Tuesday, September 01, 2015

The Treatment of Game Animals as Livestock in Michigan: Fiscal and Regulatory Issues October 5, 2010 and CWD

MEMORANDUM

Tuesday, October 5, 2010

Interested Parties '

 
FROM: William E. Hamilton, Senior Fiscal Analyst

 
RE: The Treatment of Game Animals as Livestock in Michigan: Fiscal and Regulatory Issues

 
State Regulatory Authority over the Livestock Industry

 
According to data reported by the United States Department of Agriculture (USDA) Economic Research Service, the gross value of Michigan agricultural sector outputs in 2008 was $7.654 billion. Of that amount, $2.548 billion, approximately one-third, represented sales of livestock and animal products.1

 
One of the biggest threats to livestock and commercial animal production is disease? Livestock are susceptible to a number of diseases which can reduce productivity or result in animal death. Some diseases of livestock, zoonotic diseases such as rabies and influenza, can be transmitted to humans.

 
Michigan state government has supported agriculture almost from the inception of Michigan as a state.' One of the most important elements in that state support has been the control and eradication livestock disease. Public Act 182 of 1885 established a State Livestock Sanitary Commission and provided for the appointment of a state veterinary surgeon. The act stated that "it shall be the duty of the commission to protect the health of the domestic animals of the state from all contagious or infectious diseases of a malignant character, and for this purpose it is hereby authorized and empowered to establish, maintain and enforce such quarantine, sanitary and other regulations as it may deem necessary. "

 
Public Act 181 of 1919 abolished the State Live Stock Sanitary Commission, established a state Department of Animal Industry, and provided for the appointment of a Commissioner of Animal Industry and a State Veterinarian. The 1919 act was similar to the 1885 act in that it provided for the Commissioner of Animal Industry to have "general charge and oversight of the protection of the health of the domestic animals of the state and the guarding of the same from all contagious or infectious diseases." The 1919 act also provided for the use of "quarantine, sanitary and other regulations as may be deemed necessary."

 
The 1919 act was subsequently repealed and replaced with the Animal Industry Act, Public Act 466 of 1988. The stated intent of the Animal Industry Act is to ''protect the health, safety, and welfare of humans and animals. 11 The act provides for the appointment of a State Veterinarian within the Department of Agriculture, I This data was obtained from a document on the USDA Economic Research Service website, State Fact Sheets: Michigan updated July 30, 2010. In addition to the $2.548 billion related to animal industry, the $7.654 billion figure included crop output of $4.074 billion, as well as agriculture services and forestry product sales of $1.032 billion. With minor exceptions, the data in the State Fact Sheet document is the same as that presented in the Farm Economics section of Michigan Agricultural Statistics 2008-2009, a collaborative effort of the USDA's National Agricultural Statistics Service (NASS), the Michigan Department of Agriculture, and Michigan State University.

 
2 Diseases of livestock can have a catastrophic impact on the agricultural economy. One example of a high-impact disease is foot and mouth disease (FMD). According to an analysis by the Congressional Research Service (CRS), there have been nine outbreaks of FMD in the United States since 1870, "each time the disease was eradicated with strict slaughter and quarantine control procedures." The report also indicates that the most serious of those outbreaks, in 1914, originated in Michigan. The disease then spread to 22 states after it gained entry to the Chicago stockyards. Although the last outbreak of FMD in the United State was in California in 1929, FMD has appeared more recently in other counties, notably in Great Britain in 2001 and 2007, and currently in Japan. Source: CRS Report for Congress "Foot and Mouth Disease: A Threat to U. S. Agriculture." April, 16,2001, and "Disease Threatens Japan's Beef Trade," New York Times, July 11,2010.

 
3 As one example, the Michigan Constitution of 1850 provided for the establishment of a state college of agriculture. A state agricultural school, which subsequently became Michigan State University, was established in 1855.

 
snip...

 
Summary

 
Beginning in the mid-1990s, Michigan law began to recognize the privately owned cervid industry as an agricultural enterprise, and conveyed on the industry benefits enjoyed by traditional agricultural enterprises - protection from nuisance lawsuits and exemption from some local zoning restrictions under the Right to F arm Act, indemnification for diseased animals killed under the authority of the Animal Industry Act, and shelter from certain property taxes under the General Property Tax Act and the MNREPA.

 
The cervid industry differs from traditional agricultural activities in that its economic benefit is not primarily food or fiber, but rather in the hunting experience - in particular trophy deer and elk. While the commercial cervid industry undoubtedly contributes to the Michigan economy, there are also economic externalities associated with the industry - primarily the risk of disease occurring in privately held cervid herds and subsequent transmission to the free ranging deer population or to domestic cattle. Those risks have driven the state regulatory program."

 
15 The 2005 Risk-based Audit of the Captive/Privately owned Cervid Industry in Michigan included a discussion of some risks associated with the privately owned cervid industry. An extended quotation from that Audit is included as Appendix I of this analysis.

 
Treatment of Game Animals as Livestock in Michigan October 5, 2010

 
Page 9 of 10

 
As noted in the above analysis, regulatory fees established under the Cervidae Act have not covered the costs of the state regulatory program; they represent approximately 7% of on-going program costs for the seven- year period ending September 30, 2009, exclusive of indemnification payments. In fact, over that seven-year period, fee revenue was less than the amount of indemnification payments to cervid owners for destruction of diseased deer.

 
Because regulatory fees established in the Cervidae Act to do not provide sufficient revenue to maintain the regulatory and inspection programs mandated by the act, the shortfall has been made up with state General Fund revenue. With regard to the MDA, the use of General Fund revenue for the cervid regulatory program has effectively reduced General Fund support for other MDA Animal Health and Welfare activities. Those programs eliminated or significantly reduced include MDA regulatory activities related to pet shops, dog pounds, animal shelters, aquaculture, livestock dealers, and riding stables.

 
Given reductions in available state General Fund revenue, the Legislature may reduce funding for privately- owned cervidae regulatory and inspection programs. However, at reduced funding levels, it is unlikely that the MDA and the DNR could effectively perform the regulatory activities currently mandated by the Cervidae Act.

 
Sources

 
The following is a list of additional information on state recognition of the captive cervid industry as an agricultural enterprise, and related issues:

 
Analysis on the Michigan Legislature website of the Cervidae Ac4 Public Act 190 of 2000 For the original legislative analysis of House Bill 4427 of the 1999-2000 Legislative Session http://legislature.mi.gov/doc.aspx?1999-HB-4427

 
For analysis of the 2006 amendments in House Bill 6245 of the 2005-2006 Legislative Session

 
http://legislature.mi.gov/doc.aspx?2006-HB-6245

 
House Fiscal Agency Website House Fiscal Agency March 2005 Analysis of the Cervidae Act

 
http://www.house.mi.gov/hfa/PDFs/cervidae%20memo.pdf

 
House Fiscal Agency June 2008 Analysis of the Fiscal Impact of Pseudorabies and Feral Swine

 
http://www.house.mi.gov/hfa/PDFs/pseudorabies.pdf

 
Treatment of Game Animals as Livestock in Michigan October 5,2010

 
Page 10 of 10

 
APPENDIX I

 
Discussion of CWD from the 2005 Risk-Based Audit

 
Chronic Wasting Disease (CWD) is a naturally occurring progressive nervous system disorder disease of certain North American deer. It is apparently similar to other diseases such as BSE (Mad Cow Disease) and Scrapie Disease of sheep.

 
On March 10, 2005, the DNR released an audit of cervid livestock facilities. The audit, A Risk-based Audit of the Captive/Privately owned Cervid Industry in Michigan, was one of the recommendations of the Governor's CWD Task Force.

 
In discussing the risks associated with transmission of CWD in the captive cervid industry, the report stated that, "Practices which concentrate animals (such as baiting, and feeding, or maintenance in captivity) likely increase transmission rates." Although the report acknowledged that risk of human infection, if any, is low, it does note that "concern has arisen that the disease might be capable of infecting humans." Subsection 1.2.3 of the report, Relevance, further describes CWD risks as follows:

 
"CWD is contagious, and epidemics of the disease are self-sustaining in both CIP-O [i.e. captive privately owned cervids} and free-ranging deer and elk (Miller and Wild 2004; Miller et al. 1998, 2000). Currently the geographic distribution of CWD in free-ranging cervids is relatively limited and the natural rate of expansion has been slow (Williams et al. 2002). Nevertheless, there are concerns, and in the opinion of some, evidence (Nebraska Game and Parks Commission 2002; . Williams et al. 2002), that CWD can be spread much more widely and rapidly with human assistance, through movement of live animals or carcasses. Given CWD 's known persistence in the environment (Miller et al. 2004), its ability to infect over 80% of the animals in a WTD [white tail deer} herd within four years of initial exposure (Miller and Wild 2004), its high probability of becoming established once it has been introduced into a population (Miller and Williams 2003), and disease models which project high rates of death in affected populations (Gross and Miller 2001), concern for risks to the health of both C/P-O and free-ranging Michigan cervids is clearly warranted. Introduction into Michigan's C/P-OC population would result in substantial costs to producers due to quarantines and loss of sales, and indemnity costs for government. The importance of free-ranging deer and elk to both the culture and economy (Joly et al. 2003) and the threat of unsubstantiated human health concerns about CWD eroding public participation in hunter harvest (Williams et al. 2002) make the potential consequences of CWD introduction even more grave. In short, CWD clearly has the potential to impair the long-term viability of both cervid farming and wildlife management in Michigan. "

 
Although the audit, in accordance with the CWD Task Force mandate, was specific to CWD risk, the problems noted in the audit could also increase the risk of transmission of other diseases. The entire 2005 report, A Risk-based Audit of the Captive/Privately owned Cervid Industry in Michigan is available from the Michigan.gov website at http://www.michigan.gov/dnr/0,1607,7-153-10370_12150---,00.html

 
http://www.house.mi.gov/hfa/Archives/PDF/animal_industry(pub_v2).pdf

 
Thursday, August 06, 2015

 
Michigan DNR confirms third deer positive for CWD; hunter participation is critical this fall

 
http://chronic-wasting-disease.blogspot.com/2015/08/michigan-dnr-confirms-third-deer.html

 
Friday, July 17, 2015

 
Michigan confirms CWD in second free-ranging white-tailed deer

 
http://chronic-wasting-disease.blogspot.com/2015/07/michigan-confirms-cwd-in-second-free.html

 
Tuesday, May 26, 2015

 
Michigan confirms state's first case of chronic wasting disease in free-ranging white-tailed deer

 
http://chronic-wasting-disease.blogspot.com/2015/05/michigan-confirms-states-first-case-of.html

 
CWD Update Chronic Wasting Disease Eradication Program Provided by the Animal Industry Division Michigan Department of Agriculture September 5, 2008

 
Background: The Michigan departments of Agriculture (MDA) and Natural Resources (DNR) confirmed the state’s first case of Chronic Wasting Disease (CWD) in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County on Monday, August 25, 2008. The state quarantined all POC facilities, prohibiting the movement of all – dead or alive – privately-owned deer, elk, or moose. Officials do not yet know how the deer may have contracted the disease. To date, there is no evidence that CWD presents a risk to humans or to animals other than cervids. MDA Actions: The state-wide quarantine on all privately owned cervid facilities is still in place. Facilities may continue to hold shooting events, but all carcasses* must be held until testing clears the animal/or the quarantine is released. A clarification to the quarantines was published and distributed to law enforcement officials, stakeholders and other interested parties. A questions and answers sheet is available under the livestock link on the www.michigan.gov/chronicwastingdisease website.

 
The test results from the Kent County cervid breeding facility, where the index case was confirmed, found no additional diseased deer. Epidemiologists are reviewing taxidermy records on a facility related to the index case. Taxidermy operations must be licensed and operators must follow Michigan requirements when conducting business with hunters who have harvested animals from other states. Current Michigan law prohibits the import of free-ranging deer or elk carcasses from states or provinces with CWD. Only de-boned meat, antlers, antlers attached to a scull cap cleaned of all brain and muscle tissue, hides and upper canine teeth may be brought into Michigan. A person that is notified by mail or other means, that a carcass imported into Michigan tested positive for CWD must notify the Michigan DNR.

 
The first tier of traces from the index facility led to five facilities: three in Kent County, one in Montcalm County, and one in Osceola County. These facilities were quarantined by MDA. Records of sales and purchases have been reviewed and have revealed that two facilities received deer from the index case. Four deer from these two facilities were 2 euthanized, samples were tested at MSU’s DCPAH and were found to be negative on Thursday, September 04, 2008. One of the five facilities in tier one, also a Kent County facility conducts a taxidermy operation on the premises. Taxidermy is of great concern because infectious prions in the bones and spinal tissue of the carcass from CWD positive states can infect deer on the facility. MDA, DNR and USDA staff are investigating the records of the taxidermy operation. The second tier investigation to this point, has quarantined four facilities in Bay, Kent, Mecosta, and Saginaw counties. These facilities only sold to the tier one facilities and did not receive anything. They are quarantined as terminal operations and any deer that die, are culled, or shot for sport must be submitted for CWD testing. POC Facilities Quarantined: All POC facilities, except those that only have reindeer, are under quarantine in Michigan until the disease investigation is complete. Epidemiologists are developing a policy for records review and release of quarantines based on management practices and risk.

 
Disease Surveillance Table: Index facility Depopulated Tier 1 Tier 2 1 Entire index herd tested negative 5 herds 2 trace outs (four test-negative animals) 3 trace ins 4 none of these 4 facilities trace directly to the index facility DNR Actions: The ban on all baiting and feeding of deer and elk in the Lower Peninsula is in effect. MSU’s Product Center for Agriculture Development is taking calls from bait growers/sellers. The Center is using Michigan Market Maker, an interactive mapping system that connects Agriculture processors and businesses with Michigan growers and marketers. http://mi.marketmaker.uiuc.edu/ Information on the baiting and feeding ban is available on the CWD page of the Emerging Diseases website. A mandatory deer check for hunters who take a deer within the Kent County townships of Tyrone, Solon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield, and Cannon, is in effect for the 2008 hunting season. The deer heads will be collected and tested for CWD. All transport of live wild deer, elk, and moose is prohibited statewide, including transport for rehabilitation purposes. Education and Outreach: A town hall meeting is scheduled to take place in Kent County on September 9, 2008 at 6:30 p.m. near Grand Rapids. Representatives from MDA, USDA, DNR and MSU will be there to answer questions about CWD, quarantines and the baiting ban. An update on the disease investigation will be presented to the House of Representatives Committee on Outdoor Recreation and Natural Resources on September 9, 2008 and the Senate Natural Resources, Agriculture, and Hunting and Fishing committees on September 10, 2008. 3 Questions and Answers regarding POC facility quarantines were sent via email to legislative offices, POC facility executive directors, and DNR law enforcement. They are also posted to the MDA, and Emerging Diseases websites. A coordinated communications action plan is in place. MSU Extension, Michigan Deer and Elk Breeders, MUCC, and many other special interest groups have volunteered to assist with information distribution. Information on CWD may be found on the Michigan Emerging Diseases website at www.michigan.gov/emergingdiseases. Corrected on September 8, 2008 – changed from “meat” to “carcasses”.

 
http://www.michigan.gov/documents/e...WD_Update_September_5_2008_final_248172_7.pdf

 
http://www.michigan.gov/emergingdiseases/0,1607,7-186-25806_26356---,00.html

 
Summary of Michigan Wildlife Chronic Wasting Disease Surveillance Updated May 1, 2008 by Michigan Department of Natural Resources, Wildlife Disease Laboratory

 
http://www.michigan.gov/documents/emergingdiseases/CWDTable082508_246523_7.pdf

 
http://www.michigan.gov/images/emergingdiseases/cwdcum1998_2002-050108_246525_7.jpg

 
Consumer Warning September – December 2008

 
The state's first case of Chronic Wasting Disease (CWD) was confirmed in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County on August 25, 2008. As a result, all POC facilities in Michigan were quarantined. Chronic Wasting Disease (CWD) is a fatal neurological disease that affects deer, elk and moose. Infected animals display abnormal behavior, progressive weight loss and physical debilitation. CWD is believed to be caused by infectious, self-multiplying proteins (prions). Prions are normal cell proteins whose shape has been transformed, causing CWD. To date, CWD is not known to cause or be associated with disease in humans. No increase in human prion disease has been observed in areas of the western United States where CWD has been endemic in cervid populations for decades.

 
However, because much is still unknown about prion diseases, the Centers for Disease Control and Prevention and the World Health Organization advise that humans do NOT consume animals that have been tested and are known to be infected with CWD. In general, people should not handle or consume wild animals that appear sick or act abnormally, regardless of the cause. CWD prions are primarily found in central nervous system tissues (e.g. brain and spinal cord) and the lymphatic system (e.g. tonsils, lymph nodes and spleen) of infected cervids. Humans should avoid the handling or consumption of these tissues. Hunters should wear disposable gloves while field dressing and de-boning meat from the carcass. Recent research has shown that CWD prions may also be found in the saliva and urine of the infected animal. Experiments conducted suggest that CWD prions can persist in the environment and may indirectly infect other susceptible animals that come into contact with the contaminated environment. The meat product you are receiving has come from a quarantined facility under surveillance for CWD. MDA recommends you take de-boned meat from the carcass, hold the meat product in a freezer and consume it only after the facility of origin receives clarification from MDA that the animal was negative for CWD.

 
http://www.michigan.gov/documents/emergingdiseases/Meat_-_CWD_Consumer_Warning_final_248038_7.pdf

 
http://www.michigan-sportsman.com/forum/threads/cwd-michigan-update-september-5-2008.250638/

 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

 
O18

 
Zoonotic Potential of CWD Prions

 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

 
P.105: RT-QuIC models trans-species prion transmission

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

 
Additionally, human rPrP was competent for conversion by CWD and fCWD.

 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

 
https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

 
Friday, August 28, 2015

 
Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection

 
http://chronic-wasting-disease.blogspot.com/2015/08/chronic-wasting-disease-cwd-tse-prion.html

 
Monday, August 24, 2015

 
Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests CWD

 
http://chronic-wasting-disease.blogspot.com/2015/08/ohio-wildlife-officials-ramp-up-fight.html

 
Sunday, August 23, 2015

 
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas

 
http://chronic-wasting-disease.blogspot.com/2015/08/tahc-chronic-wasting-disease-cwd-tse.html

 
Thursday, August 20, 2015

 
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD

 
http://chronic-wasting-disease.blogspot.com/2015/08/texas-captive-deer-industry-pens.html

 
Tuesday, August 11, 2015

 
Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker

 
http://chronic-wasting-disease.blogspot.com/2015/08/wisconsin-doing-what-it-does-best.html

 
Thursday, July 23, 2015

 
*** Chronic Wasting Disease (CWD) 101 Drs. Walter Cook & Donald S. Davis

 
http://chronic-wasting-disease.blogspot.com/2015/07/chronic-wasting-disease-cwd-101-drs.html

 
Monday, August 31, 2015

 
Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date

 
http://chronic-wasting-disease.blogspot.com/2015/08/illinois-loosing-ground-to-chronic.html

 
Friday, August 14, 2015

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

 
http://chronic-wasting-disease.blogspot.com/2015/08/susceptibility-of-cattle-to-agent-of.html

 
Friday, August 14, 2015

 
Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015

 
http://transmissiblespongiformencephalopathy.blogspot.com/2015/08/carcass-management-during-mass-animal.html

 
http://chronic-wasting-disease.blogspot.com/



Terry S. Singeltary Sr.

Monday, August 31, 2015

Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date

Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date
 
 
Chronic Wasting Disease Page Content Update July 1, 2015: We now have a total of 538 cases of CWD
 
Note: Years are reported by fiscal year: 2015 is the period from July 1, 2014 through June 30, 2015, etc.
 
Total CWD Cases per year:
 
Year Cases

​2015 ​71

2014 59

2013 36

2012 36

2011 42

2010 37

2009 30

2008 38

2007 42

2006 51

2005 31

2004 51

2003 14

Total 538
 
 
 
see history of CWD in Illinois here
 
Saturday, February 08, 2014
 
Illinois CWD confirmed in Will County deer
 
Chronic Wasting Disease Illinois
 
Update July 1, 2013:
 
We now have a total of 408 cases of CWD.
 
Note: Years are reported by fiscal year: 2013 is the period from July 1, 2012 through June 30, 2013, etc.
 
 
Illinois CWD-Infected Sections - August 15, 2013
 
 
 
Friday, August 28, 2015
 
Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection
 
 
Monday, August 24, 2015
 
Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests CWD
 
 
Sunday, August 23, 2015
 
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas
 
 
Thursday, August 20, 2015
 
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD
 
 
Tuesday, August 11, 2015
 
Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker
 
 
Friday, August 14, 2015
 
Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation
 
 
Friday, August 14, 2015
 
Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015
 
 
CWD TO HUMAN RISK FACTOR RISES !
 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
Zoonotic Potential of CWD Prions
 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
 
P.105: RT-QuIC models trans-species prion transmission
 
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
 
Additionally, human rPrP was competent for conversion by CWD and fCWD.
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
 
 
Thursday, July 23, 2015
 
Chronic Wasting Disease (CWD) 101 Drs. Walter Cook & Donald S. Davis
 
 
 
Terry S. Singeltary Sr.

Friday, August 28, 2015

Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection

Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection

Article | Open

Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of Prion Infection

A. Christy Wyckoff , Nathan Galloway , Crystal Meyerett-Reid , Jenny Powers , Terry Spraker , Ryan J. Monello , Bruce Pulford , Margaret Wild , Michael Antolin , Kurt VerCauteren & Mark Zabel

Scientific Reports 5, Article number: 8358 (2015) doi:10.1038/srep08358 Download Citation Molecular ecology | Proteins | Statistics

Received:27 June 2014Accepted:19 January 2015Published online:10 February 2015 Article Tools

Abstract

Prions are unique infectious agents that replicate without a genome and cause neurodegenerative diseases that include chronic wasting disease (CWD) of cervids. Immunohistochemistry (IHC) is currently considered the gold standard for diagnosis of a prion infection but may be insensitive to early or sub-clinical CWD that are important to understanding CWD transmission and ecology. We assessed the potential of serial protein misfolding cyclic amplification (sPMCA) to improve detection of CWD prior to the onset of clinical signs. We analyzed tissue samples from free-ranging Rocky Mountain elk (Cervus elaphus nelsoni) and used hierarchical Bayesian analysis to estimate the specificity and sensitivity of IHC and sPMCA conditional on simultaneously estimated disease states. Sensitivity estimates were higher for sPMCA (99.51%, credible interval (CI) 97.15–100%) than IHC of obex (brain stem, 76.56%, CI 57.00–91.46%) or retropharyngeal lymph node (90.06%, CI 74.13–98.70%) tissues, or both (98.99%, CI 90.01–100%). Our hierarchical Bayesian model predicts the prevalence of prion infection in this elk population to be 18.90% (CI 15.50–32.72%), compared to previous estimates of 12.90%. Our data reveal a previously unidentified sub-clinical prion-positive portion of the elk population that could represent silent carriers capable of significantly impacting CWD ecology.

snip...

Our data demonstrate that previous IHC-based studies are possibly missing early stage or sub-clinical cases in sampled populations. It is widely accepted that IHC is sensitive enough to detect pre-clinical cases, but we propose that sPMCA can detect additional cases even earlier, possibly soon after infection. In previous work we found sPMCA had a detection limit of 10−9 35,46 which is much more sensitive than the sensitivity of a mouse bioassay at 10−4. This suggests that animals found positive by sPMCA have much lower levels of PrPCWD than animals with clinical disease, but are indeed infected. The detection of very early sub-clinical cases raises the question of biological relevance at the population level. We propose that this sub-clinical subset of the population may be ecologically important to the disease transmission cycle because of potential preclinical vertical transmission from mother to offspring47, horizontal transmission through direct contact, or indirect transmission through environmental deposits of prions.

It remains unclear when animals begin shedding prions into the environment. Through the use of a mouse bioassay Tamguney et al.22,24,44,45 showed asymptomatic deer were capable of shedding infectious levels of CWD as early as 10 months prior to clinical disease. Bioassays, both in mice and deer, have limited sensitivity so shedding could be occurring much earlier than 10 months post-infection but at levels insufficient to cause clinical disease in the infected host. It is also unclear if genotype plays a role in prion shedding, as well as disease course. Our data suggest that having at least one L allele at codon 132 does not alter the disease prevalence within the ML genotype, supporting data reported by Perucchini et al.27. The slow disease course and the potential existence of a carrier state facilitate a high prevalence and frequent opportunity for transmission between animals with the MM and ML genotypes.

It is commonly stated in the literature that CWD is an invariably fatal disease, but it may be more accurate to state that once animals begin to show clinical signs they are certain to succumb to CWD or other associated causes of death such as predation4,24,48. Perhaps other carrier states exist within the population, which may or may not contribute to the transmission and deposition of prions in the population and the environment. Further research is required to address the role of a carrier state in the ecology of CWD transmission.

The application of sPMCA will be important both to research and for diagnostic investigation, and may improve state and federal surveillance programs for CWD in both naïve and endemic host populations. Increased sensitivity, and the need for only obex tissue, may lead to detection of new focal points prior to clinical disease emerging in otherwise CWD-free populations. Additionally, in the economically and politically difficult scenario of culling captive herds that tested positive for CWD, extremely sensitive assays such as sPMCA of prions from tissue and excreta are essential to verify that more animals besides the index case were infected, and if any sub-clinical carriers may have been shedding into the environment.

Overall, our data contribute to the increasing evidence that a portion of a herd may be infected, but die from other causes while infected with PrPCWD because of age, genetic susceptibility or other unknown factors. However, the contribution of prions shed into the environment from this sub-clinical population may be important and requires further investigation. The existence of an infectious PrPCWD carrier state aligns with disease ecology theory, which proposes balance between transmissibility and pathogenesis of a pathogen. As such, through selection pressures from the host and external environment the pathogen will tend towards the greatest transmissibility strategy. CWD transmission may be more complicated than disease ecology might predict, since prolonged persistence and indirect transmission of prions in the environment may potentiate spread without affecting pathogenesis.

Despite the fact that prions are only protein, studies continue to point at evolutionary behavior and selection pressures of prions which indicate that like other pathogens, prions are capable of evolving and adapting to their environment4,27,48,49. With increasing prevalence at the population level, as is reported in this study, sPMCA will continue to be an important tool to investigate CWD in wildlife.



P170

Clinical Stage of Infection is Critical in the Antemortem Diagnosis of Chronic Wasting Disease in Deer and Elk

Chris Siepker1, Nicholas Haley1, W. David Walter2, Matteo Manca3, Laura Hoon-Hanks4, Ryan Monello5, Jenny Powers5, Justin Greenlee6 , Bruce Thomsen7 , Aaron Lehmkuhl7, Gordon Mitchell8, Tracy Nichols9,Byron Caughey3, Edward Hoover4, and Juergen Richt1.

1. Department of Diagnostic Medicine and Pathobiology, Kansas State University, Manhattan KS USA 2. United States G e o l o g i c a l Survey, P e n n s y l v a n i a Cooperative Fish and Wildlife Research Unit, University Park PA USA 3. TSE/Prion Biochemistry Section, Rocky Mountain Laboratories, National Institutes of Health, Hamilton, MT USA 3. Department of MIP, Colorado State University, Fort Collins CO USA 4. National Park Service, Wildlife Health Branch, Fort Collins CO USA 5. Virus and Prion Research Unit, National Animal Disease Center, ARS, USDA, Ames IA USA 6. USDA, APHIS, VS, STAS, National Veterinary Service Laboratories, Ames IA USA 7. National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa ON Canada 8. National Wildlife Research Center Wildlife Services, APHIS, USDA, Fort Collins CO USA

Chronic wasting disease (CWD) is an e f f i c i e n t l y t r a n s mi t t e d s p o n g i f o r m encephalopathy of cervids (e.g. deer, elk, and moose), and is the only known prion disease affecting both free-ranging wildlife and captive animals. The antemortem detection of CWD and other prion diseases has proven difficult, due in part to difficulties in identifying an appropriate peripheral tissue specimen and complications with conventional test sensitivity. At present, biopsies of the recto-

Prion2015 Program Guide 22

anal mucosal-associated lymphoid tissues (RAMALT) have shown promising sensitivity and are not impractical to collect in live animals. Nasal brush collections have likewise proven both sensitive and practical for identification of prion infections in humans. In this study, we evaluated both RAMALT and nasal brush collections by real time quaking-induced conversion (RT-QuIC), and compared our findings to RAMALT immu n o h i s t o c h emi s t r y a s we l l a s conventional postmortem evaluation of obex and retropharyngeal lymph node tissues from over 700 captive and free-ranging deer and elk in areas with endemic CWD. We correlated our results with various clinical findings, including pathological stage of infection as determined by obex scoring, PrP genotype, age, and sex. While the sensitivity of RAMALT RT-QuIC analyses exceeded that of RAMALT IHC (69-80% vs. >44%) and nasal brush collections (15-30%), the sensitivity of both biopsy and nasal brush analyses were dependent primarily on clinical stage of disease, although PrP genotype was also an important predictor of sample positivity. Our findings further demonstrate the potential and limitations of antemortem sample analyses by RT-QuIC in the identification and management of prion diseases.



J Vet Sci. 2015 Jun; 16(2): 179–186.

Published online 2015 Jun 17. doi: 10.4142/jvs.2015.16.2.179

PMCID: PMC4483501

Classical natural ovine scrapie prions detected in practical volumes of blood by lamb and transgenic mouse bioassays

Rohana P. Dassanayake,corresponding author1 Thomas C. Truscott,2 Dongyue Zhuang,2 David A. Schneider,2 Sally A. Madsen-Bouterse,1 Alan J. Young,3 James B. Stanton,1 William C. Davis,1 Katherine I. O'Rourke1


J Virol. 2013 May; 87(10): 5895–5903. doi: 10.1128/JVI.03469-12 PMCID: PMC3648199

Dissociation between Transmissible Spongiform Encephalopathy (TSE) Infectivity and Proteinase K-Resistant PrPSc Levels in Peripheral Tissue from a Murine Transgenic Model of TSE Disease

Karen Dobie and Rona Barroncorresponding author Neurobiology Division, The Roslin Institute & R(D)SVS, Easter Bush, Midlothian, United Kingdom corresponding authorCorresponding author. Address correspondence to Rona Barron, Email: ku.ca.de.nilsor@norrab.anor. Author information ► Article notes ► Copyright and License information ► Received 2012 Dec 19; Accepted 2013 Mar 7. Copyright © 2013, American Society for Microbiology. All Rights Reserved. This article has been cited by other articles in PMC. Go to:

Abstract

Most current diagnostic tests for transmissible spongiform encephalopathies (TSE) rely on the presence of proteinase K (PK)-resistant PrPSc (PrP-res) in postmortem tissues as an indication of TSE disease. However, a number of studies have highlighted a discrepancy between TSE infectivity and PrP-res levels in both natural and experimental cases of TSE disease. Previously, we have shown high TSE infectivity levels in the brain tissue of mice that have a clinical TSE disease with associated vacuolar pathology but little or no detectable PrP-res. Here, the levels of TSE infectivity and PrP-res within a peripheral tissue of this mouse model were investigated. Biochemical analysis showed that low levels of PrP-res were present in the spleen tissue in comparison to the levels observed in the spleen of mice infected with ME7 or 79A. However, upon subpassage of brain and spleen tissue from clinically ill mice with little or no PrP-res detectable, similar short incubation periods to disease were observed, indicating that infectivity levels were similarly high in both tissues. Thus, the discrepancy between PrP-res and TSE infectivity was also present in the peripheral tissues of this disease model. This result indicates that peripheral tissues can contain higher levels of infectivity given the correct combination of host species, PrP genotype, and TSE agent. Therefore, the assumption that the levels of peripheral infectivity are lower than those in the central nervous system is not always correct, and this could have implications for current food safety regulations.

SNIP...

Several recent studies have identified the presence of quasispecies within individual cases of TSE disease in humans (23, 24) and animals (25) and in cell-culture models (26). Indeed, it has been hypothesized that subvariants of disease-associated PrP replicate preferentially in specific tissue types, with a dependence on tissue-specific host factors (25, 27). The biochemical and immunohistochemical analyses of the recipient mice from the 101LL/GSS subpassage demonstrated that PrP-res deposition was lower in the brain tissue of mice that received the spleen homogenate inocula than in those that received the brain homogenate inocula (Fig. 6), while in contrast, the vacuolation score in mice was greater in those that received the spleen homogenate than in those that received the brain homogenate (Fig. 4). These results indicate that a potentially heterogeneous population of PrP-res was present. It is hypothesized that tissue-specific conditions supported the replication of different subvariants that showed different replication efficiencies upon subpassage. If heterogeneous populations of PrP-res exist that include variants that have different replication capabilities, a variant present in peripheral tissues may have a higher level of infectivity than the corresponding brain-derived variant. Therefore, assessment of the peripheral infectivity levels from novel and emerging isolates is urgently required to ensure that an accurate titer is established to maintain food safety.

Together, these results indicate that a form of the infectious agent may be present in this disease model that remains undetectable by current standard analysis. Given the increasing costs of bioassay to identify the presence of TSE infectivity, the majority of disease cases are being confirmed by biochemical techniques specific for the presence of PrP-res, without confirmation of the presence of infectivity. This current reliance on PrP-res as indicative of TSE disease may not detect all cases of TSE disease, with the possible emergence of cases with high infectivity levels associated with low levels or an absence of PrP-res. Indeed, the discovery of significant levels of TSE infectivity despite the absence of PrP-res in spleens from sheep infected with atypical scrapie (13) indicates that this disease phenomenon can occur in natural cases of TSE disease present in the environment. Furthermore, a recent study by Gonzalez and colleagues highlighted the discrepancy between levels of PrP-res and TSE infectivity in sheep scrapie and sheep BSE and indicated that quantitative laboratory tests to detect disease-associated PrP could not be used to accurately predict infectious titers (28). While TSEs remain in the environment, the emergence of novel isolates or the possibility that a known isolate could infect a different host species remains. Our data show that a combination of host species, PrP genotype, and TSE isolate that could produce a novel disease phenotype with high levels of TSE infectivity in the absence of PrP-res has the potential to occur. Therefore, if the infectivity levels in the peripheral tissues of disease cases with low levels of PrP-res are higher than originally hypothesized from previous research into classical isolates and current biochemical tests, the emergence of a novel isolate could pose a major risk to food safety if tissues were able to enter the food chain. Together with the discrepancy between PrP-res and TSE infectivity levels presented here, the estimation of infectious titer should not rely on the detection of PrP-res as the sole indicator of TSE disease.


 
P.153: An independent and blinded confirmation of real-time quakinginduced conversion (RT-QuIC) analysis of cervid rectal biopsies for detection of chronic wasting disease

Sireesha Manne1,*, Naveen Kondru1, Nicholas Haley2, Tracy Nichols3, Bruce Thomsen4, Roger Main5, Patrick Halbur5, Arthi Kanthasamy1, and Anumantha Kanthasamy1 1Biomedical Sciences; Iowa State University; Ames, IA USA; 2Kansas State University; Manhattan, KS USA; 3United States Department of Agriculture; Fort Collins, CO USA; 4National Veterinary Service Laboratories; Ames, IA USA; 5VDPAM; Iowa State University; Ames, IA USA

Prion diseases are transmissible spongiform encephalopathies (TSEs) characterized by an always fatal, progressive neuronal degeneration in the brain due to infectious misfolded prion proteins whose prolonged incubation periods often make ante-mortem diagnosis difficult. Chronic wasting disease (CWD) is a TSE affecting both wild and captive populations of mule deer, whitetailed deer, elk and moose. CWD in cervids was first identified in Rocky Mountain States and has recently spread to several other states including Iowa. In this current study, we attempted to independently confirm the results of a Real-Time Quaking-Induced Conversion (RT-QuIC) assay to diagnose CWD using rectal biopsy sections from farmed white-tailed deer. First, we generated recombinant prion protein substrate and then validated the quality of protein for RT-QuIC using a reference prion protein kindly provided by Dr. Caughey’s lab. After validating the assay, we blindly evaluated approximately 350 rectal biopsy samples analyzed previously by another institution. All assay plates included positive and negative controls and were analyzed in triplicate. Samples were analyzed using the Biotek Cytation-3 multimode plate reader for 24-hrs duration. Our RT-QuIC assays showed 55% positivity for 356 rectal samples analyzed. Comparison of RT-QuIC results with the immunohistochemical results of obex revealed 93% sensitivity (95% confidence limits: 88.05–95.78%) and 96% specificity (95% CL: 91–99%), confirming that the RT-QuIC assay may be one of the most promising rapid assays for detecting CWD prions. We are currently working on applying the RT-QuIC assay to other test samples (ISU Presidential Wildlife initiative, ISU-CVM Diagnostic lab and ES10586).

P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum

Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State University; Ames, IA USA

The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.


cwd diagnostics


 

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

 

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

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

SUMMARY:


For Immediate Release Thursday, October 2, 2014

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).



*** see history of this CWD blunder here ;




The overall incidence of clinical CWD in white-tailed deer was 82%

Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)



J Vet Diagn Invest 20:698–703 (2008)

Chronic wasting disease in a Wisconsin white-tailed deer farm

Delwyn P. Keane,1 Daniel J. Barr, Philip N. Bochsler, S. Mark Hall, Thomas Gidlewski, Katherine I. O’Rourke, Terry R. Spraker, Michael D. Samuel

Abstract.

In September 2002, chronic wasting disease (CWD), a prion disorder of captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus virginianus) from a captive farm in Wisconsin. The facility was subsequently quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty animals (79%) were found to be positive by immunohistochemical staining for the abnormal prion protein (PrPCWD) in at least one tissue; the prevalence of positive staining was high even in young deer. Although none of the deer displayed clinical signs suggestive of CWD at depopulation, 49 deer had considerable accumulation of the abnormal prion in the medulla at the level of the obex. Extraneural accumulation of the abnormal protein was observed in 59 deer, with accumulation in the retropharyngeal lymph node in 58 of 59 (98%), in the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of 58 (83%). The retina was positive in 4 deer, all with marked accumulation of prion in the obex. One deer was considered positive for PrPCWD in the brain but not in the extraneural tissue, a novel observation in white-tailed deer. The infection rate in captive deer was 20- fold higher than in wild deer. Although weakly related to infection rates in extraneural tissues, prion genotype was strongly linked to progression of prion accumulation in the obex. Antemortem testing by biopsy of recto– anal mucosal-associated lymphoid tissue (or other peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for surveillance in captive herds at risk for CWD infection.

Key words: Cervids; chronic wasting disease; prion; transmissible spongiform encephalopathy.


 

> the prevalence of positive staining was high even in young deer



Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.

"This is the first intensive sampling for CWD in fawns anywhere," said Dr. Julie Langenberg, Department of Natural Resources wildlife veterinarian, "and we are trying to learn as much as we can from these data".



Saturday, February 04, 2012

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



Articles of Significant Interest Selected from This Issue by the Editors Next Section Prions in the Blood of Infected Hosts: Early and Persistent Prions circulate in the blood of prion-infected hosts, including humans with variant Creutzfeldt-Jakob disease. Determining the parameters of blood-borne prions during the long asymptomatic phase of disease characteristic of all prion diseases has been a long-standing problem in prion biology. Elder et. al (p. 7421–7424) have demonstrated amyloid formation, a biomarker for prions, in the blood of prion-infected rodent and cervid hosts as early as 15 minutes post-mucosal or -intravenous infection. This prionemia persists throughout the disease course, indicating a role for hematogenous prions throughout the preclinical stage of illness.



***Immediate and Ongoing Detection of Prions in the Blood of Hamsters and Deer following Oral, Nasal, or Blood Inoculations

Alan M. Eldera, Davin M. Hendersona, Amy V. Nallsa, Edward A. Hoovera, Anthony E. Kincaidb,c, Jason C. Bartzb and Candace K. Mathiasona aDepartment of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, USA bMedical Microbiology and Immunology, Creighton University, Omaha, Nebraska, USA cDepartment of Pharmacy Sciences, Creighton University, Omaha, Nebraska, USA S. Perlman, Editor + Author Affiliations



 

 TSS

Monday, August 24, 2015

Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests CWD

Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests

 

By D'Arcy Egan, The Plain Dealer The Plain Dealer

 

on August 21, 2015 at 3:36 PM, updated August 21, 2015 at 5:10 PM

 

CLEVELAND, Ohio – Ohio wildlife officials proposed a need for the ability to create "disease surveillance zones" with special rules should a white-tailed deer test positive for Chronic Wasting Disease (CWD), a fatal brain disease that continues to spread among deer and elk in Ohio and around the country. Chief Scott Zody of the Ohio Division of Wildlife revealed a large number of positives for CWD on a Holmes County deer breeding farm when he proposed the system to the Ohio Wildlife Council at its meeting Wednesday. The areas would generally have a radius of about six miles. The first zone would cover parts of Homes and Wayne counties where two captive deer tested positive last October at World Class Whitetails, a deer farm and high-fence hunting operation.

 

Triggering the proposal were 17 additional deer testing positive for CWD in June after the World Class Whitetails herd of approximately 300 deer was euthanized. The exceptionally large number of positives for CWD were not revealed by the Ohio Department of Agriculture, which did the testing since the deer are considered livestock.

 

"We now need to move forward, take proactive tests of deer and ramp up our monitoring and surveillance of wild deer near the facility," said Zody, whose agency manages wild deer.

 

The biggest fear is CWD will be transmitted to wild Ohio deer, since 24 captive deer have escaped from the facility owned by Daniel Yoder. Many of the escaped deer have been killed and tested for CWD. While none tested positive, state wildlife experts say they can no longer assume CWD is confined to a fenced facility.

 

The special zone regulations proposed to the Ohio Wildlife Council on Wednesday would:

 

Require submission of harvested deer carcasses to ODOW inspection stations during deer gun and muzzleloading rifle seasons;

 

Prohibit the placement of salt, mineral supplements, grain, fruit, vegetables or other feed;

 

Prohibit hunting with the aid of salt, mineral supplements, grain, fruit, vegetables or other feed; and

 

Prohibit the removal of deer carcasses killed by a motor vehicle unless the carcass complies with special regulations. "We've also undertaken some culling of deer in the Holmes County area around World Class Whitetails to sample for CWD," said Zody. "With landowner permission, over the last two weeks we've killed 15 of a total of 50 deer we want to sample."

 

The Ohio Wildlife Council will vote on the proposal at its October meeting. It approved it would take effect Nov. 9. It would not affect normal agricultural activities, including feeding of domestic animals or hunting deer over food plots, naturally occurring or cultivated plants and agricultural crops.

 

Wildlife officials said if CWD is detected at a location, it does not mean it would automatically become a designated disease surveillances area. The rule would give the head of the ODOW the ability to designate an area if additional surveillance is required.

 

A map of any surveillance area would be posted on the ODOW web site, wildohio.com. The ODOW is encouraging comments on the proposal at the site.

 

snip...

 


 

Wednesday, August 05, 2015

 

Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases to date

 


 

Monday, June 11, 2012

 

*** OHIO Captive deer escapees and non-reporting ***

 


 

Thursday, October 23, 2014

 

FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE

 


 

Thursday, April 02, 2015

 

OHIO CONFIRMS SECOND POSTIVE CHRONIC WASTING DISEASE CWD on Yoder's properties near Millersburg

 


 

Wednesday, February 11, 2015

 

World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with two counts of tampering with evidence

 


 

the tse prion aka mad cow type disease is not your normal pathogen.

 

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.

 

you cannot cook the TSE prion disease out of meat.

 

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.

 

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

 

the TSE prion agent also survives Simulated Wastewater Treatment Processes.

 

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.

 

you can bury it and it will not go away.

 

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.

 

it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

 

CWD, spreading it around...

 

for the game farm industry, and their constituents, to continue to believe that they are _NOT_, and or insinuate that they have _NEVER_ been part of the problem, will only continue to help spread cwd. the game farming industry, from the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet mills, shooting pens, to large ranches, are not the only problem, but it is painfully obvious that they have been part of the problem for decades and decades, just spreading it around, as with transportation and or exportation and or importation of cervids from game farming industry, and have been proven to spread cwd. no one need to look any further than South Korea blunder ;

 

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

 

spreading cwd around...

 

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

 

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

 


 

spreading cwd around...

 

Friday, May 13, 2011

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 


 


 


 


 

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

 

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

 

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

 

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

 

SUMMARY:

 


 

For Immediate Release Thursday, October 2, 2014

 

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

 

*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

 

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).

 


 

*** see history of this CWD blunder here ;

 


 

On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.

 


 

The overall incidence of clinical CWD in white-tailed deer was 82%

 

Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)

 


 

*** 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.

 


 

Friday, January 30, 2015

 

*** Scrapie: a particularly persistent pathogen ***

 


 

Friday, December 14, 2012

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 

snip...

 

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

 

Animals considered at high risk for CWD include:

 

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

 

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

 

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

 

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

 

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

 

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

 

snip...

 

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

 

snip...

 

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

 

snip...

 

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

 

snip...

 

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

 

snip...

 

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

 

snip...

 


 

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

 

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.

 


 

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

 

Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.

 


 

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

 

The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.

 


 

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

 

Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE

 

In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.

 


 

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

 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

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

 

98 | Veterinary Record | January 24, 2015

 

EDITORIAL

 

Scrapie: a particularly persistent pathogen

 

Cristina Acín

 

Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’

 

From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).

 

Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.

 

Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.

 

The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).

 

In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.

 

Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).

 

In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.

 

The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).

 

Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).

 

So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?

 

What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.

 

References

 

snip...

 

98 | Veterinary Record | January 24, 2015

 


 

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

 

Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations

 

1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.

 

SNIP...

 

Discussion

 

Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.

 

Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.

 

The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.

 

Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014

 


 

Monday, November 3, 2014

 

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

 


 

PPo3-22:

 

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

 

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

 

Key words: scrapie, evironmental persistence, sPMCA

 

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.

 


 

cwd environmental load factor in the land and surrounding plants and objects.

 

transportation of cervids and HUMANS from cwd zone should be regarded as a great risk factor, and environmental contamination.

 

PL1

 

Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.

 

Claudio Soto

 

Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.

 

Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

 

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

 

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

 

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

 

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.

 


 

see ;

 


 


 


 


 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

Terry S. Singeltary Sr.

 

Friday, January 30, 2015

 

*** Scrapie: a particularly persistent pathogen ***

 


 

PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

 

*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

 

O18

 

Zoonotic Potential of CWD Prions

 

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

 

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

 

P.105: RT-QuIC models trans-species prion transmission

 

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

 

Additionally, human rPrP was competent for conversion by CWD and fCWD.

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

 


 

From: Terry S. Singeltary Sr.

 

Sent: Saturday, November 15, 2014 9:29 PM

 

To: Terry S. Singeltary Sr.

 

Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984

 

THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE

 

R. G. WILL

 

1984

 

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

 

snip...

 


 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

 


 

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

 


 

Friday, August 14, 2015

 

Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015

 


 

Thursday, August 20, 2015

 

*** TEXAS TAHC DEER BREEDER CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE ***

 


 

Thursday, August 20, 2015

 

TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD

 


 


 

Sunday, August 23, 2015

 

TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas

 

from the other side of the fence... today’s Singeltary Sunday School class ‘thinking outside of the box’ at the bottom. ...tss

 


 

Friday, August 07, 2015

 

Texas CWD Captive, and then there were 4 ?

 


 

Thursday, August 06, 2015

 

WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY

 


 

Tuesday, July 21, 2015

 

Texas CWD Medina County Herd Investigation Update July 16, 2015

 

• 66 Texas sites, 2 Mexico sites

 


 

Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas

 

Under Texas law, though, breeder deer belong to the state, not the permittee. See, e.g., TEX. PARKS & WILD. CODE §§ 1.011 (“All wild animals . . . inside the borders of this state are the property of the people of this state.”); 43.364 (“All breeder deer . . . are under the full force of the laws of [Texas] pertaining to deer . . . .”). While a permittee may have possession of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351. Nowhere do the statutes or regulations state that breeder deer become the property of a permit holder.4 Regardless, even if they did give ownership of breeder deer to permit holders, the Andertons were not permit holders when the deer were killed.

 


 

While a permittee may have possession of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351

 


 

S.B. No. 820

 


 


 

Texas Senate Bill

 

Relating to the management, breeding, and destruction of deer and to procedures regarding certain deer permits.

 

View latest bill text Session:83rd Legislature (2013)

 


 

Sunday, August 23, 2015

 

TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas

 

from the other side of the fence... today’s Singeltary Sunday School class ‘thinking outside of the box’ at the bottom. ...tss

 


 

Sunday, August 02, 2015

 

TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?

 


 

Wednesday, March 18, 2015

 

Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015

 


 

Wednesday, March 25, 2015

 

Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015

 


 

Thursday, May 02, 2013

 

*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING

 


 

Monday, February 11, 2013

 

TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos

 


 

Tuesday, July 10, 2012

 

Chronic Wasting Disease Detected in Far West Texas

 


 

Monday, March 26, 2012

 

Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas

 


 

***for anyone interested, here is some history of CWD along the Texas, New Mexico border, and my attempt to keep up with it...terry

 

snip...

 

see history CWD Texas, New Mexico Border ;

 

Monday, March 26, 2012

 

3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER

 


 

Sunday, October 04, 2009

 

CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic Wasting Disease in New Mexico New Mexico Department of Game and Fish

 


 

 Tuesday, June 16, 2015

 

Missouri MDC changes deer hunting regs to help slow CWD

 


 

Wednesday, March 11, 2015

 

MDC reports 11 new cases of Chronic Wasting Disease CWD in Missouri deer

 


 

Monday, January 26, 2015

 

Missouri MDC reports two new cases of CWD found in Adair and Macon counties

 


 

Tuesday, December 09, 2014

 

Missouri MDC reports one new case of CWD, found in Adair County

 


 

Friday, October 17, 2014

 

Missouri Final action on Orders of Rule making Breeders and Big Game Hunting Preserves

 


 

Thursday, September 11, 2014

 

Missouri Nixon's Veto Stands Overide Fails on Agriculture Legislation

 

How they voted: attempt to override veto of ag bill fails in the House

 


 

Thursday, May 01, 2014

 

Missouri DNR CWD prevention and captive cervid farming Update

 


 

Tuesday, March 26, 2013

 

CWD Missouri remains confined to Linn-Macon-County Core Area with four new cases

 


 

Wednesday, January 23, 2013

 

Missouri sixth case CWD documented northwest Macon County

 


 

Tuesday, January 24, 2012

 

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

 


 

Friday, February 26, 2010

 

Chronic wasting disease found in Missouri deer

 


 

Sunday, March 25, 2012

 

Three more cases of CWD found in free-ranging deer in Macon County

 


 

From: Terry S. Singeltary Sr.

 

Sent: Thursday, March 29, 2012 6:26 PM

 

To: warhovert@missouri.edu

 

Cc: abbottjm@missouri.edu ; waltermr@missouri.edu ; John.McLaughlin@missouri.edu ; connerek@missouri.edu ; contact@dnr.mo.gov ; Shelly.Witt@mda.mo.gov ; Animal.Health@mda.mo.gov ; acfa@mda.mo.gov ; animalid@mda.mo.gov ; Linda.Hickam@mda.mo.gov

 

Subject: re-Missouri officials seek states' advice on chronic wasting disease in deer

 


 

Thursday, May 31, 2012

 

Missouri MDC staff will provide information on five recently found cases of CWD in free-ranging deer in northwest Macon County June 2, 2012

 


 

Wednesday, September 05, 2012

 

Missouri MDC seeks hunters’ help when processing harvested deer and preventing CWD

 


 

Thursday, December 20, 2012

 

MISSOURI Initial CWD sampling test results available online from MDC so far one adult buck has tested positive for the disease

 


 

Friday, October 21, 2011

 

Chronic Wasting Disease Found in Captive Deer Missouri

 


 

The Missouri Department of Agriculture discovers the state's first case of CWD in a captive white-tailed deer.

 


 

Friday, February 26, 2010

 

Chronic wasting disease found in Missouri deer February 25, 2010

 

Chronic Wasting Disease Found in Captive Deer

 

The Missouri Departments of Agriculture, Conservation and Health and Senior Services and the U.S. Department of Agriculture announced today that a captive white-tailed deer in Linn County, Missouri has tested positive for Chronic Wasting Disease (CWD). CWD is a neurological disease found in deer, elk and moose.

 

"There is no evidence that CWD poses a risk to domestic animals or humans," said State Veterinarian Dr. Taylor Woods. "We have protocols in place to quickly and effectively handle these situations."

 

The animal that tested positive for CWD was a white-tailed deer inspected as part of the State's CWD surveillance and testing program. Preliminary tests were conducted by the USDA National Veterinary Services Laboratory in Ames, Iowa.

 

Upon receiving the confirmed CWD positive, Missouri's departments of Agriculture, Conservation and Health and Senior Services initiated their CWD Contingency Plan. The plan was developed in 2002 by the Cervid Health Committee, a task force comprised of veterinarians, animal health officers and conservation officers from USDA, MDA, MDC and DHSS working together to mitigate challenges associated with CWD.

 

CWD is transmitted by live animal to animal contact or soil to animal contact. The disease was first recognized in 1967 in captive mule deer in the Colorado Division of Wildlife captive wildlife research facility in Fort Collins, Colorado. CWD has been documented in deer and/or elk in Colorado, Illinois, Kansas, Michigan, Minnesota, Montana, Nebraska, New Mexico, New York, Oklahoma, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and the Canadian Provinces of Alberta and Saskatchewan. There has been no evidence that the disease can be transmitted to humans.

 

"Missouri's proactive steps to put a testing protocol in place and create a contingency plan years ago is proving beneficial. We are in a solid position to follow pre-established steps to ensure Missouri's valuable whitetail deer resource remains healthy and strong," said Jason Sumners Missouri's Deer Biologist.

 

For more information regarding CWD, please contact Dr. Taylor Woods at (573) 751-3377.

 


 


 

Friday, September 20, 2013

 

*** Missouri State records show gaps in oversight of captive deer farms, ranches ***

 


 

TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS) BURNS

 

Tuesday, August 11, 2015

 

Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker

 


 

Wednesday, March 04, 2015

 

*** Disease sampling results provide current snapshot of CWD in Wisconsin finding 324 positive detections statewide in 2014

 


 

Tuesday, October 07, 2014

 

*** Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve

 


 

Thursday, June 25, 2015

 

Wisconsin CWD-positive white-tailed deer found on Eau Claire County farm

 


 

Tuesday, July 14, 2015

 

TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin CWD postive farm Yellow ear tag

 


 

Tuesday, November 27, 2012

 

Pennsylvania ‘Pink 23’ Adams County exposed CWD Escaped Deer shot, but where are the other escapees ?

 


 

Saturday, June 29, 2013

 

PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA

 


 

Tuesday, June 11, 2013

 

CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania

 


 

Sunday, July 13, 2014 Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape http://chronic-wasting-disease.blogspot.com/2014/07/louisiana-deer-mystery-unleashes.html

 

Tuesday, May 28, 2013

 

Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013

 

*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.

 


 

Sunday, January 06, 2013

 

USDA TO PGC ONCE CAPTIVES ESCAPE

 

*** "it‘s no longer its business.”

 


 

”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.

 


 

Wednesday, November 14, 2012

 

PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO LOUISIANA and INDIANA

 


 

Tuesday, October 23, 2012

 

PA Captive deer from CWD-positive farm roaming free

 


 

Thursday, October 11, 2012

 

Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive

 


 

Monday, March 23, 2015

 

North Dakota Documents Two More Cases of Chronic Wasting Disease CWD TSE Prion

 


 

Thursday, April 02, 2015

 

Kansas Chronic Wasting Disease CWD Spreads 9 Confirmed Positive including first-time cases in six southwest counties

 


 

Tuesday, January 20, 2015

 

Four Maryland Deer Test Positive for Chronic Wasting Disease

 


 

Wednesday, February 12, 2014

 

VIRGINIA VDGIF Reports Two New CWD Positives in Frederick County

 


 

Monday, October 08, 2012

 

VDGIF has discovered four positive cases of CWD in Virginia Updated 9/24/2012

 


 

Thursday, March 15, 2012 CWD VIRGINIA TWO NEW CASES

 


 

Friday, December 17, 2010

 

CWD positive in western Frederick County VA VDGIF December 16, 2010

 


 

Thursday, January 21, 2010

 

Chronic Wasting Disease Found in White-tailed Deer in Virginia

 


 

Wednesday, July 01, 2015

 

DRAFT Virginia Deer Management Plan 2015-2024 (bans urine scents do to CWD 2015)

 


 

Monday, August 25, 2008 CWD FIRST DOCUMENTED IN MICHIGAN

 

 Michigan's First Case of Chronic Wasting Disease Detected at Kent County Deer Breeding Facility Contact: Bridget Patrick (MDA) or Mary Dettloff (DNR) 517-241-2669 or 517-335-3014 Agency: Natural Resources

 

August 25, 2008 LANSING - The Michigan departments of Agriculture (MDA) and Natural Resources (DNR) today confirmed the state's first case of Chronic Wasting Disease (CWD) in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County.

 


 

Tuesday, May 26, 2015

 

Michigan confirms state's first case of chronic wasting disease in free-ranging white-tailed deer

 


 


 

 Friday, July 17, 2015

 

Michigan confirms CWD in second free-ranging white-tailed deer

 


 

 Thursday, August 06, 2015

 

Michigan DNR confirms third deer positive for CWD; hunter participation is critical this fall

 


 

Sunday, June 29, 2014

 

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

 


 

Saturday, February 08, 2014

 

Illinois CWD confirmed in Will County deer

 

Chronic Wasting Disease Illinois

 

Update July 1, 2013:

 

We now have a total of 408 cases of CWD.

 

Note: Years are reported by fiscal year: 2013 is the period from July 1, 2012 through June 30, 2013, etc.

 


 

Illinois CWD-Infected Sections - August 15, 2013

 


 


 

 Wednesday, October 30, 2013

 

Regulations Issued to Protect NYS Deer Population from Chronic Wasting Disease

 


 

 IN THE UNITED STATES DISTRICT COURT FOR THE NORTHERN DISTRICT OF INDIANA SOUTH BEND DIVISION UNITED STATES OF AMERICA, vs. RUSSELL G. BELLAR, Defendant.

 

___________________________

 

)))))))))

 

Cause No.: 3:04cr00068-AS South Bend, Indiana January 4, 2005 9:30 a.m.

 

TRANSCRIPT EXCERPT OF JURY TRIAL (TESTIMONY OF: RONNIE DUNN AND RUSTY CAMP) BEFORE THE HONORABLE ALLEN SHARP

 

snip...

 

Ronnie Dunn Cross Examination

 

Q. Mr. Dunn, at one point I believe you told the federal agents that Mr. Bellar told you that this was a private deer farm and shooting deer on that farm was like slaughtering cattle; is that correct?

 

A. I don't know if I used the word "slaughter," but it was, yeah, like that.

 

Q. You don't know if that was your word, "slaughtering cattle"?

 

A. I don't know that.

 

Q. Well, did he give you the idea of killing cattle?

 

A. Yes, it was the same principle.

 

snip...

 

see full text ;

 


 


 


 

BUCK FEVER

 


 

Tuesday, January 20, 2015

 

Iowa Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee County

 


 

 Tuesday, February 10, 2015

 

Alberta Canada First case of chronic wasting disease found in farm elk since 2002

 


 

SHOCKING ONES CONSCIENCE VIDEO

 

*** Danger of Canned Hunting Indiana Wildlife VIDEO ***

 


 

LATE-BREAKING ABSTRACTS

 

O18

 

Zoonotic Potential of CWD Prions

 

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

 

Chronic wasting disease (CWD) is a widespread and expanding prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern. Current literature generated with in vitro methods and in vivo animal models (transgenic mice, macaques and squirrel monkeys) reports conflicting results. The susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. In our earlier bioassay experiments using several humanized transgenic mouse lines, we detected protease-resistant PrPSc in the spleen of two out of 140 mice that were intracerebrally inoculated with natural CWD isolates, but PrPSc was not detected in the brain of the same mice. Secondary passages with such PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient prion transmission with clear clinical and pathological signs in both humanized and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD isolates in a new humanized transgenic mouse line led to clinical prion infection in 2 out of 20 mice. These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.

 

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

 

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

 

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

 

P.105: RT-QuIC models trans-species prion transmission

 

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

 

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious. Studies of the effects of primary or tertiary prion protein structures on trans-species prion transmission have relied primarily upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect. As an alternative strategy, we used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species prion conversion.

 

To assess trans-species conversion in the RT-QuIC system, we compared chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions, as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each prion was seeded into each host recombinant PrP (full-length rPrP of white-tailed deer, bovine or feline). We demonstrated that fCWD is a more efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests adaptation to the new host.

 

Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD. ***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.

 

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

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

 

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

 

Willingham, Erin McNulty, Kelly Anderson, Jeanette Hayes-Klug, Amy Nalls, and Candace Mathiason Colorado State University; Fort Collins, CO USA

 

Chronic wasting disease (CWD) is the transmissible spongiform encephalopathy (TSE), of free-ranging and captive cervids (deer, elk and moose).

 

The presence of infectious prions in the tissues, bodily fluids and environments of clinical and preclinical CWD-infected animals is thought to account for its high transmission efficiency. Recently it has been recognized that mother to offspring transmission may contribute to the facile transmission of some TSEs. Although the mechanism behind maternal transmission is not yet known, the extended asymptomatic TSE carrier phase (lasting years to decades) suggests that it may have implications in the spread of prions.

 

Placental trafficking and/or secretion in milk are 2 means by which maternal prion transmission may occur. In these studies we explore these avenues during early and late infection using a transgenic mouse model expressing cervid prion protein. Na€ıve and CWD-infected dams were bred at both timepoints, and were allowed to bear and raise their offspring. Milk was collected from the dams for prion analysis, and the offspring were observed for TSE disease progression. Terminal tissues harvested from both dams and offspring were analyzed for prions.

 

We have demonstrated that

 

(1) CWDinfected TgCerPRP females successfully breed and bear offspring, and

 

(2) the presence of PrPCWD in reproductive and mammary tissue from CWD-infected dams.

 

We are currently analyzing terminal tissue harvested from offspring born to CWD-infected dams for the detection of PrPCWD and amplification competent prions. These studies will provide insight into the potential mechanisms and biological significance associated with mother to offspring transmission of TSEs.

 

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

 

P.157: Uptake of prions into plants

 

Christopher Johnson1, Christina Carlson1, Matthew Keating1,2, Nicole Gibbs1, Haeyoon Chang1, Jamie Wiepz1, and Joel Pedersen1 1USGS National Wildlife Health Center; Madison, WI USA; 2University of Wisconsin - Madison; Madison, WI USA

 

Soil may preserve chronic wasting disease (CWD) and scrapie infectivity in the environment, making consumption or inhalation of soil particles a plausible mechanism whereby na€ıve animals can be exposed to prions. Plants are known to absorb a variety of substances from soil, including whole proteins, yet the potential for plants to take up abnormal prion protein (PrPTSE) and preserve prion infectivity is not known. In this study, we assessed PrPTSE uptake into roots using laser scanning confocal microscopy with fluorescently tagged PrPTSE and we used serial protein misfolding cyclic amplification (sPMCA) and detect and quantify PrPTSE levels in plant aerial tissues. Fluorescence was identified in the root hairs of the model plant Arabidopsis thaliana, as well as the crop plants alfalfa (Medicago sativa), barley (Hordeum vulgare) and tomato (Solanum lycopersicum) upon exposure to tagged PrPTSE but not a tagged control preparation. Using sPMCA, we found evidence of PrPTSE in aerial tissues of A. thaliana, alfalfa and maize (Zea mays) grown in hydroponic cultures in which only roots were exposed to PrPTSE. Levels of PrPTSE in plant aerial tissues ranged from approximately 4 £ 10 ¡10 to 1 £ 10 ¡9 g PrPTSE g ¡1 plant dry weight or 2 £ 105 to 7 £ 106 intracerebral ID50 units g ¡1 plant dry weight. Both stems and leaves of A. thaliana grown in culture media containing prions are infectious when intracerebrally-injected into mice. ***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.

 

===========

 

***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.***

 

SEE ;

 

Friday, May 15, 2015

 

Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions

 

Report

 


 

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

 

P.19: Characterization of chronic wasting disease isolates from freeranging deer (Odocoileus sp) in Alberta and Saskatchewan, Canada

 

Camilo Duque Velasquez1, Chiye Kim1, Nathalie Daude1, Jacques van der Merwe1, Allen Herbst1, Trent Bollinger2, Judd Aiken1, and Debbie McKenzie1 1Centre for Prions and Protein Folding Diseases; University of Alberta; Edmonton, Canada; 2Western College of Veterinary Medicine; University of Saskatchewan; Saskatoon, Canada

 

Chronic wasting disease (CWD) is an emerging prion disease of free ranging and captive species of Cervidae. In North America, CWD is enzootic in some wild cervid populations and can circulate among different deer species. The contagious nature of CWD prions and the variation of cervid PRNP alleles, which influence host susceptibility, can result in the emergence and adaptation of different CWD strains. These strains may impact transmission host range, disease diagnosis, spread dynamics and efficacy of potential vaccines. We are characterizing different CWD agents by biochemical analysis of the PrPCWD conformers, propagation in vitro cell assays1 and by comparing transmission properties and neuropathology in Tg33 (Q95G96) and Tg60 (Q95S96) mice.2 Although Tg60 mice expressing S96- PrPC have been shown resistant to CWD infectivity from various cervid species,2,3

 

***these transgenic mice are susceptible to H95 C CWD, a CWD strain derived from experimental infection of deer expressing H95G96-PrPC. The diversity of strains present in free-ranging mule deer (Odocoileus hemionus) and white-tailed deer (Odocoileus virginianus) from Alberta and Saskatchewan is being determined and will allow us to delineate the properties of CWD agents circulating in CWD enzootic cervid populations of Canada.

 

References

 

1. van der Merwe J, Aiken J, Westaway D, McKenzie D. The standard scrapie cell assay: Development, utility and prospects. Viruses 2015; 7(1):180–198; PMID:25602372; http://dx.doi.org/10.3390/v7010180

 

2. Meade-White K, Race B, Trifilo M, Bossers A, Favara C, Lacasse R, Miller M, Williams E, Oldstone M, Race R, Chesebro B. Resistance to chronic wasting disease in transgenic mice expressing a naturally occurring allelic variant of deer prion protein. J Virol 2007; 81(9):4533–4539; PMID: 17314157; http://dx. doi.org/10.1128/JVI.02762-06

 

3. Race B, Meade-White K, Miller MW, Fox KA, Chesebro B. In vivo comparison of chronic wasting disease infectivity from deer with variation at prion protein residue 96. J Virol 2011; 85(17):9235–9238; PMID: 21697479; http://dx.doi.org/10.1128/JVI.00790-11

 

=========

 

***these transgenic mice are susceptible to H95 C CWD, a CWD strain derived from experimental infection of deer expressing H95G96-PrPC.

 

==========

 

P.136: Mother to offspring transmission of CWD—Detection in fawn tissues using the QuIC assay

 

Amy Nalls, Erin McNulty, Clare Hoover, Jeanette Hayes-Klug, Kelly Anderson, Edward Hoover, and Candace Mathiason Colorado State University; Fort Collins, CO USA

 

To investigate the role mother to offspring transmission plays in chronic wasting disease (CWD), we have employed a small, polyestrous breeding, indoor maintainable cervid model, the Reeves’ muntjac deer. Muntjac doe were inoculated with CWD and tested positive by lymphoid biopsy at 4 months post inoculation. From these CWD-infected doe, we obtained 3 viable fawns. These fawns tested IHC-positive for CWD by lymphoid biopsy as early as 40 d post birth, and all have been euthanized due to clinical disease at 31, 34 and 59 months post birth. The QuIC assay demonstrates sensitivity and specificity in the detection of conversion competent prions in peripheral IHC-positive tissues including tonsil, mandibular, partotid, retropharyngeal, and prescapular lymph nodes, adrenal gland, spleen and liver. In summary, using the muntjac deer model, we have demonstrated CWD clinical disease in offspring born to CWD-infected doe and found that the QuIC assay is an effective tool in the detection of prions in peripheral tissues. ***Our findings demonstrate that transmission of prions from mother to offspring can occur, and may be underestimated for all prion diseases.

 

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

 

***Our findings demonstrate that transmission of prions from mother to offspring can occur, and may be underestimated for all prion diseases.

 

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

 


 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

31 Jan 2015 at 20:14 GMT

 


 

 Saturday, January 31, 2015

 

European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

 


 

 Friday, May 22, 2015

 

*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual Meeting 12-14 May 2014 ***

 


 

Saturday, May 30, 2015

 

PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 


 


 

Wednesday, June 10, 2015

 

Zoonotic Potential of CWD Prions

 

LATE-BREAKING ABSTRACTS

 


 

PRION CONFERENCE 2014 HELD IN ITALY RECENTLY CWD BSE TSE UPDATE

 

> First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)

 

PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping up the future of prion research

 

Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)

 


 

Friday, August 14, 2015

 

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

 


 

Friday, May 22, 2015

 

*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual Meeting 12-14 May 2014

 


 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

31 Jan 2015 at 20:14 GMT

 


 

Envt.07:

 

Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease

 

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

 


 

Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...

 

Abstract The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.

 


 

***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********

 

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

 

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)

 

These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

 

Table 9 presents the results of an analysis of these data.

 

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

 

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

 

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

 

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

 

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

 

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

 

snip...

 

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

 

snip...

 

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

 

snip...

 

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

 

snip...see full report ;

 


 

CJD9/10022

 

October 1994

 

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

 

Dear Mr Elmhirst,

 

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

 

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

 

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

 

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

 

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

 

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

 


 

Wednesday, March 18, 2009

 

Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

 


 

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

 

From:

 

Sent: Sunday, September 29, 2002 10:15 AM

 

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

 

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

 

Thursday, April 03, 2008

 

A prion disease of cervids: Chronic wasting disease

 

2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.

 

snip...

 

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

 

snip... full text ;

 


 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target.

 

*** Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

 


 

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

 


 

*** 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.

 


 

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

 

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

 

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

 


 

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

 

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

 


 

White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation

 

snip...

 

It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that

 

1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and

 

2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.

 

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.

 


 


 

2012

 

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

 

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

 

snip...

 

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.

 

*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

 

Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

 


 

2011

 

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.

 


 

 I was listening to a radio show the other day here in the Galveston bay area, and outdoor show, they had a breeder or someone from the industry on, and I was amazed at the false information he was spewing. the part about the poor little girl with her pet deer crying in the breeder pen, ......cry me a friggen river, they are raising the damn deer to put in a pen to slaughter, or to breed for that purpose, AND you ought to see a human die from this shit. my mother did everything Linda Blair did in that movie the exorcist except spin her head 360 degrees. she DID levitate in bed because she would jerk so bad, where it took three grown strong adults to hold her down to keep her from hurting herself, all the while screaming God why can’t I stop this. so cry me a fucking river on a damn deer they are raising to have slaughtered, but whine because the TPWD et al are going to kill it to try and prevent the spread of disease cwd. if the TPWD et al had a better way of confirming or not whether those cervid had CWD, they would do it. the live tests they have to date do not work 100%, so there for they have not been validated. oh that’s fine with the pen owners, but it’s not fine for Texas. you don’t want a cwd test that just works part of the time. it’s total ignorance out there now, and they will put lipstick on this pig and take her to the dance, just like TAHC did with mad cow disease, and that’s well documented. they will change what ever law to meet their needs$$$ I will agree with this much of what the industry said this morning, that cwd has been in Texas for a long time, and in the pens to, and that the TAHC has not tested enough, that much he got correct. I have been saying this year, after year, after year, since back to 2001, to the TAHC, and told them exactly where they should be testing back in 2001, and then year after year after year, up and until 2012, where they finally did test there in enough numbers to find it a decade later, exactly where I been saying it was. the cwd deer have been waltzing across Texas from there for over a decade. it does not matter if I am pro-pen or not. that will not and does not change the science. why in the hell did they speak about the 4 confirmed deer from that index herd, yes, I said 4 now. why is not the TAHC TPWD telling that to the public now. why did not that guy today speak of 4? all the newspapers are reporting it, and I ask about the 4th case weeks and weeks ago? where is that information at on TAHC site? I am a meat eater, I am pro-hunt, and extremely pro-gun, I am however anti-stupid and anti-prion, prions can kill you, I don’t want to eat prions, you should not either. but here is the kicker, you eat meat infected with CWD TSE prion, your exposed, however you never go clinical in your life........BBBUT, your exposed and if you go on to have surgical, dental, tissue, blood donations, etc. you risk exposing my family and others...I will simply post this one short abstract of an old study the late great Dr. Gibbs did, an old friend of mine I corresponded with many times before his passing.

 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

 

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

 


 

Thursday, August 13, 2015

 

Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years

 


 

Monday, August 17, 2015

 

FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS

 

*** I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;

 


 

 Singeltary Sunday School Class

 

o.k. I’m going to get Biblical today, it’s Sunday. I think the way I have interpreted the Bible to date, from the parts I have read and understood. God gave Man the duty of caretaker of the animals, and in that, we could eat them, while taking care of them. I think we have failed terribly in the way we take care of animals, the way we raise them for consumption. we failed God, and I think God is trying to tell us something here with CWD TSE prion. even with the scorched earth policy that I still say we must go by to date as much as I hate it, to eradicate CWD TSE prion, I think it’s all a part of Gods wrath, in that we have failed terribly as the stewards of the animails he told us to be, and has brought his wrath upon us, in the form of CWD TSE prion disease. we went from the hunt for food, the hunt to fill our freezers that God gave us, and in plenty. we went from that, to an industry crying about all those headless deer in Texas due to the fact it’s the only sure fire way to test for CWD with accuracy, to try and prevent a deadly disease in both animal and man, and to save the environment from further spread of CWD, yet these same people crying about all those headless deer will all rush to the taxidermist with a head to have mounted to fill ones wall full of heads. or you will have some poor breeder family, urine mill family, antler deer family, pen owner family, high/low fence owner family, sperm mill straw bred buck family, all crying because their pet deer are being slaughtered, yet in the long run, that’s just what they are raising the deer for anyone, to be slaughtered. I guess I don’t understand that part. ...I’m just thinking out of the box today, please understand I am still a meat eater, I guess just a bit disgusted with myself and others today. Sunday School class is over. carry on...

 

Sunday, August 23, 2015

 

TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas

 


 

 

old Indian Saying

 

When white man find land, Indians running it.

 

No taxes, no debt, plenty buffalo, plenty beaver, clean water; women did all the work, medicine man free. Indian man spend all day hunting and fishing; all night having sex.

 

Only white man dumb enough to think he can improve system like that.

 

 

Terry S. Singeltary Sr.