"The source herd is now under a hold order as we identify animals of
interest within the herd," USDA Chief Veterinarian John Clifford said in a
prepared statement. Investigators will look for cattle born within a year before
or after the BSE-infected cow and any of the cow's offspring born within the
past 2 years, he explained.
"If the age of the animal cannot be pinpointed, then we may expand our
inquiry to include all animals in this herd before the feed ban went into place
in 1997," Clifford said. To prevent BSE, the government banned putting cattle
protein into cattle feed in August 1997.
The infected cow was incinerated, and no parts were used in human food or
animal feed, according to the USDA. "The safety of our food supply is not in
question," Clifford stated.
Because of the cow's age, the USDA suspects it became infected by eating
contaminated feed before the government ban began in 1997. The USDA and the Food
and Drug Administration (FDA) will try to trace the source herd's feed history,
officials said.
The FDA will also check whether firms that may have processed meat-and-bone
meal from animals from that herd have complied with the 1997 feed ban, Dr. Steve
Sundlof, director of the FDA's Center for Veterinary Medicine, said at a news
conference last night.
The Texas case is the first US BSE case in a native-born animal; Clifford
said the cow lived on one farm all its life. The previous US case, found in
December 2003, involved a Canadian-born dairy cow in Washington state.
An initial screening test on the Texas cow last November was inconclusive,
and two confirmatory immunohistochemistry tests were negative. But early this
month the USDA's inspector general ordered a Western blot test, which came back
positive. Further confirmatory tests at an international reference lab in
Britain were also positive, prompting the USDA to announce the findings last
week.
The USDA waited for the results of DNA tests before announcing that the
infected cow came from Texas. The step was necessary because parts of the
infected cow were stored with those of four other cattle, causing some
uncertainty, officials said.
"We felt that we had the correct herd; we wanted to identify that
appropriately with DNA," Clifford said at the news conference. Investigators
analyzed DNA from the infected animal and then looked for relatives in the
presumed source herd by analyzing DNA from members of the herd, he said. The
investigation turned up two cattle that are related to the infected cow, he
added.
The AP report said Champion Pet Food is under contract to take samples from
animals in poor health. The company's owner, Benjy Bauer, told the AP that his
workers took samples from the cow and sent them to the Texas Veterinary
Diagnostic Laboratory at Texas A&M University. The lab is one of several the
USDA uses to screen cattle for BSE, the story said.
See also:
USDA news release http://www.aphis.usda.gov/lpa/issues/bse/BSE_statement6-29-05.pdf
USDA fact sheet on BSE epidemiologic investiation
USDA press conference transcript
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED
;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve
Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick
to assure the public earlier this week that the third case of mad cow disease
did not pose a risk to them, but what federal officials have not acknowledged is
that this latest case indicates the deadly disease has been circulating in U.S.
herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is thought
that cows usually contract the disease from contaminated feed they consume as
calves. The concern is that humans can contract a fatal, incurable,
brain-wasting illness from consuming beef products contaminated with the mad cow
pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the National
Institutes of Health's Laboratory for Central Nervous System Studies and an
expert on mad cow-like diseases, told United Press International. "The question
was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before one
year ago" because of the agency's reluctance to retest the Texas cow that
initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector
general.
"Everything they did on the Texas cow makes everything they did before 2005
suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as
bovine spongiform encephalopathy, or BSE, did not significantly threaten human
or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk
either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers
should be troubled by the USDA's secrecy and its apparent plan to dramatically
cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the
USDA's surveillance program and the failure of the USDA to reveal really
important details," Halloran told UPI. "Consumers have to be really concerned if
they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it
has proposed, even in light of a third case, scaling back the program to 40,000
tests annually.
"They seem to be, in terms of actions and policies, taking a lot more
seriously the concerns of the cattle industry than the concerns of consumers,"
Halloran said. "It's really hard to know what it takes to get this
administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow
tissue into cattle feed (which is thought to spread the disease) and removal of
the most infectious parts of cows, such as the brain and spinal cord, protect
consumers. But the agency glosses over the fact that both of these systems have
been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has
been criticized by the Government Accountability Office in two reports, the most
recent coming just last year. The GAO said the FDA's enforcement of the ban
continues to have weaknesses that "undermine the nation's firewall against
BSE."
USDA documents released last year showed more than 1,000 violations of the
regulations requiring the removal of brains and spinal cords in at least 35
states, Puerto Rico and the Virgin Islands, with some plants being cited
repeatedly for infractions. In addition, a violation of similar regulations that
apply to beef exported to Japan is the reason why Japan closed its borders to
U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system.
The USDA insists the prevalence of mad cow disease is low, but the agency has
provided few details of its surveillance program, making it difficult for
outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without
having a breakdown of the tested population by age and risk status," Elizabeth
Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern,
Switzerland, a company that provides advice on reducing mad cow risk to industry
and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be
able to go away a little bit for (the USDA) if they would just publish a
breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's
surveillance plan via the Freedom of Information Act in May 2004 but nearly two
years later has not received any corresponding documents from the agency,
despite a federal law requiring agencies to comply within 30 days. This leaves
open the question of whether the USDA is withholding the information, does not
have the information or is so haphazardly organized that it cannot locate
it.
Mumford said the prevalence of the disease in U.S. herds is probably quite
low, but there have probably been other cases that have so far gone undetected.
"They're only finding a very small fraction of that low prevalence," she
said.
Mumford expressed surprise at the lack of concern about the deadly disease
from American consumers. "I would expect the U.S. public to be more concerned,"
she said.
Markus Moser, a molecular biologist and chief executive officer of
Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is
that if people are infected, the mad cow pathogen could become "humanized" or
more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical
procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul
Brown is Senior Research Scientist in the Laboratory of Central Nervous System
... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy detailed
critiques and recommendations to both the USDA and the Canadian Food Agency."
........TSS
OR, what the Honorable Phyllis Fong of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform
Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and
Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat
Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
FDA STATEMENT FOR IMMEDIATE RELEASE May 4, 2004 Media Inquiries:
301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30th, the Food and Drug Administration learned that a cow
with central nervous system symptoms had been killed and shipped to a processor
for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the animal
came from, and the processor that initially received the cow from the
slaughterhouse.
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That material is
being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as "mad
cow disease," can exhibit such symptoms. In this case, there is no way now to
test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit
the feeding of its rendered protein to other ruminant animals (e.g., cows,
goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing
the firm that FDA will not object to use of this material in swine feed only. If
it is not used in swine feed, this material will be destroyed. Pigs have been
shown not to be susceptible to BSE. If the firm agrees to use the material for
swine feed only, FDA will track the material all the way through the supply
chain from the processor to the farm to ensure that the feed is properly
monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the U.K.
showed that the disease spreads by feeding infected ruminant protein to
cattle.
Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action specifying
that the material go only into swine feed means also that it will not be fed to
poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely
with the U.S. Department of Agriculture on all BSE issues. The animal feed rule
provides crucial protection against the spread of BSE, but it is only one of
several such firewalls. FDA will soon be improving the animal feed rule, to make
this strong system even stronger.
#
SEE FULL TEXT OF ALL THIS HERE ;
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
ALABAMA MAD COW CASE
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
(see COPIOUS AMOUNTS OF mad cow feed in COMMERCE IN ALABAMA...TSS)
Texas BSE Investigation Final Epidemiology Report August 2005
State-Federal Team Responds to Texas BSE Case
JUNE 30, 2005
(please note 7+ month delay in final confirmation so the BSE MRR policy
could be set in stone first. $$$...tss)
SEE ATTEMPTED COVER-UP BEFORE THE END AROUND BY FONG ET AL OF THE O.I.G
The U.S. Department of Agriculture confirmed June 29 that genetic testing
had verified bovine spongiform encephalopathy (mad cow disease) in a 12-year-old
cow that was born and raised in a Texas beef cattle herd.
Subsequent epidemiological investigations resulted in the culling and
testing of 67 adult animals from the index herd. Bio-Rad tests for BSE were
conducted on all 67 animals by the National Veterinary Services Laboratory
(NVSL) in Ames, Iowa. All tests were negative.
On July 12, Texas officials lifted the quarantine on the source herd. At
press time, USDA's Animal and Plant Health Inspection Service was tracing
animals of the same age that had left the ranch.
Timeline
The BSE-positive animal was a Brahman-cross cow born and raised in a single
Texas herd. The location of the ranch was not disclosed.
On Nov. 11, 2004, the 12-year-old cow was taken to a Texas auction market.
Because of its condition, the cow was sent to Champion Pet Foods in Waco, Texas.
The company produces several blends of dog food, primarily for the greyhound
industry.
On Nov. 15, the animal arrived dead at Champion. Under procedures
established by USDA's intensive surveillance program, a sample was sent to the
USDA-approved Texas Veterinary Medical Diagnostic Testing Laboratory (TVMDL) at
Texas A&M University.
Between June 1, 2004, and June 1, 2005, TVMDL tested nearly 34,000 samples
from Texas, New Mexico, Arkansas and Louisiana. They tested the sample from
Champion on Nov. 19 using a Bio-Rad ELISA rapid test for BSE. Initial results
were inconclusive.
Because of the inconclusive results, a representative from USDA took the
entire carcass to TVMDL where it was incinerated. USDA's Animal and Plant Health
Inspection Service (APHIS) began tracing the animal and herd.
The sample was then sent to the National Veterinary Services Laboratory for
further testing. Two Immunohistochemistry (IHC) tests were conducted and both
were negative for BSE. At that point APHIS stopped their trace.
USDA scientists also ran an additional, experimental IHC "rapid" tissue
fixation test for academic purposes. This test has not been approved
internationally.
Some abnormalities were noted in the experimental test, but because the two
approved tests came back negative, the results were not reported beyond the
laboratory.
Monitoring by OIG
USDA's Office of Inspector General (OIG) has been monitoring implementation
of the BSE expanded surveillance program and evaluating the following:
* Effectiveness of the surveillance program;
* Performance of BSE laboratories in complying with policies and procedures
for conducting tests and reporting results;
* Enforcement of the ban on specified risk materials in meat
products;
* Controls to prevent central nervous system tissue in advanced meat
recovery products;
* Ante mortem condemnation procedures; and
* Procedures for obtaining brain tissue samples from condemned
cattle.
While reviewing voluminous records, OIG auditors noticed conflicting test
results on one sample-rapid inconclusive, IHC negative, experimental
reactive.
Sample retested
At the recommendation of the Inspector General, the sample was retested
during the week of June 5 with a second confirmatory test, the Western Blot. The
results were reactive.
USDA scientists then conducted an additional IHC confirmatory test, using
different antibodies from the November 2004 test. On Friday, June 10, Secretary
of Agriculture Mike Johanns publicly announced the results as a "weak
positive."
On June 16 an official with USDA's National Veterinary Services Laboratory
hand-carried samples for further testing to the Veterinary Laboratory Agency
(VLA) in Weybridge, England. Since 1991, the VLA has been a BSE reference
laboratory for the World Organization for Animal Health (OIE).
Experts from the Weybridge lab confirmed the accuracy of the results of
USDA's November confirmatory IHC test, concurring that the case could not have
been confirmed on the basis of this sample. They also examined the November
experimental IHC test and interpreted the results to be positive.
Weybridge also conducted additional tests, including IHC, OIE-prescribed
Western Blot, NaTTA Western Blot and Prionics Western Blot tests.
To better understand the conflicting results, USDA also conducted Bio-Rad
and IDEXX rapid screening tests, IHC and OIE-prescribed Western Blot. USDA also
used DNA sequencing to determine the prion protein gene sequence of the
animal.
Texas even had a 'secret' test that showed that mad cow positive;
experimental IHC test results, because the test was not a validated procedure,
and because the two approved IHC tests came back negative, the results were not
considered to be of regulatory significance and therefore were not reported
beyond the laboratory. . A Western blot test conducted the week of June 5, 2005,
returned positive for BSE.
48 hr BSE confirmation turnaround took 7+ months to confirm this case, so
the BSE MRR policy could be put into place. ...TSS
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov,
contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at
OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully
request a full inquiry into the cover-up of TSEs in the United States of America
over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff,
Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to:
Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding
further analysis of BSE Inconclusive Test Results
posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days
later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary
for Marketing and Regulatory Programs resigns. Three days later same mad cow
found in November turns out to be positive. Both resignation are unexpected.
just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004. ...TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 -0600
From: "Terry S. Singeltary Sr."
To: Carla EverettReferences: [log in to unmask]; [log in to unmask] ;
Greetings Carla, still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food
chain?
and i see the TEXAS department of animal health is ramping up for
something, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...
can you confirm??? terry
============================================================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."References;[log in to unmask];
The USDA has made a statement, and we are referring all callers to the USDA
web site. We have no information about the animal being in Texas.
Carla
At 09:44 AM 11/19/2004, you wrote:
Greetings Carla,
i am getting unsubstantiated claims of this BSE 'inconclusive' cow is
from
TEXAS. can you comment on this either way please?
thank you,
Terry S. Singeltary Sr
======================================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."References: <[log in to unmask]><[log
in to unmask] us><[log in to unmask]> <[log in to unmask]us>
<[log in to unmask]>
our computer department was working on a place holder we could post USDA's
announcement of any results. There are no results to be announced tonight by
NVSL, so we are back in a waiting mode and will post the USDA announcement when
we hear something.
At 06:05 PM 11/22/2004,
you wrote:
why was the announcement on your TAHC site removed?
Bovine Spongiform Encephalopathy:
November 22: Press Release title here
star image More BSE information
terry
Carla Everett wrote:
no confirmation on the U.S.'inconclusive test...
no confirmation on location of animal. ;
FROM HERE, IT TOOK 7 MONTHS TO CONFIRM THIS MAD COW, while the BSE MRR
policy was being bought and sold...(in my opinion...tss)
Saturday, August 16, 2008
Qualitative Analysis of BSE Risk Factors in the United States February 13,
2000 at 3:37 pm PST (BSE red book)
TEXAS OFFICIALS DEAD WRONG ON AMOUNT OF INFECTIVITY TO CAUSE A TSE PRION
DISEASE ;
"FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams – approximately a quarter ounce — of prohibited
material. These animals weigh approximately 600 pounds."
5.5 GRAMS OF INFECTIOUS PROHIBITED MAD COW FEED FOR EACH OF THE 1,222
ANIMALS (5.5 GRAMS X 1,222 ANIMALS) IS ENOUGH INFECTIOUS MAD COW FEED TO KILL A
SMALL HERD OF COWS...TSS
U.S. Food and Drug Administration FDA News | Today the Food and Drug
Administ…U.S. Food and Drug Administration FDA News
Today the Food and Drug Administration announced the results of tests taken
on feed used at a Texas feedlot that was suspected of containing meat and bone
meal from other domestic cattle — a violation of FDA’s 1997 prohibition on using
ruminant material in feed for other ruminants. Results indicate that a very low
level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams – approximately a quarter ounce — of prohibited
material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin
(therefore not likely to contain infected material because there is no evidence
of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated.
According to Dr. Bernard Schwetz, FDA’s Acting Principal Deputy
Commissioner, “The challenge to regulators and industry is to keep this disease
out of the United States. One important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined with
other steps, like U.S. Department of Agriculture’s (USDA) ban on the importation
of live ruminant animals from affected countries, these steps represent a series
of protections, to keep American cattle free of BSE.”
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing
that it is voluntarily purchasing all 1,222 of the animals held in Texas and
mistakenly fed the animal feed containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA believes any
cattle that did not consume feed containing the prohibited material are
unaffected by this incident, and should be handled in the beef supply clearance
process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting
the human error that resulted in the misformulation of the animal feed
supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food supply and that continued vigilance
needs to be taken, by all concerned, to ensure these rules are followed
routinely.
FDA will continue working with USDA as well as State and local officials to
ensure that companies and individuals comply with all laws and regulations
designed to protect the U.S. food supply.
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242
Consumer Inquiries: 888-INFO-FDA
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken
on feed used at a Texas feedlot that was suspected of containing meat and bone
meal from other domestic cattle -- a violation of FDA's 1997 prohibition on
using ruminant material in feed for other ruminants. Results indicate that a
very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams - approximately a quarter ounce -- of prohibited
material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin
(therefore not likely to contain infected material because there is no evidence
of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy
Commissioner, "The challenge to regulators and industry is to keep this disease
out of the United States. One important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined with
other steps, like U.S. Department of Agriculture's (USDA) ban on the importation
of live ruminant animals from affected countries, these steps represent a series
of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing
that it is voluntarily purchasing all 1,222 of the animals held in Texas and
mistakenly fed the animal feed containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA believes any
cattle that did not consume feed containing the prohibited material are
unaffected by this incident, and should be handled in the beef supply clearance
process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting
the human error that resulted in the misformulation of the animal feed
supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food supply and that continued vigilance
needs to be taken, by all concerned, to ensure these rules are followed
routinely.
FDA will continue working with USDA as well as State and local officials to
ensure that companies and individuals comply with all laws and regulations
designed to protect the U.S. food supply.
PRION 2009 CONGRESS BOOK OF ABSTRACTS
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral
transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard
Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera
and Vaccines, Germany; 2Department of Neuropathology, Georg-August University,
Göttingen, Germany, 3Department of Virology and Immunology, German Primate
Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal
model to study the pathogenesis of variant Creutzfeldt-Jacob disease
(vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase
of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time
points during the incubation period and 7 orally BSE-dosed macaques were
sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues
were tested for the presence of proteinase-K-resistant prion protein (PrPres) by
western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres
deposits were widely spread in neuronal tissues (including the peripheral
sympathetic and parasympathetic nervous system) and in lymphoid tissues
including tonsils. In asymptomatic disease carriers, PrPres deposits could be
detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were
negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and
medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas
sympathetic trunk and all thoracic/cervical segments of the spinal cord were
still negative for PrPres. However, tonsil samples were negative in all
asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via
autonomic fibres of the splanchnic and vagus nerves indicating that
trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils
were predominantly negative during the main part of the incubation period
indicating that epidemiological vCJD screening results based on the detection of
PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of
vCJD among humans.
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. .........
It is clear that the designing scientists must also have shared Mr
Bradley's surprise at the results because all the dose levels right down to 1
gram triggered infection.
6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100 grams) was probably given with the benefit of hindsight;
particularly if one considers that later in the same answer Mr Bradley expresses
his surprise that it could take as little of 1 gram of brain to cause BSE by the
oral route within the same species. This information did not become available
until the "attack rate" experiment had been completed in 1995/96. This was a
titration experiment designed to ascertain the infective dose. A range of
dosages was used to ensure that the actual result was within both a lower and an
upper limit within the study and the designing scientists would not have
expected all the dose levels to trigger infection. The dose ranges chosen by the
most informed scientists at that time ranged from 1 gram to three times one
hundred grams. It is clear that the designing scientists must have also shared
Mr Bradley's surprise at the results because all the dose levels right down to 1
gram triggered infection.
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus
Macaque
"BSE-L in North America may have existed for decades"
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...
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
now if you don’t believe how screwed up USDA inc. BSE mad cow testing
is/was. when USDA inc. contracts out for someone to pick up suspect BSE mad cow
cattle heads for testing, you would hope they would be from suspect BSE mad cow
cattle. NOT WITH THE USDA INC., they hired someone to pick up HEALTHY CATTLE
THEY KNEW DID NOT HAVE MAD COW DISEASE BSE TO BE TESTED FOR MAD COW DISEASE BSE.
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
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and
BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
From: Terry S. Singeltary Sr. (216-119-138-129.ipset18.wt.net)
Subject: Emergency Operations...BSE Red Book Date: March 13, 2000 at 1:30
pm PST
BSE Red Book 2.1-35
7.0 Emergency Operations
The section below would be implemented only after a first case of BSE is
confirmed in the United States.
7.1 READEO Activation
Prelimanary Notification
The director of NVSL is responsible for immediately notifying the APHIS,
Veterinary Services (VS) deputy administrator when tests suggest a presumptive
diagnosis of BSE. Once NVSL has made a presumptive diagnosis of BSE, APHIS and
FSIS field activities will also be initiated. APHIS will receive notification
(either confirming or not confirming NVSL's diagnosis) from the United Kingdom
anywhere between 24 and 96 hours
IT TOOK 7 MONTHS AND AN ACT OF CONGRESS TO GET THIS 2ND TEXAS BSE MAD COW
CONFIRMED !
now, someone please tell me why I should expect anything different with
Chronic Wasting Disease CWD TSE Prion testing in Texas $$$
the good old boy system is still alive and well in Texas i.e. shoot,
shovel, and shut the hell up i.e. SSS POLICY...
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
to be continued...TSS
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
12:06 PM
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