Sunday, March 30, 2014

Chronic Wasting Disease Agents in Nonhuman Primates

Volume 20, Number 5—May 2014
 
Dispatch
 
Chronic Wasting Disease Agents in Nonhuman Primates
 
Brent RaceComments to Author , Kimberly D. Meade-White, Katie Phillips, James Striebel, Richard Race, and Bruce Chesebro
 
Author affiliations: National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA
 
Abstract
 
Chronic wasting disease is a prion disease of cervids. Assessment of its zoonotic potential is critical. To evaluate primate susceptibility, we tested monkeys from 2 genera. We found that 100% of intracerebrally inoculated and 92% of orally inoculated squirrel monkeys were susceptible, but cynomolgus macaques were not, suggesting possible low risk for humans.
 
snip...
 
The Study
 
Squirrel monkeys were inoculated intracerebrally or orally with CWD inocula (7). We initially reported that 11/13 intracerebrally infected monkeys died of CWD at 41 months postinoculation (mpi) on average, and disease developed in 2/12 orally infected squirrel monkeys on average of 69 mpi (7). Disease developed in the 2 remaining intracerebrally infected squirrel monkeys at 61 and 75 mpi, respectively, changing the intracerebral attack rate to 100% (Figure 1, Table 1). Of the 10 remaining orally inoculated squirrel monkeys, disease developed in 9, bringing the overall oral attack rate to 92% and the average incubation period to 68 mpi (Figure 1, Table 1). Clinical signs were subtle; the most prominent finding was gradual weight loss (Table 1). A final diagnosis of CWD agent infection was made by using immunoblotting and immunohistochemical testing to determine accumulation of abnormal, disease-associated prion protein (PrPres) in brain tissue (wwwnc.cdc.gov/EID/article/20/5/13-0778-Techapp1.pdf Adobe PDF file [PDF - 52 KB - 4 pages]).
 
To compare the neuropathologic changes in intracerebrally and orally infected squirrel monkeys, we analyzed 10 brain regions for spongiform lesion severity and PrPres deposition (Figure 1, panels B, C). No statistically significant differences were noted between the 2 routes of infection (p<0 .05="" 1="" 2="" 30="" 40="" 46="" 60="" adjacent="" affected="" agent="" aggregates.="" all="" and="" appeared="" appendix="" areas="" at="" brain.="" cerebellum="" commonly="" consistent="" cortical="" cwd="" d="" degeneration="" dense="" deposition="" deposits="" div="" e="" except="" extracellular="" f="" for="" forms:="" frequently="" frontal="" g="" generally="" gray="" h="" had="" igure="" in="" infected="" intracerebrally="" involvement="" j="" least="" lesions="" less="" little="" lobes="" lymph="" matter="" monkeys="" most="" node="" normal="" not="" observed="" occipital="" of="" orally="" panel="" parietal="" pericellular="" plaques="" positive="" prominent="" prpres="" punctate="" regions="" severe="" showed="" spleens="" spongiform="" squirrel="" striatum="" studied="" technical="" temporal="" that="" the="" throughout="" to="" vacuolation.="" was="" were="">
 
Of the squirrel monkeys under study, 3 PRNP genotypes were represented (7). In the group of orally infected squirrel monkeys, 3 had a unique heterozygous genotype that encoded either 4 or 5 octapeptide repeats. Two of these monkeys were the last orally infected monkeys to be euthanized because of clinical disease (80 and 107 mpi), and the third heterozygote was clinically normal at 108 mpi. Heterozygosity within the PRNP gene has been shown to delay or prevent prion disease (8) and may play a role in this study.
 
We inoculated cynomolgus macaques as another nonhuman primate model for cross-species transmission of CWD. Compared with squirrel monkeys, cynomolgus macaques are biologically closer to humans, and cynomolgus macaque PrP is more homologous to human PrP (7). Nine cynomolgus macaques were inoculated orally and 6 were inoculated intracerebrally with 1 of 3 CWD pools as described (7). Our first report included negative data from 1 cynomolgus macaque euthanized at 49 mpi (7). Since then, we have euthanized and screened 6 cynomolgus macaques for TSE (Table 2). No evidence of prion infection was detected by immunoblot and immunohistochemical methods (data not shown).
 
The lack of CWD transmission during >10 years suggests that a substantial species barrier exists between cervids and cynomolgus macaques. In most TSE animal models, PrPres can be detected by 1/3–1/2 of the known incubation periods. If we extrapolate this to the cynomolgus macaques in this study, negative test results at 9 years would suggest that the incubation period would be >18 years. Other prion studies of cynomolgus macaques reported clinical disease within 2–3 years after inoculation with variant Creutzfeldt-Jakob disease agents (9), 3 years after inoculation with bovine spongiform encephalopathy agents (10,11), and 5 years after inoculation with sporadic Creutzfeldt-Jakob disease agents (9,12). In contrast, our findings indicate that CWD is unlikely to develop in cynomolgus macaques.
 
The cause of susceptibility to CWD agents in squirrel monkeys and resistance to them in cynomolgus macaques is uncertain. Prnp/PRNP gene sequence variation has been linked to disease susceptibility (8), and differences in the PRNP genes of cynomolgus macaques and the genes of squirrel monkeys could play a major role. Comparison of PRNP sequences among cynomolgus macaques and squirrel monkeys showed differences exist at 5 codons (56, 100, 108, 159, and 182) (7). It is not clear which difference or combination of changes might confer protection to cynomolgus macaques, or if resistance is caused by other factors. Of the 5 codon differences described above, those of cynomolgus macaques and humans are identical at positions 56, 159, and 182.
 
Two SM-CWD brain samples were inoculated into squirrel monkeys and cynomolgus macaques to verify that SM-CWD was infectious, test for further adaptation, and to see if SM-CWD was infectious to a broader range of nonhuman primates. Two squirrel monkeys inoculated intracerebrally with SM-CWD brain homogenates (SMP2-CWD) died as a result of infection at 23–24 mpi (Table 1). These incubation periods decreased by >11 months compared with that of the donor squirrel monkey. Neurologic signs in the 2 SMP2-CWD were more pronounced than observed during the first passage; however, weight loss was reduced. Neuropathologic examination and Western blot for PrPres confirmed TSE in both squirrel monkeys. In contrast to SM-CWD infections, the SMP2-CWD-infected brains had spongiform lesions and PrPres deposition in the occipital lobe (Figure 2, panels A, B). Biochemical comparison of glycoform patterns among CWD, SM-CWD, and SMP2-CWD were made by using 3 different anti-PrP antibodies (L42, 6H4, and 3F4) (Technical Appendix Adobe PDF file [PDF - 52 KB - 4 pages]). In all cases, SM2-CWD had a greater proportion of unglycosylated PrPres and a lower proportion of double glycosylated PrPres than did SM-CWD (Figure 2, panel C). The decreased time of manifestation of disease, differences in glycoform patterns, and distribution of PrPres in brain tissue suggested that the CWD agent was still adapting within the squirrel monkey. However, similar to CWD, SM-CWD had not caused prion disease in cynomolgus macaques by 72 mpi (Table 2).
 
Conclusion
 
Our studies have shown that squirrel monkeys, but not cynomolgus macaques, were susceptible to CWD. Although these nonhuman primates are not exact models of human susceptibility, they support the data from transgenic mouse studies (3–6), in vitro experiments (13), and epidemiologic evidence (14,15) that suggest humans are at a low risk of contracting CWD. Nevertheless, it remains sensible to minimize exposure to tissues potentially contaminated with the CWD agent.
 
Dr Race is a staff scientist in the Laboratory of Persistent Viral Diseases, National Institute of Allergy and Infectious Diseases. His research interests are infectious diseases of humans and animals.
 
Acknowledgment
 
We thank Byron Caughey, Kim Hasenkrug, and James Carroll for critical review of the manuscript; Nancy Kurtz, Lori Lubke, and Dan Long for assistance with histology preparation; Don Gardner and Dana Scott for necropsy assistance and lesion interpretation; Ed Schreckendgust, Rocky Rivera, Michael Wagner, Leslie Trail, and Richard Cole for animal husbandry; Michael Parnell, Douglas Brining, and RMVB staff for assistance with nonhuman primate inoculations and health care; and Mike Miller, Terry Kreeger, Jean Jewell, and Lynn Creekmore for CWD-agent positive and negative cervid tissues. This research was supported by the Intramural Research Program of the NIH, NIAID.
 
References
 
snip... see full text ;
 



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


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

snip...

R. BRADLEY

http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf


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

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

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

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

snip...

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease. PMID: 6997404


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
 
 
*** 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.
 
 
The chances of a person or domestic animal contracting CWD are “extremely remote,” Richards said. The possibility can’t be ruled out, however. “One could look at it like a game of chance,” he explained. “The odds (of infection) increase over time because of repeated exposure. That’s one of the downsides of having CWD in free-ranging herds: We’ve got this infectious agent out there that we can never say never to in terms of (infecting) people and domestic livestock.”
 
 
P35
 
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD
 
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5
 
The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.
 
 
PPo3-7:
 
Prion Transmission from Cervids to Humans is Strain-dependent
 
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA
 
Key words: CWD, strain, human transmission
 
Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains.
 
*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,
 
*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.
 
Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.
 
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
 
PPo2-27:
 
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
 
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA
 
Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain.
 
*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
 
PPo2-7:
 
Biochemical and Biophysical Characterization of Different CWD Isolates
 
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany
 
Key words: CWD, strains, FT-IR, AFM
 
Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates.
 
*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.
 
 
UPDATED DATA ON 2ND CWD STRAIN
 
Wednesday, September 08, 2010
 
CWD PRION CONGRESS SEPTEMBER 8-11 2010
 
 
Envt.07:
 
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
 
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2 Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany †Presenting author; Email: dausm@rki.de
 
Chronic wasting disease (CWD) is a contagious, rapidly spreading transmissible spongiform encephalopathy (TSE) occurring in cervids in North America. Despite efficient horizontal transmission of CWD among cervids natural transmission of the disease to other species has not yet been observed. Here, we report a direct biochemical demonstration of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected cervids. The presence of PrPTSE was detected by Western- and postfixed frozen tissue blotting, while the seeding activity of PrPTSE was revealed by protein misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal muscles of CWD-infected WTD was estimated to be approximately 2000- to 10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE was located in muscle- associated nerve fascicles but not, in detectable amounts, in myocytes.
 
***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.
 
 
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<
 
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
 
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
 
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
 
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
 
Wednesday, January 01, 2014
 
Molecular Barriers to Zoonotic Transmission of Prions
 
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
 
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
 
 
 
PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
Sunday, August 25, 2013
 
HD.13: CWD infection in the spleen of humanized transgenic mice
 
Liuting Qing and Qingzhong Kong
 
Case Western Reserve University; Cleveland, OH USA
 
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals.
 
***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.
 
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system
 
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1
 
1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK
 
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.
 
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.
 
Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.
 
Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay.
 
***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.
 
PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
Sunday, August 25, 2013
 
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
 
 
Friday, November 09, 2012
 
*** Chronic Wasting Disease CWD in cervidae and transmission to other species
 
 
Sunday, November 11, 2012
 
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012
 
 
Friday, December 14, 2012
 
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012
 
 
Saturday, March 09, 2013
 
Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest Incubation Time Model for Prion Diseases
 
 
*** 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. ***
 
 
Thursday, January 2, 2014
 
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
 
 
Thursday, March 20, 2014
 
CHRONIC WASTING DISEASE CWD TSE PRION OF CERVID AND THE POTENTIAL FOR HUMAN TRANSMISSION THEREFROM 2014
 
 
Saturday, March 15, 2014
 
Potential role of soil properties in the spread of CWD in western Canada
 
 
Friday, February 08, 2013
 
*** Behavior of Prions in the Environment: Implications for Prion Biology
 
 
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...
 
 
 
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. ...
 
also, see where even decades back, the USDA had the same thought as they do today with CWD, not their problem...see page 27 below as well, where USDA stated back then, the same thing they stated in the state of Pennsylvania, not their damn business, once they escape, and they said the same thing about CWD in general back then ;
 
”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.
 
”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.
 
sound familiar $$$
 
Sunday, January 06, 2013
 
USDA TO PGC ONCE CAPTIVES ESCAPE
 
*** "it‘s no longer its business.”
 
 
Wednesday, September 04, 2013
 
*** cwd - cervid captive livestock escapes, loose and on the run in the wild
 
 
Singeltary submission ;
 
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
 
*** DOCUMENT ID: APHIS-2006-0118-0411
 
 
Friday, March 28, 2014
 
BUCK FEVER What can happen if preserve owners make the rules
 
BUCK FEVER
 
 
Saturday, March 29, 2014
 
Game Farm, CWD Concerns Rise at Boone and Crockett Club
 
 
TSS
 


Saturday, March 29, 2014

Game Farm, CWD Concerns Rise at Boone and Crockett Club

Game Farm, CWD Concerns Rise at Boone and Crockett Club

 

Friday, March 28, 2014 Concerned about captive deer operations transmitting diseases to wild herds, the Boone and Crockett Club now officially supports state bans on commercial import and export of deer or elk.

 

The Club also opposes efforts to relax regulation of captive cervid breeding operations or to remove management authority over such operations from state wildlife agencies.

 

A full position statement, posted here, was passed at the Club’s December meeting.

 

The Club’s concerns were reinforced at the recent Whitetail Summit hosted by the Quality Deer Management Association (QDMA), the first summit to focus on key issues and challenges facing free-ranging white-tailed deer.

 

“Of all the presentations, seminars and findings, I was most pleased to see the attention given to the connections between chronic wasting disease (CWD) and the game farming industry. This has been on our radar, and on the radar of QDMA, other conservation groups, state agencies and sportsmen for quite some time,” said Richard Hale, chairman of the Club’s Records Committee.

 

Hale added, “Congratulations to QDMA on one of the most impressive and well-run summits I’ve had the pleasure of attending and for keeping this issue front and center.”

 

CWD is a degenerative brain disease that affects elk, mule deer, white-tailed deer, and moose. The disease can be transmitted by direct animal-to-animal contact through saliva, feces and urine, and indirectly through environmental contamination. CWD is fatal in deer, elk and moose, but there is no evidence that CWD can be transmitted to humans, according to the CDC and The World Health Organization.

 

Documented cases of CWD have been found in captive and/or wild deer and elk in 22 states and two Canadian provinces. In some, but not all, cases where the disease has been found in wild populations, the disease is present in captive populations within these regions.

 

In 2002, the Boone and Crockett Club, Rocky Mountain Elk Foundation and the Mule Deer Foundation formed the CWD Alliance. Its purpose was to pool resources, share information and collaborate on ways to positively address the CWD issue. Other organizations have since joined the Alliance, including QDMA and the Wildlife Management Institute, which now administers the Alliance website www.cwd-info.org.

 

“Evidence strongly suggests that captive animals infected with CWD can serve as the source for the spread of the disease to other captive animals, and between captive animals and wild populations,” said Hale. “To reduce the risk to wild deer populations, several states passed laws prohibiting game farming or live captive deer and elk importation, but now they are fighting efforts to expand captive deer and elk breeding and shooting operations within their jurisdictions. The captive cervid industry is persistent in proposing new legislations to overturn these laws, or transfer the authority of captive deer and elk from state fish and game agencies to their respective departments of agriculture.”

 

No vaccine or treatment is available for animals infected with CWD and once established in a population, culling or complete depopulation to eradicate CWD has provided only marginal results. In fact, the prevalence of CWD is rising at an alarming rate in some infected wild deer populations. Prevention is the only truly effective technique for managing diseases in free-ranging wildlife populations. Consequently, what can be done is minimizing the spread of CWD by restricting intra- and interstate transportation captive, privately owned wildlife, which frequently occurs in game farming.

 


 

 boone and crockett club position statement

 

REGULATION OF GAME FARMS First Adopted December 7, 2013 - Updated December 7, 2013

 

Situational Overview

 

The captive cervid industry, also referred to as game farming, uses artificial means to breed captive deer, elk, and other cervids for sale in shooting preserve operations. These game farms commonly transport captive deer and elk to other shooting preserves in a state or in other states.

 

Transportation of captive, game farm animals has been shown to increase the risk of spreading parasites and infectious, diseases, such as chronic wasting disease (CWD) and bovine tuberculosis, to other captive and wild cervids in new locations. There is currently no way of testing live animals for CWD, and infected animals show no signs for at least 16-18 months post-infection. There is no vaccine, and despite fenced enclosures, captive animals often come in contact with wild populations thereby spreading diseases. Once CWD is present, the area cannot be decontaminated even if infected animals are removed. As a result, many states have banned or are attempting to ban the importation of captive cervids (as well as intact carcasses of hunter-killed, wild cervids) to lower the risk of spreading CWD and other infectious diseases.

 

Position

 

The Boone and Crockett Club supports state bans on importing or exporting captive deer and elk by game farming operations in order to protect the health of native populations. The Club opposes any legislation aimed at relaxing regulations governing captive cervid breeding operations or removing management authority over such operations from state wildlife agencies. The Club does not oppose the transportation of wild cervids by state agencies and non-governmental organizations for the purpose of re-establishing wild game animals to their historic, open ranges.

 

The breeding of captive deer, elk, and other cervids for profit to create abnormally large “trophy” animals for fenced shoots under non-fair chase conditions are addressed in the Boone and Crockett Club’s positions on “Genetic Manipulation of Game” and “Canned Shoots.”

 


 

 BUCK FEVER

 

What can happen if preserve owners make the rules

 

Damning investigation by Mr. Sabalow et al @ IndyStar, that shows what we have known for decades about, an industry run amuck, an industry that will eventually self regulate itself, if they get their way, an industry that in my opinion, has been spreading cwd to hell and back for decades, i.e. the shooting pen industry. ...tss

 

BUCK FEVER

 

What can happen if preserve owners make the rules

 

What can happen if preserve owners make the rules

 

At one Indiana high-fence operation, deer — some ill or appearing drugged — were hunted in what prosecutors called 'killing pens.' Today, laws like those that sent the owner to prison are under assault in many states.

 

Ryan Sabalow, ryan.sabalow@indystar.com

 

"I think the DNR was so jealous 'cause I was selling deer for hundreds of thousands of dollars, and it would take 10 years for them to make what I was making in one day." — Russ Bellar

 

Buck Fever

 

Chapter 4

 

The nation's deer farmers are aggressively lobbying for regulatory changes that would benefit their industry. One Indiana case serves as a warning of what could happen if the industry is allowed to set its own rules. Robert Scheer/The Star

 

PERU, Ind. – For seven days in January 2005, a jury in a federal courtroom heard tales from a now-notorious Indiana hunting preserve of deer being drugged and even a sick deer propped up in a 1-acre pen so a hunter could shoot a $15,000 trophy.

 

Jurors heard testimony from an outdoor television celebrity, a corporate CEO, a country music star and an ex-NFL quarterback, some of whom paid substantial sums to shoot deer in enclosures so small that prosecutors dubbed them "killing pens." One shot his deer only minutes after it was released from a trailer. ...

 

snip...see full text, videos of interviews and such ;

 


 

Overview: Trophy industry breeds risk disease, costs taxpayers millions

 

The pursuit of deer bred for enormous antlers and shot in hunting pens is compromising our ethics and laws, and comes with growing risk and costs. http://www.indystar.com/longform/news/investigations/2014/03/27/buck-fever-intro/6865031/

 

Chapter 1: A troubling industry is born

 

Amish farmer unwittingly helped give rise to a booming new business — and ethical and legal quandaries.

 

"I am the king behind my fence. These are my deer." — Marty Berry, Texas deer breeder

 


 

Chapter 3: How fair is the chase?

 


 

Chapter 4: What can happen if preserve owners make the rules

 


 

Is the rack worth the risk?

 

The search for the source of a deadly disease often leads to deer farms.

 

The interstate movement of deer has been linked to the spread of disease. What are we risking for trophies? Robert Scheer/The Star

 

SEYMOUR, Ind. – In April 2012, a tree fell on a fence in Southern Indiana and 20 white-tailed deer bounded through the gap, their tails raised like stark white flags.

 

One of the deer in the pen had been shipped from a Pennsylvania herd where two deer tested positive for chronic wasting disease, a neurological disorder that's always fatal to deer and elk and has been found in 22 states — but never in Indiana.

 

Not yet, anyway.

 

That buck — which state officials call Yellow 47, for the color and number of the tag in his ear — has never been found. And because there is no reliable way to test for the disease until an animal dies, no one knows whether Yellow 47 had CWD when he arrived in Indiana, or whether he could be spreading it to his wild brethren today. ...

 

BUCK FEVER

 


 

A MUST READ !!!

 

BUCK FEVER

 


 

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

 


 

Monday, June 24, 2013

 

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

 


 

Tuesday, June 11, 2013

 

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

 


 

Tuesday, May 28, 2013

 

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

 

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

 


 

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

 

also, see where even decades back, the USDA had the same thought as they do today with CWD, not their problem...see page 27 below as well, where USDA stated back then, the same thing they stated in the state of Pennsylvania, not their damn business, once they escape, and they said the same thing about CWD in general back then ;

 

”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.

 


 

”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.

 

sound familiar $$$

 

Sunday, January 06, 2013

 

USDA TO PGC ONCE CAPTIVES ESCAPE

 

*** "it‘s no longer its business.”

 


 

Wednesday, September 04, 2013

 

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

 


 

how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ???

 

Tuesday, December 20, 2011

 

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

 

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

 

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

 

SUMMARY:

 


 


 

Friday, March 07, 2014

 

37th Annual Southeast Deer Study Group Meeting in Athens, Georgia (CWD TSE Prion abstracts)

 


 

Tuesday, March 25, 2014

 

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

 


 

Saturday, March 15, 2014

 

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

 


 

Thursday, March 20, 2014

 

CHRONIC WASTING DISEASE CWD TSE PRION OF CERVID AND THE POTENTIAL FOR HUMAN TRANSMISSION THEREFROM 2014

 

 
 
 
Friday, November 09, 2012

 

*** Chronic Wasting Disease CWD in cervidae and transmission to other species

 


 

Sunday, November 11, 2012

 

*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012

 


 

Friday, December 14, 2012

 

Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012

 


 

Saturday, March 09, 2013

 

Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest Incubation Time Model for Prion Diseases

 


 

Thursday, January 2, 2014

 

*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***

 


 

how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ???

 

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:

 


 


 

OLD HISTORY ON CWD AND GAME FARMS IN USA

 


 


 


 


 


 


 


 

 THE LANCET Infectious Diseases Vol 3 August 2003

 

Tracking spongiform encephalopathies in North America

 


 

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...

 


 

Singeltary submission ;

 

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

 

*** DOCUMENT ID: APHIS-2006-0118-0411

 


 

 Friday, March 28, 2014

 

BUCK FEVER What can happen if preserve owners make the rules

 

BUCK FEVER

 


 

 TSS

Friday, March 28, 2014

BUCK FEVER What can happen if preserve owners make the rules

BUCK FEVER

What can happen if preserve owners make the rules

Damning investigation by Mr. Sabalow et al @ IndyStar, that shows what we have known for decades about, an industry run amuck, an industry that will eventually self regulate itself, if they get their way, an industry that in my opinion, has been spreading cwd to hell and back for decades, i.e. the shooting pen industry. ...tss

BUCK FEVER

What can happen if preserve owners make the rules

What can happen if preserve owners make the rules

At one Indiana high-fence operation, deer — some ill or appearing drugged — were hunted in what prosecutors called 'killing pens.' Today, laws like those that sent the owner to prison are under assault in many states.

Ryan Sabalow, ryan.sabalow@indystar.com

"I think the DNR was so jealous 'cause I was selling deer for hundreds of thousands of dollars, and it would take 10 years for them to make what I was making in one day." — Russ Bellar

Buck Fever

Chapter 4

The nation's deer farmers are aggressively lobbying for regulatory changes that would benefit their industry. One Indiana case serves as a warning of what could happen if the industry is allowed to set its own rules. Robert Scheer/The Star

PERU, Ind. – For seven days in January 2005, a jury in a federal courtroom heard tales from a now-notorious Indiana hunting preserve of deer being drugged and even a sick deer propped up in a 1-acre pen so a hunter could shoot a $15,000 trophy.

Jurors heard testimony from an outdoor television celebrity, a corporate CEO, a country music star and an ex-NFL quarterback, some of whom paid substantial sums to shoot deer in enclosures so small that prosecutors dubbed them "killing pens." One shot his deer only minutes after it was released from a trailer. ...

snip...see full text, videos of interviews and such ;

http://www.indystar.com/longform/news/investigations/2014/03/27/buck-fever-chapter-four/6867811/

Overview: Trophy industry breeds risk disease, costs taxpayers millions

The pursuit of deer bred for enormous antlers and shot in hunting pens is compromising our ethics and laws, and comes with growing risk and costs.

http://www.indystar.com/longform/news/investigations/2014/03/27/buck-fever-intro/6865031/

Chapter 1: A troubling industry is born

Amish farmer unwittingly helped give rise to a booming new business — and ethical and legal quandaries.

"I am the king behind my fence. These are my deer." — Marty Berry, Texas deer breeder

http://www.indystar.com/longform/news/investigations/2014/03/27/buck-fever-chapter-one/6865283/

Chapter 3: How fair is the chase?

http://www.indystar.com/longform/news/investigations/2014/03/27/buck-fever-chapter-three/6865399/

Chapter 4: What can happen if preserve owners make the rules

http://www.indystar.com/longform/news/investigations/2014/03/27/buck-fever-chapter-four/6867811/

Is the rack worth the risk?

The search for the source of a deadly disease often leads to deer farms.

The interstate movement of deer has been linked to the spread of disease. What are we risking for trophies? Robert Scheer/The Star

SEYMOUR, Ind. – In April 2012, a tree fell on a fence in Southern Indiana and 20 white-tailed deer bounded through the gap, their tails raised like stark white flags.

One of the deer in the pen had been shipped from a Pennsylvania herd where two deer tested positive for chronic wasting disease, a neurological disorder that's always fatal to deer and elk and has been found in 22 states — but never in Indiana.

Not yet, anyway.

That buck — which state officials call Yellow 47, for the color and number of the tag in his ear — has never been found. And because there is no reliable way to test for the disease until an animal dies, no one knows whether Yellow 47 had CWD when he arrived in Indiana, or whether he could be spreading it to his wild brethren today. ...

BUCK FEVER

http://www.indystar.com/longform/news/investigations/2014/03/27/buck-fever-chapter-two/6867301/

A MUST READ !!!

BUCK FEVER

http://www.indystar.com/longform/news/investigations/2014/03/27/buck-fever-chapter-two/6867301/

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

http://chronic-wasting-disease.blogspot.com/2013/06/pennsylvania-captive-cwd-index-herd.html

Monday, June 24, 2013

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

http://chronic-wasting-disease.blogspot.com/2013/06/the-effects-of-chronic-wasting-disease.html

Tuesday, June 11, 2013

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

http://chronic-wasting-disease.blogspot.com/2013/06/cwd-gone-wild-more-cervid-escapees-from.html

Tuesday, May 28, 2013

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

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

http://chronic-wasting-disease.blogspot.com/2013/05/chronic-wasting-disease-cwd-quarantine.html

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

also, see where even decades back, the USDA had the same thought as they do today with CWD, not their problem...see page 27 below as well, where USDA stated back then, the same thing they stated in the state of Pennsylvania, not their damn business, once they escape, and they said the same thing about CWD in general back then ;

”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.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

”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.

sound familiar $$$

Sunday, January 06, 2013

USDA TO PGC ONCE CAPTIVES ESCAPE

*** "it‘s no longer its business.”

http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html

Wednesday, September 04, 2013

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

http://chronic-wasting-disease.blogspot.com/2013/09/cwd-cervid-captive-livestock-escapes.html

how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ???

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:

http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Friday, March 07, 2014

37th Annual Southeast Deer Study Group Meeting in Athens, Georgia (CWD TSE Prion abstracts)

http://chronic-wasting-disease.blogspot.com/2014/03/37th-annual-southeast-deer-study-group.html

Tuesday, March 25, 2014

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

 http://chronic-wasting-disease.blogspot.com/2014/03/transmission-of-chronic-wasting-disease.html

Saturday, March 15, 2014

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

 http://chronic-wasting-disease.blogspot.com/2014/03/potential-role-of-soil-properties-in.html

Thursday, March 20, 2014

CHRONIC WASTING DISEASE CWD TSE PRION OF CERVID AND THE POTENTIAL FOR HUMAN TRANSMISSION THEREFROM 2014

http://chronic-wasting-disease.blogspot.com/2014/03/chronic-wasting-disease-cwd-tse-prion.html

Friday, November 09, 2012

*** Chronic Wasting Disease CWD in cervidae and transmission to other species

http://chronic-wasting-disease.blogspot.com/2012/11/chronic-wasting-disease-cwd-in-cervidae.html

Sunday, November 11, 2012

*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012

http://chronic-wasting-disease.blogspot.com/2012/11/susceptibilities-of-nonhuman-primates.html

Friday, December 14, 2012

Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012

http://chronic-wasting-disease.blogspot.com/2012/12/susceptibility-chronic-wasting-disease.html

Saturday, March 09, 2013

Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest Incubation Time Model for Prion Diseases

http://chronic-wasting-disease.blogspot.com/2013/03/chronic-wasting-disease-in-bank-voles.html

Thursday, January 2, 2014

*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***

http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/cwd-tse-prion-in-cervids-to-htgmice.html

TSS

Tuesday, March 25, 2014

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

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

 

Christopher S. Jennelle mail,

Viviane Henaux,

Gideon Wasserberg,

Bala Thiagarajan,

Robert E. Rolley,

Michael D. Samuel

 

Published: March 21, 2014 •DOI: 10.1371/journal.pone.0091043

 

 

Abstract

 

Few studies have evaluated the rate of infection or mode of transmission for wildlife diseases, and the implications of alternative management strategies. We used hunter harvest data from 2002 to 2013 to investigate chronic wasting disease (CWD) infection rate and transmission modes, and address how alternative management approaches affect disease dynamics in a Wisconsin white-tailed deer population. Uncertainty regarding demographic impacts of CWD on cervid populations, human and domestic animal health concerns, and potential economic consequences underscore the need for strategies to control CWD distribution and prevalence. Using maximum-likelihood methods to evaluate alternative multi-state deterministic models of CWD transmission, harvest data strongly supports a frequency-dependent transmission structure with sex-specific infection rates that are two times higher in males than females. As transmissible spongiform encephalopathies are an important and difficult-to-study class of diseases with major economic and ecological implications, our work supports the hypothesis of frequency-dependent transmission in wild deer at a broad spatial scale and indicates that effective harvest management can be implemented to control CWD prevalence. Specifically, we show that harvest focused on the greater-affected sex (males) can result in stable population dynamics and control of CWD within the next 50 years, given the constraints of the model. We also provide a quantitative estimate of geographic disease spread in southern Wisconsin, validating qualitative assessments that CWD spreads relatively slowly. Given increased discovery and distribution of CWD throughout North America, insights from our study are valuable to management agencies and to the general public concerned about the impacts of CWD on white-tailed deer populations.

 

snip...

 

Discussion

 

CWD Transmission

 

Using white-tailed deer harvest data from south-central Wisconsin, we show that FD CWD transmission is the best supported model for both sexes (with higher infection rates for males) at a broad spatial scale, whereas our earlier efforts to model this system could not discriminate between FD and DD transmission [18]. It has been suspected that FD was a dominant transmission mechanism in mule deer [5], [17]; [ but see 6], and more recently in white-tailed deer [28], [46]. Furthermore, our modeling results suggest a more recent and biologically plausible time since CWD introduction in south-central Wisconsin compared with earlier analysis [18]. As demonstrated in previous work in this CWD system [21], [22], [25] and in Colorado [7], [47], adult males have higher CWD infection rates than females. Although the mechanism for higher CWD infection and prevalence in males is unknown, these differences may be driven by sex-specific social behavior [7], [21]. Males typically have larger home ranges, longer dispersal distances, interactions with other males, or rut-related behavior [48] that could result in more contacts with infectious deer. In contrast, females generally interact within a much smaller matrilineal group [27], [28], [49], and only briefly with males during rut [47].

 

Given the simplicity of our model, our estimated infection coefficients are likely a function of several different (and largely unknown) mechanisms that may vary between/among sexes, seasons, and the environment. These infection rates represent a weighted average of many potential drivers as summarized by Potapov et al. [39]. Our models do not account explicitly for indirect transmission from the environment where prions can persist for years [50], [51], although our infection rates implicitly subsume both direct and indirect routes of infection. The importance of environmental transmission has been demonstrated in captive mule deer [52], [53] and theoretical modeling indicates that population impacts can be driven by the length of time that prions remain infectious in the environment [54]. In the long term, the potential accumulation of an environmental reservoir of infectious prions may become an increasingly important component of CWD transmission; however, the relative contribution of direct and indirect transmission in wild deer populations remains unknown and requires further research. Although we expect infectious contact likely varies by sex and season, harvest data were insufficient to account for intra-annual complexity in sex-specific transmission. Additional insights for CWD management given directional sex-specific transmission (i.e., female-to-male, female-to-female) may require focal research studies that determine differences in infectious contact between and among sexes [49], [55]–[57] and how these influence the risk of disease transmission [28]. In particular, understanding the mechanisms that lead to rates of male infection twice as high as females could provide crucial insights on management strategies designed to reduce male CWD prevalence as an alternative to high male harvest.

 

Assuming CWD originated in the core area and environmental accumulation of prions contributes significantly to transmission, we would expect higher infection rate estimates in the core compared with surrounding areas. We are uncertain why infection rate is apparently greater in males for some areas to the west and southwest of the core. These surrounding areas have similar habitat characteristics with the core, and we would not expect deer abundance to vary significantly prior to CWD discovery. Heterogeneous harvest management conducted among areas may be one potential explanation. However, this difference also suggests that unidentified environmental characteristics or management actions may influence the current and future trends in CWD prevalence. Regardless, these patterns suggest that our model predictions for the core area may underestimate the rate of CWD increase in other areas. Future research is needed to understand the drivers of CWD transmission, how these vary spatially, and their influence on future patterns of infection. The identification of potential environmental reservoirs (e.g., common feeding areas, mineral licks) and evaluation of the significance of indirect transmission in free-ranging deer populations would also enhance our ability to predict future trends in infection and allow a better evaluation of alternative control strategies.

 

In concept QAIC should help account for overdispersion in our data, which might result from missing covariates in the model and/or a lack of independence in the data (e.g., [58]). Such lack of independence may be due to spatial and/or temporal autocorrelation, and while we do not explicitly account for such effects, we rely on QAIC to generally accommodate a portion of these impacts. While we detected significant temporal autocorrelation in residuals for predicted female prevalence, other research in the same study area [44], [46] found no spatial autocorrelation in model residuals using a 93.6 km2 or 2.6 km2 spatial frame, respectively. We caution that despite use of QAIC, our model parameter estimates may still be overly precise.

 

Rate of spread

 

Several studies indicate that the southwestern core area of WI is the likely point of origin for CWD in our study area, with an inverse relationship between distance-to-core and prevalence as would be expected from an introduced disease spreading across the landscape [20], [22], [44]. To our knowledge, we present the first empirical estimate of CWD geographic spread, based on sex-specific FD transmission, which indicated a low average rate (1.13 km year−1) during initial phases of the epizootic. There is no current evidence to suggest that CWD spread in our study area was facilitated by humans (via movements of infectious animals between game farms or preserves); however, the anecdotal evidence of such events warrants further investigation. Though DD transmission was not supported by our data, the estimated rate of geographic spread was similar for this model structure. Our results suggest that in the south-central Wisconsin endemic area, CWD has slowly moved across the landscape and is probably not a recent development. Clearly this estimated rate of spread must be considered unique to the outbreak in south-central Wisconsin.

 

Rates of CWD spread in other regions are likely influenced by a number of factors including habitat features [44], [59], mode of disease transmission, host species (e.g., white-tailed or mule deer), population structure, host movements [60], dispersal [61], and possibly the environment [54]. For example, recent analyses [44] indicate that CWD may be spreading faster from the outbreak in eastern Wisconsin and northern Illinois than from south-central Wisconsin. Our simple estimate also assumes an average uniform diffusion from the point of origin and ignores potential disease movement via longer distance dispersal [60], although recent discovery of CWD in north-west Wisconsin does not appear to be linked to long-distance dispersal from southern Wisconsin based on genetic analysis (S. Robinson Pers. Comm.). In addition, our analysis does not account for habitat heterogeneity and physical barriers (natural or anthropogenic) that influence landscape scale movement and interaction of deer populations [62], [63] or CWD distribution [44], [63]. We also note that despite a highly significant R2 value, our simple regression utilizes only six data points (including the core, which we assume is the origin of the epizootic), with uncertainty that is not accounted for in the regression. As such, there is likely higher variance associated with our estimated rate of spread.

 

Despite these limitations, our estimate provides a starting place to conceptualize early CWD spread across the southern Wisconsin landscape. In the context of CWD, we believe the areas surrounding the core are currently in relatively early stages of the epizootic with low, but increasing prevalence. Under FD transmission and barring effective management efforts, CWD prevalence is predicted to increase over time, and we suspect that the rate of spread may also increase because more young males will become infected prior to dispersal [46]. As such, we consider our spread estimate as a lower bound that is likely to increase as the epizootic progresses.

 

Harvest strategies

 

As a consequence of FD transmission, our simulations predict that in the next decade CWD prevalence can increase to relatively high levels (25% in females and 50% in males) in the absence of significant management actions to reduce infection rates. Of the three harvest strategies we evaluated, only male-focused harvest succeeded in reducing CWD prevalence below current levels. Prevalence is reduced because this strategy removes animals from the highest prevalence class (reducing infection rates), while allowing dilution of population-level CWD prevalence by recruitment of more females [64]. In contrast, CWD increased under female-focused and herd-control harvest strategies. By focusing harvest on the portion of the population with highest prevalence and infection rates, our simulation suggests that harvest management can effectively reduce prevalence despite FD disease transmission. Although disease eradication may not be possible, prevalence reduction (especially in higher risk groups), which reduces force of infection, is the key to mediating disease impacts on host populations in the long term. Effective disease management by sex-specific differential harvest has also been explored for bovine tuberculosis in deer [55].

 

The density-dependent harvest structure we imposed produced much lower average realized harvest (RH) rates for the female-focused and herd-control strategies, compared with male-focused harvest. High female harvest reduces population size, which requires lower realized harvest rates to maintain stable population goals (based on societal tolerance for deer). While this density-dependent harvest structure is artificial, it is intended to represent hunter effort in response to perceived deer densities. In the absence of such a mechanism, static harvest rates over the simulated time frame of 50 years resulted in host and disease extinction, as predicted in theoretical models of FD disease transmission [14]. In addition, our results show that deer demography and CWD dynamics are sensitive to changes in harvest. Estimation of unbiased harvest rates requires accurate information on both the distribution of harvested animals and the distribution of the underlying population. Although harvest-based estimates for deer populations have various limitations [9], [65], the importance of this parameter for monitoring the performance of CWD management programs suggests future research to improve estimation procedures should be considered.

 

The demographic implications of alternative harvest strategies for disease management are also important as they affect deer densities, recreational opportunities (e.g., hunting or observation), and potential disease spread. While male-focused harvest reduces CWD prevalence in the long term, it results in lower densities of adult males (compared with herd-control), which are usually of primary interest to deer hunters. For the herd-control harvest strategy (current deer management goals) nearly 50% of adult males and 25% of adult females are expected to become infected within another decade. Even worse, for female-focused harvest not only are deer densities expected to be low, but more than 50% of surviving adult males and 30% of adult females would be infected. In general, these harvest strategies are characterized by accelerating rates of infection in all deer, and higher prevalence, particularly in males. Considering the constraints of our model the tradeoff between strategies is clear; CWD can eventually be reduced with fewer opportunities to harvest healthy adult bucks, or more adult bucks may be available for harvest, but with higher rates of CWD infection. Given that quality deer management practices focus on production of older bucks with large antlers, management agencies could face difficult alternatives from these competing interests. However, if an efficacious CWD vaccine was available and cost-effectively distributed to broad segments of a deer population (particularly males), managers would have more flexibility to employ a disease control strategy combining harvest and vaccination to provide adequate recreational opportunities to harvest CWD-free deer.

 

The mechanism for density-dependent population regulation in deer is not well known, but one hypothesis is that deer reduce body size and maintain survival rates while lowering reproduction [66]. Therefore, we used density-dependent fecundity to regulate population size in our no-harvest simulations. The goal of these simulations was to illustrate the rapid increase in CWD prevalence and eventual impact on deer populations in the absence of harvest or other factors that remove infected animals prior to mortality from CWD. Such situations might be likely in high density urban deer populations, national parks, captive deer farms, or other areas where deer harvest or removal is limited. This simulation is not designed to represent current conditions in Wisconsin, and we consider this a worst-case disease scenario in areas without harvest.

 

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

 

snip...

 

Conclusions

 

Given our model structure and data, our results provide strong support for FD transmission of CWD with the force of infection driven by changes in prevalence, which we suggest is a vital metric for focused control efforts. Generally as prevalence increases, as found in Wisconsin, infection rate also increases in the absence of intervention, producing an accelerating pattern of infection. Assuming that frequency-dependent transmission predominates (as our evaluation indicates), management to reduce prevalence will mediate potential CWD population impacts. The higher rate of infection and prevalence in males, thus, provides the basis for effective CWD management using deer harvest focused on this sex. Management to reduce prevalence might be accomplished through the synergistic effects of targeted harvest and vaccination of males. Unfortunately, we know little about the mechanisms for male infection and further research is needed before alternative management strategies to reduce male infection rates can be developed. Spatial differences in CWD infection rates, despite similar habitat and pre-CWD deer abundance, suggest that unidentified environmental or management factors may also influence disease dynamics and future trends in prevalence. Future research to understand the drivers of CWD transmission, how these vary spatially, and the relative importance of environmental and direct transmission is critical to understanding future CWD dynamics in wild deer.

 

Our results also indicate that even with high deer densities CWD has been spreading at a relatively slow rate across the landscape; in agreement with larger scale spatial patterns for prevalence [44]. However, as disease prevalence continues to increase, the rate of infection in yearling bucks will also increase [46]. Because dispersing bucks may be an important source of disease spread, these patterns suggest that CWD prevalence outside the core area will continue to grow and the disease may spread at an increasing rate. Although the drivers of CWD spatial spread are not generally known (see [44] for identification of landscape features that affect spread), management efforts to reduce both local prevalence and deer abundance will likely reduce dispersal of infected yearling bucks. However, the relative impact of reducing deer abundance versus prevalence in lowering the number of infected yearling bucks likely depends on disease prevalence and deer density [46]. Further research is needed to determine the factors that affect spatial spread and develop effective management strategies.

 

 

Figures






 

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

 

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

 

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***

 


 

Sunday, October 13, 2013

 

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

 


 

Sunday, March 09, 2014

 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

 

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

 


 

Wednesday, December 11, 2013

 

*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease ***

 


 

Monday, February 10, 2014

 

18 Forsyth Medical Center patients exposed to CJD; apology issued...OOOPS, SORRY, TOO BAD $$$

 


 

Tuesday, February 11, 2014

 

Novant Health Forsyth Medical Center Information on potential CJD exposure

 


 

Monday, February 3, 2014

 

*** Evaluation of the zoonotic potential of transmissible mink encephalopathy TSE Prion disease

 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 


 

Sunday, March 23, 2014

 

APHIS USDA National Scrapie Eradication Program February 2014 Monthly Report Fiscal Year 2014

 


 

Monday, March 3, 2014

 

*** Gov. C.L. "Butch" Otter of Idaho signs bill that will force consumers to eat dead stock downers and whatever else the industry decides

 

see updated Rancho CLASS 1 HIGH RISK dead stock cancer downer recall for IDAHO

 


 


 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 

OAI 2012-2013

 

OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.

 

ATL-DO 1035703 Newberry Feed & Farm Ctr, Inc. 2431 Vincent St. Newberry SC 29108-0714 OPR DR, FL, FR, TH HP 9/9/2013 OAI Y

 

DET-DO 1824979 Hubbard Feeds, Inc. 135 Main, P.O. Box 156 Shipshewana IN 46565-0156 OPR DR, FL, OF DP 8/29/2013 OAI Y

 

ATL-DO 3001460882 Talley Farms Feed Mill Inc 6309 Talley Rd Stanfield NC 28163-7617 OPR FL, TH NP 7/17/2013 OAI N

 

NYK-DO 3010260624 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007 OPR FR, OF NP 7/16/2013 OAI Y

 

DEN-DO 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N

 

CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y

 

*** DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N

 

Ruminant Feed Inspections Firms Inventory (excel format)

 


 

PLEASE NOTE, the VAI violations were so numerous, and unorganized in dates posted, as in numerical order, you will have to sift through them for yourselves. ...tss

 

snip...see full text ;

 

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

 


 

Saturday, December 15, 2012

 

Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012

 


 

Sunday, February 2, 2014

 

The Presence of Disease-Associated Prion Protein in Skeletal Muscle of Cattle Infected with Classical Bovine Spongiform Encephalopathy

 

NOTE Pathology

 


 

Saturday, December 21, 2013

 

**** Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle ****

 


 

Wednesday, December 4, 2013

 

*** Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products; Final Rule Federal Register / Vol. 78 , No. 233 /

 

Wednesday, December 4, 2013

 


 

Saturday, November 2, 2013

 

*** APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe

 


 

 

 

*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.

 


 


 


 


 

 

Friday, March 21, 2014

 

Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014 ?

 

“As of March 20, 2014, FSIS has completed all checks (effectiveness checks and disposition verification checks) for recalls 002-2014 and 013-2014 regarding Rancho Feeding Corporation. FSIS has determined that based on the number of successful checks (see Directive 8080.1, Attachment 1, Table 3) where businesses were notified of the recall and removed affected products from commerce that the recall activities were effective.”

 

say what $$$

 


 

Monday, December 1, 2008

 

When Atypical Scrapie cross species barriers

 


 

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

 

snip...

 

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

 

snip...

 

R. BRADLEY

 


 

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

 

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

 

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

 

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

 

snip...

 

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

 

PMID: 6997404

 


 

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

 

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

 

snip...

 

76/10.12/4.6

 


 

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

 

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). Gibbs CJ Jr, Gajdusek DC.

 

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

 

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

 

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

 

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

 

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

 


 


 

 Re: vCJD in the USA * BSE in U.S. 15 November 1999 Terry S Singeltary, NA

 

CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie.

 

It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses.

 


 

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...

 

2 January 2000 Terry S Singeltary

 

The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;

 

"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."

 

Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.

 

Something else I find odd, page 16;

 

"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."

 

A few more factors to consider, page 15;

 

"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."

 

"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."

 

"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."

 

Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.

 

To be continued...

 

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

 

Competing interests: None declared

 


 

Letters

 

JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Terry S. Singeltary, Sr Bacliff, Tex

 

Since this article does not have an abstract, we have provided the first 150 words of the full text.

 

KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

 

References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.

 


 

Published March 26, 2003

 

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States

 

Terry S. Singeltary, retired (medically)

 

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

 

Published March 26, 2003

 


 

14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114

 

Session: International Scientific Exchange

 

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

 

T. Singeltary Bacliff, TX, USA

 

Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

 

Methods: 12 years independent research of available data

 

Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

 

Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

 


 

The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI

 

Tracking spongiform encephalopathies in North America

 

Original

 

Xavier Bosch

 

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...

 


 


 

SEE FULL TEXT ;

 

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

 

Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003

 

Date: Tue, 29 Jul 2003 17:35:30 –0500

 

From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de

 

Volume 3, Number 8 01 August 2003

 

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Tracking spongiform encephalopathies in North America

 

Xavier Bosch

 

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.

 

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

 

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.

 

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

 

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

 

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

 

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

 

Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.

 

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.

 

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

 

CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.

 


 

LANCET SINGELTARY ET AL CWD TSE PRION NORTH AMERICA

 


 

Singeltary submission to PLOS ;

 

No competing interests declared.

 

see full text ;

 


 

Owens, Julie

 

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

 

Sent: Monday, July 24, 2006 1:09 PM

 

To: FSIS RegulationsComments

 

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98

 


 

FSIS, USDA, REPLY TO SINGELTARY

 


 

Sunday, August 09, 2009

 

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

 


 

Tuesday, August 18, 2009

 

* BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009

 


 

Monday, March 10, 2014

 

Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014

 


 

Wednesday, May 16, 2012

 

*** Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

Proposal ID: 29403

 


 

CJD QUESTIONNAIRE USA

 


 


 

CJD VOICE

 


 


 


 


 


 


 


 


 


 


 

 

never break a promise to your mom. DOD 12/14/97 CONFIRMED hvCJD...

 

layperson

 

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net