Sunday, June 29, 2014

Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014

Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014

 

Transmissible Spongiform Encephalopathy TSE Prion Disease have now been discovered in a wide verity of species across North America. typical C-BSE, atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine, typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98 Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD in cervid is slowly spreading without any stopping it in Canada and the USA and now has mutated into many different strains. Transmissible Mink Encephalopathy TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease have been silently mutating and spreading in different species in North America for decades.

 

The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion Firewall, of which we now know without a doubt, that it was nothing but ink on paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of banned mad cow feed has been put out into commerce, never to return, as late as December of 2013, serious, serious breaches in the FDA mad cow feed ban have been documented. The 2004 enhanced BSE surveillance program was so flawed, that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; 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. see ; http://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/UPI-12841142465253/

 

The BSE surveillance and testing have also been proven to be flawed, and the GAO and OIG have both raised serious question as to just how flawed it has been (see GAO and OIG reports). North America has more documented TSE prion disease, in different documented species (excluding the Zoo BSE animals in the EU), then any other place on the Globe. This does not include the very likelihood that TSE prion disease in the domestic feline and canine have been exposed to high doses of the TSE prion disease vid pet food. To date, it’s still legal to include deer from cwd zone into pet food or deer food. Specified Risk Material i.e. SRM bans still being breach, as recently as just last month.

 

nvCJD or what they now call vCJD, another case documented in Texas last month, with very little information being released to the public on about this case? with still the same line of thought from federal officials, ‘it can’t happen here’, so another vCJD blamed on travel of a foreign animal disease from another country, while ignoring all the BSE TSE Prion risk factors we have here in the USA and Canada, and the time that this victim and others, do spend in the USA, and exposed to these risk factors, apparently do not count in any way with regard to risk factor. a flawed process of risk assessment.

 

sporadic CJD, along with new TSE prion disease in humans, of which the young are dying, of which long duration of illness from onset of symptoms to death have been documented, only to have a new name added to the pot of prion disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be sporadic with no genetic link to any family member? when the USA is the only documented Country in the world to have documented two different cases of atypical H-type BSE, with one case being called atypical H-G BSE with the G meaning Genetic, with new science now showing that indeed atypical H-type BSE is very possible transmitted to cattle via oral transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old excuse, better surveillance. You can only use that excuse for so many years, for so many decades, until one must conclude that CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a blip or a reason of better surveillance, it is a mathematical rise in numbers. More and more we are seeing more humans exposed in various circumstance in the Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same time in North America, more and more humans are becoming exposed to the TSE prion disease via consumption of the TSE prion via deer and elk, cattle, sheep and goats, and for those that are exposed via or consumption, go on to further expose many others via the iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I pondered this mode of transmission via the victims of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or sGSS ? what if?

 

Two decades have passed since Dr. Ironside first confirmed his first ten nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is transmissible. yet all these TSE prion disease and victims in the USA and Canada are being pawned off as a spontaneous event, yet science has shown, the spontaneous theory has never been proven in any natural case of TSE prion disease, and scientist have warned, that they have now linked some sporadic CJD cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about this in the public domain. We must make all human and animal TSE prion disease reportable in every age group, in ever state and internationally, we must have a serious re-evaluation and testing of the USA cattle herds, and we must ban interstate movement of all cervids. Any voluntary effort to do any of this will fail. Folks, we have let the industry run science far too long with regards to the TSE prion disease. While the industry and their lobbyist continues to funnel junk science to our decision policy makers, Rome burns. ...end

 

REFERENCES

 

[all scientific peer review studies and other scientific information I have put into blogs, to shorten reference data. I DO NOT advertise or make money from this, this information is for education use...lost my mom to the hvCJD, and just made a promise, never forget, and never let them forget. ...TSS]

 

Saturday, June 14, 2014

 

Rep. Rosa DeLauro (D-CT) Calls for Briefing on Beef Recalled for Mad Cow Potential Rep. Rosa DeLauro (D-CT)

 


 

Thursday, June 12, 2014

 

Missouri Firm Recalls Ribeye and Carcass Products That May Contain Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal root ganglia may not have been completely removed

 


 

Monday, June 02, 2014

 

Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas

 


 

Monday, June 9, 2014

 

TEXAS MAD COW COVER UP (human BSE) AGAIN IN TEXAS, Mr. President Sir, we need your help please

 


 

Monday, June 23, 2014

 

PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES

 


 

P.28: Modeling prion species barriers and the new host effect using RT-QuIC

 

Kristen A Davenport, Davin M Henderson, Candace K Mathiason, and Edward A Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

 

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious. Studies of the effects of primary or tertiary prion protein www.landesbioscience.com Prion 37 structures on trans-species prion transmission have relied upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect. As an alternative strategy, we are using real-time quaking-induced conversion (RT-QuIC) to investigate the propensity for and the kinetics of trans-species prion conversion. RT-QuIC has the advantage of providing more defined conditions of seeded conversion to study the specific role of native PrP:PrPRES interactions as a component of the species barrier.

 

We are comparing chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions by seeding each prion into its native host recPrP (full-length bovine recPrP, or white tail deer recPrP) vs. into the heterologous species. Upon establishing the characteristics of intra-species and inter-species prion seeding for CWD and BSE prions, we will evaluate the seeding kinetics and cross-species seeding efficiencies of BSE and CWD passaged into a common new host—feline—shown to be a permissive host for both CWD and BSE.

 

*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.

 


 

PROCEEDINGS ONE HUNDRED AND SEVENTEENTH ANNUAL MEETING of the UNITED STATES ANIMAL HEALTH ASSOCIATION BSE, CWD, SCRAPIE, TSE, PRION DISEASE October 17 – 23, 2013

 

Scrapie

 

REPORT OF THE COMMITTEE ON SCRAPIE

 

Chair: Charles Palmer, CA

 

Vice Chair: Kristine Petrini, MN

 

Deborah Brennan, GA; Beth Carlson, ND; John Clifford, DC; Thomas Conner, OH; Walter Cook, WY; Stephen Crawford, NH; Linda Detwiler, NJ; Nancy East, CA; William Edmiston, TX; Anita Edmondson, CA; Dee Ellis, TX; Keith Forbes, NV; Michael Gilsdorf, MD; William Hartmann, MN; Carl Heckendorf, CO; Susan Keller, ND; James Leafstedt, SD; Mary Lis, CT; Jim Logan, WY; Michael Marshall, UT; Shirley McKenzie, NC; Cheryl Miller, IN; Ronald Miller, PA; Elisabeth Patton, WI; Jewell Plumley, WV; Justin Roach, OK; Suelee Robbe-Austerman, IA; Paul Rodgers, WV; Joan Dean Rowe, NC; Ben Smith, WA; Scott Stuart, CO; Diane Sutton, MD; Manoel Tamassia, NJ; Stephen White, WA; Nora Wineland, MO; David Winters, TX; Cindy Wolf, MN.

 

The Committee met on October 22, 2013 at the Town and Country Hotel, San Diego, California, from 9:00 to 11:46 a.m. There were 12 members and 9 guests present. The meeting began with a review of the of the Committee purpose.

 

Attendees did not elect to make any changes to the current language. The following presentations and reports were given.

 

USDA-APHIS Scrapie Program Update and Scrapie Surveillance Projects

 

Alan Huddleston, Associate National Scrapie Program Director

 

United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services (USDA-APHIS-VS) (Presented by TJ Myers Associate Deputy Administrator, USDA-APHIS-VS)

 

Scrapie Eradication Program Results

 

• There has been a 90 percent decrease in the percent positive sheep sampled at slaughter adjusted for face color, from 0.15 to 0.015 percent, since the start of Regulatory Scrapie Slaughter Surveillance (RSSS) in FY 2003 thru September 30, 2013.

 

• There were 11 new infected or source flocks reported in FY 2013 as of September 30, 2013. FY 2013 is the first year since FY 2005 when a reduction in the number of new scrapie infected and source flocks was not observed. Now that the program is in the tail end of the eradication effort it is likely that the numbers will go up and down from year to year due to the difficulty in accurately measuring the frequency of uncommon events. Slaughter Surveillance

 

• The number of animals sampled through slaughter surveillance in FY 2013, through September 30, 2013 was 42,888 compared to 40,776 in FY 2012; this represents an increase of 5 percent. The increase was due to increased sampling of goats.

 

Scrapie Surveillance Plan

 

• Implementation

 

o States with regulatory scrapie slaughter surveillance (RSSS) collection sites will continue to sample all targeted sheep and goats.

 

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o States have State-of-origin sampling minimums for sheep.

 

o VS plans to require annual State-of-origin sampling minimum for goats to be met once the proposed rule revising title 9, Code of Federal Regulations (9 CFR) parts 54 and 79 is finalized. Proposed sampling minimums were provided for FY 2013 and FY 2014.

 

o The annual State-of-origin sampling minimum for sheep is 20 percent of the number required to detect a scrapie prevalence of 0.1 percent with 95 percent confidence or 1 percent of the breeding flock in the State, whichever is less. The objective is to sample sufficient sheep in a 5-year period to detect a scrapie prevalence of 0.1 percent with 95 percent confidence or 5 percent of the breeding flock in the State, whichever is less.

 

o The annual State-of-origin sampling minimum for goats is determined based on the States’ goat scrapie case incidence.

 

o If a State has not had a goat scrapie case in the previous ten years, its annual goat sampling minimum is its prorated share of 3,000 samples, based on its proportion of the U.S. goat population as determined by the National Agricultural Statistics Survey (NASS) Sheep and Goat annual report.

 

o If a State has had a goat scrapie case in the previous ten years, its annual goat sampling minimum is determined using the same method as is used for determining its annual sheep sampling minimum.

 

o Beginning in FY 2013, sheep and goat sampling minimums were calculated separately. As a result, a higher percentage of States will not achieve their sheep sampling minimums in FY 2013 compared with FY 2012. Approximately 40% will not achieve the sheep sampling minimums this fiscal year, compared to approximately 20% in FY 2012. States that did not meet their sheep sampling minimum in FY 2013 through RSSS but will be expected to find other sampling sources to meet the minimum in FY 2014.

 

Note: These are minimums. Plans are to continue to collect samples from the maximum number of targeted animals given the available budget.

 

FY 2014 Priorities

 

• VS priorities for scrapie are to focus on improving the effectiveness and cost efficiency of surveillance and to increase animal identification compliance. This will be accomplished in part by publishing a proposed rule that would address gaps in identification and require States to meet reasonable surveillance targets to remain consistent States. States must meet these targets for VS to demonstrate geographically appropriate surveillance to meet the criteria for freedom and have confidence that all of the remaining cases have been found.

 

• The rule would propose to:

 

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o Give the APHIS Administrator authority to relieve requirements for sheep and goats exposed to scrapie types, such as Nor98-like, that do not pose a significant risk of transmission;

 

o Increase flexibility in how investigations can be conducted and allow the epidemiology in a specific flock to be given more consideration in determining flock and animal status;

 

o Add a genetic-based approach to regulation;

 

o Make goat identification requirements similar to those for sheep to support ongoing slaughter surveillance in goats (no changes will be made in the consistent State requirements regarding identification of goats in intrastate commerce);

 

o Tighten the definition of slaughter channels;

 

o Expand the individual identification requirement to all sexually intact animals unless moving as a group/lot (allows mixed-source groups moving in slaughter channels under 18 months);

 

o Limit the use of tattoos and implants to animals not moving through markets and not in slaughter channels; and

 

o Reduce recordkeeping requirements by making them similar to the current uniform methods and rules compliance guidance.

 

• APHIS is also revising its scrapie import regulations to bring them more in line with the World Animal Health Organization (OIE) scrapie chapter. This will ensure that we meet OIE criteria for free status and prevent the reintroduction of scrapie after free status is achieved.

 

Scrapie Flock Certification Program (SFCP) Standards

 

On May 3, 2013 APHIS announced its intention to revise the SFCP. The comment period closed June 3, and the revised program has gone into effect. The SFCP standards were revised to increase the program’s ability to identify infected flocks quicker and to prevent infected flocks from becoming certified, to reduce costs associated with the program, and to increase SFCP contribution to scrapie surveillance. Scrapie program staff collected input from SFCP enrolled producers, industry representatives, and State and federal stakeholders. The public had a final opportunity to comment on the revised standards through a Federal Register notice.

 

In the revised SFCP the Complete category is eliminated. Additionally, the Select category is revised, and the Export category is slightly modified.

 

• Select category: APHIS has redirected monitoring from inspections to sampling. Select category flocks do not become certified. Specifics for this category include:

 

o There are no annual inspections.

 

o Owners must report clinical signs of scrapie.

 

o Herd owners follow 9 CFR 79 requirements for recordkeeping and animal ID for their flocks.

 

o Flock owners can acquire animals from any other flock, whether or not

 

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that flock is enrolled in the SFCP.

 

o The sampling and testing requirements include:

 

 Sheep or goats displaying clinical signs over 12 months of age;

 

 Animals of any age that either test suspect, inconclusive or positive on a live animal scrapie test or have been determined to be a scrapie suspect by a State, Federal or accredited veterinarian; and  A minimum of one animal per 1-3 years, depending on flock size.

 

• Export Category: APHIS continues a high level of monitoring including inspections and sampling. Flocks can become Export Certified. Specifics for this category include:

 

o Annual inspections are required.

 

o Owners must report clinical signs of scrapie.

 

o Animals must be identified with official SFCP ID.

 

o Flock owners must meet rigorous recordkeeping requirements including maintaining records on every animal that leaves the flock for seven years.

 

o Flock owners must have all cull animals inspected, including home slaughtered animals, for clinical signs of scrapie at least 30 days before culling.

 

o Flock owners can acquire female animals and embryos only from other Export category flocks of equal or higher status.

 

o Flock owners can use sheep and goat milk and colostrum and sheep and goat milk- and colostrum-derived products only from within their own flock or from other Export category flocks of equal or higher status.

 

o The sampling and testing requirements include:

 

 Sheep or goats displaying clinical signs over 12 months of age;

 

 Animals of any age that either test suspect, inconclusive or positive on a live animal scrapie test or have been determined to be a scrapie suspect by a State, Federal or accredited veterinarian;

 

 All found dead mature animals, including euthanized animals;

 

 An annual sampling minimum of one test eligible animal tested for each year of status held (A flock will be removed from the program if the flock owner fails to submit at least one test eligible animal for two consecutive years.);

 

 To gain six years in status, 15 test eligible animals must be sampled; and

 

 The requirements for Export Certified status include:

 

 seven years in status; and

 

 Meet one of three sampling protocols

 

o Standard: 30 test eligible animals

 

o Alternative 1: test all genetically susceptible animals sold

 

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o Alternative 2: test all foundation flock animals.

 

• Participants in the Complete category had the following options: (1) join the Export category with up to 5 years of status; (2) join the revised Select category; or (3) withdraw from the program.

 

o For participants who held “Certified” status in the Complete category who convert to the Export category, APHIS will continue to publish their “Certified” status on its website for 3 years following the start date of the revised program, in addition to their new “Export Monitored” status, to allow them sufficient time to become Export Certified; and

 

o If instead they convert to the Select category or withdraw from the program, APHIS will not continue to publish their “Certified” status on its website.

 

Scrapie Surveillance Projects:

 

• Since the start of slaughter surveillance in 2003 the prevalence of scrapie in sheep has declined 85 percent from 0.2 percent to less than 0.03 percent. The prevalence in goats is estimated to be less than 0.02 percent.

 

• APHIS continues to find new approaches to increase flock level surveillance.

 

• In FY 2013 APHIS initiated an effort to provide information on sample collection and to encourage producer and accredited veterinarian submission of samples.

 

• Instructions for producers and veterinarians to submit samples are now available on the APHIS Scrapie Web Page.

 

• In FY 2014 APHIS will conduct pilot projects in New Jersey and Arkansas to evaluate the efficiency of working with accredited veterinarians to collect samples for scrapie testing.

 

Update from Agriculture Research Service

 

David Schneider

 

USDA, Agriculture Research Service (ARS), Animal Disease Research Unit (ADRU)

 

The USDA-ARS unit in Pullman, Washington, conducts an integrated research program involving studies on scrapie transmission, diagnosis and susceptibility genetics in domestic sheep and goats. Accumulation of disease-associated prion protein (PrPSc) in the placenta of sheep is a recognized source for natural transmission of classical scrapie disease and environmental contamination. Much less is known about prion accumulation in the placenta of goats but our recent study demonstrated much less PrPSc accumulates in the placenta in goats, which calls into question its role in natural transmission. In a recent follow-up study, we now demonstrate that the placenta of goats does harbor prions infectious to other goats and sheep when exposed by the oral route. A study on Nor98-like scrapie in breeding ewes is now in its 6th year.

 

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Ewes were experimentally inoculated with brain homogenate obtained from a U.S. sheep with clinical Nor98-like scrapie. Recipient ewes are bred annually to examine the placenta for evidence of a transmissible agent. Placentas shed 2009-2013 were negative. In 2013, one recipient ewe developed an unrelated disease. At postmortem examination, abundant accumulation of PrPSc was observed only in the cerebellum of this ewe with much less accumulation in the hindbrain obex. This confirms that initial inoculation of these ewes has been successful. Monitoring continues in the remaining ewes of this study. Improvements in tissue-based (rectal biopsy) live animal testing for scrapie with focus on application to goats continue. In addition, efforts toward developing a live-animal blood test have demonstrated the presence of prions (infectivity) in the blood of sheep and goats, even those with preclinical disease and within blood sample volumes routinely used in veterinary diagnostic work. A recent study also demonstrates PrPSc accumulation in lymphoid tissues of hemal nodes, small lymphoid organs that filter blood but not lymph. Collectively, these findings confirm that blood is a relevant target for continued assay development. We continue to develop methods for enriching the relevant blood fractions for assay and are now making efforts to adapt novel in vitro assays for detecting infectivity and prion-associated misfolding activity. A long term study examining the effect of prion genotype on susceptibility to goat scrapie and the effect of genetic changes on accuracy of live animal testing continue. Following oral infection at birth with placenta and brain-derived scrapie, goats with the highly susceptible genotype all developed clinical disease around 24 months. Goats with the less susceptible or long incubation genetics today remain clinically normal. Monitoring continues.

 

Prion Transmission Through Milk

 

Christina Sigurdson

 

University of California, San Diego School of Medicine, Department of Pathology

 

Prion disorders are caused by misfolded proteins that are naturally transmitted, causing a fatal neurological disease in animals. In sheep with classical scrapie, prions accumulate in the follicles of lymphoid tissues in addition to the brain and spinal cord. Follicular dendritic cells (FDCs) form a network within the follicles and accumulate high levels of prions during disease. Previous work in mice has revealed that follicular inflammation in non-lymphoid organs, such as kidney, results in prion accumulation and can lead to prion shedding, such as into the urine. We have found sheep with follicular mastitis and scrapie that have accumulated prions within the follicles of the mammary gland.

 

In follow-up studies, we found that sheep with scrapie and lentiviral mastitis secrete prions into the milk and infect nearly 90% of naïve suckling lambs. Taken together, lentiviruses may enhance prion transmission and conceivably sustain prion infections in flocks for generations. Work by other groups has also shown prion infectivity in all three milk fractions, cells, casein whey, and cream. Prion infectivity has also been detected in milk from sheep having the VRQ/VRQ genotype with no evidence of mastitis.

 

References

 

1. Konold, T., Moore, S.J., Bellworthy, S.J. & Simmons, H.A. Evidence of scrapie transmission via milk. BMC Vet Res 4, 14 (2008).

 

2. Konold, T., et al. Evidence of effective scrapie transmission via colostrum and milk in sheep. BMC Vet Res 9, 99 (2013).

 

3. Ligios, C., et al. Sheep with Scrapie and Mastitis Transmit Infectious Prions through the Milk. J Virol 85, 1136-1139 (2011).

 

4. Ligios, C., et al. PrPSc in mammary glands of sheep affected by scrapie and mastitis. Nat Med 11, 1137-1138 (2005).

 

5. Lacroux, C., et al. Prions in milk from ewes incubating natural scrapie. PLoS Pathog 4, e1000238 (2008).

 

Committee Business:

 

The final response from the Committee’s 2012 Resolution (26, 9 and 30 Combined) relating to the export of sheep and goats was reviewed. In this response the USDA-APHIS-VS agreed to ask the World Organization for Animal Health (OIE) to modify the Scrapie Chapter to consider options such as genotyping to qualify animals for export. USDA-APHIS-VS agreed to make this request by Spring 2014, and would expect to see the Scrapie Chapter amended in Spring 2015 or 2016 if their revisions were to be accepted by OIE.

 

One of the Committee members updated the group on progress related to a 2010 Resolution #48. This resolution requested USDA, Food Safety Inspection Service (FSIS) to work with USDA-APHIS-VS and industry to identify and approve appropriate sites for radio frequency identification implants for goats and sheep. As a result, both the underside of the tail and the base of the ear are now approved sites for these implants. No new resolutions or recommendations were introduced.

 

The Committee briefly discussed the challenges of obtaining scrapie surveillance samples from certain flocks and herds. Several members mentioned that one barrier to sample collection is the problem that the producers have with carcass disposal after the head has been removed. Members agreed that offering options to producers to help them properly dispose of these carcasses could significantly increase voluntary participation in surveillance. Options include to transporting carcasses to diagnostic laboratories or providing payment to the producers to offset the cost of carcass disposal.

 

RESOLUTION NUMBER: 22 – APPROVED

 

SOURCE: COMMITTEE ON SHEEP AND GOATS

 

SUBJECT MATTER: SEPARATE SHEEP AND GOAT COMMODITY HEALTH LINE ITEM

 

BACKGROUND INFORMATION:

 

In FY2011, the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) primarily addressed sheep and goat health/disease issues through the National Scrapie Eradication Program (NSEP) and National Animal Health Monitoring System (NAHMS) studies. For FY2012, USDA-APHIS-VS requested that Congress approve commodity-based funding which would include horses, cervids, sheep, and goats in a single line item where funding could be transferred between the commodities based on priorities identified by USDA-APHIS-VS and its partners. The proposed grouping of these species is reminiscent of the failed Miscellaneous Diseases line item in the USDA-APHIS-VS budget of over 20 years ago.

 

NOMINATIONS AND RESOLUTIONS

 

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The United States Animal Health Association is concerned that sheep and goat funding may be diverted to address needs of other species, which could jeopardize the eradication of scrapie from the United States and the health and well-being of sheep and goats.

 

The currently proposed species grouping of Equines, Cervids, and Small Ruminants (sheep and goats) is not appropriate to serve the health and disease needs of such a diverse group of animals. Equines and Cervids have very few common health and disease issues with Sheep and Goats. Emerging diseases in each of the species in the proposed grouping will most likely result in even less commonality in disease/health priorities among these species.

 

RESOLUTION:

 

The United States Animal Health Association (USAHA) urges the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) to establish a separate funding line item for Sheep and Goat Health.

 

*****

 

REPORT OF THE COMMITTEE ON SHEEP AND GOATS

 

Chair: William Edmiston Jr., TX

 

Vice Chair: Don Knowles, WA

 

Scott Bender, AZ; Deborah Brennan, GA; John Clifford, DC; Thomas Conner, OH; Walter Cook, WY; Stephen Crawford, NH; Linda Detwiler, NJ; Nancy East, CA; Effingham Embree, Jr., IL; Chester Gipson, MD; Joseph Huff, CO; Paul Jones, AL; Eileen Kuhlmann, MN; James Leafstedt, SD; Howard Lehmkuhl, IA; Mary Lis, CT; Jim Logan, WY; Linda Logan, TX; Francine Lord, CAN; David Marshall, NC; Michael Marshall, UT; Chuck Massengill, MO; Cheryl Miller, IN; Ronald Miller, PA; Jeffrey Nelson, IA; Charles Palmer, CA; Kris Petrini, MN; Suelee Robbe-Austerman, IA; Paul Rodgers, WV; Joan Dean Rowe, NC; Mo Salman, CO; A. David Scarfe, IL; William Shulaw, OH; Diane Sutton, MD; Peter Timm, CA; Stephen White, WA; Margaret Wild, CO; Ellen Mary Wilson, CA; William Wilson, KS; Nora Wineland, MO; David Winters, TX; Cindy Wolf, MN.

 

The Committee met on October 22, 2013 at the Town and Country, San Diego, California, from 1:00 to 4:30 p.m. There were 9 members and 12 guests present. The meeting proceeded with the following presentations and reports.

 

Overview of Schmallenburg Virus: Lessons from a European Outbreak

 

Rob Cordery-Cotter, Dept. of Animal Science, University of Wyoming

 

Dr. Cordery-Cotter presented the history of Schmallenberg Virus (SBV) incursion into Europe and the United Kingdom (U.K.), with excellent photos and case histories of clinical signs and symptoms. A complete power point of this presentation is available on the Committee web page, at www.usaha.org.

 

Regulatory Updates for Sheep and Goat Importations

 

Joyce Bowling-Heyward, NCIE, USDA-APHIS

 

Discussion initiated with discussion of bovine spongiform encephalopathy (BSE), Scrapie and other Transmissible spongiform encephalopathies (TSEs) in Ruminants, and impact on regulations concerning these. Schmallenburg Virus and potential for incursion was discussed, and need for surveillance and vigilance. A complete copy of this presentation is included at the end of this report.

 

Chronic Wasting Disease CWD

 

Goals for CWD Herd Certification Program

 

Lee Ann Thomas, Ruminant Health Programs, USDA-APHIS–VS

 

An overview was presented of the voluntary national Chronic Wasting Disease (CWD) herd certification program for farmed deer, elk, and moose as well as established minimum standards for interstate movement of cervids. The purpose of the Herd Certification Program (HCP) is to provide clarification and guidance on how to comply with and meet requirements of the CWD rule and contains two Parts: Part A – Herd Certification and Part B – Guidance on Response to CWD-affected herds.

 

Funding for the program is through APHIS-VS Equine, Cervids, Small Ruminants (ECSR) Commodity Health Line which funds essential activities for surveillance and program operations with flexibility to respond to new and emerging health concerns.

 

A review of the FY 2013/14 Program Activities of APHIS-VS which included federal oversight of the voluntary national CWD HCP as well as the principle activities conducted that pertain to the HCP.

 

Based on available resources, APHIS will serve in an advisory capacity to Approved States for 1) epidemiological investigations of positive findings; 2) development of herd plans (newly infected herds); 3) quarantine, depopulations, cleaning and disinfection; and 4) assistance with annual herd inspections and tri-annual physical herd inventories.

 

FY 2013/14 Program Activities required for Approved States included 1) compliance with CWD rule; 2) annual reports; 3) management of HCP data; 4) reporting positive cervid herds to APHIS; 5) respond, investigate, and manage any positive, suspect, and exposed animals/herds; and 6) develop herd plans for positive/exposed herds.

 

The CWD Interim Final Rule (CWD Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose) was published in the Federal Register June 13, 2012 with a public comment period. The effective date of the rule was August 13, 2012.

 

Part 81 of the Rule delayed enforcement until December 10, 2012. Public comments have been considered and affirmation of a final rule is in development. The Revised federal rule applies only to the following genera known to be susceptible to CWD by natural infection including, Cervus (elk, red deer, sika deer), Odocoileus (white-tailed deer (WTD), mule deer (MD), black-tailed deer (BTD) and Alces (moose). States may have requirements for other cervid species.

 

The objectives of the CWD rule are to 1) provide uniform minimum requirements for state CWD herd certification programs (HCPs); 2) provide uniform minimum requirements for interstate movement of CWD susceptible species; 3) provide a regulatory framework to support domestic and international markets for farmed cervids and cervid products; and 4) provide a consistent approach towards minimizing risk of introduction and transmission of CWD in cervid populations. Provisions of the CWD rule include 1) Part 55 (Subpart A): Indemnity, Laboratory Approval, Official Laboratory Testing; 2) Part 55 (Subpart B): Voluntary national Approved State CWD HCP for farmed cervids (deer and elk) (fencing requirements, animal ID and herd inventory requirements, surveillance - testing mortalities >12 months, and herd status – based on years of surveillance and participation in HCP), 3) Part 81: Interstate movement minimum requirements ) establishes minimum requirements for interstate movement of cervids.

 

The CWD rule does not include international movement regulations.

 

States having a CWD HCP may request federal approval of their State program which will be approved by APHIS in accordance with CWD rule (9 CFR 55.23). As of October 2013, there are 29 Approved State HCPs. Approved states must have a signed memorandum of understanding (MOU) with APHIS that addresses 1) authority to restrict animal movement; 2) enforces and monitors quarantines; 3) surveillance and disease reporting capability; 4) animal identification; 5) designated CWD HCP coordinator; 6) mortality surveillance; 7) recordkeeping and data management; 8) ability to conduct epidemiologic investigations; 8) education/ outreach for producers; 9) herd plans (CWD positive/exposed herds); and 10) annual reports to renew Approved status.

 

Herd owners already participating in State CWD programs will keep initial State enrollment date (first date of participation) when State is designated an Approved State CWD HCP. There is no available funding projected for FY2014 to support direct herd owner enrollment in the national program. Herd owners must comply with animal identification, fencing requirements, reporting escapes & mortalities and mortality testing for certified status, herd records and inventories, separation from other herds, and status of herd additions.

 

A CWD Working Group was formed to review and provide input on revisions to the CWD Program Standards (2012 USAHA Resolution). Members included representatives from the cervid industry, state animal health officials, state wildlife agencies/ Association of Fish and Wildlife Agencies (AFWA), and diagnostic laboratories (AAVLD/NAHLN), and APHIS-VS. Meetingwere conducted through weekly teleconferences and topics discussed included – physical inventory, sample collection, missing samples, reporting mortalities and escapes, transiting, herd plans, trace outs, animal identification, fencing, and interstate movement.

 

Further information can be found at: http://www.aphis.usda.gov/animal_health/animal_diseases/cwd.

 

CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK

 

171

 

Committee Business:

 

There was one resolution presented and passed by the Committee regarding a National Review of Research Needs for Chronic Wasting Disease. The resolution was submitted requesting that the USAHA request the USDA, and the U.S. Department of Interior (DOI) to arrange a diversified blue-ribbon panel (which would include industry stakeholders, university and federal researchers, and Federal and State regulatory agencies) to determine research needs and identify and prioritize intervention strategies for the control of Chronic Wasting Disease. The resolution was moved by member Warren Bluntzer and seconded by Glen Zebarth, and forwarded to the Committee on Nominations and Resolutions.

 

A recommendation was presented to the Committee on Captive Wildlife and Alternative Livestock to create a new Committee on farmed cervidae. The motion to form the new Committee was moved by Richard Winters and seconded by Paul Anderson. A vote following discussion was tied 13 to 13. The following is a copy of the recommendation with some preliminary edits. It was felt by many of the members that if this Committee was approved that there should be some significant modifications to the mission statement, which was proposed as follows:

 

Background:

 

The farmed cervidae industry is unique in that producers deal with diseases, regulations and political issues which are unlike any other animal agricultural industry.

 

To effectively address these issues requires a national forum for discussion. The creation of a new USAHA committee where farmed cervidae producers can work together with state and federal regulatory officials and scientists to solve the problems faced by the industry is critical.

 

Mission:

 

“The purpose of the Committee on Farmed Cervidae is to provide a national forum to (1) discuss scientific, regulatory and political issues affecting the farmed cervidae industry, (2) evaluate state and federal regulatory programs, (3) develop effective programs to control diseases, and (4) recommend regulatory programs that contribute to the growth and prosperity of the farmed cervidae industry while mitigating disease risks.” The Committee adjourned at 12:47 p.m.

 

RESOLUTION NUMBER: 16 – APPROVED

 

SOURCE: COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK

 

SUBJECT MATTER: NATIONAL REVIEW OF RESEARCH NEEDS FOR CHRONIC WASTING DISEASE

 

BACKGROUND INFORMATION:

 

In the absence of an approved live animal test, vaccine, or recognition of genetically resistant animals, depopulation and indemnity of the herd mates is

 

NOMINATIONS AND RESOLUTIONS

 

289

 

our only method of prevention to stop the spread of Chronic Wasting Disease (CWD) to other animals.

 

A Federal CWD Rule has been implemented with the purpose of controlling the spread of CWD versus eradication. To insure a successful program more tools are needed to manage this disease.

 

RESOLUTION:

 

The United States Animal Health Association (USAHA) requests that the United States Department of Agriculture, and United States Department of Interior arrange a diversified blue-ribbon panel (including: industry stakeholders, university and federal researchers, Federal and State regulatory agencies) to determine research needs and identify and prioritize intervention strategies for the control of Chronic Wasting Disease.

 

*****

 

Chronic Wasting Disease Ecology and Epidemiology of Mule Deer and White-tailed Deer in Wyoming

 

Dr. Brant Schumaker of the University of Wyoming reported that the effects of high chronic wasting disease (CWD) prevalence in free-ranging deer populations are unknown. In south-central Wyoming, CWD prevalence exceeds 50% in hunter harvested deer. We hypothesized that 1) vital rates are depressed by CWD and the finite rate of population growth (λ) is subsequently lowered, 2) CWD alters normal deer behavior during preclinical and clinical disease, and 3) genetic differences associated with CWD incubation periods drives natural selection to favor less susceptible deer. To test these hypotheses, we radio-collared white-tailed deer (Odocoileus virginianus) and mule deer (Odocoileus hemionus) and monitored them to determine a) survival probability, pregnancy rates, and annual recruitment, b) cause of death, c) home range area and habitat use, d) migration patterns, e) dispersal behavior, and f) genetic variation in incubation period based on CWD-status. Deer were tested for CWD using tonsil tissue collected by biopsy at capture and immunohistochemistry. White-tailed deer positive for CWD were 4.5 times more likely to die annually compared to CWD-negative deer. High CWD prevalence depressed survival of young females and resulted in an unsustainable white-tailed deer population (λ < 1.0); however, when female harvest was eliminated, the population became stable (λ =1.0). Female CWD-positive white-tailed deer maintain locally high CWD incidence as they migrated less and occupied smaller home ranges compared to other deer. Male CWD-positive white-tailed deer migrated at the highest proportion and likely contributed to spread of CWD to disparate populations. In the last nine years, mule deer genetically associated with prolonged incubation periods to CWD have increased in frequency in the population. However, it is still unknown whether or not this change will counteract the negative impacts of CWD on the population. The white-tailed deer population is adversely affected by high CWD prevalence; however, implementing management techniques to increase annual survival of females may maintain deer populations. The impact of CWD on mule deer populations is currently unknown; however, the present study is in its final stages with results to be completed in the near future.

 

snip...

 

BSE

 

A comment was posted regarding bovine spongiform encephalopathy (BSE) indicating the possible need to review the present protocol for renderers so that carcasses which are submitted for rabies, are flagged at the render and held until testing for rabies and BSE is completed.

 

Regulatory Updates for Sheep and Goat Importations

 

Joyce Bowling-Heyward, NCIE, USDA-APHIS

 

Discussion initiated with discussion of bovine spongiform encephalopathy (BSE), Scrapie and other Transmissible spongiform encephalopathies (TSEs) in Ruminants, and impact on regulations concerning these. Schmallenburg Virus and potential for incursion was discussed, and need for surveillance and vigilance. A complete copy of this presentation is included at the end of this report.

 

• Three new Scrapie/chronic wasting disease (CWD) testing platforms have been approved by NVSL/VS for use in the 21 NAHLN laboratories performing surveillance to replace the Ventana NexES (being obsoleted). Laboratories may select from: Biocare Medical’s IntelliPATH FLX®, Leica Microsystem’s BOND MAX, or the Ventana Discovery XT. NVSL- Pathobiology Laboratory (PL) will continue to provide standard operating procedures (SOP), proficiency testing (PT), reagent quality assurance (QA) and confirmatory testing on each of the platforms.

 


 

Formation of a Committee on Farmed Cervids

 

A recommendation was presented to the Committee on Captive Wildlife and Alternative Livestock to create a new Committee on farmed cervidae. The motion to form the new Committee was moved by Richard Winters and seconded by Paul Anderson. A vote following discussion was tied 13 to 13. Attached is a copy of the recommendation with some preliminary edits in track changes. It was felt by many of the Committee members that if this committee was approved that there should be some significant modifications to the mission statement, which was proposed as follows: Background:

 

The farmed cervidae industry is unique in that producers deal with diseases, regulations and political issues which are unlike any other animal agricultural industry.

 

To effectively address these issues requires a national forum for discussion. The creation of a new USAHA committee where farmed cervidae producers can work together with state and federal regulatory officials and scientists to solve the problems faced by the industry is critical. Mission:

 

“The purpose of the Committee on Farmed Cervidae is to provide a national forum to

 

(1) discuss scientific, regulatory and political issues affecting the farmed cervidae industry,

 

(2) evaluate state and federal regulatory programs,

 

(3) develop effective programs to control diseases, and

 

(4) recommend regulatory programs that contribute to the growth and prosperity of the farmed cervidae industry while mitigating disease risks.”

 

The Committee adjourned at 12:47 p.m.

 


 

SEE MORE ;

 


 

 P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)

 

Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA

 

Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein

 

Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.

 

Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.

 

Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.

 

Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

 

P.89: Prions survive long-term burial in soil with some groundwater dissemination

 

Allister JA Smith,1 Karen Fernie,1 Ben Maddison,2 Keith Bishop,2 Kevin Gough,3 and Robert A Somerville1 1The Roslin Institute; University of Edinburgh; Edinburgh, UK; 2ADAS Biotechnology Group, University of Nottingham; Nottingham, UK; 3University of Nottingham; Nottingham, UK

 

An intrinsic property of prions is their extreme resistance to degradation. When they are deposited within the environment, whether from inappropriate disposal by man or from fallen diseased livestock, there is the potential to further propagate cases of disease for many years. It is evidenced that the spread of scrapie in sheep and chronic wasting disease in deer have occurred in this manner.

 

We mimicked such scenarios under large-scale field conditions to determine the extent to which TSE infectivity survives or disseminates in soil and soil water over five years. The mouse passaged BSE strain, 301V, was used to spike buried bovine heads, or was buried as an uncontained bolus in large soil-filled lysimeters. Two soils were examined, a free-draining sandy loam and a water-retentive clay loam.

 

Infectivity, determined by bioassay in mice, was recovered from all heads exhumed annually for 5 years from both soil types, with little reduction in the amount of infectivity over time. Small amounts of infectivity were found in soil samples immediately surrounding the heads but not in samples remote from them. Commensurate with this there was no evidence of significant lateral movement of infectivity from the bolus buried in a large soil mass. However large amounts of infectivity were recovered at the original bolus burial site in both soils. There was limited vertical upward movement of infectivity from the bolus buried in clay and downward movement from the bolus buried in sand perhaps reflecting the clay soils propensity to flood.

 

Throughout the course of the experiment rainwater particulate from several lysimeters was trapped on glass-fibre filters. Extracts from these filters were subject to serial PMCA (protein misfolding cyclic amplification) which was optimised using 301V-spiked samples and blinded controls. All positive and negative control samples were correctly determined. We have tested 44 samples from rainwater passed through the clay lysimeter filters, and found 9 positive samples, mainly from the initial 8 months of the experiment.

 

We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSErelated material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

 

P.121: Efficient transmission of prion disease through environmental contamination

 

Sandra Pritzkow, Rodrigo Morales, and Claudio Soto Mitchell Center for Alzheimer’s disease and related Brain disorders; University of Texas Medical School at Houston; Hourston, TX USA

 

Chronic wasting disease (CWD) is a prion disorder effecting captive and free-ranging deer and elk. The efficient propagation suggests that horizontal transmission through contaminated environment may play an important role. It has been shown that infectious prions enter the environment through saliva, feces, urine, blood or placenta tissue from infected animals, as well as by carcasses from diseased animals and can stay infectious inside soil over several years.

 

82 Prion Volume 8 Supplement

 

We hypothesize that environmental components getting in contact with infectious prions can also play a role for the horizontal transmission of prion diseases. To study this issue, surfaces composed of various environmentally relevant materials were exposed to infectious prions and the attachment and retention of infectious material was studied in vitro and in vivo. We analyzed polypropylene, glass, stainless steel, wood, stone, aluminum, concrete and brass surfaces exposed to 263K-infected brain homogenate. For in vitro analyses, the material was incubated in serial dilutions of 263K-brain homogenate, washed thoroughly and analyzed for the presence of PrPSc by PMCA. The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

 

In addition, in order to study the transmission in a more natural setting, we exposed a group of hamster to habit in the presence of spheres composed of various materials that were pretreated with 263K prions. Many of the hamsters exposed to these contaminated materials developed typical signs of the disease that were confirmed by immunohistological and biochemical analyses.

 

These findings suggest that various surfaces can efficiently bind infectious prions and act as carriers of infectivity, suggesting that diverse elements in the environment may play an important role in horizontal prion transmission.

 

P.138: Phenotypic diversity in meadow vole (Microtus pennsylvanicus) prion diseases following challenge with chronic wasting disease isolates

 

Christopher J Johnson,1 Christina M Carlson,1,2 Jay R Schneider,1 Jamie K Wiepz,1 Crystal L Meyerett-Reid,3 Mark D Zabel,3 Joel A Pedersen,2 and Dennis M Heisey1 1USGS National Wildlife Health Center; Madison, WI USA; 2University of Wisconsin— Madison; Madison, WI USA; 3Colorado State University; Fort Collins, CO USA

 

Chronic wasting disease (CWD), a prion disease of cervids (deer, elk and moose), is spreading unchecked through large sections of North America. Transmission of CWD among cervids is especially facile and can occur through direct animal-toanimal contact and indirectly through contact with prions shed from infected animals. The disease transmission threat posed by CWD to other wildlife species remains unknown, but other species are inevitably exposed to CWD by consumption of infectious materials and through contact with environmental CWD contamination.

 

In this study, we investigated the transmission and adaptation of various white-tailed deer CWD isolates in the meadow vole (Microtus pennsylvanicus), a native North American rodent that is sympatric with current CWD epizootics that we have previously established is susceptible to CWD. We found that serial subpassage of CWD from white-tailed deer homozygous for glycine at position 96 (96GG) of the prion protein in meadow voles resulted in the selection of a single prion strain that was characterized by homogeneity in incubation period, abnormal prion protein (PrPTSE) glycoform ratio, lesion profile and PrPTSE deposition pattern. In contrast, passage of CWD from heterozygous 96GS genotype deer produced four unique disease phenotypes upon first passage. Subpassage of these types ultimately resulted in selection of a single strain by third passage that was distinct from the 96GG genotype CWD-derived strain.

 

We also establish that meadow voles are susceptible to CWD via peripheral challenge, albeit with lower attack rates and longer incubation periods. Interestingly, oral challenge of meadow voles with CWD resulted in subclinical infection in primary passage animals, but manifested as clinical prion disease upon subpassage.

 

Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.

 

P.141: Abundant prion shedding in CWD-infected deer revealed by Realtime conversion

 

Edward A Hoover,1 Davin M Henderson,1 Nathaniel D Denkers,1 Candace K Mathiason,1 Matteo Manca,2,3 and Byron Caughey2 1Prion Research Center, Colorado State University; Fort Collins, CO USA; 2Laboratory of Persistent Viral Diseases, NI AID; Hamilton, MT USA; 3Department of Biomedical Sciences, University of Cagliari; Monserrato, Italy

 

Background/Introduction. Chronic wasting disease (CWD) is unique among prion diseases in its efficient lateral transmission in nature. While the presence of infectious prions in body fluids and excreta of infected cervids has been demonstrated by bioassay, the dynamics, magnitude, and consequences of prion shedding remain unknown. The present studies were undertaken to determine the kinetics, duration, and magnitude of prion shedding in infected white-tailed deer.

 

Materials and Methods. Longitudinal samples were collected from white-tailed deer over a 2-year span after either oral (n=11)] aerosol (n = 6) CWD exposure. The assay protocol employed phosphotungstic acid precipitation of either whole saliva or the pelleted fraction of urine to seed recombinant Syrian hamster prion PrP substrate in RT-QuIC reactions. Prion seeding activity was assayed in 8 replicates of each sample employing thioflavin T detection in a 96-well plate-based fluorometer. Prion seeding reaction rate was determined by taking the inverse of the time at which samples exceeded a threshold of 5 standard deviations above the mean fluorescence of negative controls (1/time to threshold). Seeding activity was quantitated by comparing the realtime conversion reaction rate to a standard curve derived from a reference bioassayed brain pool homogenate from deer with terminal CWD.

 

Results. We analyzed >200 longitudinally collected, blinded, then randomized saliva and urine samples from 17 CWDinfected and 3 uninfected white-tailed deer. We detected prion shedding as early as 3 months post exposure and sustained thereafter throughout the disease course in both aerosol and orally exposed deer. The incidence of non-specific false positive results from >500 saliva and urine samples from negative control deer was 0.8%. By comparing real-time reaction rates for these body fluids to a bioassayed serially diluted brain control, we estimated that ≤1 ml of saliva or urine from pre-symptomatic infected deer constitutes a lethal infectious prion dose.

 

Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.

 

Acknowledgments. Support: NIH-RO1-NS-061902; Morris Animal Foundation D12ZO-045

 

P.154: Urinary shedding of prions in Chronic Wasting Disease infected white-tailed deer

 

Nathaniel D Denkers,1 Davin M Henderson, 1 Candace K Mathiason,1 and Edward A Hoover1 1Prion Research Center, Department of Microbiology, Immunology, and Pathology, Colorado State University; Fort Collins, CO USA

 

Background/Introduction. Chronic wasting disease (CWD) is unique among prion diseases in its efficient lateral transmission in nature, yet the dynamics and magnitude of shedding and its immediate and long term consequences remain unknown. The present study was designed to determine the frequency and time span in which CWD prions are shed in urine from infected white-tailed deer using adapted real-time quaking-induced conversion (RT-QuIC) methodology.

 

Materials and Methods. Longitudinal urine samples were collected by free catch or catheterization over a 2-year period from oral-route infected [CWD+ (n = 11)] and aerosol-route-infected [CWD+ (n = 6); CWD- (n = 3)] white-tailed deer. High speed centrifugation pelleted material from 500 µl of urine was treated with sodium phosphotungstic acid (Na-PTA), resuspended in 0.05% SDS buffer, and used as seed in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Eight (8) replicates of each sample were run and prion seeding activity was recorded as thioflavin T binding fluorescence (480 nm emission) using a fluorimeter-shaker. Samples were considered positive if they crossed an established threshold (5 standard deviations above the negative mean fluorescence).

 

Results. In our oral-route inoculation studies, prion seeding activity has been demonstrated in urine collected at 6 months post-inoculation in 6 of 10 deer (11 of 80 replicates; 14%), and intermittently at later time points in all 11 CWD+ exposed deer. Our aerosol-route inoculation studies also showed prion seeding activity in urine collected at 6 months post-inoculation in 1 of 2 deer (3 of 16 replicates; 19%), and intermittently at later time points in 4 of 6 CWD+ exposed deer. Urine from sham-inoculated control deer and all baseline samples yielded 3 false-positive prion seeding activities (3 of 352 replicates; 0.8%).

 

Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.

 

Acknowledgments. Support: NIH: RO1-NS-061902 and Morris Animal Foundation: D12ZO-045

 

P.158: Structurally and phenotypically different prions in CWD-infected white-tailed deer

 

Martin L Daus, Peter Lasch, and Michael Beekes Robert Koch-Institut; Berlin, Germany

 

Prions can exist as multiple strains within mammals. We could detect, for the first time, two distinct chronic wasting disease (CWD) isolates in white-tailed deer (WTD).

 

WTD had been challenged with CWD from either mule deer (MD) or WTD. Brain-derived prions from MD-infected WTD and WTD-infected WTD could be distinguished by biochemical, biophysical and biological methods. PK-mediated limited proteolysis at different pH-values indicated conformational differences between pathological prion proteins (PrPTSE) from MD-infected WTD and WTD-infected WTD. More specifically, Fouriertransform infrared microspectroscopy revealed secondary structure differences between highly purified PrPTSE extracts from MD-infected WTD and WTD-infected WTD. Different sedimentation velocities of PrPTSE in gradient centrifugations provided additional evidence for structure differences between prions from MD-infected WTD and WTD-infected WTD. Brain homogenate from WTD-infected WTD showed a substantially lower seeding activity on cellular prion protein (PrPC) of Syrian hamsters in protein misfolding cyclic amplification (PMCA) than its conformationally distinct counterpart from MD-infected WTD. When hamsters were intracerebrally inoculated with brain tissue from MD-infected WTD disease could be transmitted, which was not observed after similar inoculation with brain homogenate from WTD-infected WTD. In an ongoing macaque-study both CWD-isolates are currently being further tested for their transmissibility to primates.

 

P.163: Bayesian hierarchical modeling of chronic wasting disease in free-ranging white-tailed deer in the eastern U.S.

 

Tyler S Evans1 and W David Walter2 1Pennsylvania Cooperative Fish and Wildlife Research Unit; The Pennsylvania State University; University Park, PA USA; 2US Geological Survey; Pennsylvania Cooperative Fish and Wildlife Research Unit; The Pennsylvania State University; University Park, PA USA

 

Introduction. Chronic wasting disease (CWD) is a prion disease that affects both free-ranging and captive cervid populations. In the past 45 years, CWD has spread from a single region in Colorado to all bordering states, as well as Canada, the Midwest and the northeastern United States. In 2005, CWD was detected in the eastern U.S. in a free-ranging white-tailed deer (Odocoileus virginianus) killed by a vehicle in West Virginia followed by positives from Virginia, Maryland, and Pennsylvania. Although considerable information has been learned about CWD in wildlife from several areas of the U.S. and Canada, little information is available on spatial epidemiology of disease in the eastern U.S.

 

Materials and Methods. In order to develop a CWD surveillance plan for the region, we determined covariates and the best scale for analysis by exploring habitat use and estimating the mean size of home range for deer in the central Appalachian region (6 km2). We conducted Bayesian hierarchical modeling in WinBUGS on 24 a priori models using 11,320 free-ranging white-tailed deer (69 positive, 11,251 negative) that have been tested for CWD since 2005. Testing for CWD was conducted using standard protocols on a variety of tissues extracted from hunter-harvested deer that included retropharyngeal lymph nodes, tonsil lymph nodes, and the medulla oblongata sectioned at the obex.

 

Results. We found 94% of models weights were accounted for in our top model that identified habitats such as developed and open as covariates that increased the odds of infection for CWD in this region. Contrary to research in the endemic area of Colorado, we did not identify clay soil as a significant predictor of disease even though clay soil ranged from 9% to 19% in our study samples. Furthermore, contrary to results from the recent expansion of CWD into the agricultural Midwestern U.S. (Wisconsin, Illinois), we identified developed and open habitats were better predictors of disease occurrence compared to forest habitat considered more critical to deer population dynamics in the U.S.

 

Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.

 

P.178: Longitudinal quantitative analysis of CWD prions shed in saliva of deer

 

Davin M Henderson, Nina Garbino, Nathaniel D Denkers, Amy V Nalls, Candace K Mathiason, and Edward A Hoover Prion Research Center, College of Veterinary Medicine and Biomedical Sciences, Colorado State University; Fort Collins, CO USA

 

Background/Introduction. Chronic Wasting Disease (CWD) is an emergent rapidly spreading fatal prion disease of cervids (deer, elk and moose). CWD has now been identified in 22 States (including two new states within the last year), 2 Canadian provinces, and South Korea. Shedding of infectious prions in excreta (saliva, urine, feces) may be an important factor in CWD transmission. Here we apply an adapted version of a rapid in vitro assay [real-time quaking-induced conversion (RT-QuIC)] to determine the time of onset, length, pattern, and magnitude of prion shedding in saliva of infected deer.

 

Materials and Methods. The RT-QuIC assay was performed as previously described in Henderson et al. PLoS-One (2013). Saliva samples were quantitated by comparison to a RT-QuIC reaction rate standard curve of a bioassayed obex sample from a terminally ill cervid.

 

Results. To better understand the onset and length of CWD prion shedding we analyzed >150 longitudinally collected, blinded, then randomized saliva samples from 17 CWD-infected and 3 uninfected white-tailed deer. We observed prion shedding, as detected by the RT-QuIC assay, as early as 3 months from inoculation and sustained shedding throughout the disease course in both aerosol and orally exposed deer. We estimated the infectious lethal dose of prions shed in saliva from infected deer by comparing real-time reaction rates of saliva samples to a bioassayed serially diluted brain control. Our results indicate that as little as 1 ml of saliva from pre-symptomatic infected deer constitutes a lethal CWD prion dose.

 

Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.

 

Acknowledgments. Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal Foundation.

 


 

Monday, June 23, 2014

 

PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES

 


 

Sunday, June 22, 2014

 

Governor Nixon Missouri Urged to VETO Legislation turning over captive shooting pens to USDA

 

snip...

 

PLEASE WATCH THIS VIDEO OF A CAPTIVE SHOOTING PEN HUNT.

 

THIS IS NOT HUNTING FOLKS, THIS IS JUST SLAUGHTERING A DEFENSELESS ANIMAL, AND HAVING TO PROP IT UP TO DO THAT $$$

 

Michigan 2005 237 captive shooting pens not in compliance

 

March 2005 DNR Audit

 

37 % or 237 captive pens not in compliance.

 

96% that died were not tested for CWD, as was required.

 

700 captive pens had inadequate fencing.

 

tranquilizing target deer...

 

Measuring antlers to verify scores for record book.

 

Scooping up with front in loading tractor, and dumping into small 3 to 5 acre pen to be shot for up to $20,000.00

 

how did the fix the problem, turned the DNR over to the USDA et al, problem solved...

 

‘’The rich...who are content to buy what they have not the skill to get by their own exertions, these are the real enemies of game’’

 

Theodore Roosevelt’s Principles of the Hunt

 


 

snip...see full text ;

 


 

Infectious agent of sheep scrapie may persist in the environment for at least 16 years

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

 


 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

 


 

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

 


 

A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

 


 

Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals

 


 

PPo4-4:

 

Survival and Limited Spread of TSE Infectivity after Burial

 


 

Sunday, September 01, 2013

 

hunting over gut piles and CWD TSE prion disease

 


 

Sunday, April 13, 2014

 

Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer

 

Environmental Geochemistry and Health

 


 

Alkaline Hydrolysis

 

The alkaline hydrolysis process has been through a validation study by the Institute of Animal Health, and an Opinion has been issued by the Scientific Steering Committee of the European Commission (EC 2002) on the effectiveness of the process. There was detectable infectivity from samples held for 3 hours, but not from samples held for 6 hours. The committee concluded that the by-products after 3 hours of processing could contain some residual TSE infectivity and that this risk may decrease with increased duration of processing.

 

Glossary

 

snip...see ;

 


 

Alkaline Hydrolysis

 


 


 

========================================

 

There are many disposal options for dead livestock currently in use throughout the world; however, the knowledge that TSEs and some pathogens may not be completely destroyed may limit their utility in the wake of changing legislation (e.g. the amended EU Animal By-Products Regulation (1069/2009) which comes into effect in March 2011). On-farm disposal methods are favoured by the farming community due to the perceived environmental, practical, economical and biosecurity benefits, therefore processes such as composting and anaerobic digestion have found favour in countries such as the USA and Canada. Under the ABPR in the EU, these options are not deemed safe;

 

========================================

 

Review

 

The environmental and biosecurity characteristics of livestock carcass disposal methods: A review

 

Ceri L. Gwyther a, A. Prysor Williams a,⇑, Peter N. Golyshin b, Gareth Edwards-Jones a, David L. Jones a a School of Environment, Natural Resources and Geography, College of Natural Sciences, Bangor University, Gwynedd, LL57 2UW, UK b School of Biological Sciences, College of Natural Sciences, Bangor University, Gwynedd, LL57 2UW, UK

 

a b s t r a c t

 

Livestock mortalities represent a major waste stream within agriculture. Many different methods are used throughout the world to dispose of these mortalities; however within the European Union (EU) disposal options are limited by stringent legislation. The legal disposal options currently available to EU farmers (primarily rendering and incineration) are frequently negatively perceived on both practical and economic grounds. In this review, we assess the potential environment impacts and biosecurity risks associated with each of the main options used for disposal of livestock mortalities in the world and critically evaluate the justification for current EU regulations. Overall, we conclude that while current legislation intends to minimise the potential for on-farm pollution and the spread of infectious diseases (e.g. transmissible spongiform encephalopathies, bacterial pathogens), alternative technologies (e.g. bioreduction, anaerobic digestion) may provide a more cost-effective, practical and biosecure mechanism for carcass disposal as well as having a lower environmental footprint. Further social, environmental and economic research is therefore warranted to assess the holistic benefits of alternative approaches for carcass disposal in Europe, with an aim to provide policy-makers with robust knowledge to make informed decisions on future legislation.

 

snip...

 

4. Conclusions

 

There are many disposal options for dead livestock currently in use throughout the world; however, the knowledge that TSEs and some pathogens may not be completely destroyed may limit their utility in the wake of changing legislation (e.g. the amended EU Animal By-Products Regulation (1069/2009) which comes into effect in March 2011). On-farm disposal methods are favoured by the farming community due to the perceived environmental, practical, economical and biosecurity benefits, therefore processes such as composting and anaerobic digestion have found favour in countries such as the USA and Canada. Under the ABPR in the EU, these options are not deemed safe; however, the legal alternatives are not favoured by the farming community leading to widespread non-compliance and potentially greater environmental risk (due to illegal dumping, etc. (Kirby et al., 2010)). There is therefore a real need for new methods to be developed and validated and the legislation reconsidered following submission of new evidence. From this perspective, bioreduction and freezing seems to be promising on-farm storage methods for livestock mortalities, limiting the need for off farm transport thus reducing associated biosecurity risks. While the implementation of highly precautionary, risk-averse mortality disposal systems is admirable in many ways, similar risk assessments and legislation do not apply to other components of the livestock sector which may pose a similar or even greater risk to human health or environmental contamination (e.g. spreading of animal waste, animal access to watercourses, public access to grazing land). It is important therefore that mortality disposal systems are based on a realistic and proportionate level of acceptable risk in comparison to other components of the food chain, rather than the current zero-risk approach. It is clear that more evidence is needed on each disposal and storage method in order to make substantiated risk assessments, e.g. the effects of spreading carcass ash on crops or the potential of leachate from burial to contaminate ground or surface water. This review has initiated this process by applying a simple five-star award system to each livestock disposal and storage method (Table 3 and Table 4, respectively) in order to rudimentarily classify various biosecurity and environmental factors based on current scientific evidence. Methods in need of greater research have also been highlighted where there is either limited or no existing published literature. Further research into the economic impacts of dead livestock disposal is necessary for legislators to appreciate the cost implications on the livestock sector, whilst life-cycle assessments are needed to help provide more environmentally sustainable disposal solutions.

 


 

Sunday, November 3, 2013

 

Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044]

 


 

Saturday, March 15, 2014

 

Potential role of soil properties in the spread of CWD in western Canada

 


 

Friday, February 08, 2013

 

*** Behavior of Prions in the Environment: Implications for Prion Biology

 


 

OPINION AND REPORT ON : THE TREATMENT OF ANIMAL WASTE BY MEANS OF HIGH TEMPERATURE (150°C, 3 HOURS) AND CORRESPONDING HIGH PRESSURE ALKALINE HYDROLYSIS.

 

ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 16 MAY 2002

 


 

FINAL OPINION AND REPORT ON : A TREATMENT OF ANIMAL WASTE BY MEANS OF HIGH TEMPERATURE (150°C, 3 HOURS) AND HIGH PRESSURE ALKALINE HYDROLYSIS.

 

ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 10-11 APRIL 2003

 


 

BSE INQUIRY 1989 TO ...

 

The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester Issued 06/08/1999 (not scheduled to give oral evidence)

 

SECOND STATEMENT TO THE BSE INQUIRY

 

Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences & Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s Hospital London and William Harvey Hospital Ashford April 1999

 

snip...

 

88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed. 89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence. 90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.

 

91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.

 

92. This review and recommendations from Brown have particular importance. Brown is one of the world's foremost authorities on TSEs and is a senior researcher in the US National Institutes of Health (NIH). It is notable that such a respected authority is forthright in acknowledging the existence of potential risks, and in identifying the appropriate measures necessary to safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical distribution of variant CJD in the UK (excluding Northern Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41 (02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD (variant CJD) might live closer to rendering factories than would be expected by chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were studied. The incubation period of vCJD is not known but by analogy with other human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure to rendering products, such exposure might plausibly have occurred 8-10 years before the onset of symptoms. The authors were able to obtain the addresses of all rendering plants in the UK which were in production in 1988. For each case of vCJD, the distance from the place of residence on 1st January 1998 to the nearest rendering plant was calculated

 

snip...

 


 

BSE INQUIRY DATA 1989 through the 1990’s REPORT ON BOVINE CARCASE INCINERATION, incinerations temps., plume, etc. ...tss

 

some unofficial info. from a source on the inside looking out;

 

Confidential!!!!

 

As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

 

xxxxxxxxxxx

 

you can take that with however many grains of salt you wish, and we can debate these issues all day long, but bottom line, this is not rocket-science, all one has to do is some experiments and case studies, but for the life of me, i don't know what they are waiting on?

 

kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA

 

more here;

 


 


 

INCINERATION TEMPS

 

requirements include;

 

a. after burning to the range of 800 to 1000*C to eliminate smell;

 

well heck, this is just typical public relations fear factor control. do you actually think they would spend the extra costs for fuel, for such extreme heat, just to eliminate smell, when they spread manure all over your veg's. i think not. what they really meant were any _TSE agents_.

 

b. Gas scrubbing to eliminate smoke -- though steam may be omitted;

 

c. Stacks to be fitted with grit arreaters;

 

snip...

 

1.2 Visual Imact

 

It is considered that the requirement for any carcase incinerator disign would be to ensure that the operations relating to the reception, storage and decepitation of diseased carcasses must not be publicly visible and that any part of a carcase could not be removed or interfered with by animals or birds.

 

REPORT ON BOVINE CARCASE INCINERATION

 

IF GOD DEMANDED

 

full text;

 


 


 

snip...see more ;

 


 

spreading cwd around...tss

 

Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

 

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.

 


 

spreading cwd around...tss

 

Friday, May 13, 2011

 

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

 

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

 

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

 

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

 

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

 

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

 

Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

 

Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

 

In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

 

Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

 

All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.

 

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

 

In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

 

In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.

 

: Corresponding author: Dr. Hyun-Joo Sohn (+82-31-467-1867, E-mail: shonhj@korea.kr) 2011 Pre-congress Workshop: TSEs in animals and their environment 5

 


 


 


 

Friday, May 13, 2011

 

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

 


 

how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and this is just one cwd infected farm, which had the highest documented infection rate of cwd, documented at 80%.

 

Tuesday, December 20, 2011

 

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

 

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

 

SUMMARY:

 


 

Friday, April 04, 2014

 

Wisconsin State officials kept silent on CWD discovery at game farm

 


 

Tuesday, March 25, 2014

 

Transmission of Chronic Wasting Disease in Wisconsin White-Tailed Deer: Implications for Disease Spread and Management

 

*** However, we also note that CWD transmission rates and prevalence are much higher in captive deer farms than has been reported in wild populations [67].

 


 

Tuesday, February 11, 2014

 

*** Wisconsin tracks 81 deer from game farm with CWD buck to seven other states

 


 

Monday, December 02, 2013

 

WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING PRESERVE

 


 

Tuesday, December 17, 2013

 

Wisconsin Second CWD positive deer found in Grant County

 


 

Friday, February 03, 2012

 

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

 


 

2010 WISCONSIN CAPTIVE DEER ESCAPES

 

There were 26 reported escape incidents so far this year, this amounted to 20 actual confirmed escape incidents because 3 were previously reported, 2 were confirmed as wild deer, and 1 incident was not confirmed. ...

 

snip...

 

C. & D. Captive Cervid and Law Enforcement Update (11:10 AM)- Warden Pete Dunn gave the captive cervid farm update.

 

There were 26 reported escape incidents so far this year, this amounted to 20 actual confirmed escape incidents because 3 were previously reported, 2 were confirmed as wild deer, and 1 incident was not confirmed. Approximately 30% of these escapes were caused by gates being left open and the other 70% resulted from bad fencing or fence related issues. The 20 actual confirmed escape incidents amounted to 77 total animals. 50 of the escaped animals were recovered or killed and 27 were not recovered and remain unaccounted for. Last year the CWD Committee passed a resolution to require double gates, but this has not gone into effect yet. Questions were raised by the committee about double fencing requirements? Pete responded that double fencing has not been practical or accepted by the industry. The DNR has the authority to do fence inspections. ? If a fence fails to pass the inspection the fencing certificate can be revoked and the farmer can be issued a citation. This year three citations and one warning have been issued for escapes. Pete reviewed the reporting requirements for escape incidents that these must be reported within 24 hours. The farmer then has 72 hours to recover the animals or else it will affect the farm’s herd status and ability to move animals. Davin proposed in the 15 year CWD Plan that the DNR take total control and regulatory authority over all deer farm fencing. Larry Gohlke asked Pete about the reliability for reporting escapes? Pete said that the majority of escapes were reported by the farmer, but it is very difficult to determine when an escape actually occurred. Pete said that they are more concerned that an escape is reported and not that it is reported at the exact time that it happened.

 


 

Wisconsin : 436 Deer Have Escaped From Farms to Wild

 

Date: March 18, 2003 Source: Milwaukee Journal Sentinel

 

Contacts: LEE BERGQUIST lbergquist@journalsentinel.com

 

State finds violations, lax record keeping at many sites, report says

 

A state inspection of private deer farms, prompted by the discovery of chronic wasting disease, found that 436 white-tailed deer escaped into the wild, officials said Tuesday

 

The Department of Natural Resources found that captive deer have escaped from one-third of the state's 550 deer farms over the lifetime of the operations. The agency also uncovered hundreds of violations and has sought a total of 60 citations or charges against deer farm operators.

 

snip...

 

CWD found on 2 farms

 

Seven deer have tested positive for the disease on game farms - one on a Portage County farm and six on a Walworth County farm - since the disease was discovered in three wild deer killed near Mount Horeb in western Dane County. One deer that tested positive on the Walworth County farm escaped and roamed free for six months.

 

snip...

 

The audit found that most farms were in compliance, but the DNR found many violations and instances of poor record keeping. Also in numerous instances, fences did not stop wild and captive deer from intermingling.

 

At least 227 farms conducted part of their business on a cash basis, making it hard to track animal movement with financial records.

 

For example, both the Internal Revenue Service and the state Department of Revenue have been contacted about a deer farm near Wild Rose in Waushara County that is suspected of selling six large bucks for $45,000 in cash and not using live deer shipping tags as required.

 

The DNR found that game farm operators have more deer in captivity than their records show, which is "due in part because the owners of a number of large deer farm operations were! unable to accurately count the number of deer within their fences," the audit found.

 

Hundreds of deer escape

 

The DNR found a total of 671 deer that escaped farms - 436 of which were never found - because of storm-damaged fences, gates being left open or the animals jumping over or through fences.

 

In one example in Kewaunee County, a deer farmer's fence was knocked down in a summer storm. Ten deer escaped, and the farmer told the DNR he had no intention of trying to reclaim them. The DNR found five of the deer, killed them and cited the farmer for violation of a regulation related to fencing.

 

Another deer farmer near Mishicot, in Manitowoc County, released all nine of his whitetails last summer after he believed the discovery of chronic wasting disease was going to drive down the market for captive deer.

 

The DNR found 24 instances of unlicensed deer farms and issued 19 citations.

 

Journal Sentinel correspondent Kevin Murphy contributed to this report.

 

Game Farms Inspected

 

A summary of the findings of the Department of Natural Resources' inspection of 550 private white-tailed deer farms in the state: The deer farms contained at least 16,070 deer, but the DNR believes there are more deer in captivity than that because large deer farms are unable to accurately count their deer. 671 deer had escaped from game farms, including 436 that were never found.

 

24 farmers were unlicensed. One had been operating illegally since 1999 after he was denied a license because his deer fence did not meet minimum specifications.

 

Records maintained by operators ranged from "meticulous documentation to relying on memory." At least 227 farms conducted various portions of their deer farm business with cash. Over the last three years, 1,222 deer died on farms for various reasons. Disease testing was not performed nor required on the majority of deer. Farmers reported doing business with people in 22 other states and one Canadian province. Click these links for more information

 


 

The initial discovery at Wilderness Whitetails was the first in five years. In trying to explain the sudden appearance, McGraw cited several possibilities for transmission, including the chance it occurred spontaneously.

 

That drew attention of Clausen and wildlife staff at the DNR. Clausen said he knew of no peer-reviewed research showing the disease turned up that way.

 

Tami Ryan, wildlife health section chief with the DNR, asked the agriculture department to back up the claim.

 

Richard Bourie, a veterinarian, pointed to a paper by Nobel Laureate Stanley Prusiner of the University of California, San Francisco, who discussed spontaneous occurrence in TSEs.

 

*** Ryan wrote back and said, "to the best of our collective knowledge, spontaneous CWD in wild deer has not been substantiated," although she said the DNR wasn't trying to pick a fight.

 

Said McGraw: "There is no battle going on here. We all read science here. Everybody looks at different possibilities."

 


 

Saturday, February 04, 2012

 

*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

 

Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month.

 

*** Two of the six fawns with CWD detected were 5 to 6 months old.

 

All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.

 


 

Wednesday, September 04, 2013

 

***cwd - cervid captive livestock escapes, loose and on the run in the wild...

 


 

”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.

 


 

Sunday, January 06, 2013

 

USDA TO PGC ONCE CAPTIVES ESCAPE

 

*** "it‘s no longer its business.”

 


 

Monday, June 24, 2013

 

The Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry Following its Discovery

 


 

Tuesday, May 20, 2014

 

“Atypical” Chronic Wasting Disease in PRNP Genotype 225FF Mule Deer

 


 

Tuesday, May 27, 2014

 

New Missouri CWD regulations... You know where we stand... What are your thoughts?

 


 

Friday, May 30, 2014

 

Wisconsin Waushara County hunting preserve ordered to pay civil forfeiture in CWD case

 


 

Monday, May 05, 2014

 

Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing

 


 

Sunday, June 29, 2014

 

Chronic Wasting Disease Ecology and Epidemiology of Mule Deer and White-tailed Deer in Wyoming

 


 

Sunday, June 29, 2014

 

Chronic wasting disease spreads in West Virginia

 


 

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose DOCUMENT ID: APHIS-2006-0118-0411

 

***Singeltary submission

 


 


 

*** 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.

 


 

Sunday, May 18, 2014

 

*** Chronic Wasting Disease CWD TSE PRION DISEASE and the transmission to other species

 


 

*** 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).

 


 

Saturday, April 19, 2014

 

Exploring the zoonotic potential of animal prion diseases: In vivo and in vitro approaches

 


 

Monday, June 23, 2014

 

PRION 2014 CHRONIC WASTING DISEASE CWD

 


 

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

 

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

 

see full text ;

 


 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

 

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 


 


 

Wednesday, February 16, 2011

 

IN CONFIDENCE

 

SCRAPIE TRANSMISSION TO CHIMPANZEES

 

IN CONFIDENCE

 


 

Chronic Wasting Disease Susceptibility of Four North American Rodents

 

Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu

 

We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.

 


 

please see ;

 


 

UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

 

----- Original Message -----

 

From: David Colby To: flounder9@verizon.net

 

Cc: stanley@XXXXXXXX

 

Sent: Tuesday, March 01, 2011 8:25 AM

 

Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

 

Dear Terry Singeltary,

 

Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware

 

===========END...TSS==============

 

 SNIP...SEE FULL TEXT ;

 


 

UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010

 


 

 *** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 

VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $

 

OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles

 

Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA

 

Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.

 

Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.

 

Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.

 

In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.

 

Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.

 

The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 


 

Wednesday, March 28, 2012

 

VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up again $

 


 

 CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss

 

PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase.

 

please see ;

 

 > 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.

 

CJD Deaths Reported by CJDSS1, 1994-20122

 

As of May 31, 2012

 

Deaths of Definite and Probable CJD

 

Year Sporadic Iatrogenic Familial GSS FFI vCJD Total

 

1994 2 0 0 1 0 0 3

 

1995 3 0 0 0 0 0 3

 

1996 13 0 0 0 0 0 13

 

1997 16 0 1 1 0 0 18

 

1998 22 1 0 1 0 0 24

 

1999 26 2 2 1 0 0 31

 

2000 32 0 0 3 0 0 35

 

2001 27 0 2 1 0 0 30

 

2002 31 0 2 2 0 1 36

 

2003 27 1 1 0 0 0 29

 

2004 42 0 1 0 0 0 43

 

2005 42 0 0 2 0 0 44

 

2006 39 0 1 3 1 0 44

 

2007 35 0 0 4 0 0 39

 

2008 48 0 1 0 0 0 49

 

2009 48 0 3 2 0 0 53

 

2010 34 0 3 0 0 0 37

 

2011 37 0 2 1 0 1 41

 

2012 1 0 0 0 0 0 1

 

Total 525 4 19 22 1 2 573

 

1. CJDSS began in 1998

 

2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional

 

3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.

 

CJD Deaths Reported by CJDSS1, 1994-20122

 

As of May 31, 2012

 


 


 

 SEE DECEMBER 2012 CANADA

 


 

USA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss

 

National Prion Disease Pathology Surveillance Center

 

Cases Examined1

 

(May 18, 2012)

 

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

 

1996 & earlier 50 32 28 4 0 0

 

1997 114 68 59 9 0 0

 

1998 88 52 44 7 1 0

 

1999 123 74 65 8 1 0

 

2000 145 103 89 14 0 0

 

2001 210 120 110 10 0 0

 

2002 248 149 125 22 2 0

 

2003 266 168 137 31 0 0

 

2004 326 187 164 22 0 13

 

2005 344 194 157 36 1 0

 

2006 382 196 166 28 0 24

 

2007 377 213 185 28 0 0

 

2008 396 232 206 26 0 0

 

2009 423 256 212 43 1 0

 

2010 413 257 216 41 0 0

 

2011 410 257 213 43 0 0

 

2012 153 82 51 15 0 0

 

TOTAL 44685 26406 2227 387 6 3

 

1 Listed based on the year of death or, if not available, on year of referral;

 

2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;

 

3 Disease acquired in the United Kingdom;

 

4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;

 

5 Includes 14 cases in which the diagnosis is pending, and 18 inconclusive cases;

 

6 Includes 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).

 

Rev 5/18/2012

 


 

> 6 Includes

 

> 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded.

 

> The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).

 

WELL, it seems the USA mad cow strains in humans classified as type determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased over the years, and the same old song and dance continues with sporadic CJD cases $$$

 


 

 *** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 

Increased Atypical Scrapie Detections

 

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

 


 

Thursday, March 29, 2012

 

*** atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

 


 

Monday, April 25, 2011

 

Experimental Oral Transmission of Atypical Scrapie to Sheep

 

Volume 17, Number 5-May 2011 However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40).

 


 

Monday, December 14, 2009

 

Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types

 

(hmmm, this is getting interesting now...TSS)

 

Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits,

 

see also ;

 

All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

 


 

see full text ;

 

Monday, December 14, 2009

 

Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types

 


 

***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion

 

Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada

 

Keywords: Atypical BSE, oral transmission, RT-QuIC

 

The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.

 

The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.

 

Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.

 

Monday, June 23, 2014

 

PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES

 


 

Friday, March 09, 2012

 

Experimental H-type and L-type bovine spongiform encephalopathy in cattle: observation of two clinical syndromes and diagnostic challenges

 

Research article

 


 

Thursday, June 23, 2011

 

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

 


 

P03.141

 

Aspects of the Cerebellar Neuropathology in Nor98

 

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

 

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 


 

PR-26

 

NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS

 

R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway

 

Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.

 

*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.

 

119

 


 

A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

 

Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations

 

*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

 

***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)

 

Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice.

 

*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

 


 

Monday, December 1, 2008

 

When Atypical Scrapie cross species barriers

 

Authors

 

Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.

 

Content

 

Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.

 

The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.

 

Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.

 

Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

 

(i) the unsuspected potential abilities of atypical scrapie to cross species barriers

 

(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

 

These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.

 


 

Friday, February 11, 2011

 

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

 


 

CENSORSHIP IS A TERRIBLE THING $$$

 

Wednesday, April 10, 2013

 

CFIA investigated for muzzling scientists

 


 

Canada has had a COVER-UP policy of mad cow disease since about the 17th case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored $$$

 

THIS proves there is indeed an epidemic of mad cow disease in North America, and it has been covered up for years and years, if not for decades, and it’s getting worse $$$

 


 

Thursday, February 10, 2011

 

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

 


 

Wednesday, August 11, 2010

 

REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

 


 

Thursday, August 19, 2010

 

REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

 


 

Friday, March 4, 2011

 

Alberta dairy cow found with mad cow disease

 


 

Tuesday, May 21, 2013

 

Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$

 


 

Increased Atypical Scrapie Detections

 

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

 


 

Monday, April 07, 2014

 

Saskatchewan’s first chronic wasting disease case of the year has been confirmed 2014

 


 

why do we not want to do TSE transmission studies on chimpanzees $

 

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

 

snip...

 

R. BRADLEY

 


 

1: J Infect Dis 1980 Aug;142(2):205-8

 

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

 

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

 

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

 

snip...

 

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

 

PMID: 6997404

 


 

Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"

 

Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

 

snip...

 

76/10.12/4.6

 


 

Nature. 1972 Mar 10;236(5341):73-4.

 

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

 

Gibbs CJ Jr, Gajdusek DC.

 

Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

 

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

 

C. J. GIBBS jun. & D. C. GAJDUSEK

 

National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

 

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

 


 


 

Wednesday, February 16, 2011

 

IN CONFIDENCE

 

SCRAPIE TRANSMISSION TO CHIMPANZEES

 

IN CONFIDENCE

 


 

Sunday, December 12, 2010

 

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

 


 

Sunday, April 18, 2010

 

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

 


 

 Saturday, May 2, 2009

 

APHIS AND WHO PLAN TO EXEMPT THE ATYPICAL SCRAPIE NOR-98 FROM REGULATIONS AT MEETING THIS MONTH

 


 

Monday, November 30, 2009

 

USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE

 


 

RESEARCH

 

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011

 

Experimental Oral Transmission of Atypical Scrapie to Sheep

 

Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos

 

To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specific prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These findings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.

 

SNIP...

 

Although we do not have epidemiologic evidence that supports the effi cient spread of disease in the fi eld, these data imply that disease is potentially transmissible under fi eld situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing fi nding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.

 

How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantified, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confirmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.

 

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011

 


 

Monday, June 23, 2014

 

PRION 2014 CHRONIC WASTING DISEASE CWD

 


 

Monday, June 23, 2014

 

PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES

 


 

TSS

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