Friday, August 31, 2012

COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review

COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review



COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK 2011



The Committee met on October 2, 2011 at the Adams Mark Hotel in Buffalo, New York from 12:30-5:3 0p.m. There were 25 members and 31 guests present. Dr. John Fischer presided as acting chair for the Committee due to unavoidable conflicts of Drs. Miller and Hilsenroth. Bovine TB



snip...



USDA-APHIS-VS Chronic Wasting Disease National Program


Patrice N. Klein of USDA APHIS VS – National Center for Animal Health Programs provided an update on the agency’s CWD–related activities:


CWD Rule Update: The amended final rule on chronic wasting disease (CWD) is currently in departmental clearance. The rule will set minimum standards for interstate movement and establish the national



___voluntary___



Herd Certification Program (HCP). Farmed/captive cervid surveillance testing: Through FY2010, VS conducted surveillance testing on approximately 20,000 farmed /captive cervids by the immunohistochemistry (IHC) standard protocol. As of September 15, 2011, approximately 19,000 farmed /captive cervids were tested by IHC for CWD with funding to cover lab costs provided through NVSL.


Farmed/captive cervid CWD status: The CWD positive captive white-tailed deer (WTD) herd reported in Missouri (February 2010) was indemnified and depopulation activities were completed in June 2011. All depopulated animals were tested for CWD and no additional CWD positive animals were found.


In FY 2011, CWD was reported in two captive elk herds in Nebraska (December, 2010 and April 2011, respectively). To date, 52 farmed/captive cervid herds have been identified in 11 states: CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI. Thirty-nine were elk herds and 13 were WTD herds. At this time, eight CWD positive herds remain – six elk herds in Colorado and the two elk herds in Nebraska.


Wild Cervid surveillance: In FY 2009 funding supported surveillance in approximately 74,330 wild cervids in 47 cooperating States. Wild cervid CWD surveillance totals are pending for fiscal year 2010 (2010 – 2011 calendar year) due to seasonal surveillance activities and completion of final cooperative agreement reporting to APHIS.


In fiscal year 2011, there are 15 ‘tier 1’ States, 20 ‘tier 2’ States, and 15 ‘tier 3’ States. Two new ‘tier 1’ States, Minnesota and Maryland, were added in fiscal year 2011 based on the new CWD detections in a free-ranging white-tailed deer in southeastern Minnesota and in western Maryland. Consequently, Delaware was upgraded to ‘tier 2’ status as an adjacent State to Maryland. For FY 2011, 45 States and 32 Tribes will receive cooperative agreement funds to complete wild cervid surveillance and other approved work plan activities. Based on FY 2012 projected budget reductions, future cooperative agreement funds will be eliminated.


APHIS CWD Funding: In FY2011, APHIS received approximately $15.8 million in appropriated funding for the CWD Program. The President’s FY 2012 budget proposes to reduce program funding for CWD by $13.9 million, leaving the program with a request of $1.925 million to provide some level of Federal coordination for the national herd certification program (HCP).


Consequently, APHIS is planning to amend its role in the program to one of Federal coordination. Based on the projected FY 2012 budget, funding for CWD cooperative agreements and indemnity funding for States and Tribes will be eliminated. Under this scenario, the States or cervid industry producers will likely be responsible for the costs of surveillance testing and indemnity for appraisal, depopulation, and disposal of CWD-positive animals.


Commodity Health Line Structure: In the FY 2012 budget, livestock commodities regulated by USDA have been organized into ‘Commodity Health Line’ structures or groupings. APHIS’ Equine, Cervid and Small Ruminant (ECSR) Health line supports efforts to protect the health and thereby improve the quality and productivity of the equine, cervid and small ruminant industries. Activities supported by the ECSR Health line range from monitoring and surveillance to investigation and response actions undertaken when health issues relevant to the industry are identified. APHIS also maintains regulations and program standards which guide ECSR activities at both the Federal and State/Tribal level.


The ECSR Health line funds essential activities necessary to maintain current ECSR surveillance and program operations while providing the flexibility to respond to new and emerging industry-specific health concerns. APHIS’ current activities include Scrapie, Chronic Wasting Disease (CWD), Slaughter Horse Transport, and Brucellosis/Tuberculosis in cervids. Overall, APHIS will use funding from the ECSR Health Line Item to support Agency efforts in the following mission areas: prevention, preparedness and communication; monitoring, surveillance and detection; response and containment; and continuity of business, mitigation and recovery



Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)



Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie and CWD in inoculated deer. Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. We inoculated white-tailed deer intracranially (IC) and by a natural route of exposure (concurrent oral and intranasal inoculation) with a US scrapie isolate. All deer inoculated by the intracranial route had evidence of PrPSc accumulation and those necropsied after 20 months post-inoculation (PI) (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6 months PI did not have clinical signs, but had widespread distribution of PrPSc. This highlights the facts that 1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and 2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile consistent with CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.



Committee Business:


The Committee discussed and approved three resolutions regarding CWD. They can be found in the report of the Reswolutions Committee. Essentially the resolutions urged USDA-APHIS-VS to:


Continue to provide funding for CWD testing of captive cervids


• Finalize and publish the national CWD rule for Herd Certification and Interstate Movement


• Evaluate live animal test, including rectal mucosal biopsy, for CWD in cervids









BACKGROUND INFORMATION:


The proposed rule for Chronic Wasting Disease (CWD) Herd Certification and Interstate Movement of Captive Cervids in farmed cervidae requires that all farmed cervidae greater than 12 months of age that die or are slaughtered must be tested for CWD. Farmed cervidae producers across the nation have complied with testing requirements, in large part because laboratory costs for CWD testing have traditionally been paid with United States Department of Agriculture (USDA) funds.


The CWD testing protocol that is recommended for farmed cervidae is the immunohistochemistry (IHC) test using formalin fixed samples of brain stem and retropharyngeal lymph node from each animal. It is the most sensitive and specific test for detecting CWD. The test is expensive and costs at least $25.00 per slide to perform at USDA approved laboratories.


There is an urgency to maintain USDA funding to cover the costs of CWD testing for farmed cervidae. If USDA funding for CWD tests ends and farmed cervidae producers are forced to cover the cost of such tests, there is a real possibility that producer compliance with CWD testing requirements will decrease. Without producer cooperation, the national CWD control program for farmed cervidae could collapse.


RESOLUTION:


The United States Animal Health Association urges the United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services to continue to provide funding to cover the laboratory costs of testing farmed cervidae for Chronic Wasting Disease by immunohistochemistry at all approved laboratories.


INTERIM RESPONSE:


The U.S. Department of Agriculture (USDA), Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) recognizes the concerns of the United States Animal Health Association (USAHA) and appreciates the opportunity to respond.


Resolution 14 / pg 2


In fiscal year 2012, the congressional appropriation for the chronic wasting disease (CWD) program was reduced by $13.9 million, to approximately $1.9 million. Consequently, VS no longer has funds to cover testing costs for farmed cervids. Laboratories and industry were informed that this funding ended on December 31, 2011; all such costs must now be borne by the producers. VS will continue to cover only confirmatory testing on any presumptive CWD positive samples from farmed and wild cervidae at the National Veterinary Services Laboratories.


VS will direct remaining program funds to the publication of the CWD final rule and the administrative costs associated with implementation of the national CWD herd certification program.







UNITED STATES ANIMAL HEALTH ASSOCIATION


115th Annual Meeting


September 29- October 5, 2011


Buffalo, New York


_________________________________________________________



RESOLUTION NUMBER: 15 APPROVED


SOURCE: COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK


SUBJECT MATTER: CHRONIC WASTING DISEASE HERD CERTIFICATION AND INTERSTATE MOVEMENT FINAL RULE


BACKGROUND INFORMATION:


Implementation of rules for Chronic Wasting Disease (CWD) that define the CWD herd certification program (9 CFR 55 Subpart B) and requirements for interstate movement of farmed cervidae (9 CFR 81) has been delayed since 2006. There is an urgency to finalize these rules to ensure that CWD certification programs are uniformly administered in all states and that all farmed cervidae that move from state to state meet the same requirements. These rules are critically important to the survival of the farmed cervidae industry. These rules are needed to preserve the ability of producers to move farmed cervidae and their products interstate and internationally without unnecessary restrictions.


RESOLUTION:


The United States Animal Health Association urges the United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services to finalize rules for Chronic Wasting Disease herd certification programs (9 CFR 55 Subpart B) and interstate movement of farmed cervidae (9 CFR 81).


INTERIM RESPONSE:


The U.S. Department of Agriculture (USDA), Animal and Plant Health Inspection Service, Veterinary Services appreciates your interest in the rulemaking for chronic wasting disease (CWD).


The CWD amended final rule was cleared by USDA and is in clearance in the Office of Management and Budget (OMB). Once OMB clearance is completed, the CWD amended rule would become effective 60 days after its publication.







UNITED STATES ANIMAL HEALTH ASSOCIATION


115th Annual Meeting


September 29- October 5, 2011


Buffalo, New York



_________________________________________________________




RESOLUTION NUMBER: 16 APPROVED


SOURCE: COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK


SUBJECT MATTER: LIVE ANIMAL TESTING FOR CHRONIC WASTING DISEASE


BACKGROUND INFORMATION:


Detection of Chronic Wasting Disease (CWD) in live animals is an important component of CWD Prevention and Control Programs.


With the funding decrease for CWD indemnification, the need has increased for additional diagnostic tools to monitor CWD positive herds and epidemiologically linked herds that may be maintained in quarantine rather than depopulated. The use of recto-anal mucosa associated lymphoid tissue (RAMALT) has been approved as a live animal test for Scrapie. There have been numerous studies evaluating the sensitivity and specificity of RAMALT in cervids. There are several additional advantages to RAMALT sampling. There is a large amount of suitable tissue to sample and multiple sites can be sampled allowing repeat sampling over time.


RESOLUTION:


The United States Animal Health Association requests that the United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services evaluate live animal tests, including the rectal biopsy (RAMALT), as a live animal test for Chronic Wasting Disease.


INTERIM RESPONSE:


The U.S. Department of Agriculture, Animal and Plant Health Inspection Service (APHIS), Veterinary Services appreciates your interest in live animal tests for chronic wasting disease (CWD).


APHIS is completing analysis of a multi-year study evaluating recto-anal mucosa associated lymphoid tissue (RAMALT) biopsy testing as a diagnostic tool for CWD detection in captive white-tailed deer. This is a collaborative study with APHIS Wildlife Services, Agricultural Research Service, Canadian Food Inspection Agency, Colorado State University, and others to evaluate the existing collective data on white-tailed deer relative to diagnostic testing and interpretation of the immunohistochemistry test for CWD


Resolution 16 / pg 2


on rectal biopsy testing in the United States and Canada. Currently, there is insufficient data available to evaluate this technique on other captive Cervidae.


After this analysis is completed, APHIS will determine the applicability of RAMALT for use in a CWD Herd Certification Program (HCP). We plan to complete this determination by September 30, 2012. APHIS also will continue to evaluate other live animal tests for CWD, as they are developed, to assess appropriate use in a CWD HCP.








Friday, August 24, 2012



Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America



The overall diagnostic specificity was 99.8%. Selective use of antemortem rectal biopsy sample testing would provide valuable information during disease investigations of CWD-suspect deer herds.













(E) Beginning one hundred-eighty days after the effective date of this rule,








(K) All monitored captive deer, three hundred sixty-five days of age or older which die from injury, illness, slaughter, hunting, or any other cause, shall be reported within twenty-four hours of discovery to an approved accredited licensed veterinarian or if not available, the Chief, Division of Animal Health or his representative. Monitored captive deer in hunting preserves are exempt from the twenty-four hour requirement for notification.


Monitored captive deer shall be tested for chronic wasting disease according to the following:


(1) Herds with ten head or less must test all deaths.


(2) Herds with eleven heads or more must annually test thirty percent or thirty head of deaths, whichever is less.


(L) The owner of all captive whitetail deer being tested for chronic wasting disease, is responsible for arranging for the submission of the required brain tissue and any other tissues as directed by the Chief, Division of Animal Health or his representative, to a department approved laboratory for chronic wasting disease testing. The submission form for CWD shall be signed by an approved accredited licensed veterinarian and shall accompany the sample. Owners are responsible for the cost of collecting and submitting, and testing of samples.


The animal’s official identification tag must accompany the sample; if the animal does not have a tag at time of death, a tag must be issued and accompany the sample.










Q. What does the 2012 amended CWD final rule entail?



A. The interim final rule responds to the concerns raised to APHIS in 2006 and finalizes the changes to the CWD program APHIS proposed in March, 2009.


It establishes a ___voluntary___ national CWD Herd Certification Program (HCP), providing consistent minimum standards for participating states and minimum requirements for the interstate movement of cervids.


States that participate in the HCP must establish programs that are approved by APHIS.




snip...




Q. What are the requirements for a State to become a CWD HCP participant?



A. States interested in having their State CWD HCP approved should submit the required application and supporting documents to APHIS for review and approval. Application materials should be sent to the Area Veterinarian in Charge (AVIC) in the APHIS Veterinary Service (VS) Area Office in the requesting State. Information provided must describe the State’s CWD prevention and control activities, and the deer, elk, and moose herd certification activities, and cite relevant State statutes, regulations, and directives pertaining to animal health activities and reports and publications of the State.



This must include:



• Movement restrictions,



• Surveillance and disease reporting capabilities,



• Herd/animal identification requirements



• Diagnostic testing capacities,



• Recordkeeping and data management,



• Ability to conduct epidemiologic investigations and trace-outs



• Education and outreach Details of requirements are described in 9 CFR Part 55.23.




Q. What must a herd owner do to become a CWD HCP participant?




A. Herd owners seeking approval to participate in their Approved State CWD HCP should contact their State agency for information on herd owner enrollment United States Department of Agriculture



• Animal and Plant Health Inspection Service



• Safeguarding American Agriculture and State requirements. In general, herd owners may be eligible to enroll in an Approved State CWD HCP if they:



• Add to their herds only animals that are from herds enrolled in the CWD Herd Certification Program, to ensure that animals added to herds are of known risk. Additions to the herd should be from other enrolled herds of equal or greater status in the program.



• Maintain perimeter fencing adequate to prevent entry or exit of cervids, and to minimize the possibility of CWD transmission by direct contact between farmed and free-ranging wild cervid populations.



• Report to APHIS or the State all animals that escape or disappear, and report to APHIS or the State all animals that die or are killed and make their carcasses available for tissue sampling and testing. Minimum federal standards for herd owner enrollment in their State CWD HCP are described in the 9 CFR Part 55.22.




snip...




Q. Do I have to be enrolled in an Approved State CWD HCP if the cervid species I raise is not known to be susceptible to CWD?


A. No. The federal rule establishes federal standards for a voluntary Approved State CWD HCP and includes cervids in the genera Cervus, Odocoileus, and Alces and their hybrids. These genera represent cervids known to be susceptible to CWD. Individual States may have additional requirements for other cervid species not included in the federal rule.










never say never...tss





5. A positive result from a chimpanzee challenged severely 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.














Monday, June 18, 2012



natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red deer crossbreeds captive Korea and Experimental oral transmission to red deer (Cervus elaphus elaphus)








Tuesday, June 19, 2012



Experimental Oral Transmission of Chronic Wasting Disease to Reindeer (Rangifer tarandus tarandus)









USAHA Committee on Captive Wildlife and Alternative Livestock


Tuesday October 23, 2012 8:00 AM–12:00 PM


Grandover West, Sheraton Greensboro


Greensboro, North Carolina


Chronic Wasting Disease


9:00-9:30AM Review and Updates of the USDA/APHIS Veterinary Services National CWD Program


Patrice Klein


9:30-10:00AM CWD surveillance using the RAMALT (rectal biopsy) method Bruce Thomsen


10:00-10:30AM Break









2010




Status: CWD was detected in one captive white-tailed deer (WTD) herd in Missouri in February 2010. To date, 50 farmed/captive cervid herds have been identified in 11 states: CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI. Thirty-seven were elk herds and 13 were WTD herds. At this time, six CWD positive elk herds remain in Colorado and one WTD herd remains in MO. VS has continued to offer indemnity for appraised value of the animals and to cover costs of depopulation, disposal, and testing of CWD-positive and exposed herds. Indemnity is provided based on availability of federal funding.







2009



Status: Five positive farmed cervid herds were detected in FY 2009: Two white-tailed deer herds in Wisconsin, one elk herd in Minnesota, and two elk herds in Colorado. The Wisconsin and Minnesota facilities have been depopulated. This brings to 47 the number of positive herds that have been identified since 1997. At this time, six positive elk herds remain in Colorado. Also, CWD was detected at slaughter for the first time in FY 2009. VS continues to offer indemnity and cover depopulation, disposal and testing costs for CWD-positive and exposed herds and trace animals.








Saturday, June 09, 2012


USDA Establishes a Herd Certification Program for Chronic Wasting Disease in the United States
















CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).



SNIP...



Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).



PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS







Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012


CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).







Tuesday, June 05, 2012


Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session






Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting






Saturday, February 04, 2012


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






Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE






Friday, February 03, 2012


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






Monday, November 14, 2011


WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011






Sunday, November 13, 2011


COLORADO CWD CJD TSE PRION REPORTING 2011






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 ;


CWD to cattle figures CORRECTION



Greetings,


I believe the statement and quote below is incorrect ;


"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."


Please see ;


Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.





" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "


shouldn't this be corrected, 86% is NOT a low rate. ...



kindest regards,



Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518




Thank you!


Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.






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


1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu






Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.


snip...








----- 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






Sunday, August 19, 2012


Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012


Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit






PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)

















Thursday, May 31, 2012



CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more







Wednesday, August 29, 2012

SUMNER COUNTY DEER DID NOT HAVE CHRONIC WASTING DISEASE

SUMNER COUNTY DEER DID NOT HAVE CHRONIC WASTING DISEASE Aug. 30, 2012


Initial test was false-positive


PRATT— In July, the Kansas Department of Wildlife, Parks and Tourism (KDWPT) reported that nine deer had tested positive for chronic wasting disease (CWD) during the 2011-12 testing period. The agency now reports that the National Veterinary Services Laboratory in Ames, Iowa, after two different tests, did not detect CWD prions in the Sumner County deer, so initial testing in this case yielded a false-positive result. This reduces the total 2011-2012 positives to eight. Counties where CWD was detected during the 2011-2012 surveillance period include Wallace (one), Rawlins (one), Decatur (one), Norton (two), Trego (one), Ford (one), and Stafford (one).


The white-tailed deer in question was taken from Sumner County last winter. This result brings the total number of confirmed CWD cases in Kansas to 48 since testing began in 1996. In total, 2,446 animals were tested for CWD during the 2011-2012 surveillance period, Aug. 1, 2011, through July 31, 2012.


Annual testing is part of an ongoing effort by KDWPT to monitor the prevalence and spread of CWD. The fatal disease was first detected in the Kansas free-ranging deer herd in 2005 in Cheyenne County.


More information on CWD can be found on KDWPT’s website, ksoutdoors.com, or at the Chronic Wasting Disease Alliance website, www.cwd-info.org.


-30-







Thursday, July 19, 2012


NINE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE








TSS


Saturday, August 25, 2012

Missouri Suspends Issuing Permits for New Deer Breeders and Big-game Hunting Facilities

Commission approves suspension of issuing permits for new deer breeders and big-game hunting facilities


Published on: Aug. 24, 2012


Posted by Joe Jerek


JEFFERSON CITY, Mo. – At its Aug. 24 meeting in Jefferson City, the Missouri Conservation Commission approved changes to the Wildlife Code of Missouri that indefinitely suspend issuing permits for new big-game hunting facilities and new wildlife breeding facilities in Missouri that hold white-tailed deer or mule deer.


The regulation changes to suspend the issuance of new permits do not apply to wildlife breeders and game ranches with existing permits. The suspension of issuing permits does not include wildlife-breeders or game ranches who wish to hold approved wildlife species other than white-tailed deer or mule deer. Renewal of existing permits for hunting and breeding facilities will be considered under established requirements of the Wildlife Code.


“The Missouri Department of Conservation (MDC) is responsible for managing and protecting the wildlife resources of the state and we take that responsibility very seriously,” says MDC Deputy Director Tom Draper. “With Chronic Wasting Disease now in Missouri, this suspension of issuing permits for new deer breeders and hunting ranches is one of several actions we are taking to help protect free-ranging deer from CWD, and to help ensure the health of captive deer and other cervids.”


MDC permit records show there are 27 permitted big-game hunting preserves in Missouri with white-tailed deer, and 277 permitted wildlife breeders with white-tailed deer.


MDC has held numerous open houses to share information and get public feedback on the issue of Chronic Wasting Disease (CWD) and Department actions to contain the disease.


MDC provided current information on CWD and the proposed suspension of issuing permits for new big-game ranches and wildlife breeders that hold white-tailed deer or mule deer to members of the Missouri Whitetail Breeders and Hunting Ranch Association at the Association’s annual conference on Aug. 4.


Draper adds that MDC continues to work with landowners, deer hunters, members of the captive cervid industry and others on the issue of CWD and welcomes related comments at mdc.mo.gov/node/17901.


Chronic Wasting Disease is a fatal disease that attacks the nervous systems of cervids, such as white-tailed, mule and other types of deer. It is transmitted by animal-to-animal contact or soil-to-animal contact. It can spread through activities that unnaturally concentrate animals, the natural movement and dispersal of infected free-ranging deer, the transportation of live captive deer with CWD or the transportation and improper disposal of infected carcasses.


According to the Missouri Department of Agriculture, there is no evidence from existing research that CWD can spread to domestic livestock, such as sheep or cattle. According to the Missouri Department of Health and Senior Services (MDHSS), there is no evidence that CWD can infect people.


The first two cases of CWD in the state were found in 2010 and 2011 at two private big-game hunting preserves in Linn and Macon counties. Following those discoveries, the first two cases of CWD in free-ranging deer were confirmed in 2012 in Macon County. Missouri’s confirmed cases of CWD total 11 in captive deer from the private hunting preserves and five in free-ranging deer harvested in Macon County.


With the help of hunters, MDC has tested more than 35,000 free-ranging deer for CWD from all parts of the state since 2002 and up to 2012. As a result of that testing, MDC scientists have determined it is highly unlikely that CWD has been present in the state prior to its recent discovery in northeast Missouri.


Draper says that the Code changes allow time for MDC to further assess the CWD situation, continue to engage stakeholders, plan for the future and identify and utilize the best and most current science to manage the disease.


New federal regulations for the interstate movement and disease certification of captive deer and other cervids were recently open for review and comment through the Federal Register at www.federalregister.gov. Additional information is pending publication. Draper says that the Code changes also give MDC, deer breeders and others time to review these new regulations.


“Conservation efforts such as providing good habitat and progressive deer management practices on both public and private land make Missouri a great place to hunt deer,” Draper says. “The cultural, social and economic importance that white-tailed deer provide the people of our state is, and will continue to be, one of our top priorities.”


According to MDC, Missouri has more than 507,000 deer hunters who spend about $690 million in the state each year on deer hunting and related activities. This has an overall economic impact of $1.1 billion in Missouri each year and supports almost 12,000 jobs. Many Missourians also enjoy viewing deer. A 2009 Gallup survey found that about 91% of Missourians are somewhat or very interested in observing deer in the outdoors.


Other actions the Conservation Commission and MDC have taken to limit the spread of CWD in Missouri include regulation changes, recommendations and continuing sampling of harvested deer to test for CWD.


The Conservation Commission approved a regulation change in May that restricts activities that are likely to unnaturally concentrate white-tailed deer and promote the spread of CWD. The regulation will become effective Oct. 30. It bans the placement of grain, salt products, minerals and other consumable natural or manufactured products in the CWD Containment Zone, which consists of Adair, Chariton, Linn, Macon, Randolph and Sullivan counties. The regulation includes exceptions for backyard feeding of wildlife and normal agricultural, forest management, crop and wildlife food production practices.


The Conservation Commission also approved a regulation change in May that rescinds the antler-point restriction (four-point rule) in the CWD Containment Zone, which became effective July 1. Yearling and adult male deer have been found to exhibit CWD at higher rates than female deer so a reduction in the number of male deer can help limit the spread of CWD. The dispersal of yearling males from their natal or birth range in search of territory and mates is also one of the primary means of expanding the distribution of CWD.


MDC also encourages hunters who harvest deer in the CWD Containment Zone not to take whole deer carcasses or certain carcass parts out of the area.


MDC will also continue to work with hunters who harvest deer in the CWD Containment Zone to collect samples for CWD testing.


Detailed information can be found in MDC’s “2012 Fall Deer & Turkey Hunting Regulations and Information” booklet available at MDC offices, from permit vendors and online at












Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting






Saturday, February 04, 2012


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






Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting







Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE







Tuesday, June 05, 2012


Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session







Saturday, June 09, 2012


USDA Establishes a Herd Certification Program for Chronic Wasting Disease in the United States







Oral.29: Susceptibility of Domestic Cats to CWD Infection


Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu


Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature. www.landesbioscience.com Prion















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 ProfessorDepartment of Chemical EngineeringUniversity of Delaware



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



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UPDATED DATA ON 2ND CWD STRAIN



Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010







Thursday, May 31, 2012


CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more






Tuesday, January 24, 2012


CWD found in two free-ranging deer from Macon County Missouri







Friday, October 21, 2011


Chronic Wasting Disease Found in Captive Deer Missouri







Friday, February 26, 2010


Chronic wasting disease found in Missouri deer






Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission







*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***



Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012


CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).


SNIP...


Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).



PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS







Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012







Friday, August 24, 2012


Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America







TSS

Friday, August 24, 2012

Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America

Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America



Effects of age, sex, polymorphism at PRNP codon 96, and disease progression


Bruce... V. Thomsen1 David A. Schneider Katherine I. O’Rourke Thomas Gidlewski James McLane Robert W. Allen Alex A. McIsaac Gordon B. Mitchell Delwyn P. Keane Terry R. Spraker Aru Balachandran


U.S. Department of Agriculture, National Veterinary Services Laboratories, Ames, IA (Thomsen)


U.S. Department of Agriculture, Agricultural Research Service, Pullman, WA (Schneider, O’Rourke)


U.S. Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, Fort Collins, CO (Gidlewski)


Canadian Food Inspection Agency, Battleford, Saskatchewan, Canada (McLane)


Canadian Food Inspection Agency, Prince Albert, Saskatchewan, Canada (Allen)


Canadian Food Inspection Agency, Saskatoon, Saskatchewan, Canada (McIsaac)


National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa Laboratory–Fallowfield, Ottawa, Ontario, Canada (Mitchell, Balachandran)


University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory, Madison, WI (Keane)


Colorado State University Diagnostic Laboratory, Fort Collins, CO (Spraker)


↵1 Bruce V. Thomsen, National Veterinary Services Laboratories, 1920 Dayton Avenue, Ames, IA 50010. bruce.v.thomsen@aphis.usda.gov



Abstract



An effective live animal diagnostic test is needed to assist in the control of chronic wasting disease (CWD), which has spread through captive and wild herds of white-tailed deer (Odocoileus virginianus) in Canada and the United States. In the present study, the diagnostic accuracy of rectal mucosa biopsy sample testing was determined in white-tailed deer from 4 CWD-infected captive herds. Specifically, the current study compared the immunohistochemical detection of disease-associated prion protein in postmortem rectal mucosa biopsy samples to the CWD status of each deer as determined by immunodiagnostic evaluations of the brainstem at the obex, the medial retropharyngeal lymph node, and the palatine tonsil. The effects of age, sex, genotype, and disease progression were also evaluated. Diagnostic sensitivity on rectal biopsy samples for CWD in white-tailed deer ranged from 63% to 100%; the pooled estimate of sensitivity was 68% with 95% confidence limits (95% CLs) of 49% and 82%. However, diagnostic sensitivity was dependent on genotype at prion protein gene (PRNP) codon 96 and on disease progression as assessed by obex grade. Diagnostic sensitivity was 76% (95% CLs: 49%, 91%) for 96GG deer but only 42% (95% CLs: 13%, 79%) for 96GS deer. Furthermore, diagnostic sensitivity was only 36% for deer in the earliest stage of disease (obex grade 0) but was 100% for deer in the last 2 stages of preclinical disease (obex grades 3 and 4). The overall diagnostic specificity was 99.8%. Selective use of antemortem rectal biopsy sample testing would provide valuable information during disease investigations of CWD-suspect deer herds.







*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.


(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)





Wednesday, February 16, 2011


IN CONFIDENCE


SCRAPIE TRANSMISSION TO CHIMPANZEES


IN CONFIDENCE






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






PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)








High-Fence 226-Inch Whitetail Escapes, Shot in Louisiana


by Dylan Polk•December 1, 2011






Volume 18, Number 3—March 2012



Synopsis


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


Samuel E. Saunders1, Shannon L. Bartelt-Hunt, and Jason C. Bartz Author affiliations: University of Nebraska-Lincoln, Omaha, Nebraska, USA (S.E. Saunders, S.L. Bartelt-Hunt); Creighton University, Omaha (J.C. Bartz)


snip...


CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B). Except in South Korea, CWD has not been detected outside North America. In most locations reporting CWD cases in free-ranging animals, the disease continues to emerge in wider geographic areas, and prevalence appears to be increasing in many disease-endemic areas. Areas of Wyoming now have an apparent CWD prevalence of near 50% in mule deer, and prevalence in areas of Colorado and Wisconsin is <15 0="0" 10="10" 5="5" according="according" adult="adult" age="age" agencies.="agencies." and="and" appear="appear" areas="areas" between="between" but="but" cwd="cwd" data="data" deer.="deer." deer="deer" div="div" elk="elk" factors="factors" for="for" from="from" gene="gene" genetic="genetic" highest="highest" however="however" in="in" include="include" influence="influence" influences="influences" is="is" known="known" less="less" lower="lower" male="male" many="many" obtained="obtained" of="of" parts="parts" polymorphisms="polymorphisms" prevalence="prevalence" provincial="provincial" prp="prp" reaches="reaches" remain="remain" remains="remains" reports="reports" risk="risk" scrapie.="scrapie." sex="sex" show="show" state="state" strong="strong" susceptibility="susceptibility" than="than" the="the" to="to" understood="understood" wildlife="wildlife" wyoming.="wyoming.">

snip...


Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5). In addition, CWD-infected deer are selectively preyed upon by mountain lions (5), and may also be more vulnerable to vehicle collisions (10).


snip...


Conclusions


Much remains unknown about prion diseases and CWD in particular, especially about CWD strains (which may have varied zoonotic potentials) and the long-term effects of CWD on cervid ecosystems. CWD prevalence and geographic range appear likely to continue to increase. Moreover, the disease is inevitably fatal, and no effective therapeutic measures are presently available. As such, it would seem wise to continue research and surveillance of CWD to elucidate the details of its transmission, pathogenesis, and continued emergence in cervid populations in hopes that strategies for mitigating its negative effects on humans and cervid ecosystems can be identified.









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.



Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.


However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.


Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <








SNIP...SEE FULL TEXT ;








50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE CWD


2012


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.


Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.


However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.


Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought




SNIP...SEE FULL TEXT ;









Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE







Friday, February 03, 2012


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








Saturday, February 04, 2012


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







Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting








Ohio's testing is spontaneous and voluntary, and is limited to 16 month old only, and only after found dead. so, the flaws there are obvious. anything voluntary is useless, and the voluntary mad cow feed ban proved just how useless anything voluntary is. ...








Friday, July 20, 2012


CWD found for first time in Iowa at hunting preserve











TSS

Sunday, August 19, 2012

Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit
Title: Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation
Authors
Greenlee, Justin Nicholson, Eric Smith, Jodi Kunkle, Robert Hamir, Amirali
Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 12, 2012 Publication Date: N/A
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Cattle could be exposed to chronic wasting disease (CWD) by contact with infected farmed or free-ranging cervids. The purpose of this study was to assess the potential transmission of CWD from elk to cattle after intracranial inoculation, the most direct route to test the potential of a host to replicate an isolate of the prion agent. This study reports that only 2 of 14 calves inoculated with CWD from elk had clinical signs or evidence of abnormal prion protein accumulation. These results suggest that cattle are unlikely to be susceptible to CWD if inoculated by a more natural route. This information could have an impact on regulatory officials developing plans to reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas where CWD may be present.
Technical Abstract: Cattle could be exposed to the agent of chronic wasting disease (CWD) through contact with infected farmed or free-ranging cervids or exposure to contaminated premises. The purpose of this study was to assess the potential for CWD derived from elk to transmit to cattle after intracranial inoculation. Calves (n=14) were inoculated with brain homogenate derived from elk with CWD to determine the potential for transmission and define the clinicopathologic features of disease. Cattle were necropsied if clinical signs occurred or at the termination of experiment (49 months post-inoculation (MPI)). Clinical signs of poor appetite, weight loss, circling, and bruxism occurred in two cattle (14%) at 16 and 17 MPI, respectively. Accumulation of abnormal prion protein (PrP**Sc) in these cattle was confined to the central nervous system with the most prominent immunoreactivity in midbrain, brainstem, and hippocampus with lesser immunoreactivity in the cervical spinal cord. The rate of transmission was lower than in cattle inoculated with CWD derived from mule deer (38%) or white-tailed deer (86%). Additional studies are required to fully assess the potential for cattle to develop CWD through a more natural route of exposure, but a low rate of transmission after intracranial inoculation suggests that risk of transmission through other routes is low. A critical finding here is that if CWD did transmit to exposed cattle, currently used diagnostic techniques would detect and differentiate it from other prion diseases in cattle based on absence of spongiform change, distinct pattern of PrP**Sc deposition, and unique molecular profile.
Last Modified: 08/16/2012
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 ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.
" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.
snip...
----- Original Message -----
From: David Colby
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
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B). SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
PLEASE READ THIS CDC 2012 UPDATE ON CWD RISK FACTORS ;
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).
SNIP...
CWD Zoonotic Potential, Species Barriers, and Strains
Current Understanding of the CWD Species Barrier Strong evidence of zoonotic transmission of BSE to humans has led to concerns about zoonotic transmission of CWD (2,3). As noted above, CWD prions are present nearly ubiquitously throughout diseased hosts, including in muscle, fat, various glands and organs, antler velvet, and peripheral and CNS tissue (2,14,15). Thus, the potential for human exposure to CWD by handling and consumption of infectious cervid material is substantial and increases with increased disease prevalence. Interspecies transmission of prion diseases often yields a species-barrier effect, in which transmission is less efficient compared with intraspecies transmission, as shown by lower attack rates and extended incubation periods (3,28). The species barrier effect is associated with minor differences in PrPc sequence and structure between the host and target species (3). Prion strain (discussed below) and route of inoculation also affect the species barrier (3,28). For instance, interspecies transmission by intracerebral inoculation is often possible but oral challenge is completely ineffective (29). Most epidemiologic studies and experimental work have suggested that the potential for CWD transmission to humans is low, and such transmission has not been documented through ongoing surveillance (2,3). In vitro prion replication assays report a relatively low efficiency of CWD PrPSc-directed conversion of human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are resistant to CWD infection (31); these findings indicate low zoonotic potential. However, squirrel monkeys are susceptible to CWD by intracerebral and oral inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans than squirrel monkeys, are resistant to CWD infection (32). Regardless, the finding that a primate is orally susceptible to CWD is of concern. Interspecies transmission of CWD to noncervids has not been observed under natural conditions. CWD infection of carcass scavengers such as raccoons, opossums, and coyotes was not observed in a recent study in Wisconsin (22). In addition, natural transmission of CWD to cattle has not been observed in experimentally controlled natural exposure studies or targeted surveillance (2). However, CWD has been experimentally transmitted to cattle, sheep, goats, mink, ferrets, voles, and mice by intracerebral inoculation (2,29,33). CWD is likely transmitted among mule, white-tailed deer, and elk without a major species barrier (1), and other members of the cervid family, including reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD infection. Black-tailed deer (a subspecies of mule deer) and European red deer (Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34). Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation (35). Continued study of CWD susceptibility in other cervids is of considerable interest.
Reasons for Caution There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD. Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation. Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified,
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
SOME HISTORY ON THIS ;
ANOTHER COW GOES DOWN WITH CWD IN LAB STUDIES;
Subject: Re: CWD TO CATTLE by inoculation (ok, is it three or four???)

Date: Wed, 11 Dec 2002 23:20:41 +0000
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy
Organization: Netscape Online member
To: BSE-L
References:

Dear Dr Miller,

I have to admit it was difficult to me to believe either....but in the end I just had to realise that it was true.
When I investigated the age at which cattle actually were becoming infected it was shocking to find that the majority were infected under 1 month of age (and many of them seemed to be within the first week, although the data on this was more shakey, and the rest seemed to be infected in a decreasing slope up to the 7th month.
The question was: just how could the cattle be infected simply so young? What also was turning out was that I could not find any obvious sign of multipoint inoculation and it was as if either there was a major dose arriving at one point or not at all. Again the maths on that was difficult but would probably stand up to the logic. These figures could only be certain in the period on either of the feed ban in the UK in 1988: but then again there was no change in the age distrubution after some other factors are removed since that point.
For a long time we had been wondering why, during the epidemic, the age distribution of cases did not change greatly, when the actual amount of infectivity in the total diet of the battle population may have gone up 10,000fold. Surely, if infection was taking place at many points in an animal's life then they would have been becoming younger when dying of disease as the epidemic progressed?..but this was not seen.
So...when you argue that a lamb is unlikely to have been infected naturally at a single point....I think that this is almost certainly incorrect and that they are indeed infected when exceedingly young and probably at a single point. Also I now believe that the amount of infectivity needed to infect these animals is likely to be very low compared with adults when given orally. (this was all published in the British Food Journal in 2001)

Steve Dealler


"Janice M. Miller" wrote:

> ######## Bovine Spongiform Encephalopathy
#########


>
> I did not mean to imply that it wouldn't be possible for an animal to
> consume that amount of material, especially over a lifetime. I was
> merely pointing out that it is unlikely a lamb would be naturally
> exposed to that amount of material at a single time point early in its
> life and therefore such a short incubation period would not be expected
> to occur under non-experimental conditions.
>
> >>> flounder@WT.NET 12/09/02 12:35PM >>>
>
>
> hello Dr. Miller,
>
> i was curious about this statement;
>
> > It was not a true natural exposure, however, because they fed
>
> > the lambs 2-5 grams of infectious brain, which is very likely a
>
> > much larger dose than would occur under natural conditions.
>
> how do you come to the conclusion that 2-5 grams is a
> 'much larger dose than would occur under natural conditions',
> considering 1/2 to 1 gram is lethal for a cow ?
>
> "FDA has determined that each animal could have consumed, at most and
> in
> total, five-and-one-half grams - approximately a quarter ounce -- of
> prohibited material. These animals weigh approximately 600 pounds."
>
> http://www.fda.gov/bbs/topics/news/2001/new00752.html
>
> if we look at these studies, we will find that
> the 5.5 grams would be more than sufficient to
> infect a cow, if the feed was tainted with TSEs...TSS
>
> please read page 4, 5 and 6 of some 53;
>
> Scientific Steering Committee
> ORAL EXPOSURE OF HUMANS TO THE BSE AGENT:
> INFECTIVE DOSE AND SPECIES BARRIER
>
> http://europa.eu.int/comm/food/fs/sc/ssc/out79_en.pdf
>
> 9 DR. BROWN: If I am not mistaken, and I can be
> 10 corrected, I think a half a gram is enough in a cow, orally;
> 11 in other words, one good dietary-supplement pill.
>
> [FULL TEXT ABOUT 600 PAGES]
> 3681t2.rtf
> http://www.fda.gov/ohrms/dockets/ac/cber01.htm
>
> thank you,
>
> kind regards,
> terry
>
> Janice M. Miller wrote:
> >
> > With scrapie it's believed that most infections occur at or
> shortly
> > after birth, either from exposure to placenta from the lamb's own
> > infected dam or from another placent of another infected ewe that is
> > lambing at the same time. There are several experiments reported,
> > however, in which older sheep from scrapie-free flocks have been put
> in
> > contact with lambing ewes from scrapie flocks and transmission has
> > occurred. In these cases the incubation period appears to be
> longer.
> > Recently we heard in England that they have been able to reproduce
> > scrapie within 6 months (an incredibly short incubation period for
> that
> > disease) by oral exposure of 2-week old lambs. It was not a true
> > natural exposure, however, because they fed the lambs 2-5 grams of
> > infectious brain, which is very likely a much larger dose than would
> > occur under natural conditions. The effect of age on incubation
> period
> > may reflect the amount of lymphoid tissue available in the
> intestinal
> > tract of lambs because they experience a significant amount of
> atrophy
> > in that tissue diromg the first year of life. I don't remember
> anyone
> > suggesting that age plays a role in either the success of
> transmissions
> > or incubation periods when sheep are inoculated initracerebrally.
> That
> > seems to depend mostly on infectious titer of the inoculum and the
> > genetics of the recipient sheep.
> > In CWD no one has found any evidence that placenta is
> infectious
> > so the source of infectivity for transmission is unknown. In the
> highly
> > contaminated wildlife research facility at Colorado they lose over
> 90%
> > of their deer by about 2 years of age so it is likely that those
> animals
> > are infected at a very young age. In the wild, however, they are
> > reporting some positive animals that are much older so while there
> might
> > be some development of resistance with age, it certainly isn't
> complete.
> > I don't know that anyone has reported doing experiments where
> CWD-free
> > deer of different ages were put into a contaminated environment to
> see
> > if the transmission rates or incubation periods would be influenced
> by
> > age.
> >
> >
> >>>>taotm@EARTHLINK.NET 11/26/02 08:24AM >>>
> >>>
> >
> > Dr. Miller,
> >
> > About a year ago there was a report of from a Colorado DoW staffer
> who
> > recalled seeing scrapie sheep in
> > pens near the sickly-looking deer at the Ft. Collins research
> facility.
> > Although there's some debate about
> > whether those sheep actually had scrapie, given the results of the
> > intercerebral tests-- "... The other
> > sheep, necropsied 35 months after inoculation, showed clinical signs
> > and histopathologic lesions that were
> > indistinguishable from scrapie..."-- has there been any attempt to
> > recreate the alleged conditions at Ft.
> > Collins? In other words, an environmental test where scrapie sheep
> > would be put in close proximity to
> > healthy deer? Clearly there's a huge questions about the mechanics
> of
> > jumping the species barrier. But is
> > it possible that this was the way the CWD prion fire was initially
> lit?
> > Farmed sheep to wild cervids?
> >
> > Also, have there been any tests looking at the age at which an
> animal
> > becomes infected? Are younger,
> > smaller animals more at risk? Does the same dose of infectious
> material
> > as given an adult affect them
> > faster or more intensely?
> >
> > thank you,
> >
> > Janet Ginsburg
> >
> > "Terry S. Singeltary Sr." wrote:
> >
> >>hello Janice,
> >>
> >>many thanks for this update.
> >>
> >> > we do not know if the CWD agent in white-tailed deer
> >> > would be equivalent to that obtained from mule deer.
> >>
> >>i was just reading some data where it states;
> >>
> >>Although few white tailed deer were available for biopsy,
> >>findings were consistent with those in mule deer and
> >>support similarity in lymphoid accumulation of PrPCWD
> >>between the species that has been observed post-mortem.
> >>However, because PrPCWD does not appear to accumulate
> >>in lymphoid tissue to the same degree in elk as deer
> >>(T.R. Spraker, unpublished data)
> >>
> >>i am confused?
> >>
> >>thank you,
> >>kind regards,
> >>
> >>terry
> >>
> >>Janice M. Miller wrote:
> >>
> >
> >>> The statement that 4 cattle have developed evidence of CWD
> >>
> > transmission
> >
> >>>following intracerebral inoculation is correct because an
> >>
> > additional
> >
> >>>animal has been found prion positive subsequent to the 2001 paper
> >>
> > that
> >
> >>>presented preliminary findings after only 2 and a half years of
> >>>observation. Following this message is a summary of the current
> >>
> > status
> >
> >>>of our CWD cross-species transmission experiments in cattle and
> >>
> > sheep.
> >
> >>>This information was prepared in anticipation of questions about
> >>
> > these
> >
> >>>studies that we expected would be raised at the recent annual
> >>
> > meeting of
> >
> >>>the U.S. Animal Health Association.
> >>> I would like to correct one statement in the newspaper
> >>
> > article
> >
> >>>that was attributed to me that is in error. I did not imply that
> >>
> > our
> >
> >>>work thus far could be extrapolated to the situation with
> >>
> > white-tailed
> >
> >>>deer and dairy cattle. While there is no indication that there
> >>
> > should
> >
> >>>be any difference in susceptibility of beef versus dairy cattle, we
> >>
> > do
> >
> >>>not know if the CWD agent in white-tailed deer would be equivalent
> >>
> > to
> >
> >>>that obtained from mule deer. For that reason Dr. Hamir is now
> >>>repeating the original experiment in cattle with brain suspension
> >>
> > from
> >
> >>>affected white-tails as inoculum.
> >>>
> >>>Experimental Transmission of Chronic Wasting Disease (CWD) to
> >>
> > Cattle
> >
> >>>and Sheep
> >>>Progress report - October 15, 2002
> >>>
> >>>Transmission of CWD (mule deer) to cattle:
> >>>
> >>>Background:
> >>>In 1997, 13 calves were inoculated intracerebrally with brain
> >>>suspension from mule deer naturally affected with CWD. During the
> >>
> > first
> >
> >>>3 years, 3 animals were euthanized 23, 24, and 28 months after
> >>>inoculation because of weight loss (2) or sudden death (1).
> >>
> > Although
> >
> >>>microscopic examination of the brains did not show classical
> >>
> > lesions of
> >
> >>>transmissible spongiform encephalopathy (TSE), a specific TSE
> >>
> > marker
> >
> >>>protein, PrPres, was detected by immunohistochemistry (IHC) and
> >>
> > western
> >
> >>>blot . Detailed information on these animals has been published
> >>>previously (A Hamir et al., J Vet Diagn Invest 13: 91-96, 2001).
> >>>
> >>>Update:
> >>>During the 3rd and 4th years of observation, 5 additional animals
> >>
> > have
> >
> >>>been euthanized because of health concerns (primarily chronic joint
> >>
> > and
> >
> >>>foot problems). Although all tests for PrPres are not complete,
> >>
> > IHC
> >
> >>>results indicate that 1 of these animals, necropsied 59 months
> >>
> > after
> >
> >>>inoculation, was positive for PrPres. This animal (# 1746) had not
> >>
> > been
> >
> >>>eating well for approximately 1 week prior to being found
> >>
> > recumbent. At
> >
> >>>necropsy, significant gross lesions consisted of an oblique
> >>
> > fracture of
> >
> >>>L1 vertebral arch with extension into the body, and moderate
> >>
> > multifocal
> >
> >>>hemorrhagic ulceration in the abomasum. Microscopic examination
> >>
> > of
> >
> >>>brain revealed a few isolated neurons with single or multiple
> >>
> > vacuoles,
> >
> >>>but neither neuronal degeneration nor gliosis was observed. IHC
> >>>revealed the presence of PrPres in sections from several areas of
> >>
> > the
> >
> >>>brain.
> >>>
> >>>Summary of findings on this case and data from previous animals:
> >>>
> >>> Necropsy Survival Disease Clinical
> >>>Histo- IHC SAF WB
> >>> No. Route date period course signs
> >>
> > pathology
> >
> >>>________________________________________________________________
> >>>
> >>>1745 i/c 8/18/99 23m 2m +
> >>>+/- + - +
> >>>
> >>>1768 i/c 9/22/99 24m 3m +
> >>>+/- + + +
> >>>
> >>>1744 i/c 1/29/00 28m 3d ±
> >>>- + + +
> >>>
> >>>1749 i/c 5/20/01 44m NA -
> >>> - - NT NT
> >>>
> >>>1748 i/c 6/27/01 45m NA -
> >>>- - NT NT
> >>>
> >>>1743 i/c 8/21/02 59m NA -
> >>>- - Pending Pending
> >>>
> >>>1741 i/c 8/22/02 59m NA -
> >>>- - Pending Pending
> >>>
> >>>1746 i/c 8/27/02 59m 7d ±
> >>>+/- + Pending Pending
> >>>
> >>>NT = not tested; IHC = immunohistochemistry for PrPres; SAF =
> >>
> > scrapie
> >
> >>>associated fibrils; NA = not applicable; WB = Western blot
> >>>(Prionics-Check); + = lesions or antigen present; - = lesions or
> >>>antigen absent; ± = signs/lesions equivocal; i/c = intracerebral;
> >>
> > m =
> >
> >>>months; d = days.
> >>>
> >>>Summary:
> >>>After 5 years of observation we have 4 CWD transmissions to cattle
> >>
> > from
> >
> >>>a group of 13 inoculates. These animals, which were necropsied 23,
> >>
> > 24,
> >
> >>>28, and 59 months after inoculation, did not show the clinical
> >>
> > signs or
> >
> >>>histopathologic lesions typical of a TSE, but PrPres was detected
> >>
> > in
> >
> >>>brain samples. Four other animals that were necropsied during the
> >>
> > 4th
> >
> >>>and 5th years of observation have not shown evidence of prion
> >>
> > disease
> >
> >>>(although not all tests are complete) and the 5 remaining cattle
> >>
> > are
> >
> >>>apparently healthy. Note that this study involved direct
> >>
> > intracerebral
> >
> >>>inoculation of cattle with the CWD agent, which is an unnatural
> >>
> > route of
> >
> >>>exposure. It is likely that transmission by a more natural route,
> >>
> > such
> >
> >>>as oral exposure, would be much more difficult to accomplish.
> >>
> > Cattle
> >
> >>>have been inoculated orally at the University of Wyoming with the
> >>
> > same
> >
> >>>inoculum used for this experiment, and 5 years into the study
> >>
> > these
> >
> >>>animals remain healthy.
> >>>
> >>>
> >>>Experimental Transmission of CWD (mule deer) to sheep
> >>>
> >>>Eight Suffolk sheep from the NADC scrapie-free flock were
> >>
> > inoculated
> >
> >>>intracerebrally with the CWD brain suspension used to inoculate
> >>
> > cattle.
> >
> >>>PRNP genotyping showed that 4 of the sheep were QQ at codon 171 and
> >>
> > the
> >
> >>>other four were QR. Two of the QQ sheep were euthanized during the
> >>
> > 3rd
> >
> >>>year of observation. At necropsy one of these animals had a
> >>
> > urethral
> >
> >>>obstruction and PrPres was not detected in brain or lymphoid
> >>
> > tissues.
> >
> >>>The other sheep, necropsied 35 months after inoculation, showed
> >>
> > clinical
> >
> >>>signs and histopathologic lesions that were indistinguishable from
> >>>scrapie. IHC tests showed typical PrPres accumulations in brain,
> >>>tonsil, and some lymph nodes. The 2 remaining QQ sheep and all 4
> >>
> > QR
> >
> >>>sheep are apparently healthy 39 months after inoculation.
> >>>
> >>>Summary:
> >>>After 3 years of observation we have 1 transmission of CWD to a 171
> >>
> > QQ
> >
> >>>sheep. This animal, which was necropsied 35 months after
> >>
> > inoculation,
> >
> >>>showed clinical signs and histopathologic lesions that were
> >>>indistinguishable from scrapie. Another QQ sheep that was
> >>
> > necropsied
> >
> >>>during the 3rd year showed no evidence of prion disease and all
> >>>remaining sheep (2 QQ and 4 QR) are apparently healthy.
> >>>
> >>>
> >>>>>>flounder@WT.NET 11/23/02 06:54PM >>>
> >>>>>>
> >>>
> >>>1: J Vet Diagn Invest 2001 Jan;13(1):91-6
> >>>
> >>>Preliminary findings on the experimental transmission of chronic
> >>>wasting
> >>>disease agent of mule deer to cattle.
> >>>
> >>>Hamir AN, Cutlip RC, Miller JM, Williams ES, Stack MJ, Miller MW,
> >>>O'Rourke KI, Chaplin MJ.
> >>>
> >>>National Animal Disease Center, ARS, USDA, Ames, IA 50010, USA.
> >>>
> >>>To determine the transmissibility of chronic wasting disease (CWD)
> >>
> > to
> >
> >>>cattle and to provide information about clinical course, lesions,
> >>
> > and
> >
> >>>suitability of currently used diagnostic procedures for detection
> >>
> > of
> >
> >>>CWD
> >>>in cattle, 13 calves were inoculated intracerebrally with brain
> >>>suspension from mule deer naturally affected with CWD. Between 24
> >>
> > and
> >
> >>>27
> >>>months postinoculation, 3 animals became recumbent and were
> >>>euthanized.
> >>>Gross necropsies revealed emaciation in 2 animals and a large
> >>>pulmonary
> >>>abscess in the third. Brains were examined for protease-resistant
> >>>prion
> >>>protein (PrP(res)) by immunohistochemistry and Western blotting
> >>
> > and
> >
> >>>for
> >>>scrapie-associated fibrils (SAFs) by negative-stain electron
> >>>microscopy.
> >>>Microscopic lesions in the brain were subtle in 2 animals and
> >>
> > absent
> >
> >>>in
> >>>the third case. However, all 3 animals were positive for PrP(res)
> >>
> > by
> >
> >>>immunohistochemistry and Western blot, and SAFs were detected in 2
> >>
> > of
> >
> >>>the animals. An uninoculated control animal euthanized during the
> >>
> > same
> >
> >>>period did not have PrP(res) in its brain. These are preliminary
> >>>observations from a currently in-progress experiment. Three years
> >>>after
> >>>the CWD challenge, the 10 remaining inoculated cattle are alive
> >>
> > and
> >
> >>>apparently healthy. These preliminary findings demonstrate that
> >>>diagnostic techniques currently used for bovine spongiform
> >>>encephalopathy (BSE) surveillance would also detect CWD in cattle
> >>>should
> >>>it occur naturally.
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11243374&dopt=Abstract
>
> >>>Sat, Nov 23, 2002
> >>>
> >>>Scientists unsure if CWD can jump species
> >>>
> >>>By Jessica Bock
> >>>Wausau Daily Herald
> >>>jbock@wdhprint.com
> >>>
> >>>snip...
> >>>
> >>>Janice Miller, a veterinarian in charge of the experiment, said
> >>
> > she
> >
> >>>believes previous research shows it is hard for the disease to be
> >>>transmitted naturally from whitetail deer to dairy cattle.
> >>>"Our study says nothing of how it could be transmitted in natural
> >>>surroundings," she said.
> >>>
> >>>Miller has been studying the transmission of CWD from mule deer to
> >>>cattle since 1997. Since then, chronic wasting disease was
> >>
> > transmitted
> >
> >>>to four out of 13 cattle injected with brain tissue from naturally
> >>>infected mule deer, she said.
> >>>
> >>>In Wyoming, Williams has been studying cattle that were given a
> >>>concoction of diseased brain tissue orally, and five years into
> >>
> > the
> >
> >>>study the animals remain healthy, Miller said.
> >>>No one knows if chronic wasting disease could ever spread to
> >>
> > another
> >
> >>>species through natural surroundings.
> >>>
> >>>"Our experience is that it's pretty hard to predict," Miller said.
> >>>
> >>>http://www.wausaudailyherald.com/wdhlocal/277564794712612.shtml
> >>>
> >>>greetings list,
> >>>
> >>> > Since then, chronic wasting disease was
> >>>
> >>> > transmitted to four out of 13 cattle
> >>>
> >>>is this a typo by the media or has another cow gone down
> >>>with CWD since the preliminary findings were found?
> >>>
> >>>TSS
=======================================================
-------- Original Message --------
Subject: Re: CWD TO CATTLE by inoculation (ok,is it three or four OR NOW FIVE???)
Date: Mon, 23 Jun 2003 12:36:59 –0500
From: "Janice M. Miller"
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
I am happy to provide an update on the experimental inoculation of cattle and sheep with CWD. These are ongoing experiments and updates are normally provided via presentations at meetings. Dr. Hamir has prepared a poster of the following information that will be displayed at 4 upcoming meetings this summer and fall.
Experimental Transmission of Chronic Wasting Disease (CWD) to Cattle and Sheep Progress report - June 23, 2003
Experimental Transmission to Cattle
Background: In 1997, 13 calves were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD. During the first 3 years, 3 animals were euthanized 23, 24, and 28 months after inoculation because of weight loss (2) or sudden death (1). Although microscopic examination of the brains did not show classical lesions of transmissible spongiform encephalopathy (TSE), a specific TSE marker protein, PrPres, was detected by immunohistochemistry (IHC) and western blot. Detailed information on these animals has been published previously (A Hamir et al., J Vet Diagn Invest 13: 91-96, 2001).
Update: During the 3rd, 4th and 6th years of observation, 7 additional animals have been euthanized due to a variety of health concerns (primarily chronic joint and foot problems). IHC and western blot results indicate that 2 of these animals, necropsied 59 and 63 months after inoculation, were positive for PrPres. One animal (# 1746) had not been eating well for approximately 1 week prior to being found recumbent. At necropsy, significant gross lesions consisted of an oblique fracture of L1 vertebral arch with extension into the body, and moderate multifocal hemorrhagic ulceration in the abomasum. Microscopic examination of brain revealed a few isolated neurons with single or multiple vacuoles, but neither neuronal degeneration nor gliosis was observed. IHC revealed the presence of PrPres in sections from several areas of the brain. The other PrPres positive animal (#1742) was euthanized after being found in lateral recumbency with a body temperature of 104.6 F. It had not shown prior clinical signs except for some decreased appetite for 2 days. Necropsy revealed only moderate hepatitis and a small renal infarct due to intravascular thrombosis.
Summary of findings on all necropsied animals to date:
Ear tag Date of Survival Disease Clinical Histo- IHC WB no. necropsy period course signs pathology _____________________________________________________________________ 1745 8/18/99 23m 2m + +/- + + 1768 9/22/99 24m 3m + +/- + + 1744 1/29/00 28m 3d +/- - + + 1749 5/20/01 44m NA - - - - 1748 6/27/01 45m NA - - - - 1743 8/21/02 59m NA - - - - 1741 8/22/02 59m NA - - - - 1746 8/27/02 59m 7d +/- +/- + + 1765 11/27/02 62m 1d +/- +/- - - 1742 12/28/02 63m 2d +/- - + + NT = not tested; IHC = immunohistochemistry for PrPres; SAF = scrapie associated fibrils; NA = not applicable; WB = Western blot (Prionics-Check); + = lesions or antigen present; - = lesions or antigen absent; +/- = signs/lesions equivocal; i/c = intracerebral; m = months; d = days.
Summary: After 5.75 years of observation we have 5 CWD transmissions to cattle from a group of 13 inoculates. These animals, which were necropsied 23, 24, 28, 59, and 63 months after inoculation, did not show the clinical signs or histopathologic lesions typical of a TSE, but PrPres was detected in brain samples by both immunohistochemistry and western blot. Five other animals necropsied during the 4th, 5th and 6th years of observation have not shown evidence of PrPres and the remaining 3 cattle are apparently healthy. Note that this study involved direct intracerebral inoculation of cattle with the CWD agent, which is an unnatural route of exposure. Likely, it would be more difficult to infect cattle by the oral route. Cattle have been inoculated orally at the University of Wyoming with the same inoculum used in this experiment, and 5.75 years into the study the animals remain healthy (personal communication, Dr. Beth Williams).
Experimental Transmission of CWD to sheep
Eight Suffolk sheep from the NADC scrapie-free flock were inoculated intracerebrally with the CWD brain suspension used to inoculate cattle. PRNP genotyping showed that 4 of the sheep were QQ at codon 171 and the other four were QR. Two of the QQ sheep were euthanized during the 3rd year of observation. At necropsy one of these animals had a urethral obstruction and PrPres was not detected in brain or lymphoid tissues. The other sheep, necropsied 35 months after inoculation, showed clinical signs and histopathologic lesions that were indistinguishable from scrapie. IHC tests showed typical PrPres accumulations in brain, tonsil, and some lymph nodes. The 2 remaining QQ sheep and all 4 QR sheep are apparently healthy 47 months after inoculation.
Summary: After 4 years of observation we have 1 transmission of CWD to a 171 QQ sheep. This animal, which was necropsied 35 months after inoculation, showed clinical signs and histopathologic lesions that were indistinguishable from scrapie. Another QQ sheep that was necropsied during the 3rd year showed no evidence of prion disease and all remaining sheep (2 QQ and 4 QR) are apparently healthy.
-------- Original Message --------
Subject: Re: CWD TO CATTLE by inoculation (ok, is it three or four OR NOW FIVE???)
Date: Mon, 23 Jun 2003 09:25:27 –0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
Greetings List Members,
i hear now that a 5th cow has gone done with CWD from the studies of Amir Hamir et al. will Dr. Miller please confirm or deny this please, and possibly explain why this has not made the news, if in fact this is the case?
seems these cows infected with CWD/TSE did not display the usual BSE symptoms. i wonder how many more are out there in the field? course, we will never know unless someone starts rapid TSE/BSE testing in sufficient numbers to find...
thank you, kind regards, terry
Date: Sat, 23 Nov 2002 18:54:49 -0600 Reply-To: BSE Sender: BSE From: "Terry S. Singeltary Sr." Subject: CWD TO CATTLE by inoculation (ok, is it three or four???)
1: J Vet Diagn Invest 2001 Jan;13(1):91-6
Preliminary findings on the experimental transmission of chronic wasting disease agent of mule deer to cattle.
Hamir AN, Cutlip RC, Miller JM, Williams ES, Stack MJ, Miller MW, O'Rourke KI, Chaplin MJ.
National Animal Disease Center, ARS, USDA, Ames, IA 50010, USA.
To determine the transmissibility of chronic wasting disease (CWD) to cattle and to provide information about clinical course, lesions, and suitability of currently used diagnostic procedures for detection of CWD in cattle, 13 calves were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD. Between 24 and 27 months postinoculation, 3 animals became recumbent and were euthanized. Gross necropsies revealed emaciation in 2 animals and a large pulmonary abscess in the third. Brains were examined for protease-resistant prion protein (PrP(res)) by immunohistochemistry and Western blotting and for scrapie-associated fibrils (SAFs) by negative-stain electron microscopy. Microscopic lesions in the brain were subtle in 2 animals and absent in the third case. However, all 3 animals were positive for PrP(res) by immunohistochemistry and Western blot, and SAFs were detected in 2 of the animals. An uninoculated control animal euthanized during the same period did not have PrP(res) in its brain. These are preliminary observations from a currently in-progress experiment. Three years after the CWD challenge, the 10 remaining inoculated cattle are alive and apparently healthy. These preliminary findings demonstrate that diagnostic techniques currently used for bovine spongiform encephalopathy (BSE) surveillance would also detect CWD in cattle should it occur naturally.
Sat, Nov 23, 2002
Scientists unsure if CWD can jump species
By Jessica Bock Wausau Daily Herald jbock@wdhprint.com
snip...
Janice Miller, a veterinarian in charge of the experiment, said she believes previous research shows it is hard for the disease to be transmitted naturally from whitetail deer to dairy cattle. "Our study says nothing of how it could be transmitted in natural surroundings," she said.
Miller has been studying the transmission of CWD from mule deer to cattle since 1997. Since then, chronic wasting disease was transmitted to four out of 13 cattle injected with brain tissue from naturally infected mule deer, she said.
In Wyoming, Williams has been studying cattle that were given a concoction of diseased brain tissue orally, and five years into the study the animals remain healthy, Miller said. No one knows if chronic wasting disease could ever spread to another species through natural surroundings.
"Our experience is that it's pretty hard to predict," Miller said.
greetings list,
> Since then, chronic wasting disease was
> transmitted to four out of 13 cattle
is this a typo by the media or has another cow gone down with CWD since the preliminary findings were found?
TSS
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease in the United States
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
Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. The purpose of these experiments was to determine susceptibility of white-tailed deer (WTD) to scrapie and to compare the resultant clinical signs, lesions, and molecular profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate.
All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer that was necropsied at 15.6 months had widespread distribution of PrPSc highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues prior to the onset of clinical signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues.
The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
After a natural route of exposure, 100% of WTD were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
PO-041: Susceptibility of domestic cats to CWD infection
Amy Nalls, Jeanette Hayes-Klug, Kelly Anderson, Davis Seelig, Kevin Carnes, Susan Kraft, Edward Hoover, Candace Mathiason
Colorado State University; Fort Collins, CO USA
Domestic and non-domestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE); very likely due to consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain homogenate.
Between 40 and 43 months two IC-inoculated cats developed slowly progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors, and ataxia”’ultimately mandating euthanasia. PrPCWD was detected in the brains of these animals by western blot, immunohistochemistry (IHC), and quaking-induced conversion (RT-QuIC) assays. No clinical signs of TSE were detected in the remaining primary passage cats at 86 months pi. Feline-adapted CWD (FelCWD) was sub-passaged into groups (n = 4 or 5) of cats by IC, PO, and IP/SQ routes.
All 5 IC inoculated cats developed symptoms of disease 20–24 months pi (approximately half the incubation period of primary passage). Additional symptoms in these animals included increasing aggressiveness and hyper responsiveness. FelCWD was demonstrated in the brains of all the affected cats by western blot and IHC. Currently, 3 of 4 IP/SQ, and 1 of 4 PO inoculated cats have developed abnormal behavior patterns consistent with the early stage of feline CWD. Magnetic resonance imaging (MRI) has been performed on 11 cats (6 clinically ill, 2 asymptomatic, and 3 age-matched negative controls). Abnormalities were detected in 4 of 6 clinically ill cats and included multifocal signal changes consistent with inflammation, ventricular size increases, more prominent sulci, and white matter tract cavitation.
These results demonstrate that CWD can be transmitted and adapted to the domestic cat, and raise the potential for cervid-to-feline transmission in nature.
SEE ;
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more