Saturday, December 12, 2015

NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE Prion REPORT December 14, 2015

NOTICE: Environmental Impact Statement on Large Livestock Carcasses USDA Animal and Plant Health Inspection Service sent this bulletin at 12/12/2015 01:01 AM EST

 

The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service (APHIS) is issuing a final environmental impact statement (EIS) for carcass management alternatives that could be implemented during an animal health emergency.

 

Livestock carcasses in large numbers can present a potential environmental risk. The agency must effectively manage carcasses in a mass animal health emergency to reduce potential risks to humans, livestock, and the surrounding environment.

 

In the EIS, the agency evaluated three alternatives, including:

 

Taking no action, under which APHIS would manage carcasses in a mass animal health emergency in accordance with the existing regulations in 9 CFR 53.4, using either unlined burial or open-air burning. Using standard procedures, which would consider four additional carcass-management options – landfill, rendering, fixed incineration, and composting – in addition to those listed in the no action alternative. Adaptive management, chosen as the preferred alternative, which allows for all high-capacity, widely-available carcass management options – including unlined burial, open-air burning, landfill, rendering, incineration, composting, and other nonstandard options – to be considered and potentially used during a mass animal health emergency. This chosen alternative is expected to provide greater flexibility for using the best available resources in such an event. The EIS finds that carcasses resulting from an animal health emergency can be disposed of safely using a variety of available methods. The EIS is not specific to any one animal disease. The findings of the EIS will be used to support animal health emergency planning and decision-making.

 


 

The U.S. Environmental Protection Agency (EPA) will publish a notice of availability in the Federal Register on Friday, December 18, 2015. APHIS will consider all comments received on or before January 17, 2016 in the Record of Decision. Comments regarding the EIS may be submitted at http://www.regulations.gov/#!docketDetail;D=APHIS-2013-0044 or sent to:

 

USDA APHIS Policy and Program Development Environmental and Risk Analysis Services 4700 River Road, Unit 149 Riverdale MD 20737

 

 ***

 

Please share the following link with others who may be interested in these updates. Click here to subscribe to the VS Animal Health Stakeholder Registry. This link will also allow you to change or cancel your subscriptions.

 


 

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

 

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

 


 

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

 

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

 


 

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

 

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

 


 

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

 

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

 

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

 


 

PL1

 

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

 

Claudio Soto

 

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

 

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

 

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

 

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

 

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

 

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

 


 

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

 

Alsu Kuznetsova1*, Debbie McKenzie2, Pamela Banser2, Tariq Siddique1, and Judd M. Aiken2 1Department of Renewable Resources; University of Alberta; Edmonton, AB Canada; 2Centre for Prions and Protein Folding Diseases; University of Alberta; Edmonton, AB Canada

 

Keywords: CWD expanding, prion, soil texture, soil organic matter, soil pH

 

Chronic wasting disease (CWD) is a horizontally transmissible prion disease of free ranging deer, elk and moose. Recent experimental transmission studies indicate caribou are also susceptible to the disease. CWD is present in southeast Alberta and southern Saskatchewan. This CWDendemic region is expanding, threatening Manitoba and areas of northern Alberta and Saskatchewan, home to caribou. Soil can serve as a stable reservoir for infectious prion proteins; prions bound to soil particles remain infectious in the soils for many years. Soils of western Canada are very diverse and the ability of CWD prions to bind different soils and the impact of this interaction on infectivity is not known. In general, clay-rich soils may bind prions avidly and enhance their infectivity comparable to pure clay mineral montmorillonite. Organic components of soils are also diverse and not well characterized, yet can impact prion-soil interaction. Other important contributing factors include soil pH, composition of soil solution and amount of metals (metal oxides). In this review, properties of soils of the CWD-endemic region in western Canada with its surrounding terrestrial environment are described and used to predict bioavailability and, thus, potential spread of CWD. The major soils in the CWD-endemic region of Alberta and Saskatchewan are Chernozems, present in 60% of the total area; they are generally similar in texture, clay mineralogy and soil organic matter content, and can be characterized as clay loamy, montmorillonite (smectite) soils with 6 - 10% organic carbon. The greatest risk of CWD spread in western Canada relates to clay loamy, montmorillonite soils with humus horizon. Such soils are predominant in the southern region of Alberta, Saskatchewan and Manitoba, but are less common in northern regions of the provinces where quartz-illite sandy soils with low amount of humus prevail.

 

snip...

 

Conclusions Soils can serve as an environmental reservoir for infectious prions and contribute to CWD expansion. Soil compounds (organic and inorganic) can bind and intercalate with infectious prions; many of these interactions affect maintenance of prion bioavailability and infectivity. The diversity of soil types in western Canada with their extreme variability in both organic and inorganic composition would suggest distinct outcomes of interactions of soil with PrPCWD. The potential contribution of northern soils (Luvisols and Brunisols) in the maintenance and bioavailability of CWD is unknown. Vertical transport of bound prions with clay particles in Luvisols into underlying horizons could limit transmission of prions through soil consumption. Differences in mineralogical composition, clay content, pH, amount and composition of SOM and other soil properties indicate a large number of variables in soil/prion interaction, a complexity that can impact prion persistence and infectivity levels in the environment.

 


 

Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted Infectivity from Complex Solutions (BASICS) A. Christy Wyckoff,

 

Krista L. Lockwood, Crystal Meyerett-Reid, Brady A. Michel, Heather Bender, Kurt C. VerCauteren, Mark D. Zabel

 

PLOS

 

Published: March 4, 2013 •DOI: 10.1371/journal.pone.0058630

 


 

Behavior of Prions in the Environment: Implications for Prion Biology

 

Shannon L. Bartelt-Hunt1*, Jason C. Bartz2* 1 Department of Civil Engineering, University of Nebraska-Lincoln, Peter Kiewit Institute, Omaha, Nebraska, United States of America, 2 Department of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, United States of America

 

Emergence of Prion Diseases Prion diseases are infectious, potentially zoonotic neurodegenerative diseases of animals including humans that are inevitably fatal and are caused by prions. Prions are comprised of a misfolded isoform of the normal prion protein, PrPC, into the infectious conformation, PrPSc [1]. Of the known prion diseases, chronic wasting disease (CWD) of deer, elk, and moose is emerging. CWD was first identified in captive deer in the front range of Colorado and Wyoming in the 1960s and has since been identified in captive and free-ranging cervids in 20 states, two Canadian provinces, and South Korea (for latest disease distribution please see http://www. nwhc.usgs.gov/disease_information/chronic_wasting_disease/index. jsp).While there is evidence of the spread ofCWDalong known cervid home ranges, the mechanism underlying the emergence of CWD in geographically isolated areas is not understood. The prevalence of CWD within an affected population is generally lower than 5%; however, there are reports of incidence rates that approach 50%. Transmission of CWD can occur horizontally or through CWD contaminated environments, but the relative contribution of each mode in the overall transmission of CWD is unknown [2]. Since effective control measures are not available, it is likely that CWD will continue to spread in North America. The effect of this on the wellbeing of the cervid

 


 

Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of Prion Infection

 

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

 

 & Mark Zabel

 

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

 

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

 

 Abstract

 

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

 


 

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

 

Authors Sandra Pritzkow, Rodrigo Morales, ..., Edward Hoover, Claudio Soto Correspondence claudio.soto@uth.tmc.edu

 

In Brief Prions are the proteinaceous infectious agents responsible for prion diseases. Pritzkow et al. report that prions from brain and excreta can bind grass plants and remain attached to living plants for a long time and that contaminated plants can infect animals. In addition, grass plants can uptake and transport prions from infected soil. Pritzkow et al., 2015, Cell Reports 11, 1168–1175 May 26, 2015 ª2015 The Authors http://dx.doi.org/10.1016/j.celrep.2015.04.036

 


 

98 | Veterinary Record | January 24, 2015

 

EDITORIAL

 

Scrapie: a particularly persistent pathogen

 

Cristina Acín

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

References

 

snip...

 

98 | Veterinary Record | January 24, 2015

 


 

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

 

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

 

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

 

SNIP...

 

Discussion

 

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

 

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

 

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

 

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

 


 

Monday, November 3, 2014

 

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

 


 

PPo3-22:

 

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

 

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

 

Key words: scrapie, evironmental persistence, sPMCA

 

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

 


 

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

 


 

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

 

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

 

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

 

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

 

SUMMARY:

 


 

For Immediate Release Thursday, October 2, 2014

 

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

 

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

 

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

 


 

*** see history of this CWD blunder here ;

 


 

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

 


 

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

 

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

 


 

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

 


 

Saturday, December 05, 2015

 

CWD Prions Remain Infectious after Passage Through the Digestive System of Coyotes (Canis latrans)

 


 

COMERCIAL IN CONFIDENCE

 

SPREADING OF UNPROCESSED BLOOD ON LAND

 


 

The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences & Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s Hospital London and William Harvey Hospital Ashford April 1999

 

snip...

 

88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed. 89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence. 90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.

 

91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.

 

92. This review and recommendations from Brown have particular importance. Brown is one of the world's foremost authorities on TSEs and is a senior researcher in the US National Institutes of Health (NIH). It is notable that such a respected authority is forthright in acknowledging the existence of potential risks, and in identifying the appropriate measures necessary to safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical distribution of variant CJD in the UK (excluding Northern Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41 (02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD (variant CJD) might live closer to rendering factories than would be expected by chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were studied. The incubation period of vCJD is not known but by analogy with other human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure to rendering products, such exposure might plausibly have occurred 8-10 years before the onset of symptoms. The authors were able to obtain the addresses of all rendering plants in the UK which were in production in 1988. For each case of vCJD, the distance from the place of residence on 1st January 1998 to the nearest rendering plant was calculated

 

snip...

 


 

Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).

 


 

PAUL BROWN SCRAPIE SOIL TEST

 


 

Published online 11 February 2011 | Nature | doi:10.1038/news.2011.87

 

News

 

Livestock plagues are spreading As farming intensifies, researchers warn that the developing world is "dangerously behind" on controlling animal diseases.

 

Natasha Gilbert

 


 


 

snip...

 

please see full text ;

 

Thursday, February 17, 2011

 

Environmental Sources of Scrapie Prions

 


 


 

INCINERATION TEMPS

 

Requirements include:

 

a. after burning to the range of 800 to 1000*C to eliminate smell;

 

well heck, this is just typical public relations fear factor control. do you actually think they would spend the extra costs for fuel, for such extreme heat, just to eliminate smell, when they spread manure all over your veg's. i think not. what they really meant were any _TSE agents_.

 

b. Gas scrubbing to eliminate smoke -- though steam may be omitted;

 

c. Stacks to be fitted with grit arreaters;

 

snip...

 

1.2 Visual Imact

 

It is considered that the requirement for any carcase incinerator disign would be to ensure that the operations relating to the reception, storage and decepitation of diseased carcasses must not be publicly visible and that any part of a carcase could not be removed or interfered with by animals or birds.

 

full text;

 


 

Part II, page 5, final para – continued on page 6.

 

The precautionary principle, as set out in PPG 23, requires that where there is perceived to be an unacceptable risk, which cannot be scientifically quantified, the precautionary principle should be applied. This was the case with the landfill of untreated carcasses. If there were no perception of such a risk, as was the case with Thruxted Mill, then the precautionary principle does not apply. ...

 


 

Knacker's yard link to Queniborough nvCJD cluster

 

Sun, 13 Aug 2000 Jonathan Leake and Dipesh Gadher

 

Sunday Times Additional reporting: Graham Hind

 

BRITAIN'S worst outbreak of the human form of mad-cow disease may be linked to a nearby knacker's yard that sold meat from diseased animals. The yard operated just eight miles from Queniborough, the Leicestershire village where health officials are investigating the first known cluster of CJD cases.

 

Three people who spent time in the village died from CJD in 1998, and a fourth person is suspected of having the degenerative brain disease. Another victim lived just three miles away.

 

The possible link to the knacker's yard - which recycled animals unfit for human consumption into pet food and other products - dates back 20 years, to about the time when scientists now believe the BSE epidemic may have begun.

 

Two meat traders from Bedfordshire were convicted in 1982 of buying unapproved beef from W E Mason & Sons of Wigston, near Leicester, and selling it to an unsuspecting butcher in Hertfordshire.

 

Last week officials seized council documents and court reports relating to the company to determine whether any unfit meat may have entered the human food chain locally.

 

"We have had a very useful series of conversations about this with Oadby and Wigston council," said Philip Monk, a consultant in communicable disease control at Leicestershire health authority, who is heading the Queniborough investigation. "I am ruling nothing in and nothing out. Anything we have that is potentially helpful in explaining local meat trading practices has to be examined."

 

The case heard by Leicester magistrates in 1982 was the culmination of Operation Meat Hook, a joint investigation between detectives and environmental health officers from three counties.

 

The teams covertly observed Peter Fletcher, a partner in a wholesale butcher's business near Dunstable, on four occasions in 1980 when he visited Leonard Mason, the yard's owner. He loaded beef carcasses from the yard into an un-marked van, which had been contaminated by a cow's head "fouled by stomach contents", according to evidence given in court. One of the carcasses was later found to have been infected with pleurisy.

 

Fletcher marked the meat with a fake inspector's stamp, and then left it with a retail butcher near Hemel Hempstead, Hertfordshire.

 

"A knacker's yard may, and frequently will, deal with diseased cattle," the prosecutor had told an earlier hearing. "Meat may be partly decomposed and contaminated. Disease is rife in such premises and could include anthrax and tuberculosis."

 

Fletcher was jailed for three months and fined ?500. His partner, Francis Fensome, received a suspended prison sentence. Mason was cleared after telling the court that he had been told the meat was to be used to feed animals at Whipsnade zoo [site of two cheetah BSE fatalities -- webmaster]

 

The knacker's yard, which had been run by the Mason family since 1947, was closed the same year and now stands derelict. Mason has since died.

 

Last week his brother, Jack Mason, said: "I am confident there is no connection with us and the outbreak in Queniborough. Most of the meat went to zoos. Any meat that was sold locally went to dog owners as pet food."

 

There is no proof that Mason dealt in cattle infected with BSE, which was not recognised at the time. But such yards commonly dealt in "downer" cows - those displaying symptoms of illness - so any animals that did have BSE were likely to have ended up in such places.

 

The Queniborough inquiry team is also examining slaughtering techniques at Leicestershire abattoirs and childhood eating habits of those who grew up in the village, although school meals have been ruled out as a possible cause of the CJD outbreak.

 

Arthur Beyless lost his daughter, Pamela, 24, a bank worker, to the disease after a two-year struggle for survival. Although the Beylesses live in nearby Glenfield, Pamela regularly visited her grandparents in Queniborough and the family often bought meat from Ian Bramley, the village butcher, in the late 1970s and early 1980s.

 

Beyless said: "On one occasion I was buying some meat when Ian told me he'd got it for 'a good deal'. It does make you wonder when you consider this theory about the knacker's yard. This disease is something that might never have happened if people weren't always grasping for that last penny."

 

The other two named victims with links to Queniborough are Stacey Robinson, 19, who lived there for 12 years before moving to another part of the county, and Glen Day, 34, who worked on a farm in the area. He regularly ate at the Horse and Groom pub, which was supplied with meat by Bramley.

 

Bramley died in a car crash. His stepmother, Hazel Bramley, said she knew nothing about Mason's yard. "We bought our meat directly from local farmers," she said. "The animals were slaughtered in Leicester and delivered to us. I don't know anything about this place in Wigston."

 


 


 

18 Jun 00 - CJD - Risk of CJD is higher in north Jonathan Leake

 

Sunday Times ... Sunday 18 June 2000

 

Northerners could be at several times more risk from variant CJD , the human form of "mad cow" disease, than those living in the Midlands and south, a study by government scientists has found, writes.

 

The research, carried out by the Creutzfeldt-Jakob disease Surveillance Unit, also shows that the rate of incidence of the disease, which is always fatal, is rising across Britain .

 

The figures remain too low to estimate accurately how many people will ultimately be affected. Estimates range from hundreds to many thousands .

 

Variations in the incidence of the disease are a matter of deep concern . In the north of England - north of Manchester and including Yorkshire and Humberside - there were 3.14 cases per million people over the five years to 1999. Scotland had the second highest rate at 2.98 cases per million .

 

The West Midlands emerged as the safest place with just 0.36 cases per million. East Anglia and the south experienced, respectively, 0.93 and 1.37 cases per

 


 


 

#18 Jun 00 - CJD - Risk of CJD is higher in north

 


 


 

Knacker's yard link to Queniborough nvCJD cluster

 

Sun, 13 Aug 2000 Jonathan Leake and Dipesh Gadher Sunday Times Additional reporting: Graham Hind

 

BRITAIN'S worst outbreak of the human form of mad-cow disease may be linked to a nearby knacker's yard that sold meat from diseased animals. The yard operated just eight miles from Queniborough, the Leicestershire village where health officials are investigating the first known cluster of CJD cases. Three people who spent time in the village died from CJD in 1998, and a fourth person is suspected of having the degenerative brain disease. Another victim lived just three miles away.

 

The possible link to the knacker's yard - which recycled animals unfit for human consumption into pet food and other products - dates back 20 years, to about the time when scientists now believe the BSE epidemic may have begun.

 

Two meat traders from Bedfordshire were convicted in 1982 of buying unapproved beef from W E Mason & Sons of Wigston, near Leicester, and selling it to an unsuspecting butcher in Hertfordshire.

 

Last week officials seized council documents and court reports relating to the company to determine whether any unfit meat may have entered the human food chain locally.

 

"We have had a very useful series of conversations about this with Oadby and Wigston council," said Philip Monk, a consultant in communicable disease control at Leicestershire health authority, who is heading the Queniborough investigation. "I am ruling nothing in and nothing out. Anything we have that is potentially helpful in explaining local meat trading practices has to be examined."

 

The case heard by Leicester magistrates in 1982 was the culmination of Operation Meat Hook, a joint investigation between detectives and environmental health officers from three counties.

 

The teams covertly observed Peter Fletcher, a partner in a wholesale butcher's business near Dunstable, on four occasions in 1980 when he visited Leonard Mason, the yard's owner. He loaded beef carcasses from the yard into an un-marked van, which had been contaminated by a cow's head "fouled by stomach contents", according to evidence given in court. One of the carcasses was later found to have been infected with pleurisy.

 

Fletcher marked the meat with a fake inspector's stamp, and then left it with a retail butcher near Hemel Hempstead, Hertfordshire.

 

"A knacker's yard may, and frequently will, deal with diseased cattle," the prosecutor had told an earlier hearing. "Meat may be partly decomposed and contaminated. Disease is rife in such premises and could include anthrax and tuberculosis."

 

Fletcher was jailed for three months and fined ?500. His partner, Francis Fensome, received a suspended prison sentence. Mason was cleared after telling the court that he had been told the meat was to be used to feed animals at Whipsnade zoo [site of two cheetah BSE fatalities -- webmaster]

 

The knacker's yard, which had been run by the Mason family since 1947, was closed the same year and now stands derelict. Mason has since died.

 

Last week his brother, Jack Mason, said: "I am confident there is no connection with us and the outbreak in Queniborough. Most of the meat went to zoos. Any meat that was sold locally went to dog owners as pet food."

 

There is no proof that Mason dealt in cattle infected with BSE, which was not recognised at the time. But such yards commonly dealt in "downer" cows - those displaying symptoms of illness - so any animals that did have BSE were likely to have ended up in such places.

 

The Queniborough inquiry team is also examining slaughtering techniques at Leicestershire abattoirs and childhood eating habits of those who grew up in the village, although school meals have been ruled out as a possible cause of the CJD outbreak.

 

Arthur Beyless lost his daughter, Pamela, 24, a bank worker, to the disease after a two-year struggle for survival. Although the Beylesses live in nearby Glenfield, Pamela regularly visited her grandparents in Queniborough and the family often bought meat from Ian Bramley, the village butcher, in the late 1970s and early 1980s.

 

Beyless said: "On one occasion I was buying some meat when Ian told me he'd got it for 'a good deal'. It does make you wonder when you consider this theory about the knacker's yard. This disease is something that might never have happened if people weren't always grasping for that last penny."

 

The other two named victims with links to Queniborough are Stacey Robinson, 19, who lived there for 12 years before moving to another part of the county, and Glen Day, 34, who worked on a farm in the area. He regularly ate at the Horse and Groom pub, which was supplied with meat by Bramley.

 

Bramley died in a car crash. His stepmother, Hazel Bramley, said she knew nothing about Mason's yard. "We bought our meat directly from local farmers," she said. "The animals were slaughtered in Leicester and delivered to us. I don't know anything about this place in Wigston."

 

Bovine spongiform encephalopathy: Epidemiological studies

 


 


 


 

The Queniborough CJD cluster

 

New claims link CJD to water supply

 


 


 

Eurosurveillance, Volume 5, Issue 12, 22 March 2001 Articles

 

--------------------------------------------------------------------------------

 

Citation style for this article: Report on Leicestershire vCJD cluster published. Euro Surveill. 2001;5(12):pii=1785. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=1785 Date of submission:

 

--------------------------------------------------------------------------------

 

Report on Leicestershire vCJD cluster published

 

The inquiry team at Leicestershire Health Authority has reported on the results of the investigation into the geographical cluster of five cases of variant Creutzfeld-Jakob Disease (vCJD) around the village of Queniborough. The investigators have concluded that the purchase and consumption of beef in the early 1980’s from butcher’s shops where the meat could have been contaminated with brain tissue from cattle affected with bovine spongiform encephalopathy (BSE) provides a plausible explanation for the cluster (1). A case control study, in which relatives of the five cases and relatives of 30 age-matched controls were interviewed, found that cases were 15 times more likely than controls to have purchased and consumed beef from a butcher who removed brains from cattle (p = 0.0058, 95% C.I. for odds ratio 1.6 – 140). The two butchers linked to four of the five cases removed the brains from cattle that were slaughtered either by the butchers themselves or in a nearby small abattoir. Pithing rods were used during slaughtering, and the carcasses were cleaned by wiping rather than by hosing. Removal of the brain was difficult and messy and the meninges were often ruptured either at removal or by the pithing rod. This led to a risk of cross contamination of carcass meat with brain tissue. Reasons are also given as to why during the early 1980’s the cattle in mixed dairy-beef herds used for the local meat trade may have had higher levels of BSE agent at slaughter than cattle raised for beef alone.

 

The practice of removing and selling the brains of cattle as food was legal in the United Kingdom throughout the 1980’s. Since 1989 it has been illegal for cattle brains to be used for human consumption and since 1996 the whole head of cattle over six months must be disposed of in a slaughterhouse as specified risk material.

 

The current number of definite and probable cases of vCJD in the UK is 97 (2). Of these, seven are probable cases who are still alive. Although there are other geographical areas with more than one case, to date Queniborough is the only area where statistical analysis suggests the association between the cases is unlikely to have occurred by chance.

 

References : Bryant G, Monk P. Summary of the final report of the investigation into the North Leicestershire cluster of variant Creutzfeld-Jakob disease. Leicester: Leicestershire NHS Health Authority, 2001. Available online at . Queniborough vCJD cluster report - Department of Health statement [press release 2001/0141]. London: Department of Health, 21 March 2001. Available online at

 


 


 


 

 Tue, 8, Aug 2000 19:39:27 -0400

 

From: jonathan leake

 

Date: Tue, 8, Aug 2000 19:39:27 -0400

 

Subject: IN CONFIDENCE (I SMELL A STORY ......)

 

Sender: jonathan leake

 

To: BSE Terry Singletary

 

Message-ID: <200008081939_mc2-af13-1bc compuserve.com=""> MIME-Version: 1.0 Content-Type: text/plain; charset=ISO-8859-1 Content-Disposition: inline Content-Transfer-Encoding: 8bit X-MIME-Autoconverted: from quoted-printable to 8bit by sys44.hou.wt.net id SAA15659 X-Mozilla-Status: 8007 X-Mozilla-Status2: 00000000 X-UIDL: ed0acd360d74370a3e06000000000000

 

Hi Terry - this is Jonathan Leake here.

 

we're thinking of doing a story on the knackers yard meat issue - is there a link to Queniborough?

 

Would you mind resending any info you have on this - I may have lost some of the stuff you sent.

 

Cd you send it to

 

jonathan.leake@suandy-times.co.uk

 

AND TO

 

dipesh.gadher@sunday-times.co.uk

 

- HE'S RESEARCHING THIS STORY FOR ME AS I'M AT A CONFERENCE

 

MANY THANKS FOR YOUR HELP - AND FOR ALL THE GOOD WORK YOU'VE BEEN DOING

 

snip...end...TSS

 

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

 

 Re: IN CONFIDENCE (I SMELL A STORY )

 

Subject: Re: IN CONFIDENCE (I SMELL A STORY )

 

Date: Tue, 08 Aug 2000 21:41:57 -0700

 

From: "Terry S. Singeltary Sr."

 

To: jonathan leake

 

Hello Jonathan,

 

yes, give me some time though. there is a shitstorm on CJD Voice, they let the Faillace's on the CJD Voice support group (TSE tainted sheep farmers) without telling anyone; and myself and other are pissed off to say the least. This was suppose to be a support group. i told them it would be like asking the Malboro Man on a Cancer List. But he is Dead. Maybe it struck a nerve.

 

Have you got the DFA 4, 5, and 7, i thought i read something about knackers or maybe babyfoods??? not sure. i can send to you. I am sure i have something in the GBR's for the states and the other countries, don't have time to read. you can read them at;

 


 

i will search as soon as i get time ....

 

kind regards, Terry

 

jonathan leake wrote:

 

Hi Terry - this is Jonathan Leake here. we're thinking of doing a story on the knackers yard meat issue - is there a link to Queniborough?

 

Would you mind resending any info you have on this - I may have lost some of the stuff you sent. ...

 

snip...END...TSS

 

Re: KNACKERS AND RENDERS

 

Subject: Re: KNACKERS AND RENDERS

 

Date: Thu, 10 Aug 2000 16:04:14 ·0700

 

From: "Terry S. Singeltary Sr."

 

To: jonathan.leake@sunday-times.co.uk, dipesh.gadher@Sunday-times.co.uk

 

do you have access to the;

 

The Veterinary-Record, December 20/27, 1997 Papers and Articles Effect of rendering procedures on the scrapie agent D. M. Taylor, S.L. Woodgate, A.J. Fleetwood, R.J.G. Cawthorne it's about 6 or 7 pages. i do not have it scanned and it's fairly fine print, however good print. also the report; The Veterinary Record, March 2, 1991 Papers and Articles Bovine Spongiform Encephalopathy: epidemiological studies on the origin there is a good section of rendering; Survey of rendering processes, solvents etc (very detailed on temps and processes) can scan copy correct and paste, but it will take some time, or fax COLLECT to you. I'm running out of quarters fast, nobody paying me to do this, and i am on disablility. so the fax will have to be collect ... regards, Terry 1 of 1 8/13/00 1 :06 PM

 

end...TSS

 

Date: Fri, 2 Mar 2001 23:27:10 +0000 (GMT)

 

From:

 

Subject: confidential

 

To: "Terry S. Singeltary Sr."

 

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at..........

 

USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........

 

if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........

 

I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........

 

forget any action........it is ALL gonna be sporadic!!!

 

And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. ....

 

It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....

 

and this may be their biggest downfall.

 

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

 

snip...

 

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

 

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

 

snip...

 

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

 


 


 


 


 


 


 


 


 

snip...

 

for anyone interested, see full text ;

 

Thursday, July 08, 2010

 

GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010

 

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

 

From: Terry S. Singeltary Sr.

 


 

Cc: BSE-L@LISTS.AEGEE.ORG ; cjdvoice@yahoogroups.com ; BLOODCJD@YAHOOGROUPS.COM

 

Sent: Thursday, July 08, 2010 9:27 PM

 

Subject: GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010

 


 

*** 2009 UPDATE WATER AND PRIONS ***

 

Wednesday, October 14, 2009

 

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

 


 

2015

 

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

 

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

 

item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -

 

Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573. Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent.

 

***The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy.

 

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. 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.

 


 

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

 


 

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

 

Title: Transmission of the agent of sheep scrapie to deer results in PrPSc with two distinct molecular profiles

 

item Greenlee, Justin item Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Kunkle, Robert

 

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: March 31, 2015 Publication Date: May 25, 2015 Citation: Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015.

 

Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum. Prion 2015. p. S62. Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes reveal PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile type readily passes to deer.

 


 

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

 

Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease Authors

 

item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -

 

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A

 

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

 


 

From: Terry S. Singeltary Sr.

 

Sent: Tuesday, December 01, 2015 5:05 PM

 

To: Terry Singeltary Sr.

 

Subject: Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission

 

*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***

 

Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats

 

SUMMARY: We are reopening the comment period for our proposed rule that would revise completely the scrapie regulations, which concern the risk groups and categories established for individual animals and for flocks, the use of genetic testing as a means of assigning risk levels to animals, movement restrictions for animals found to be genetically less susceptible or resistant to scrapie, and recordkeeping requirements. This action will allow interested persons additional time to prepare and submit comments.DATES: The comment period for the proposed rule published on September 10, 2015 (80 FR 54660-54692) is reopened. We will consider all comments that we receive on or before December 9, 2015. ...

 


 


 


 

Comment from Terry Singeltary This is a Comment on the Animal and Plant Health Inspection Service (APHIS) Proposed Rule: Scrapie in Sheep and Goats

 

For related information, Open Docket Folder Docket folder icon

 

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Show agency attachment(s) AttachmentsView All (0)

 

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Comment View document:Indeed, much science has changed about the Scrapie TSE prion, including more science linking Scrapie to humans. sadly, politics, industry, and trade, have not changed, and those usually trump sound science, as is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing animals and the OIE. we can look no further at the legal trading of the Scrapie TSE prion both typical and atypical of all strains, and CWD all stains. With as much science of old, and now more new science to back this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE, and all trading partners to take heed to the latest science on the TSE prion disease, all of them, and seriously reconsider the blatant disregards for human and animal health, all in the name of trade, with the continued relaxing of TSE Prion trade regulations through the 'NEGLIGIBLE BSE RISK' PROGRAM, which was set up to fail in the first place. If the world does not go back to the 'BSE RISK ASSESSMENTS', enhance, and or change that assessment process to include all TSE prion disease, i.e. 'TSE RISK ASSESSMENT', if we do not do this and if we continue this farce with OIE and the USDA et al, and the 'NEGLIGIBLE BSE RISK' PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they will continue to mutate and spread among species of human and animal origin, and they will continue to kill. ...

 

please see ;

 

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 longe 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***

 

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

 


 

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

***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.

 


 

please see file attachment for full submission and recent science and my deep concerns on the TSE Prion disease... No documents available. AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:

 


 

***********OCTOBER 2015*************

 

*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***

 

THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.

 

P.108: Successful oral challenge of adult cattle with classical BSE

 

Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada

 

Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only. Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.

 


 

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, Val erie 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 longe 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 study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***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.

 

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

 


 


 

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

 

***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.

 

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

 

It also appears to Mr MacLean that Mr Bradley’s answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight: particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the “attack rate” experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective

 

2

 

dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.

 

It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

it is clear that the designing scientists must have also shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

Saturday, September 12, 2015

 

The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014

 

>>>We propose that Canadian policies largely ignored the implicit medical nature of BSE, treating it as a purely agricultural and veterinary issue. In this way, policies to protect Canadians were often delayed and incomplete, in a manner disturbingly reminiscent of Britain’s failed management of BSE. Despite assurances to the contrary, it is premature to conclude that BSE (and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of Canada’s past: BSE remains very much an issue in Canada’s present. <<<

 


 

small amount of leftover contaminated feed’ ...LOL...maybe large amount in USA. see ;

 

Monday, November 30, 2015

 

*** Report on the Investigation of the Nineteenth Case of Bovine Spongiform Encephalopathy (BSE) in Canada November 2015 ***

 


 

Wednesday, September 23, 2015

 

NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15; 8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE Strains by RT-QuIC

 


 

Monday, December 7, 2015

 

STRICTLY IN CONFIDENCE WHY WE DON'T TEST ANIMAL FEED FOR ANIMAL PROTEIN BSE TSE PRION

 


 

Friday, May 29, 2015

 

GAO FEDERAL VETERINARIANS US Federal Government Is Unprepared for a Large-Scale Animal Disease Outbreak

 


 

Friday, August 14, 2015

 

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

 




Saturday, December 12, 2015

CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015


 
these blogs are for educational use. I do not advertise or make money from them.

MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget, and never let them forget...

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

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