Monday, February 02, 2015

New Jersey Assembly Bill 2903 Establishes licensing program in Department of Agriculture for farmed deer and other cervids

 

 
Sent: Monday, February 02, 2015 10:16 AM
Subject: New Jersey Assembly Bill 2903 Establishes licensing program in Department of Agriculture for farmed deer and other cervids
 

New Jersey Assembly Bill 2903 Establishes licensing program in Department of Agriculture for farmed deer and other cervids
 
 
Greetings New Jersey Politicians et al to decide New Jersey Assembly Bill 2903 Establishes licensing program in Department of Agriculture for farmed deer and other cervids.
 
USDA et al have failed terrible in the control of the Transmissible Spongiform Encephalopathy TSE Prion disease i.e. CWD of cervids, Scrapie of sheep and goats, and BSE aka mad cow disease in the bovine, both the typical and atypical strains. by letting the USDA take control of the wild cervids, and reclassify them as livestock, will be a downfall for the wild herds in more ways than one. all the USDA care about is TRADE $$$
 
by choosing USDA et al over state agencies (neither is perfect), you risk CWD spreading into the wild cervid herds. just look what happened in the state of Pennsylvania (see that history below).
 
once cwd is established in your state, once that tse prion jeannie is out of the bottle, it is very difficult to put that tse prion back in the bottle. in fact, very few have been successful at that, once cwd has been documented.
 
I have watched the USDA debacle on mad cow disease since day one. as a layperson, I have followed the TSE prion aka mad cow type disease since December 14, 1997, when I watched my mother die from Heidenhain Variant of Creutzfeldt Jakob Disease. science has now linked sporadic CJD to mad cow disease i.e. atypical BSE, and now to Scrapie, and science shows there is no species barrier for cwd to humans.
 
I thought you might need some science for the upcoming battle pitting hunter against shooting pens. these game farmers and USDA et al don’t care about science, it’s just the cash they care about, in my opinion, and in the opinion of many others. just follow the money.
 
I have put a great deal of the history of CWD TSE prion, along with much updated peer review scientific studies in my cwd blog and other TSE blogs. please take note to the sources of that data. they speak for themselves. some confidential data. I do NOT nor have I ever advertised or made money doing this. it’s for education use. please use as you wish, but if your serious about keeping Chronic Wasting Disease CWD out of New Jersey, you better think twice about turning over the captive cervid industry to the USDA, for all the following reasons...
 
kindest regards, terry
 
 
NJ A2903 | 2014-2015 | Regular Session
 
inShare0 New Jersey Assembly Bill 2903
 
NJ State Legislature page for A2903
 
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Summary Sponsors Texts Votes Research Comments Track Status Spectrum: Bipartisan Bill Status: Introduced on March 13 2014 - 25% progress Action: 2014-10-27 - Reported out of Assembly Committee, 2nd Reading Text: Latest bill text (Introduced) [HTML]
 
Summary Establishes licensing program in Department of Agriculture for farmed deer and other cervids.
 
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Monitor Legislation or view this same bill number from multiple sessions or take advantage of our national legislative search. Title Establishes licensing program in Department of Agriculture for farmed deer and other cervids.
 
Sponsors Rep Robert Andrzejczak [D] Rep John DiMaio [R]
 
History Date Chamber Action Date Chamber Action 2014-10-27 Assembly Reported out of Assembly Committee, 2nd Reading 2014-03-13 Assembly Introduced, Referred to Assembly Agriculture and Natural Resources Committee
 
Same As/Similar To S1842 (Same As) 2014-03-24 - Introduced in the Senate, Referred to Senate Economic Growth Committee
 
Subjects 2nd Reading in the Assembly
 
 
Bill Comments
 
 
Introduced
 
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Bill Title: Establishes licensing program in Department of Agriculture for farmed deer and other cervids.
 
Spectrum: Bipartisan Bill
 
Status: (Introduced) 2014-10-27 - Reported out of Assembly Committee, 2nd Reading [A2903 Detail]
 
Download: New_Jersey-2014-A2903-Introduced.html
 
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ASSEMBLY, No. 2903
 
STATE OF NEW JERSEY
 
216th LEGISLATURE
 
INTRODUCED MARCH 13, 2014
 
Sponsored by:
 
Assemblyman BOB ANDRZEJCZAK
 
District 1 (Atlantic, Cape May and Cumberland)
 
SYNOPSIS
 
Establishes licensing program in Department of Agriculture for farmed deer and other cervids.
 
CURRENT VERSION OF TEXT
 
As introduced.
 
An Act concerning Cervidae livestock operations and supplementing Titles 4 and 23 of the Revised Statutes.
 
Be It Enacted by the Senate and General Assembly of the State of New Jersey:
 
1. As used in this act:
 
"Cervid" means any member of the Cervidae family including deer, elk, moose, reindeer, and caribou, hybrids of these animals, and the germ plasm, embryos and fertile ova of these animals.
 
"Cervidae livestock operation" means a normal agricultural operation involved in the production, growing, breeding, using, harvesting, transporting, or marketing of cervid species or products.
 
"Department" means the Department of Agriculture.
 
"License" means a license issued by the Department of Agriculture to operate a Cervidae livestock operation pursuant to this act.
 
2. Notwithstanding any law, rule or regulation to the contrary, farmed cervids that are part of a Cervidae livestock operation shall be designated as agricultural livestock and shall be subject to the laws, rules and regulations governing the possession, care and breeding of that type of animal in the State.
 
3. a. There is established in the Department of Agriculture a licensing program for the operation of Cervidae livestock operations. This program shall comply with the provisions of the United States Department of Agriculture Chronic Wasting Disease Herd Certification Program.
 
b. The department shall inspect the premises of an applicant's facility and investigate each applicant for a license. An inspection may be made by the department or an agent of the department, including a licensed veterinarian accredited by the department.
 
c. The department shall issue a license if the department determines after inspection of the premises and investigation of the applicant that:
 
(1) the premises, including fences, buildings, equipment and sanitary conditions, comply with this act and the rules and regulations of the department governing farmed cervids; and
 
(2) the applicant is able to conduct a Cervidae livestock operation in compliance with this act and the rules and regulations of the department governing farmed cervids.
 
d. (1) A Cervidae livestock operation that is in operation on the effective date of this act pursuant to a valid license issued by the Department of Environmental Protection and in compliance with the applicable rules and regulations of both the Department of Environmental Protection and the Department of Agriculture concerning farmed cervids shall be granted a provisional license from the Department of Agriculture pursuant to this act.
 
(2) Within one year after the effective date of this act and prior to the expiration date of the existing license from the Department of Environmental Protection, the Department of Agriculture shall, for each provisional licensee: (a) perform the inspection and investigation required pursuant to this section; and (b) either issue a license or deny the application.
 
e. The department may charge reasonable fees to cover costs associated with implementing the licensing program established pursuant to this act.
 
4. a. A license issued by the department pursuant to this act shall be valid for a period of two years from the date of issuance.
 
b. A license shall be renewed upon application if the department determines that:
 
(1) the licensee has not been cited for a violation of this act or any rule or regulation of the department; and
 
(2) there is no reason to believe that the licensee is unable to conduct a Cervidae livestock operation in compliance with this act and the rules and regulations of the department governing farmed cervids.
 
c. The department may suspend or revoke the license of any Cervidae livestock operation violating any provision of this act or any rule or regulation adopted pursuant thereto.
 
5. a. Live cervids may be brought onto the premises of a Cervidae livestock operation through intrastate commerce, and may be removed from the premises or relocated to another premises in a manner consistent with this act and the rules and regulations of the department governing farmed cervids. Upon delivery of a live cervid, the Cervidae livestock operation shall prepare and deliver to the shipper, purchaser or consignee a receipt, detailed invoice or consignment document that clearly states the date, the name, address and telephone number of the purchaser or person to whom the cervid is sold or consigned, the quantity, sex, and species of the cervid, and the name and address of the Cervidae livestock operation.
 
b. Cervids and cervid products may be removed from the premises of a Cervidae livestock operation in a manner consistent with this act and the rules and regulations of the department governing farmed cervids. Prior to removal from the premises of a dead cervid or part of a cervid, the Cervidae livestock operation shall place the dead cervid or part of the cervid in a package or container, or attach a label to it. The package, container, or label shall have printed upon it the name, address and telephone number of the Cervidae livestock operation that produced the cervid. The Cervidae livestock operation shall also issue a receipt, detailed invoice or consignment document including the date of shipment or sale, the name of the shipper, purchaser or consignee, the quantity, sex and species of the cervid shipped or sold, and the name, address, telephone number and license number of the Cervidae livestock operation shipping, consigning or selling cervids. A dead cervid produced under the authority of the Cervidae livestock operation may not be removed from its package or container or have removed from it the label provided for in this subsection until final consumption or disposal.
 
6. The department, pursuant to the "Administrative Procedure Act," P.L.1968, c.410 (C.52:14B-1 et seq.), shall adopt rules and regulations concerning Cervidae livestock operations.
 
These rules and regulations shall include, but need not be limited to, rules and regulations governing the type of pens and enclosures used for Cervidae livestock operations, and shall require, at a minimum, that a Cervidae livestock operation:
 
a. be surrounded, along its outside perimeter, by a fenced enclosure that is designed to prevent ingress and egress, and which has a height of at least eight feet, as measured from the ground to the top of the fence; and
 
b. be established and maintained on a premises that is adequate to provide for the health and welfare of the cervids.
 
7. Nothing in sections 1 through 6 of this act shall be construed to:
 
a. affect the authority of the Department of Environmental Protection and the Fish and Game Council to promulgate rules and regulations concerning the possession of cervids that are not part of a Cervidae livestock operation; or
 
b. exempt any person from the provisions of Title 23 of the Revised Statutes, or any rules or regulations adopted pursuant thereto, concerning the release or escape of farmed cervids into the wild.
 
8. Notwithstanding the provisions of R.S.23:3-28 through R.S.23:3-39, or any rule or regulation adopted pursuant thereto, to the contrary, the Department of Environmental Protection and the Fish and Game Council shall have no authority to promulgate rules or regulations concerning Cervidae livestock operations that receive a license from the Department of Agriculture pursuant to sections 1 through 7 of P.L. , c. (C. ) (pending before the Legislature as this bill).
 
9. This act shall take effect immediately.
 
STATEMENT
 
This bill would designate farmed cervids (deer and similar hoofed mammals) that are part of a Cervidae livestock operation as agricultural livestock, and it would establish a licensing program for Cervidae livestock operations. The Department of Agriculture would be required by the bill to adopt rules governing the operation of licensed Cervidae livestock operations.
 
The bill would eliminate the authority of the DEP and the Fish and Game Council to promulgate rules or regulations concerning Cervidae livestock operations. However, the DEP and the Fish and Game Council would retain their authority to regulate the possession of cervids that are not part of a Cervidae livestock operation. In addition, the bill would not exempt any person from fish and wildlife laws, or any rules or regulations adopted pursuant thereto, concerning the release or escape of farmed cervids into the wild.
 
In 2002, the Department of Environmental Protection's (DEP) Division of Fish and Wildlife banned the importation of deer and elk into the State as a precautionary measure to prevent the spread of chronic wasting disease into the State's wild and farmed herds of animals belonging to the deer family. Under current rules, a person wishing to import cervids into the State must comply with requirements set forth by both the Department of Agriculture and the DEP's Division of Fish and Wildlife. This bill would establish the sole authority for the regulation of farmed cervid herds in the Department of Agriculture.
 
 
 
Sponsors Representative Robert Andrzejczak [D]
 
Representative John DiMaio [R]
 
Social Comments on NJ A2903
 
 
 
how much is a state and it’s taxpayers willing to pay for captives shooting pens, sperm mills, antler mills, urine mills, velvet mills, game farms, high/low fence ranches, how much is that risk worth to each and every hunter or wildlife
enthusiast in the state of New Jersey ??? well, this is too much...
 
Tuesday, December 20, 2011
 
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
 
The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.
 
SUMMARY:
 
 
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). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
 
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
 
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
 
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
 
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
 
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
 
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
 
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
 
-30-
 
 
 
*** see history of this CWD blunder here ;
 
 
 
18. 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.
 
 
 
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
 
 
 
Saturday, January 31, 2015
 
European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route
 
 
Sunday, December 28, 2014
 
CHRONIC WASTING DISEASE CWD TSE PRION DISEASE AKA MAD DEER DISIEASE USDA USAHA INC DECEMBER 28, 2014
 
 
Tuesday, January 06, 2015
 
APHIS Provides Additional Information on Chronic Wasting Disease (CWD) Indemnity Requests January 5, 2015 05:26 PM EST
 
 
Indiana SENATE BILL No. 442 Miller Pete Hunting wildlife Removes exotic mammals from the animals that may be propagated or offered for hunting at a shooting preserve Makes it a Class C misdemeanor
 
 
paying to play, just follow the money $$$
 
Thursday, January 15, 2015
 
*** INDIANA HB1453 - high fence hunting preserve bill has been introduced by Rep. Sean Eberhart and he received monetary contribution from Indiana Deer and Elk Farmers Advocates INC.
 
 
CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD $$$
 
CWD, spreading it around...
 
Tuesday, January 06, 2015
 
APHIS Provides Additional Information on Chronic Wasting Disease (CWD) Indemnity Requests January 5, 2015 05:26 PM EST
 
 
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
 
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.
 
 
 
 
 
***please read this***
 
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.
 
 
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.
 
 
*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.
 
*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.
 
PRION 2014 CONFERENCE
 
CHRONIC WASTING DISEASE CWD
 
A FEW FINDINGS ;
 
Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.
 
We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.
 
The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.
 
Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.
 
Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.
 
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.
 
Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.
 
Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.
 
see full text and more ;
 
Monday, June 23, 2014
 
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
 
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
 
 
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
 
 
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
 
 
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
 
 
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
 
 
Sunday, December 21, 2014
 
Mucosal immunization with an attenuated Salmonella vaccine partially protects white-tailed deer from chronic wasting disease
 
 
Friday, December 19, 2014
 
Pan-Provincial Vaccine Enterprise Inc. (PREVENT) Conducting a Chronic Wasting Disease (CWD) Vaccine Efficacy Trial in Elk
 
 
CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD $$$
 
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 ;
 
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...
 
 
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
 
 
FDA WARNING LETTER (14-ATL-04) adulterated under Section 402(a)(4) [21 U.S.C. 342(a)(4)] of the Act, protein derived from mammalian tissues to feeds that may be used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)]
 
Newberry Feed & Farm, Inc. 2/14/14 Department of Health and Human Services logoDepartment of Health and Human Services Public Health Service
 
Food and Drug Administration Atlanta District Office 60 8th St., NE Atlanta, GA 30309
 
February 14, 2014
 
VIA UPS
 
J. Clint Layne, President/Co-owner Rhett Baker, Secretary-Treasurer/Co-owner Newberry Feed & Farm Center, Inc. 131 Giff Street Newberry, SC 29108
 
WARNING LETTER (14-ATL-04)
 
Dear Messrs. Layne and Baker,
 
An inspection of your feed mill located at 2431 Vincent Street, Newberry, SC 29108 conducted by Investigators from the U.S. Food & Drug Administration (FDA) and South Carolina Department of Agriculture on September 5-9, 2013 revealed significant violations of Current Good Manufacturing Practice (CGMP) regulations for Medicated Feeds found in Title 21, Code of Federal Regulations, Part 225 (21 C.F.R. 225). Such violations cause the medicated feeds manufactured at your facility to be adulterated within the meaning of Section 501(a)(2)(B) of the Federal Food, Drug, and Cosmetic Act (the Act) [21 U.S.C. § 351(a)(2)(B)] in that the methods used in, or the facilities or controls used for the manufacture, processing, packing, or holding of the medicated feeds do not conform to or are not operated or administered in conformity with current good manufacturing practices.
 
The inspection also revealed significant violations of the requirements set forth in Title 21, Code of Federal Regulations, Section 589.2000 (21 C.F.R. 589.2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). Animal feeds and feed ingredients containing prohibited mammalian proteins are considered potentially injurious to ruminant and public health. Because you failed to comply with the requirements set forth in 21 C.F.R. 589.2000, the feed products manufactured and distributed by your facility are adulterated within the meaning of Section 402(a)(4) of the Act [21 U.S.C. 342(a)(4)] in that they have been prepared, packed, or held under insanitary conditions whereby they may have become contaminated with filth or rendered injurious to health. The adulterated feed was subsequently misbranded within the meaning of Section 403(a)(1) of the Act [21 U.S.C. 343(a)(1)] because it was not properly labeled with the required BSE cautionary statement.
 
Medicated Feed CGMP violations observed during the inspection include, but are not limited to, the following:
 
1. You failed to ensure that all equipment that comes in contact with the active drug component, feeds in process or finished medicated feed is subject to reasonable and effective procedures to prevent unsafe contamination of feeds with drugs. [21 C.F.R. 225.65(b)]
 
Your written equipment cleaning procedure that requires flushing with a minimum of (b)(4) does not appear to be effective to prevent unsafe contamination of your manufactured feed. During the inspection, our Investigators observed a build-up of feed residue on surfaces inside the mixer that was approximately three inches thick in accumulation. This build-up was observed on the equipment throughout the inspection, including after flushing had been performed. In addition, the cleaning procedure does not include cleaning of the hand-add chute or scoops/buckets used to handle ingredients that are then used to manufacture medicated feed. During the inspection, our Investigators observed a build-up of feed residues approximately four inches thick on the inside of the chute used to add the drug ingredients and other “hand-adds”. Considering the extent of residue accumulation—some of which would include the drug sources used in your medicated feeds—on surfaces in the mixer and the hand-add chute, it is likely that chunks of this material break off periodically, and may sometimes end up in feeds not intended to contain that drug.
 
This is a repeat observation from the July 24-26, 2012 inspection. Your response to the Form FDA 483, Inspectional Observations, issued to you following the 2012 inspection stated the buckets and scoops would be replaced, and you would schedule a regular cleaning of the equipment every (b)(4). Based on the accumulation of residual feed observed on manufacturing equipment during the inspection and which remained following flushing, you have either failed to implement the promised corrective action or you have failed to ensure that the corrective action was lasting and effective in preventing the violation from recurring.
 
On October 3, 2013, we received your response to the Form FDA 483 issued to you following the September 2013 inspection. You state in your response that you have posted signs, added cleaning of the dump chute to the (b)(4) cleaning procedure, and increased the physical cleaning of the mixer to (b)(4). You also state that dedicated scoops will be used for each component or drug and have ordered disposable liners for the buckets that will be discarded following each dumping of product. However, you did not provide any documentation to demonstrate these changes have been made, such as photos of the new sign or newly cleaned equipment, or copies of the revised cleaning procedure.
 
2. You failed to investigate and implement corrective action where the results of assays indicated that the level of drug in medicated feed was not in accord with label specifications or not within permissible assay limits. An original or copy of the record of such action must be maintained on the premises. [21 C.F.R. 225.58(d)]
 
Your firm failed to adequately investigate and implement corrective action when you received an assay result on 6/21/13 for a Type C medicated feed containing Amprolium, showing the drug present at 73% of the concentration stated on the label. This assay result is outside of the assay limits of 80-120% established in 21 C.F.R. 558.4. The subsequent review of production and inventory records conducted by your firm revealed these records were “OK”, and it was determined the feed sample was taken incorrectly. Your firm’s “\investigation sheet” dated 6/21/13 states the corrective action as “[t]rying to make sure the samples are taken correctly.” No technique or procedural changes were made in response to the described corrective action, however. Thus, your firm failed to implement any corrective action in response to the out of specification assay result.
 
Your firm also received assay results for a Type C medicated broiler feed containing a Salinomycin concentration of 75% on 7/7/12 and 78% on 8/3/12. These assay results are outside the specification tolerance of 80-120% of the concentration stated on the label. [21 C.F.R. 558.4]. Your firm did not initiate any investigation or corrective action after receiving these results. Failure to investigate and implement corrective action following an out-of-limits assay is a repeat observation from the July 24-26, 2012 inspection.
 
In your response to the Form FDA 483 issued to you following the September 2013 inspection, you state that you have instructed personnel further on completing the investigation form and have also added sampling instructions to the procedures manual. However, you did not provide copies of the new/revised investigation form or the revisions to the procedures manual discussing sampling.
 
3. Your daily inventory records fail to record the batches or production runs (or lots) of medicated feed in which each drug was used. [21 C.F.R. 225.42(b)(6)(iii)] Although your daily inventory records appear to contain all of the other required information, due to the way the form is designed, there is only space to record one batch per day per drug and no space to record the name of the product, lot number, or other identifier for that batch. Your daily inventory record must reflect every batch or lot of medicated feed manufactured each day.
 
4. You failed to document in the daily inventory record actions taken to reconcile any discrepancies in the daily inventory record. [21 C.F.R. 225.42(b)(6)(v)] For example, the drug inventory conducted on 8/30/13 revealed a discrepancy with respect to one fifty pound bag of (b)(4)(a Type A medicated article). It does not appear that your firm took any action to reconcile this discrepancy.
 
You state in your response to both #3 and #4 above that you have added an area to the inventory control sheet to report any drugs that do not reconcile, and that there is a space to make notes and/or adjustments to inventory to ensure they reconcile. However, you did not indicate that the inventory control sheet had been adjusted to provide for the possibility that any single drug may be used more than once a day, and you did not provide any documentation—such as a copy of the revised form—to demonstrate that these changes have been made.
 
5. You have failed to properly identify, store, handle, and control drugs in your mixing areas to maintain their integrity and identity [21 C.F.R. 225.42(b)(4)]. Our inspection found that your firm was storing bags of Type A Medicated Articles in a manner and location that allowed them to be covered in bird droppings.
 
This finding also relates to your obligations under 21 C.F.R. 225.20(b)(2) and (3), which requires the facility to be maintained in a reasonably clean and orderly manner, and for access by birds and other pests to be minimized. During the September 5-6, 2013 inspection, our Investigators observed birds (greater than ten) nesting, flying, perched and foraging in the mill. Your response indicated that you are investigating ways to keep birds out of the mill, but that you did not yet have a plan at that time. You indicated that you would have a plan in place by November 1, 2013, but did not provide further information regarding any plan.
 
In addition, the following violations of the Animal Proteins Prohibited in Ruminant Feed regulation [21 C.F.R. 589.2000] were observed during the inspection:
 
1. You failed to use clean out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues to feeds that may be used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)]. Your feed is therefore adulterated under Section 402(a)(4) [21 U.S.C. 342(a)(4)] of the Act.
 
Because your firm uses animal proteins prohibited from use in ruminant feeds, and also makes feeds for ruminants, you are required to have a cleanout procedure adequate to prevent carryover into ruminant feeds. As noted above, our Investigators observed a significant build-up of feed residues inside the feed mixer and the hand-add chute, which remained following your cleanout procedure. This equipment is used for processing both proteins derived from mammalian tissues and feeds for ruminants. Since flushing was ineffective in removing the accumulated feed from the equipment, your clean out procedure was inadequate to prevent carryover of protein derived from mammalian tissues to feeds intended for ruminant animals.
 
Your response indicates that your corrective actions for this item are the same as for Item 1 above. However, as noted above, you did not provide any documentation to demonstrate that the changes you discussed have been made, or that they were adequate to address this issue.
 
2. You failed to label all products which contained or may have contained prohibited materials and that are intended for use in animal feed with the BSE cautionary statement, "Do not feed to cattle or other ruminants." [21 C.F.R. 589.2000(e)(1)(i).]
 
As discussed above, your clean out procedure is inadequate to prevent carryover of protein derived from mammalian tissues to feeds intended for ruminant animals. Thus, all feeds manufactured using your mixer and hand-add chute that did not contain the BSE cautionary statement “Do not feed to cattle or other ruminants,” are misbranded under Section 403(a)(1) [21 U.S.C. 343(a)(1)] of the Act. For example, a batch of Carolina Choice Beef Conditioner Custom Mix (b)(4), manufactured on September 6, 2013, while there was a significant build-up of feed residues in the feed mixer, was misbranded as its label did not contain the required BSE cautionary statement.
 
The above is not intended to be an all-inclusive list of violations at your facility. As a medicated and non-medicated feed manufacturer, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish procedures whereby such violations do not recur. Failure to promptly correct these violations may result in regulatory and/or administrative sanctions. These sanctions include, but are not limited to, seizure, injunction, and/or notice of opportunity for a hearing on a proposal to withdraw approval of your Medicated Feed Mill License under Section 512(m)(4)(B)(ii) of the Act and 21 C.F.R. 515.22(c)(2).
 
Based on the results of the September 5-9, 2013 inspection, evaluated together with the evidence before FDA when the Medicated Feed Mill License was approved, the methods used in, or the facilities and controls used for, the manufacture, processing, and packing of medicated feeds are inadequate to assure and preserve the identity, strength, quality, and purity of the new animal drugs therein. This letter constitutes official notification under the law and provides you an opportunity to correct the above described violations.
 
You should notify this office, in writing, within fifteen (15) working days of the receipt of this letter of the steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step being taken to correct the violations and prevent their recurrence. In your response, please include the timeframe in which the corrections will be completed and provide any documentation that will effectively assist us in evaluating whether the corrective actions have been made and the adequacy of such. If you are unable to complete the corrective actions within fifteen (15) working days, identify the reason for the delay and the time within which you will complete the corrections. Include copies of any available documentation demonstrating that corrections have been made.
 
Your written response should be sent to the U.S. Food and Drug Administration, Attn: Janice L. King, Compliance Officer, at the address noted in the letterhead. If you have questions, please contact Mrs. King at 843-746-2990 or write her at the noted address.
 
Sincerely, /S/ Philip S. Campbell Acting District Director Atlanta District Office
 
cc: South Carolina Department of Agriculture, Phillip C. Trefsgar
 
 
HOLY MAD COW BATMAN, how much went out into commerce, how much was recovered, what species are consuming these adulterated under Section 402(a)(4) [21 U.S.C. 342(a)(4)] of the Act, protein derived from mammalian tissues to feeds that may be used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)] ???
 
1. You failed to use clean out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues to feeds that may be used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)]. Your feed is therefore adulterated under Section 402(a)(4) [21 U.S.C. 342(a)(4)] of the Act.
 
Because your firm uses animal proteins prohibited from use in ruminant feeds, and also makes feeds for ruminants, you are required to have a cleanout procedure adequate to prevent carryover into ruminant feeds. As noted above, our Investigators observed a significant build-up of feed residues inside the feed mixer and the hand-add chute, which remained following your cleanout procedure. This equipment is used for processing both proteins derived from mammalian tissues and feeds for ruminants. Since flushing was ineffective in removing the accumulated feed from the equipment, your clean out procedure was inadequate to prevent carryover of protein derived from mammalian tissues to feeds intended for ruminant animals.
 
Your response indicates that your corrective actions for this item are the same as for Item 1 above. However, as noted above, you did not provide any documentation to demonstrate that the changes you discussed have been made, or that they were adequate to address this issue.
 
2. You failed to label all products which contained or may have contained prohibited materials and that are intended for use in animal feed with the BSE cautionary statement, "Do not feed to cattle or other ruminants." [21 C.F.R. 589.2000(e)(1)(i).]
 
As discussed above, your clean out procedure is inadequate to prevent carryover of protein derived from mammalian tissues to feeds intended for ruminant animals. Thus, all feeds manufactured using your mixer and hand-add chute that did not contain the BSE cautionary statement “Do not feed to cattle or other ruminants,” are misbranded under Section 403(a)(1) [21 U.S.C. 343(a)(1)] of the Act. For example, a batch of Carolina Choice Beef Conditioner Custom Mix (b)(4), manufactured on September 6, 2013, while there was a significant build-up of feed residues in the feed mixer, was misbranded as its label did not contain the required BSE cautionary statement...end...TSS
 
 
Rocky Ford Pet Foods 8/27/13 Department of Health and Human Services logoDepartment of Health and Human Services Public Health Service Food and Drug Administration Denver District Office Bldg. 20-Denver Federal Center P.O. Box 25087 6th Avenue & Kipling Street Denver, Colorado 80225-0087 Telephone: 303-236-3000 FAX: 303-236-3100
 
Rocky Ford Pet Foods 8/27/13 Department of Health and Human Services logoDepartment of Health and Human Services Public Health Service Food and Drug Administration Denver District Office Bldg. 20-Denver Federal Center P.O. Box 25087 6th Avenue & Kipling Street Denver, Colorado 80225-0087 Telephone: 303-236-3000 FAX: 303-236-3100
 
August 27, 2013
 
WARNING LETTER
 
VIA UPS Overnight
 
Mr. Juan Manuel Villegas Owner Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford, CO 81067 Ref. #: DEN-13-20-WL
 
Dear Mr. Villegas:
 
On February 25-27, 2013, the U.S. Food and Drug Administration (FDA) conducted an inspection of your rendering facility located at 21693 Highway 50 East, Rocky Ford, Colorado. This inspection revealed significant deviations from the requirements set forth in FDA regulations intended to reduce the risk of bovine spongiform encephalopathy (BSE) within the United States. These regulations are found in Title 21 of the Code of Federal Regulations (CFR), Section 589.2000 (21 CFR 589.2000), Animal Proteins Prohibited in Ruminant Feed, and Section 589.2001 (21 CFR 589.2001), Cattle Materials Prohibited in Animal Food or Feed to Prevent the Transmission of Bovine Spongiform Encephalopathy. These regulations address how renderers process (1) mammalian proteins prohibited from use in ruminant food or feed and (2) materials designated as “cattle materials prohibited in animal food or feed” (CMPAF) which are prohibited from use in animal food or feed. CMPAF include, but are not limited to:
 
The brain and spinal cord of cattle 30 months of age or older; The entire carcass of cattle infected with BSE; and The entire carcass of cattle 30 months of age or older that have not been inspected and passed for human consumption if the brains and spinal cords were not removed or otherwise effectively excluded from animal feed.
 
Your facility processes CMPAF.
 
Your failure to follow certain requirements of these regulations, as described below, resulted in products manufactured and distributed by your facilities being adulterated within the meaning of Section 402(a)(4) of the Federal Food, Drug, and Cosmetic Act (the Act), [21 U.S.C. 342(a)(4)] and misbranded within the meaning of Section 403(f) of the Act, [21 U.S.C. 343(f)]. You can find the Act, and its implementing regulations on the Internet through links on the FDA’s web page at www.fda.gov1.
 
Our inspection revealed the following serious deviations from the regulations at your rendering facility:
 
Failure to prevent the inclusion of cattle materials prohibited in animal feed (CMPAF) in animal feed or feed ingredients, as required by 21 CFR 589.2001(c)(1). Specifically, on February 25, 2013, our investigator observed that the unmarked CMPAF posterior sections of vertebral columns for two cows, identified by your firm as older than 30 months of age, were separated from the rest of the marked CMPAF material from those animals. The unmarked CMPAF material was then commingled with 18 additional posterior vertebral columns and placed in a trailer for shipment to another renderer for further processing and possible use in animal feed.
 
You removed all 20 posterior vertebral columns from the trailer during the inspection and stated that you would dispose of them in a landfill.
 
Failure to maintain adequate written procedures specifying how the process of removing the brain and spinal cord from cattle not inspected and passed for human consumption or 30 months of age or older is carried out, as required by 21 CFR 589.2001(c)(2)(ii). Specifically, your written procedure “Rocky Ford Ped [sic] Food Standard Operating Procedure for handling 30 month and older Beef and CMPAF Products” indicates that the head, vertebral column, and rib cage for cattle 30 months of age and older are kept in one piece. This written procedure is not consistent with actual operations observed at your firm on February 26, 2013. Our investigator observed that posterior vertebral columns from two cows 30 months of age or older were separated from the animals’ heads and anterior vertebral columns; the posterior sections were not marked as CMPAF material. Your written procedures fail to specify how, for animals 30 months of age or older, posterior vertebral columns separated from marked anterior vertebral columns would themselves be marked as CMPAF material.
 
Failure to mark the CMPAF and products that contain or may contain CMPAF with an agent that can be readily detected on visual inspection, as required by 21 CFR 589.2001(c)(2)(v). Specifically, the posterior sections of vertebra columns from cattle identified by your firm as 30 months of age or older were separated from the head and anterior vertebral columns but then were not identified as CMPAF with an agent readily detectable on visual examination. Therefore, the CMPAF posterior vertebral columns were indistinguishable from the non-CMPAF posterior vertebral columns.
 
Failure to label containers, including vehicles when used as containers, which contain CMPAF with the required statement, “Do not feed to animals,” as required by 21 CFR 589.2001(c)(2)(iv). Specifically, the dump truck and trailer used for storage and transport of CMPAF materials did not bear the statement “Do not feed to animals.”
 
Failure to avoid cross-contamination once CMPAF have been separated from other cattle materials as required by 21 CFR 589.2001(c)(2)(iii). Specifically, both marked and unmarked CMPAF were observed to be stored on the floor of the processing area rather than in separate containers that adequately prevent contact with animal feed, animal feed ingredients, or equipment surfaces, 21 CFR 589.2001(c)(2)(iii)(B). As described in item #1 above, the unmarked materials were indistinguishable from non-CMPAF materials and could result in cross-contamination.
 
This letter is not intended to serve as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.
 
You should notify this office in writing of the steps you have taken to bring your firm into compliance with the law within fifteen (15) working days of receiving this letter. Your response should include each step that has been taken or will be taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within fifteen (15) working days, state the reason for the delay and the timeframe within which the corrections will be completed. Please include copies of supporting documentation demonstrating that corrections have been made.
 
Your written response should be sent to: U.S. Food and Drug Administration, P.O. Box 25087, 6th Ave. and Kipling St., DFC, Bldg 20, Denver, CO 80225-0087, Attn: Sarah A. Della Fave, Compliance Officer. If you have any questions about this letter, please contact Ms. Della Fave at (303) 236-3006.
 
Sincerely, /S/ LaTonya Mitchell District Director
 
cc: Ronald K. Jones, D.V.M. Denver District Manager USDA/FSIS PO Box 25387 DFC, Bldg 45 Denver, CO 80225
 
Laurel Hamling Colorado Department of Agriculture Feed Program 2331 W. 31st Avenue Denver, CO 80211 - Close Out Letter Rocky Ford Pet Foods - Close Out Letter 4/16/142
 
 
 
price of prion poker goes up again with this study. I strongly urge the United States FDA et al to revisit their failed ruminant mad cow feed ban, where still to this day, the feed ban does NOT include cervids. ...
 
Saturday, January 31, 2015
 
European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route
 
 
> 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)
 
 
P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)
 
Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA
 
Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein
 
Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.
 
Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.
 
Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.
 
Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.
 
Thursday, November 21, 2013
 
*** Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy
 
The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a 90-100% attack rates, BSE from cattle failed to transmit, indicating agent adaptation in the deer.
 
 
TSS
 
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
 
CWD to cattle figures CORRECTION
 
Greetings,
 
I believe the statement and quote below is incorrect ;
 
"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."
 
Please see ;
 
Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.
 
 
" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "
 
shouldn't this be corrected, 86% is NOT a low rate. ...
 
kindest regards,
 
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
 
Thank you!
 
Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.
 
 
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
 
1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu
 
 
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.
 
snip...
 
 
----- Original Message -----
 
From: David Colby To: flounder9@verizon.net
 
Cc: stanley@XXXXXXXX
 
Sent: Tuesday, March 01, 2011 8:25 AM
 
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
 
Dear Terry Singeltary,
 
Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware
 
===========END...TSS==============
 
SNIP...SEE FULL TEXT ;
 
 
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010
 
 
Sunday, August 19, 2012
 
Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit
 
 
these cattle ranchers supporting these shooting pens, if there are any, could be in terrible shape if a strain of cwd was to jump to cattle...just saying.
 
Tuesday, December 23, 2014
 
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION ***
 
 
Sunday, December 15, 2013
 
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
 
 
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.
 
 
*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.
 
 
Veterinary Pathology Onlinevet.sagepub.com Published online before print February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February 27, 2014 0300985814524798
 
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats
 
D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1 E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA 2Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS, 6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email address: dseelig@umn.edu
 
Abstract
 
Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and progressive prion disease of cervids with an as yet to be fully clarified host range. While outbred domestic cats (Felis catus) have recently been shown to be susceptible to experimental CWD infection, the neuropathologic features of the infection are lacking. Such information is vital to provide diagnostic power in the event of natural interspecies transmission and insights into host and strain interactions in interspecies prion infection. Using light microscopy and immunohistochemistry, we detail the topographic pattern of neural spongiosis (the “lesion profile”) and the distribution of misfolded prion protein in the primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular and subcellular associations between misfolded prion protein (PrPD) and central nervous system neurons and glial cell populations. From these studies, we (1) describe the novel neuropathologic profile of FelCWD, which is distinct from either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide evidence of serial passage-associated interspecies prion adaptation. In addition, we demonstrate through confocal analysis the successful co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and synaptophysin, which, in part, implicates each of these in the neuropathology of FelCWD. In conclusion, this work illustrates the simultaneous role of both host and strain in the development of a unique FelCWD neuropathologic profile and that such a profile can be used to discriminate between FelCWD and FSE.
 
prion chronic wasting disease immunohistochemistry interspecies cat feline spongiform encephalopathy transmissible spongiform encephalopathy adaptation species barrier
 
 
Sunday, March 09, 2014
 
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats
 
 
Monday, August 8, 2011
 
*** Susceptibility of Domestic Cats to CWD Infection ***
 
Oral.29: Susceptibility of Domestic Cats to CWD Infection
 
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†
 
Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu
 
Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness.
 
*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.
 
 
 
AD.63:
 
Susceptibility of domestic cats to chronic wasting disease
 
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA
 
Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.
 
*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.
 
 
www.landesbioscience.com
 
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
 
 
 
 
FELINE SPONGIFORM ENCEPHALOPATHY FSE
 
 
 
cwd exposure, and iatrogenic CJD, what if ???
 
*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***
 
 
snip...see full text ;
 
 
Thursday, January 2, 2014
 
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
 
 
*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.
 
 
Tuesday, November 04, 2014
 
*** Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011
 
 
Thursday, March 20, 2014
 
CHRONIC WASTING DISEASE CWD TSE PRION OF CERVID AND THE POTENTIAL FOR HUMAN TRANSMISSION THEREFROM 2014
 
 
Tuesday, July 01, 2014
 
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND POTENTIAL RISK FACTORS THERE FROM ***
 
 
Thursday, July 03, 2014
 
*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets? ***
 
 
Thursday, October 23, 2014
 
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
 
 
Tuesday, October 21, 2014
 
*** Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
 
 
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” ...page 26.
 
 
Sunday, January 06, 2013
 
USDA TO PGC ONCE CAPTIVES ESCAPE
 
*** "it‘s no longer its business.”
 
 
Sunday, July 13, 2014
 
Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape
 
 
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
 
 
Wednesday, September 04, 2013
 
***cwd - cervid captive livestock escapes, loose and on the run in the wild...
 
 
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, October 02, 2014
 
*** IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
 
 
Tuesday, April 29, 2014
 
CWD Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose FR Doc No: 2014-09714 April 29, 2014 UPDATE
 
 
*** 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.
 
 
 
when an industry is catering to the public, with products which can risk human and animal health, in my opinion, you should have NO property rights. you should not be able to hide behind property rights when you are clearly risking human and animal health from your product, or the way you handle that product. if you are going to raise, grow, produce a product for the consumer, you have an obligation NOT to risk the public domain, public property, and or the wild animal populations. just my opinion. ...
 
Thursday, July 24, 2014
 
*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations
 
 
 

Comment

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission ;

I believe that there is more risk to the world from Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from the United States and all of North America, than there is risk coming to the USA and North America, from other Countries. I am NOT saying I dont think there is any risk for the BSE type TSE prion coming from other Countries, I am just saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present mad cow risk factors in North America like they are not here?

North America has more strains of TSE prion disease, in more species (excluding zoo animals in the early BSE days, and excluding the Feline TSE and or Canine TSE, because they dont look, and yes, there has been documented evidence and scientific studies, and DEFRA Hound study, that shows the canine spongiform encephalopathy is very possible, if it has not already happened, just not documented), then any other Country in the world. Mink TME, Deer Elk cervid CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type BSE cattle, atyical HG type BSE cow (the only cow documented in the world to date with this strain), typical sheep goat Scrapie (multiple strains), and the atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical Scrapie has spread from coast to coast. sporadic CJD on the rise, with different strains mounting, victims becoming younger, with the latest nvCJD human mad cow case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL CDC.

typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al), and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. its all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$

the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing but ink on paper.

for this very reason I believe the BSE MRR policy is a total failure, and that this policy should be immediately withdrawn, and set back in place the BSE GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all TSE PRION disease in all species of animals, and that the BSE GBR risk assessments be made stronger than before.

lets start with the recent notice that beef from Ireland will be coming to America.

Ireland confirmed around 1655 cases of mad cow disease. with the highest year confirming about 333 cases in 2002, with numbers of BSE confirmed cases dropping from that point on, to a documentation of 1 confirmed case in 2013, to date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad cow feed ban, and the enforcement of that ban, has drastically reduced the number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in 2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow disease in the USA, we still have no clue as to the true number of cases of BSE mad cow disease in the USA or North America as a whole. ...just saying.

Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide* (excluding the United Kingdom)

Country/Year

snip...please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS

Attachments

 (1)

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

View Attachment:
 
 
Sunday, January 11, 2015
 
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
 
 
 
 
Saturday, January 31, 2015
 
RAPID ADVICE 17-2014 : Evaluation of the risk for public health of casings in countries with a “negligible risk status for BSE” and on the risk of modification of the list of specified risk materials (SRM) with regard to BSE
 
 
 
Terry S. Singeltary Sr.
 

posted by Terry S. Singeltary Sr. at 10:18 AM

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