SCRAPIE USA

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Location: BACLIFF, Texas, United States

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Tuesday, September 27, 2016

Classical Scrapie Diagnosis in ARR/ARR Sheep in Brazil

Acta Scientiae Veterinariae, 2015. 43(Suppl 1): 69.

 

CASE REPORT Pub. 69

 

ISSN 1679-9216

 

1

 

Received: 4 August 2014 Accepted: 19 December 2014 Published: 6 February 2015

 

1Programa de Pós-graduação em Ciências Veterinárias (PPGCV), Faculdade de Veterinária (FaVet), Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil. 2Setor de Patologia Veterinária (SPV), Departamento de Patologia Clínica Veterinária (DPCV), FAVET, UFRGS, Porto Alegre, RS, Brazil. 3Departamento de Ciências Morfológicas, Instituto de Ciências Básicas da Saúde (ICBS), UFRGS, Porto Alegre, RS. CORRESPONDENCE: J.S. Leal [julianoob@gmail.com - Tel.: +55 (51) 3308 3631]. Setor de Patologia Veterinária, FAVET, UFRGS. Av. Bento Gonçalves n. 9090, Bairro Agronomia. CEP 91540-000 Porto Alegre, RS, Brazil.

 

Classical Scrapie Diagnosis in ARR/ARR Sheep in Brazil

 

Juliano Souza Leal1,2, Caroline Pinto de Andrade2, Gabriel Laizola Frainer Correa2, Gisele Silva Boos2, Matheus Viezzer Bianchi2, Sergio Ceroni da Silva2, Rui Fernando Felix Lopes3 & David Driemeier2

 

ABSTRACT

 

Background: Scrapie is a transmissible spongiform encephalopathy (TSE) that affects sheep flocks and goat herds. The transfer of animals or groups of these between sheep farms is associated with increased numbers of infected animals and with the susceptibility or the resistance to natural or classical scrapie form. Although several aspects linked to the etiology of the natural form of this infection remain unclarified, the role of an important genetic control in scrapie incidence has been proposed. Polymorphisms of the PrP gene (prion protein, or simply prion), mainly in codons 136, 154, and 171, have been associated with the risk of scrapie. Case: One animal from a group of 292 sheep was diagnosed positive for scrapie in the municipality of Valparaíso, state of São Paulo, Brazil. The group was part of a flock of 811 free-range, mixed-breed Suffolk sheep of the two genders and ages between 2 and 7 years from different Brazilian regions. Blood was collected for genotyping (for codons 136, 141, 154 and 171), and the third lid and rectal mucosa were sampled for immunohistochemistry (IHC) for scrapie, from all 292 animals of the group. IHC revealed that seven (2.4%) animals were positive for the disease. Collection of samples was repeated for 90 animals, among which the seven individuals diagnosed positive and 83 other animals that had some degree of kinship with those. These 90 sheep were sacrificed and necropsied, when samples of brain (obex), cerebellum, third eyelid, rectal mucosa, mesenteric lymph node, palatine tonsil, and spleen were collected for IHC. The results of IHC analyses carried out after necropsy of the seven positive animals submitted to the second collection of lymphoreticular tissue and of the 83 animals with some degree of kinship with them confirmed the positive diagnosis obtained in the first analysis, and revealed that three other sheep were also positive for scrapie. Samples of 80 animals (89%) were negative for the disease in all organs and tissues analyzed. In turn, 10 sheep (11%) were positive, presenting immunoreactivity in one or more tissues. Genotyping revealed the presence of four of the five alleles of the PrP gene commonly detected in sheep: ARR, ARQ, VRQ and ARH. These allele combinations formed six haplotypes: ARR/ARR, ARR/ARQ, ARH/ARH, ARQ/ARH, ARQ/ARQ and ARQ/VRQ. Animals were classified according to susceptibility to scrapie, when 8.9% of the genotyped sheep were classified into risk group R1 (more resistant, with no restriction to breeding). In turn, 40% of the animals tested ranked in groups R4 and R5 (genetically very susceptible, cannot be used for breeding purposes). Discussion: The susceptibility of sheep flocks depends on the genetic pattern of animals and is determined by the sequence of the gene that codifies protein PrP. Additionally, numerous prion strains are differentiated based on pathological and biochemical characteristics, and may affect animals differently, depending on each individual’s genotype. Most epidemiologic data published to date indicate that animals that carry the ARR/ARR genotype are less susceptible to classical scrapie. However, in the present study, the fact that two scrapie-positive sheep presented the haplotype ARR/ARR indicates that this genotype cannot always be considered an indicator of resistance to the causal agent of the classical manifestation of the disease. The coexistence in the same environment of several crossbred animals from different flocks and farms, which characterizes a new heterogeneous flock, may have promoted a favorable scenario to spread the disease, infecting animals in the most resistant group.

 

Keywords: biopsy, scrapie, TSEs, immunohistochemistry.

 

DISCUSSION

 

The susceptibility of sheep flocks to scrapie depends largely on the genetic pattern of the animal, and is determined mainly by the sequence of the gene that codifies the PrP protein, since there are several polymorphisms that affect the conversion of the cell protein PrPC to its pathological form, PrPSc [8, 9]. Nevertheless, it is not possible to consider the occurrence of only one form of ovine prion, since there are numerous prion strains with different pathological and biochemical characteristics that may affect animals distinctively, depending on their genotypes [1, 30]. In the present study, the frequency of codon VRQ was very low (2.2%), confirming previous findings, which revealed that the alleles ARR and ARQ prevail in Suffolk sheep, and that the allele ARH sometimes is detected [12, 32]. The high sensitivity of homozygous VRQ carriers or of individuals with ARQ haplotypes has also been reported in the literature [24]. This condition raises concerns about susceptibility from the epidemiological perspective, since the allele VRQ, which is rare or absent in breeds like Suffolk, was present in two animals, one of which was positive for scrapie. Most epidemiological and genetic data published indicate that sheep carrying the haplotype ARR/ ARR are less susceptible to classical form, while animals with the haplotype VRQ in homozygosis or with ARQ haplotypes are highly susceptible [24]. This hypothesis is supported by genotyping data for thousands of sheep with the disease around the world. For example, a study carried out in Japan described a classical scrapie case in one ARR/ARR sheep [16]. Sensitivity of ARR/ARR sheep in a scenario of oral exposure to the disease has also been reported [3]. Atypical cases were observed in ARR/ARR animals [11, 42].

 

Polymorphisms at codon positions 136, 154 and 171 are not the only ones associated with resistance or susceptibility to scrapie [33]. An analysis of the variation of codon positions 136 and 171, for instance, showed that each has several adjacent polymorphic sites and may codify up to four amino acids [7, 50]. The atypical scrapie form, characterized by strain Nor98 [6], is more frequently detected in AHQ animals that carry a polymorphism in codon 141, and has not been described in Suffolk sheep in Brazil [2]. This atypical form expresses phenylalanine (F), instead of leucine (L) in the form L141F [6, 37, 46].

 

However, although it is generally acceptable that classical scrapie is an infectious and contagious disease [14], contagion with the atypical form is questionable in light of the fact that the specific marker for the atypical manifestation of the disease is detected outside the central nervous system [5, 20, 29], even in cases experimentally transmitted to transgenic mice [35] and sheep [47]. Several studies have demonstrated that susceptibility to the atypical form is consistently associated with PrP codons 141 (L/F) and 154 (R/H) [6, 42]. In fact, studies have proposed the hypothesis that this form may evolve when the animal is not exposed to the infectious agent [5, 18, 29, 48], given the limited knowledge of the physiopathology of this manifestation of the disease [19].

 

In the present study, two (2/8) positive animals presented the haplotype ARR/ARR, which is considered to be the least susceptible and therefore responsible for the lowest risk of scrapie. However, like all sheep that were genotyped, these animals did not present any change in lysine in codon position 141. This change (that is, when lysine is replaced by phenylalanine) has been associated with atypical scrapie in Suffolk sheep [6]. Therefore, these two ARR/ARR sheep do not fit in the genotypic characteristics of sheep that may commonly present the atypical form. It is possible that the presence of several crossbred animals of different flocks and farms in the same environment, which characterizes an heterogeneous flock, has created the favorable conditions for the disease to evolve and spread, infecting the more susceptible animals.

 

The variation in the frequency of the PrP genotype between flocks has been identified as a real risk factor for the disease [4]. The introduction of adult sheep free of scrapie in contaminated flocks is believed to allow lateral transmission, even between adult animals with less susceptible genotypes [40, 45], although young sheep are more predisposed [43]. Other reasons behind differences in occurrence include the stress caused during husbandry and large population numbers [26]. Additionally, the lack of a defined epidemiological pattern and the different strains of the causal agent play an important role in inter-flock variability [40]. Several models were based on the assumption that outbreak duration is influenced by flock size and by the frequency of the PrP genotype in one flock [25, 26, 38, 51]. Commercial flocks with high genetic diversity, mainly in codons other than 136, 154 and 171, are more consistently affected. In these animals, the onset of clinical manifestations occurs at significantly different ages, with means varying from 2 to 5.7 years, due to noteworthy dissimilarities in age and PrP genotype profiles [40]. The purchase of infected animals has been pointed out as the main scrapie infection mechanism in flocks [27, 41].

 

*** The diagnosis of scrapie in two homozygous ARR/ARR sheep indicates that the resistance of this genotype to the classical form of the disease is debatable. Although scrapie in these animals is rare, the cases presented in this case report lend strength to the notion that its occurrence depends on a combination of infectious factors, including differences in biological and biochemical properties in the natural hosts to this prion.

 

MANUFACTURERS 1VMRD Pullman Albion Road. Pullman, WA, USA. 2Qiagen. Hilden, Germany. 3InvitrogenTM. São Paulo, Brazil. 4Life TechnologiesTM. Gaithersburg, MD, USA. 5InvitrogenTM. Carlsbad, CA, USA. 6Applied Biosystems Inc. Foster City, CA, USA. Declaration of interest. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

 


 

Monday, May 5, 2014 Brazil 2nd BSE Mad Cow disease confirmed OIE 02/05/2014 http://bovineprp.blogspot.com/2014/05/brazil-bse-mad-cow-disease-confirmed.html Thursday, April 24, 2014

 

Brazil investigates possible BSE mad cow case

 


 

Brazil evaluate the implementation of health rules on animal by-products and derived products SRM BST TSE PRION aka MAD COW DISEASE http://bse-atypical.blogspot.com/2013/09/brazil-evaluate-implementation-of.html

 

Friday, December 07, 2012

 

ATYPICAL BSE BRAZIL 2010 FINALLY CONFIRMED OIE 2012 http://bse-atypical.blogspot.com/2012/12/atypical-bse-brazil-2010-finally.html Wednesday, December 19, 2012

 

Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Brazil http://bse-atypical.blogspot.com/2012/12/scientific-report-of-european-food.html

 

 Assessment of the PrPc amino-terminal domain in prion species barriers

 

Kristen A. Davenporta, Davin M. Hendersona, Candace K. Mathiasona and Edward A. Hoovera# + Author Affiliations

 

Prion Research Center, Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523a ABSTRACT Chronic wasting disease (CWD) in cervids and bovine spongiform encephalopathy (BSE) in cattle are prion diseases that are caused by the same protein-misfolding mechanism, but appear to pose different risks to humans. We are interested in understanding the differences between the species barriers of CWD and BSE. We used real-time, quaking-induced conversion (RT-QuIC) to model the central molecular event in prion disease, the templated misfolding of the normal prion protein, PrPc, to a pathogenic, amyloid isoform, PrPSc. We examined the role of the PrPc amino-terminal domain (NTD, aa23-90) in cross-species conversion by comparing the conversion efficiency of various prion seeds in either full-length (aa23-231) or truncated (aa90-231) PrPc. We demonstrate that the presence of white-tailed deer and bovine NTDs hindered seeded conversion of PrPc, but human and bank vole NTDs did the opposite. Additionally, full-length human and bank vole PrPc were more likely to be converted to amyloid by CWD prions than were their truncated forms. A chimera with replacement of the human NTD by the bovine NTD resembled human PrPc. The requirement for an NTD, but not for the specific human sequence, suggests that the NTD interacts with other regions of the human PrPc to increase promiscuity. These data contribute to the evidence that, in addition to primary sequence, prion species barriers are controlled by interactions of the substrate NTD with the rest of the substrate PrPc molecule.

 

Importance We demonstrate that the amino-terminal domain of the normal prion protein, PrPc, hinders seeded conversion of bovine and white-tailed deer PrPc to the prion form, but it facilitates conversion of the human and bank vole PrPc to the prion form. Additionally, we demonstrate that the amino-terminal domain of human and bank vole PrPc requires interaction with the rest of the molecule to facilitate conversion by CWD prions. These data suggest that interactions of the amino-terminal domain with the rest of the PrPc molecule play an important role in the susceptibility of humans to CWD prions.

 

snip...

 

We found that human rPrPc can be readily converted to an amyloid state by CWD prions, and that the NTD facilitates this conversion. As there is little evidence for the susceptibility of humans to CWD, the biologic significance of our observation remains to be determined. However, the role of the NTD in this in vitro phenomenon may be important to the in vivo mechanism as well. RT-QuIC, transgenic mouse bioassay, and PMCA measure different outcomes. This manuscript compares the efficiency of initial amyloid formation, while bioassay and PMCA reflect total accumulation of protease-resistant PrPSc, which may explain the difference in the apparent susceptibility of full-length human rPrPc in these models. The molecular underpinnings for species barriers and trans-species prion conversion remain a complex, yet important problem in prion biology. We propose that an interaction between the amino terminal

 

FOOTNOTES

 

↵#Address correspondence to Edward A. Hoover, edward.hoover@colostate.edu Copyright © 2016, American Society for Microbiology. All Rights Reserved.

 


 


 

‘’We demonstrate that the presence of white-tailed deer and bovine NTDs hindered seeded conversion of PrPc, but human and bank vole NTDs did the opposite. Additionally, full-length human and bank vole PrPc were more likely to be converted to amyloid by CWD prions than were their truncated forms. ‘’

 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 

Monday, May 02, 2016

 

*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***

 


 

SCRAPIE AND CWD ZOONOSIS

 

PRION 2016 CONFERENCE TOKYO

 

Saturday, April 23, 2016

 

*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X

 


 


 

Saturday, September 24, 2016

 

Assessment of the PrPc amino-terminal domain in prion species barriers

 


 

Transmission of scrapie prions to primate after an extended silent incubation period

 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 

Transmission of scrapie prions to primate after an extended silent incubation period

 

Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen , Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee , Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys

 

Abstract

 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

 

snip...

 

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.

 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 


 

2015

 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

 

***is the third potentially zoonotic PD (with BSE and L-type BSE),

 

***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

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

 

***thus questioning the origin of human sporadic cases***

 

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

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

 

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

 


 

CWD TSE PRION HUMAN ZOONOSIS POTENTIAL, has it already happened, and being masked as sporadic CJD? and what about iatrogenic, or the pass if forward, friendly fire mode of transmission of cwd to humans, same thing, sporadic cjd ?

 

*** WDA 2016 NEW YORK ***

 

We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.

 

Student Presentations Session 2

 

The species barriers and public health threat of CWD and BSE prions

 

Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University

 

Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD.

 

Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders

 

Ms. Alyssa Wetterau1, Dr. Krysten Schuler1, Dr. Elizabeth Bunting1, Dr. Hussni Mohammed1 1Cornell University

 

Chronic wasting disease (CWD) is a fatal disease of North American Cervidae. New York State (NYS, USA) successfully managed an outbreak of CWD in 2005 in both captive and wild white-tailed deer (Odocoileus virginianus) with no reoccurrence of the disease as of 2015. To attain maximum compliance and efficacy of management actions for prevention of CWD entry, understanding the varied risk perceptions will allow for targeted, proactive communication efforts to address divergences between expert-derived risk assessments and stakeholder risk perceptions. We examined perceived risks associated with CWD introduction and exposure among agricultural and wildlife agency professionals within and outside of NYS, as well as stakeholder groups (e.g., hunters and captive cervid owners). We measured perceived risk using a risk assessment questionnaire online via Qualtrics survey software and evaluated similarities within, as well as differences in, perception among participant groups. New York State biologists employed by the Department of Environmental Conservation and independent non-NYS wildlife and agricultural professionals thought CWD risks associated with captive cervids were high; captive cervid owners thought risks for wild and captive cervids were low. Agriculture and wildlife professional groups agreed on general risk perceptions. We ranked 15 individual risk hazards into high and low medium categories based on all responses. Differences between groups were most evident in hypothetical disease pathways. Any pathway involving inter-state import of live cervids received high ranking for all groups except captive cervid owners. Comparatively low risk perceptions by captive cervid operators may stem from misinformation, lack of understanding of testing programs, and indemnity payments for animal depopulation. Communication and education directed at areas of disagreement may facilitate effective disease prevention and management.

 


 


 

* No evaluation of determination of CWD risk is required for alternative livestock or captive wildlife shipped directly to slaughter or to a biosecure facility approved by the Division and the Dept. of Agriculture.

 


 

*** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. ***

 

PRION 2016 TOKYO

 

Zoonotic Potential of CWD Prions: An Update

 

Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6

 

1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.

 

4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,

 

2Encore Health Resources, 1331 Lamar St, Houston, TX 77010

 

Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.

 

PRION 2016 TOKYO

 

In Conjunction with Asia Pacific Prion Symposium 2016

 

PRION 2016 Tokyo

 

Prion 2016

 


 

Tuesday, December 16, 2014

 

Evidence for zoonotic potential of ovine scrapie prions

 

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

 

Abstract

 

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 

Subject terms: Biological sciences• Medical research At a glance

 


 

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.

 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.

 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

 

Taylor & Francis

 

Prion 2016 Animal Prion Disease Workshop Abstracts

 

WS-01: Prion diseases in animals and zoonotic potential

 

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

 

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

 

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

 

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

 

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

 

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

 

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 


 


 

2016

 

SCRAPIE AND CWD ZOONOSIS

 

PRION 2016 CONFERENCE TOKYO

 

Saturday, April 23, 2016

 

*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X

 


 

Transmission of scrapie prions to primate after an extended silent incubation period

 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 

Transmission of scrapie prions to primate after an extended silent incubation period

 

Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen , Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee , Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys

 

Abstract

 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

 

snip...

 

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.

 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 


 

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

 


 

1978 SCRAPIE IN CONFIDENCE SCJD

 


 


 


 


 


 


 


 


 


 

1979

 

SILENCE ON CJD AND SCRAPIE

 

1980

 

SILENCE ON CJD AND SCRAPIE

 

*** 1981 NOVEMBER

 


 


 

Thursday, August 04, 2016

 

*** MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD

 


 

Sunday, August 28, 2016

 

CONFIDENTIAL

 

Transmissible Spongiform Encephalopathy TSE Prion and how Politics and Greed by the Industry spread madcow type diseases from species to species and around the globe

 

TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS AND BEARS, OH MY!

 

Please be assured, the USA does NOT have any clue as to what the real perspective on the TSE prion disease in domestic feline and canine, much less our big wild cats, OR any other species including humans for that matter, but one thing for sure, the studies and history of the mad cow debacle below are deeply concerning with regards, to humans and wild big cats like mountain lions, cougars, lynx, Jaguar, and such, that feed on cervids that are infected with CWD. one thing for sure, don’t kid yourselves, all are very much susceptible to the TSE Prion disease, and if you don’t look, you don’t find, problems solved$$$

 


 

Tuesday, September 06, 2016

 

A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation

 


 

Tuesday, July 26, 2016

 

Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016

 


 

Saturday, July 23, 2016

 

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016

 


 

*** Calling Canadian beef unsafe is like calling your twin sister ugly," Dopp said. ***

 

Thursday, August 25, 2016

 

*** FSIS Green Bay Dressed Beef Recalls Beef Products Due To Possible Specified Risk Materials Contamination the most high risk materials for BSE TSE PRION AKA MAD COW TYPE DISEASE ***

 


 

Monday, June 20, 2016

 

Specified Risk Materials SRMs BSE TSE Prion Program

 


 

Friday, August 26, 2016

 

*** Journal Journal of Toxicology and Environmental Health, Part A Volume 79, 2016 - Issue 16-17 Prion Research in Perspective IV CANADA BSE CWD SCRAPIE CJD TSE Prion Disease

 


 

Saturday, July 16, 2016

 

Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10

 

WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.

 

THIS is absolutely insane. it’s USDA INC.

 


 

Monday, September 19, 2016

 

Evidence of scrapie transmission to sheep via goat milk

 


 

Saturday, April 16, 2016

 

*** APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission ***

 


 

Wednesday, January 20, 2016

 

Exportation of Live Animals, Hatching Eggs, and Animal Germplasm From the United States [Docket No. APHIS-2012-0049] RIN 0579-AE00 2016-00962

 


 

Thursday, January 14, 2016

 

EMERGING ANIMAL DISEASES Actions Needed to Better Position USDA to Address Future Risks Report to the Chairman, Committee on Energy and Commerce, House of Representatives December 2015 GAO-16-132

 

GAO

 


 

Saturday, July 23, 2016

 

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016

 


 

Wednesday, May 2, 2012

 

ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH

 


 

Saturday, June 12, 2010

 

PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse

 


 

Wednesday, July 28, 2010

 

re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010

 


 

Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net

 

Friday, September 23, 2016

North Iceland reporting more cases of Scrapie (Rida)

North Iceland reporting more cases of Scrapie (Rida)

 

Case of Scrapie in North Iceland

 

By Vala Hafstad Society about 5 hours ago

 

Icelandic sheep

 

Photo: Zoë Robert.

 

A case of scrapie has been confirmed at a farm in Skagafjörður. Scrapie is a fatal, degenerative disease, which affects the nervous systems of sheep and goats. This is the fourth confirmed case of scrapie in Northwest Iceland since February of 2015. That year, no case had been reported since 2010. Mast, the Icelandic Food and Veterinary Authority, is currently collecting data and preparing a course of action.

 

Last week, the farmer of Brautarholt in Skagafjörður suspected a case of scrapie and contacted the district’s veterinarian. The sheep was slaughtered and a specimen sent to the University of Iceland’s Institute for Experimental Pathology at Keldur, which confirmed that the animal had been affected with scrapie. Cases of the disease have come up on eleven farms in Skagafjörður in the past two decades. Sheep had to be slaughtered at the farm Brautarholt in 1987, due to scrapie. The farm currently has 290 sheep.

 

Until 2010, cases of scrapie were confirmed on a few farms in the country every year, but no cases were reported 2011-2014. Mast stresses that even though such cases are rare, we must constantly be on guard against the disease. Every year, samples are collected from about 3,000 sheep at slaughterhouses. Farmers have also been encouraged to send the heads of sheep killed by accident or disease to Keldur for examination.

 

Tags

 


 


 

Nature and Travel | Iceland Monitor | Wed 11 Mar 2015 | 10.55 GMT | Modified at 11.11

 

Scrapie outbreak

 

Three cases of scrapie have been identified in Iceland in the last month.

 

Scrapie is a fatal, degenerative disease affecting the central nervous system of sheep. Two of the confirmed cases are in Skagafjörður and the third, in Vatnsnes, both in Northern Iceland.

 

Cases not connected

 

The Icelandic Food and Veterinary Authority (IFVA) is currently gathering data and preparing further action, but so far there is not considered to be any link between the cases at the two sites. In the IFVA’s view, the current spate of cases may be attributable to greater care and attention exercised by farmers in the light of the first reported cases.

 


 

Líffræðifélag Íslands Líffræðiráðstefnan 2015

 

Erindi/veggspjald / Talk/poster V101

 

Scrapie control in Iceland – past and present Stefanía Þorgeirsdóttir (1) og Auður L. Arnþórsdóttir (2)

 

1. Tilraunastöð Háskóla Íslands í meinafræði að Keldum, 2. Matvælastofnun

 

Kynnir / Presenter: Stefanía Þorgeirsdóttir

 

Tengiliður / Corresponding author: Stefanía Þorgeirsdóttir (stef@hi.is)

 

Scrapie in sheep has been endemic in Iceland for over 130 years and has in the past caused considerable losses to sheep farming. In 1978 a rigorous scrapie control program was established and since 1986 the strategy has been to cull all scrapie flocks in order to eradicate the disease. In 1993 further enhancements of the program were made, mainly in the practical aspects of handling scrapie cases. After disinfection of premises and a three-year waiting period, farmers can restock with healthy sheep from scrapie-free zones. That plan is still in effect for classical scrapie, but in 2012 different measures for atypical/Nor98 cases were adapted. In the past the fight against other diseases in sheep has affected the control of scrapie in Iceland. In the 1930´s the country was divided into 36 movement restriction zones, in an effort to stop the spread of the so called Karakul diseases (maedi/visna and paratuberculosis). A few of these zones, marked by man-made fences or natural boundaries such as rivers and glaciers, are still scrapie-free. Marketing with live sheep is very limited, mostly from zones considered free of scrapie and import of live sheep from abroad has been banned since the middle of last century. Active surveillance for scrapie has been in practice since 1978, but no cases were detected among healthy slaughter until 2004, when rapid testing was implemented. Most classical scrapie cases in Iceland are still detected through passive surveillance, but majority of atypical cases have been detected through active surveillance. The goal of complete eradication has not yet been reached, but yearly incidence has lowered considerably and is down to a few cases per year. This is a drastic decrease from over one hundred infected farms at the height of the epidemic a few decades ago. On many farms scrapie has been detected in a repeated manner, i.e. the disease is reoccurring despite extensive cleanup and restocking.

 


 

Archives of Virology

 

April 2008, Volume 153, Issue 4, pp 637–644

 

High incidence of subclinical infection of lymphoid tissues in scrapie-affected sheep flocks

 

Authors Authors and affiliations Gudmundur GeorgssonEmail author Jona Adalheidur Adolfsdottir Astridur Palsdottir Einar Jorundsson Sigurdur Sigurdarson Stefania Thorgeirsdottir Gudmundur Georgsson 1 Email author Jona Adalheidur Adolfsdottir 1 Astridur Palsdottir 1 Einar Jorundsson 1 3 Sigurdur Sigurdarson 2 4 Stefania Thorgeirsdottir 1 1.Institute for Experimental PathologyUniversity of IcelandReykjavíkIceland 2.Laboratory of Chief Veterinary Officer, KeldurReykjavíkIceland 3.Ministry of Education, Science and CultureReykjavíkIceland 4.Agricultural Authority of IcelandSelfossIceland Original Article First Online: 29 January 2008 Received: 12 November 2007 Accepted: 27 December 2007 DOI: 10.1007/s00705-008-0035-8

 

Cite this article as: Georgsson, G., Adolfsdottir, J.A., Palsdottir, A. et al. Arch Virol (2008) 153: 637. doi:10.1007/s00705-008-0035-8

 

Abstract Prion diseases are characterized by a long incubation period. In scrapie, sheep may incubate and spread the infection for several years before clinical signs evolve. We have previously studied the occurrence of subclincal infection in the brain. Now, we have studied the occurrence of subclinical infection in the brain and several lymphoid tissues in two scrapie-affected Icelandic sheep flocks by immunohistochemistry for PrPSc, a molecular marker for infectivity, and correlated this with results of PrP genotyping. At culling, one flock had one confirmed scrapie case, while the other flock had two. Analysis of 106 asymptomatic sheep by immunostaining for PrPSc revealed that the incidence of subclinical infection was 58.3% in one flock and 42.5% in the other. PrPSc was only detected in lymphoid tissues. The youngest positive sheep were 4 months old. PrP genotyping showed that over 90% of the sheep were of a genotype which is moderately sensitive to infection and may delay neuroinvasion. Our results show that asymptomatic sheep may spread the infection during the long incubation period of several years, which constitutes an important obstacle in the eradication of scrapie. Our findings indicate that contamination of the environment plays an important part in sustaining the infection.

 

References

 


 

Epidemiology of scrapie in Iceland and experience with control measures.

 

Author(s) : Sigurdarson, S.

 

Author Affiliation : Institute for Experimental Pathology, University of Iceland, Keidur, Reykjavik, Iceland.

 

Editors : Bradley, R.; Savey, M.; Marchant, B.

 

Conference paper : Sub-acute spongiform encephalopathies. Proceedings of a seminar in the CEC Agricultural Research Programme, held in Brussels, 12-14 November 1990. 1991 pp.233-242

 

Conference Title : Sub-acute spongiform encephalopathies. Proceedings of a seminar in the CEC Agricultural Research Programme, held in Brussels, 12-14 November 1990.

 

ISBN : 0792314581

 

Record Number : 19922268331

 

Abstract : Scrapie or "rida" has been known in Iceland for more than 100 years. In 1978 a new plan was adopted in cooperation with farmers, first to reduce the losses from scrapie and prevent spreading to new areas and secondly to eradicate the disease from new places on the border of the endemic area. The final aim of the plan was full eradication of scrapie from Iceland. Earlier experiments indicated that the only possible method to accomplish this was stamping out all scrapie flocks as soon as possible after they were discovered. Restocking was supposed to take place after 2 years, only with lambs from isolated areas far away from all scrapie infected flocks. Through cleaning and disinfection of the premises was carried out one year before restocking. The result is promising. New stock has been kept for > 5 years on 76 farms and for > 4 years on 102 other farms without reappearance of the disease. Some of the restocked farms have already kept new stock for > 11 years without reappearance of scrapie. Altogether 716 flocks have been slaughtered and 397 of these have been restocked. By the end of 1990 all sheep flocks where scrapie was confirmed after 1982 will have been slaughtered. Every year since 1978 there has been an inspection of 10-15 000 brain samples of sheep possibly exposed to the infection from farms where scrapie had never been confirmed. The samples were taken in abattoirs. 15 infected farms have been identified by this method.

 

Comments… Cancel Save Annotate Rem

 

Publisher : Kluwer Academic Publishers

 

Location of publication : 3300 AA Dordrecht

 

Country of publication : Netherlands

 

Language of text : English

 

Language of summary : English

 


 

From: TSS (216-119-130-116.ipset10.wt.net)

 

Subject: ICELAND'S FIGHT AGAINST SHEEP DISEASES...

 

Date: December 9, 2000 at 3:08 pm PST

 

 ICELAND'S FIGHT AGAINST SHEEP DISEASES.

 

 By Stefanía Sveinbjarnardóttir-Dignum

 

 Copyright 1991

 

 In the last few years much has been heard about outbreaks of old and new diseases in animals in may countries around the world. TB in buffalo, Brucellosis in elk, Mad Cow disease, OPP and Scrapie in sheep and so on. One wonders if this is due to increased knowledge of diseases that have been around for a long time or if diseases are actually on the increase. All this got me looking back to my Icelandic origins and made me think about how Icelanders have responded to threats to their sheep farming, and in some cases to their very survival on this remote island, due to diseases that have hit the sheep population.

 

 After the settlement of Iceland, which took place between 800AD and 1100AD, there was no further importation of livestock for a long time. However, in the eighteen century the government became interested in improving the native sheep and in 1756 tem British rams were imported for crossbreeding. That experiment was so successful that four years later a few Merino sheep were imported from Spain. These sheep brought with them Psoroptes Ovis which are mites that live on blood and cause ill thrift and often death. These mites spread around the south and west of the island and caused severe losses. There was no cure and the only way to get rid of this pest was drastic culling of infected sheep flocks. It was made mandatory and caused incredible losses, but a victory was won. To make matters worse, in 1783 one of the biggest volcanic eruptions in recorded world history started in Iceland. The resulting poisonous gases and volcanic ash took a tremendous toll in lives of both people and animals. It is recorded that in 1760 the population of sheep in Iceland was 357,000 head and in 1784, after the eruption, it had dropped to 50,000 head, drop of over 70%. But with it the mites disappeared. This was a rather drastic way to eliminate a problem, but effective.

 

 During the next 90 years or so few importations occurred, in most cases involving only two or three animals . Crossing these seems to have been successful. In 1855 three Merino sheep and four English lambs were imported and with the English lambs the same mites as before. Again, the parasite spread and massive culling was undertaken with considerable loss, both in bloodlines and money. My great-grandfather was one of those ordered to cull his sheep in that episode. Dipping of sheep was also used in this fight with reasonably good results. After this catastrophe laws were passed in 1882 whereby all importation of sheep was forbidden. The ban lasted for fifty years.

 

 Around 1930 interest in experiments with crossbreeding surfaced again. In 1931 the Parliament passed laws allowing importation of 26 yearling from Britain. These sheep were kept for about 15 weeks in quarantine and then sent to a farm where they were bred and the offsprings sold for F-1 crossing. Under the same laws permission was given for importation of 20 Karakul sheep from Germany in 1933 for the purpose of producing crossbred lambskins. Those sheep were kept for only two months in quarantine and then released to farms around the country. The next year a strange disease, that had never before been seen in Iceland, began to appear in and around the farms where the Karakul sheep had been placed. In only one instance had the receiving farmer put his new ram into a further on farm quarantine. He did not like how the ram developed and culled it. he took the carcass a few miles out to sea and sank it there. By doing so he saved the best part of the Northwest peninsula from the worst sheep epidemic Iceland has ever experienced.

 

 By the late thirties it was clear that once again a disaster had struck the Icelandic sheep population. At that time the cause of the diseases was not known, but three different diseases had obviously come with the Karakul and were thereafter called collectively "the Karakul diseases". The first to be recognized was called Wet Mæði (pulmonary adenomatosis), and by the time this one seemed to be in remission another one appeared which got the name Dry Mæði (Maedi/Visna. OPP). Later, but only in limited area, Visna showed up. The names of these diseases were derived from the symptoms, Mæði meaning shortage of breath and Visna wasting. The third disease was Johne's.

 

 Even though these diseases had been found in other countries the causative agent was not known. By the end of the third decade it was obvious that drastic measures were needed and the old method of culling seemed to be the only possible approach. By this time the disease had spread over much of the country. The culling had to be done in an organized manner to stop the spreading of the disease and spread the unavoidable losses over time. The whole country was divided into districts by fencing or by natural barriers where possible. Some 1250 miles of fences were erected by the government and were , and still are kept up by people specifically employed for that purpose. When the barriers had be completed the culling started. All sheep in district after district were culled. After a complete eradication the area was restocked with sheep from a clean district. Most of the northwestern peninsula (areas 11 - 14) had escaped the disease as well as the isolated southeastern region between the Vatnajokull glacier and the Atlantic Ocean (area 26). The new stock came from there. In most cases the restocking was successful. The few unsuccessful cases were traced to carelessness in allowing some old sheep to escape slaughter or to infection of the new sheep en route.

 

 By 1952 the systematic slaughtering was completed. Approximately 650,000 sheep were culled during this period. Occasional outbreaks recurred up to the early sixties. It can happen, for example, that sheep are not found in the annual roundup and these can survive the winter in the mountains. Those could have been the source of infection. The last outbreak occurred in 1965 and since then Maedi/Visna (OPP) has not been found in Iceland. For decades afterwards monitoring was kept up, both on farms and in slaughterhouses but no new cases have ever been found. Iceland is now officially and in fact free of Maedi/Visna (OPP).

 

 The culling was not the only attack made on the disease. Another, and possibly more important one was the work done by Icelandic scientists. A dedicated team, headed by Dr. Björn Sigurðsson, kept looking for the causative agent and based on that work, Dr. Sigurðsson put forth his theory of ASlow Progressing Viral Diseases@ which at that time was a new concept in diseases. He and his team succeeded in isolating the Maedi virus and also proved that the same virus caused Visna. He and his colleagues, among whom were Dr. P. A. Pálsson, Dr. M. Guðnadóttir, and Dr. H. Thormar laid the base upon which AIDS research was later built, since the AIDS virus and the Maedi/Visna (OPP) virus are closely related. Dr. Sigurðsson died in 1959, only 46 years old, but his colleagues kept on the Maedi /Visna research and also studied Scrapie, another disease in some Icelandic sheep. Dr. Sigurðsson and his co-workers also studied Johne´s disease and were successful in producing a vaccine. By using that vaccine Johne´s disease has been put under control in Iceland.

 

 One might think that after all these sacrifices and losses that Icelanders were through with drastic measures; but, no. In 1878, before the van on importation in the last century, an Oxford Down ram was imported to a farm in the North of Iceland. From that farm a new disease spread through the district by selling of sons of the Oxford ram. The disease was named "riða" (tremble), we know this as Scrapie. It was confined to this area up till the early fifties when it started to spread slowly but with increasing speed as the years went by. It was not considered a serious threat at that time and it was hoped that in the Maedi/Visna culling it would disappear. It did not. The causative agent for this disease was much more resilient that the Maedi/Visna virus. After Maedi/Visna had been eradicated Scrapie was still around. In the next four years the disease appeared on 30 farms all of which and been Scrapie farms before the complete Maedi/Visna culling. Some of these farms had been out of sheep for three years. The Scrapie agent had somehow survived without sheep being on these farms. By 1978 it seemed obvious that Scrapie would overflow the whole country unless drastic measures were taken. It was decided to start a new battle against the disease, firstly by stopping the spread of it by culling all flocks where new cases appeared, on the borders of epidemic areas. Secondly, by culling all sheep in the epidemic areas. This was done with full co-operation between farmers, and the government. In addition to mandatory culling of all sheep on farms where Scrapie was confirmed or suspected, conditions for permission to restock were made stricter and minimum of two years of sheeplessness was demanded. However before full consensus was reached there was some dissent among farmers. some even suggested the losses from Scrapie were so low that they could live with it. However, culling according to the new rules was begun in 1978 and restocking from areas where Scrapie had never been found or suspected was allowed after the minimum time lapse. In most cases that was two years, ion some cases three years and in one experimental case, one year. In order to be permitted to restock, the following conditions have to be met: One year before restocking, all buildings, machinery and manure storage have to be washed and disinfected. This involves complete emptying of all buildings, scraping all floors and walls, opening all walls and ducts and all places where insects or mites could be hidden. Then the areas have to be sprayed with a jet sprayer using hypochlorite solution or some thing similar. After this has dried, the area has to be sprayed with iodine with a regular garden sprayer. After inspection by a government approved inspector the buildings are sealed until the new animals arrive. All woodwork that cannot be properly disinfected has to be burned or buried. worn tools and tools that are used to treat the animals, such as hoof clippers, marking tongs, reusable needles, etc. are to be disposed of. All areas where sheep commonly gathered have to be scraped and the soil buried. Then a minimum of four inches of gravel has to be put on these places. Manure can be spread on fields that are well fenced but not on any place where water runoff is likely. The hay taken from fields of farms where culling has taken place cannot be used for sheep feed. Hay, sod, manure etc., is not permitted to move from farm to farm. All surfaces that cannot be perfectly disinfected have to be sealed with durable paint on metal and concrete and creosote on wood. All this work has to be inspected and approved by government inspector. Restocking is not permitted without previous disinfection. Farmers do get financial assistance with cleaning and compensation while out of business due to Scrapie culling.

 

 Between 1978 and 1987 all sheep on several farms were culled and the new rules applied. Restocking was done from Scrapie-free areas. The results were promising. These were in districts where the incidence of Scrapie was just a few cases and culling was undertaken before any sign of serious spreading of the disease occurred. The disease was most widespread and serious in the eastern and northern part of the island. In the fall of 1987 the biggest onslaught was undertaken when 26,000 sheep from 130 farms were culled. In 1988 a further 20,000 sheep were culled from 100 farms. That culling left the eastern part of the country with any sheep. Last fall, in 1990 restocking in these areas began. since 1988 all confirmed and suspected cases have been culled. In some instances flocks from farms where no cases have been found have been culled on the grounds that Scrapie has been found on neighbouring farms. At present (March 1991), no cases of Scrapie are known to exist in Iceland but it is expected that some will surface in the next few years. In that case, culling of the flock, where Scrapie has been found, will be immediately undertaken. Some 280 farms have been restocked since the new regulations took effect, that is in the last 11 years, and in only two cases has Scrapie reappeared. In one case the cause could be traced o carelessness, in the other case the new stack was bought farm a farm nearby where Scrapie was later found.

 

 The veterinarians are not the only ones to report suspected cases. Farmer themselves do so also. Search is furthermore conducted in the slaughterhouses during the slaughtering season, in sheep brain samples. It seems to be that again Icelanders have gotten together to fight a disease in their sheep. Compensation to farmers is reasonable and peer pressure is very strong. Any one flock that harbors Scrapie is a threat to the whole district. Recently, the Chief Veterinarian for sheep disease control in Iceland, Dr. Sigurður Sigurðarson told me that they were pleasantly surprised over how well the fight was going. He stated that even though no known cases exist at present the battler is far from over. No country has undertaken eradication on such a large and thorough scale before. Countries such as Australia, New Zealand, Kenya and south Africa have found Scrapie and eradicated it, but in all these countries the disease has been found in recently imported animals and has been stopped before spreading into the native sheep populations. Scrapie has been known in Iceland for over 100 years and if eradication is successful, as appears to be happening, many countries may benefit from the lesson that is being learned in Iceland today.

 

 Note: I want to express my gratitude to Dr. Sigurður Sigurðarson who kindly edited this article for accuracy, as well as making available to me his paper AEpidemiology of Scrapie

 


 

P.S.-something else interesting. i have heard from several sources that the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland around 1992-3 has done long studies conducted on small pastures containing scrapie infected sheep. After leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years.... and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also came down with scrapie and passed it to their offspring.

 

a very horrifying thought, especially in light of the increase of scrapie over the years in the U.S.A., and the fact that they use scrapie for a research tool for CJD and other human/animal TSE's...

 

P.S. The U.S.A. has recently declared DECLARATIONS OF EMERGENCY'S for the following;

 

SCRAPIE regular=over 20 different strains to date

 

also

 

DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES

 


 

DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [2]

 


 

snip...end...tss

 

2015

 

update on that DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES ;

 

MAD SHEEP OF MAD RIVER VALLEY THE HISTORY AND TRUE STORY

 

A FALSE FLAG OPERATION BY THE USDA FEDERAL GOVERNMENT

 

Friday, February 20, 2015

 

***APHIS Freedom of Information Act (FOIA) Appeal Mouse Bio-Assays 2007-00030-A Sheep Imported From Belgium and the Presence of TSE Prion Disease Kevin Shea to Singeltary 2015

 


 


 

Thursday, September 22, 2016

 

*** NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION Skrantesjuke ***

 


 

Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission

 

Author

 

item Moore, Sarah item Kunkle, Robert item West greenlee, Mary item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin

 

Submitted to: Emerging Infectious Diseases Publication Type: Peer reviewed journal Publication Acceptance Date: 8/29/2016 Publication Date: N/A Citation:

 

Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.

 

Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, and CWD was recently reported in a free-ranging reindeer of Norway. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrPcwd). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel reindeer although only 2 out of 6 developed clinical disease during the study period (< 57 months PI). We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.

 

Monday, September 05, 2016

 

*** Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway ***

 


 

Monday, September 05, 2016

 

Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway

 


 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 

Monday, May 02, 2016

 

*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***

 


 

SCRAPIE AND CWD ZOONOSIS

 

PRION 2016 CONFERENCE TOKYO

 

Saturday, April 23, 2016

 

*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X

 


 


 

Monday, September 19, 2016

 

Evidence of scrapie transmission to sheep via goat milk

 


 

Monday, September 19, 2016

 

Identification of the first case of atypical scrapie in Japan

 


 

atypical scrapie NOR-98

 


 

Tuesday, December 16, 2014

 

Evidence for zoonotic potential of ovine scrapie prions

 

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

 

Abstract

 

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 

Subject terms: Biological sciences• Medical research At a glance

 


 

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.

 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.

 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

 

Taylor & Francis

 

Prion 2016 Animal Prion Disease Workshop Abstracts

 

WS-01: Prion diseases in animals and zoonotic potential

 

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

 

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

 

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

 

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

 

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

 

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

 

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 


 


 

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

 


 

SCRAPIE AND CWD ZOONOSIS

 

PRION 2016 CONFERENCE TOKYO

 

Saturday, April 23, 2016

 

*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X

 


 

Transmission of scrapie prions to primate after an extended silent incubation period

 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

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

 

Claudio Soto

 

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

 

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

 

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

 

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

 

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

 

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

 


 

see ;

 

with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion. see ;

 

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

 

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

 


 

see ;

 


 

Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles

 

Author Summary

 

Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.

 


 

tse prion soil

 


 


 


 


 

Wednesday, December 16, 2015

 

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

 


 

The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.

 


 

>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<

 

Fate of Prions in Soil: A Review

 

Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*

 

Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.

 


 

P.161: Prion soil binding may explain efficient horizontal CWD transmission

 

Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.

 


 

>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<

 

Wednesday, December 16, 2015

 

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

 

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

 

Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1

 

1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK

 

Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.

 

snip...

 

Discussion

 

Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).

 

Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.

 

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.

 

PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.

 

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.

 

Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification

 


 

Wednesday, December 16, 2015

 

*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***

 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<

 

Circulation of prions within dust on a scrapie affected farm

 

Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben C Maddison2*

 

Abstract

 

Prion diseases are fatal neurological disorders that affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk are contagious prion diseases where environmental reservoirs have a direct link to the transmission of disease. Using protein misfolding cyclic amplification we demonstrate that scrapie PrPSc can be detected within circulating dusts that are present on a farm that is naturally contaminated with sheep scrapie. The presence of infectious scrapie within airborne dusts may represent a possible route of infection and illustrates the difficulties that may be associated with the effective decontamination of such scrapie affected premises.

 

snip...

 

Discussion

 

We present biochemical data illustrating the airborne movement of scrapie containing material within a contaminated farm environment. We were able to detect scrapie PrPSc within extracts from dusts collected over a 70 day period, in the absence of any sheep activity. We were also able to detect scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m distance away from the scrapie contaminated buildings, suggesting that the chance of contamination of pasture by scrapie contaminated dusts decreases with distance from contaminated farm buildings. PrPSc amplification by sPMCA has been shown to correlate with infectivity and amplified products have been shown to be infectious [14,15]. These experiments illustrate the potential for low dose scrapie infectivity to be present within such samples. We estimate low ng levels of scrapie positive brain equivalent were deposited per m2 over 70 days, in a barn previously occupied by sheep affected with scrapie. This movement of dusts and the accumulation of low levels of scrapie infectivity within this environment may in part explain previous observations where despite stringent pen decontamination regimens healthy lambs still became scrapie infected after apparent exposure from their environment alone [16]. The presence of sPMCA seeding activity and by inference, infectious prions within dusts, and their potential for airborne dissemination is highly novel and may have implications for the spread of scrapie within infected premises. The low level circulation and accumulation of scrapie prion containing dust material within the farm environment will likely impede the efficient decontamination of such scrapie contaminated buildings unless all possible reservoirs of dust are removed. Scrapie containing dusts could possibly infect animals during feeding and drinking, and respiratory and conjunctival routes may also be involved. It has been demonstrated that scrapie can be efficiently transmitted via the nasal route in sheep [17], as is also the case for CWD in both murine models and in white tailed deer [18-20].

 

The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.

 


 

Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964

 

How Did CWD Get Way Down In Medina County, Texas?

 

Confucius ponders...

 

Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?

 

Epidemiology of Scrapie in the United States 1977

 

snip...

 

Scrapie Field Trial Experiments Mission, Texas

 

A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.

 

The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ...

 

snip...see full text ;

 


 

Thursday, June 09, 2016

 

Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964

 

How Did CWD Get Way Down In Medina County, Texas?

 


 


 

Friday, April 22, 2016

 

*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer

 


 

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 


 

Monday, May 02, 2016

 

*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***

 


 

SCRAPIE AND CWD ZOONOSIS

 

PRION 2016 CONFERENCE TOKYO

 

Saturday, April 23, 2016

 

*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***

 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X

 


 


 

Thursday, August 04, 2016

 

MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD

 


 

snip...

 


 


 


 


 


 


 

1979

 

SILENCE ON CJD AND SCRAPIE

 

1980

 

SILENCE ON CJD AND SCRAPIE

 

*** 1981 NOVEMBER

 


 


 

snip...see full text ;

 

Thursday, August 04, 2016

 

MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD

 


 

*** Calling Canadian beef unsafe is like calling your twin sister ugly," Dopp said.

 

Thursday, August 25, 2016

 

*** FSIS Green Bay Dressed Beef Recalls Beef Products Due To Possible Specified Risk Materials Contamination the most high risk materials for BSE TSE PRION AKA MAD COW TYPE DISEASE ***

 


 

Tuesday, August 9, 2016

 

*** Concurrence with OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2015-0055]

 


 

Saturday, July 23, 2016

 

*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016

 


 

Tuesday, July 26, 2016

 

*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016

 


 

Saturday, July 16, 2016

 

*** Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10

 

WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.

 

THIS is absolutely insane. it’s USDA INC.

 


 

Thursday, October 22, 2015

 

*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened those mad cows in Texas ***

 


 

Monday, June 20, 2016

 

*** Specified Risk Materials SRMs BSE TSE Prion Program ***

 


 

Tuesday, September 06, 2016

 

A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation

 


 

Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net