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 final EIS is available at: http://www.aphis.usda.gov/stakeholders/downloads/2015/eis_carcass_management.pdf.
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
***
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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
--------------------------------------------------------------------------------
Show agency attachment(s) AttachmentsView All (0)
--------------------------------------------------------------------------------
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
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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