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Monday, July 18, 2016

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.

 


 

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 Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001)

 


 

*** 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.

 


 

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 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

 

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