Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information
Greetings FDA et al, I kindly would like to make comment submission to
;
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information
A Notice by the Food and Drug Administration on 03/04/2016
This document has a comment period that ends in 54 days (05/03/2016)
Action Notice; Request For Comments And For Scientific Data And
Information.
Summary The Food and Drug Administration (FDA or we) is requesting
scientific data, information, and comments that would assist the Agency in its
plan to develop a risk assessment for produce grown in fields or other growing
areas amended with untreated biological soil amendments of animal origin
(including raw manure). The risk assessment will evaluate and, if feasible,
quantify the risk of human illness associated with consumption of produce grown
in fields or other growing areas amended with untreated biological soil
amendments of animal origin that are potentially contaminated with enteric
pathogens, such as Escherichia coli O157:H7 or Salmonella. The risk assessment
also will evaluate the impact of certain interventions, such as use of a time
interval between application of the soil amendment and crop harvest, on the
predicted risk. The risk assessment is intended to inform policy decisions with
regard to produce safety.
Table of Contents Back to Top DATES: ADDRESSES: Electronic Submissions
Written/Paper Submissions FOR FURTHER INFORMATION CONTACT: SUPPLEMENTARY
INFORMATION: I. Background A. What are the food safety concerns related to
untreated biological soil amendments of animal origin? B. How did FDA's rule on
produce safety address BSAAO? II. FDA's Risk Assessment III. Issues for
Consideration IV. Reference DATES: Back to Top Submit either electronic or
written comments and scientific data and information by May 3, 2016.
ADDRESSES: Back to Top You may submit comments and scientific data and
information as follows:
SNIP...
SUPPLEMENTARY INFORMATION: Back to Top
I. Background Back to Top A. What are the food safety concerns related to
untreated biological soil amendments of animal origin? Biological soil
amendments of animal origin (BSAAO) can be a source of contamination of produce
with pathogens that can cause human illness. Human pathogens in BSAAO, once
introduced to the growing environment, may be inactivated at a rate that is
dependent upon a number of environmental, regional, and other agricultural and
ecological factors. The rate of pathogen population decline over time is also
influenced by the types of BSAAO and application methods. Furthermore, the types
of produce and whether or not BSAAO may come into contact with a harvestable
portion of the crop influences the likelihood of pathogen transfer from the
amended soil to produce (Ref. 1).
Some produce farms use untreated BSAAO for various reasons, including that
they are inexpensive, readily available, and rich nutrient sources for growing
crops. Whether it is feasible for a farm to use untreated BSAAO as a principal
nutrient source depends on numerous factors, including whether there is a
required time interval between application and harvest and the length of such an
interval (which may affect the nutrients retained or available from BSAAO), and
crop nutrient demand (i.e., the nutrients needed to support crop growth).
Typical examples of untreated BSAAO are raw cattle manure, poultry litter, swine
slurry, and horse manure. FDA acknowledges that required application intervals
for certain uses of untreated BSAAO could influence the number of crop cycles a
farm is able to undertake each year and/or the choices farms make regarding
which type of amendment to apply (e.g., raw manure, composted manure, or other
nutrient sources).
B. How did FDA's rule on produce safety address BSAAO? In January 2013,
based in part upon authority provided by the FDA Food Safety Modernization Act,
we published a proposed Produce Safety Rule entitled “Standards for the Growing,
Harvesting, Packing, and Holding of Produce for Human Consumption” (78 FR 3504,
January 16, 2013). Among other provisions related to BSAAO, the proposed rule
included at § 112.56(a)(1)(i) (21 CFR 112.56(a)(1)(i)) a 9-month minimum
application interval for untreated BSAAO applied in a manner that does not
contact covered produce during application and minimizes the potential for
contact with covered produce after application (78 FR 3504 at 3637). In response
to public comments, we withdrew this proposed 9-month minimum application
interval in a supplemental proposed rulemaking that we published on September
29, 2014 (79 FR 58434 at 58457 through 58461). In the supplemental proposed
rule, we acknowledged the limited body of currently available scientific
evidence relating to the proposed 9-month interval and the need for additional
research in this area, and described our planned risk assessment and research
agenda (79 FR 58434 at 58460 through 58461). Accordingly, we deferred our
decision on an appropriate minimum application interval.
On November 27, 2015, we published a final Produce Safety Rule entitled
“Standards for the Growing, Harvesting, Packing, and Holding of Produce for
Human Consumption,” (80 FR 74354). The final rule is now codified at 21 CFR part
112. In the preamble to the final rule, we restated our decision with respect to
the appropriate minimum BSAAO application interval (80 FR 74354 at 74463). We
reserved one of the provisions in the final rule's Subpart F (Biological Soil
Amendments of Animal Origin and Human Waste) because we continue to believe that
a quantitative application interval standard is necessary and anticipate
locating such a future standard in that provision. As finalized, the Produce
Safety Rule establishes that there is no minimum application interval required
when untreated BSAAO are applied in a manner that does not contact covered
produce during or after application (§ 112.56(a)(1)(ii)), and the minimum
application interval is [reserved] when applied in a manner that does not
contact produce during application and minimizes the potential for contact with
produce after application (§ 112.56(a)(1)(i)).
II. FDA's Risk Assessment Back to Top FDA, in consultation with the U.S.
Department of Agriculture, is conducting a risk assessment to evaluate the risk
of human illness associated with the consumption of produce grown in growing
areas amended with untreated BSAAO that are potentially contaminated with
enteric pathogens such as E. coli O157:H7 or Salmonella. The risk assessment
will evaluate the impact of different agricultural and ecological conditions and
certain interventions, such as use of a time interval or intervals between
application of untreated BSAAO and crop harvest, on the predicted risk. The risk
assessment will take into account available data and information on relevant
steps in the produce food safety continuum including: The initial prevalence and
levels of pathogens in untreated BSAAO; the methods used to apply untreated
BSAAO to soils; pathogen survival (and growth) in untreated BSAAO and soils
amended with untreated BSAAO; pathogen transfer to produce grown in amended
soils; pathogen survival and growth on produce; and pathogen survival, growth,
and cross-contamination during storage and other steps in the supply chain
(e.g., washing). The risk assessment will include characterization of the
variability and uncertainty of pathogen survival and growth under different
agricultural and ecological conditions (e.g., soil types, application methods,
or geographic locations/climatic factors) and time intervals between application
of untreated BSAAO and crop harvest. The risk assessment is intended to inform
policy decisions with regard to produce safety.
III. Issues for Consideration Back to Top FDA is requesting comments and
scientific data and other information relevant to this risk assessment. We are
particularly interested in scientific data and information concerning, but not
limited to, the following factors that may affect the risk of human illness
associated with the consumption of produce grown in fields or other growing
areas amended with untreated BSAAO (including raw manure):
1. Data on the prevalence and levels of pathogens.
a. The frequency of detecting the presence of pathogens in untreated BSAAO
and soil amended with BSAAO, such as Salmonella in poultry litter, and E. coli
O157:H7 and other pathogenic Shiga-toxin producing E. coli in cattle manure.
Samples may be obtained at different stages of untreated BSAAO storage prior to
application, or after application. If available, for each data point, we also
invite information regarding the following:
The type of untreated BSAAO (e.g., animal origin and content);
how the untreated BSAAO, including raw manure, was sampled and handled
prior to analysis;
the size of the analytical unit (i.e., detection limit) and test
method;
the number of positives, the total number of samples, and the time period
in which the testing was conducted; and
sampling protocol (e.g., simple random, stratified random, targeted).
b. The pathogen concentration, i.e., the number of pathogen cells per
amount (unit volume or weight), in contaminated untreated BSAAO or soil amended
with untreated BSAAO, especially cattle manure and poultry litter. If available,
for each data point, we ask that the data be provided in unaggregated form and
that Most Probable Number (MPN) patterns as well as raw data (e.g., number of
positive and negative tubes per serial dilution) be provided.
2. Data and information on survival of pathogens (e.g., Salmonella, E. coli
O157:H7), and pathogen transfer to produce.
a. Kinetic data that describe the survival (or inactivation) or growth of
pathogens in untreated BSAAO, especially cattle manure and poultry litter;
b. Kinetic data that describe the survival (or inactivation) or growth of
pathogens in soil amended with untreated BSAAO, especially cattle manure and
poultry litter, as influenced by soil type, untreated BSAAO type, application
method, geographic locations/climatic factors (e.g., temperature, days of
sunlight, intensity of solar irradiation, moisture, rainfall) and other
factors;
c. The mechanisms for pathogen transfer from soils to specific types or
categories of produce, such as leafy greens, or to produce generally, and
associated transfer coefficients, including irrigation and rain water splash,
direct contact between produce and soil, machinery or people or animals
contaminated by soil and directly contacting produce during growth and harvest
of produce;
d. Pathogen transfer rates (i.e., transfer coefficients) from amended soils
to specific types or categories of produce, such as leafy greens, or to produce
generally, as influenced by soil type, untreated BSAAO type, application method,
climate factors, commodity type or any other pertinent factors not listed
here;
e. The survival of pathogens on produce in the field or other growing area
before harvest; and
f. The variability in the survival of different Salmonella serotypes,
different subtypes of E. coli O157:H7, or other pathogens of public health
significance in amended soils under field, greenhouse, or laboratory
conditions.
3. On-farm practices with regard to the use of untreated BSAAO, including,
but not limited to, the following aspects.
a. The extent to which untreated BSAAO are used in different regions in the
United States, as well outside the United States in regions that export produce
to the United States;
b. The types of untreated BSAAO and the soil type, and associated physical
and chemical parameters (including but not exclusive to nutrient content,
moisture and pH); and the crops typically grown in each BSAAO-amended soil
type;
c. Characterization of the proportion of produce farms that have one or
more soil types per geographical location;
d. The amount of untreated BSAAO applied per unit surface (e.g., per acre)
or the ratio of untreated BSAAO/soil, including typical ratio and variability by
commodity type, including, for example, row crops such as leafy greens;
e. The time of year, number of applications, and amount of untreated BSAAO
that are applied;
f. The method of application (e.g., surface, incorporated), and whether or
not the amended soil is covered (e.g., with plastic mulch);
g. Produce commodity type and cropping cycles;
h. Climate conditions and irrigation practices after soil is amended,
before and after planting; and
i. The crop density (e.g., the number of rows per bed, and the distance
between adjacent rows in a bed), distance between two crop beds (furrow width),
and the influence of such factors on pathogen transfer.
4. Harvesting, handling, and storage conditions that may affect pathogen
detection and levels, survival, growth, or inactivation between harvest and
retail sale along the farm-to-fork continuum.
a. The harvesting practices and the average conditions as well as the range
of climactic conditions prior to harvesting (e.g., time and temperature, rain
events) under which produce is handled in the field and in packing
operations;
b. The survival, growth, or inactivation of pathogens on produce
(including, for example, specific commodities or categories such as leafy
greens, or produce generally) during transportation and storage;
c. Typical storage conditions (e.g., time, temperature) for produce
(including, for example, specific commodities or categories, such as leafy
greens, or produce generally), from harvest until consumer purchase and whether
and how those storage conditions affect pathogen levels; and
d. The types and concentration of antimicrobial chemicals or other
treatments, if any, applied to the water used for wash or transport of produce
during farm or other distribution operations prior to retail, and the efficacy
of these treatments in reducing pathogen levels, as well as the likelihood of
cross-contamination during wash or transport.
5. Storage conditions such as times and temperatures that may affect
pathogen growth and/or survival during transportation and storage of produce in
the consumer's home, and consumer handling practices with respect to produce
after purchase, including data and information on consumer washing
practices.
We are also interested in other comments concerning, but not limited to,
the types of untreated BSAAO, produce commodities, relevant agricultural and
ecological conditions, and appropriate mitigation strategies that the Agency
should consider in the risk assessment.
IV. Reference Back to Top The following reference is on display in the
Division of Dockets Management (see ADDRESSES) and is available for viewing by
interested persons between 9 a.m. and 4 p.m., Monday through Friday; they are
also available electronically at http://www.regulations.gov. FDA has
verified the Web site address, as of the date this document publishes in the
Federal Register, but Web sites are subject to change over time.
1. Food and Drug Administration, 2015. “Final Qualitative Assessment of
Risk to Public Health from On-Farm Contamination of Produce.” Available at: http://www.fda.gov/downloads/Food/FoodScienceResearch/RiskSafetyAssessment/UCM470780.pdf.
Accessed January 20, 2016. Show citation box
Dated: February 29, 2016.
Leslie Kux,
Associate Commissioner for Policy.
COMMENT
Greetings FDA et al,
I kindly would like to make comment submission to Docket No.
FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated with Pathogens
from Produce Grown in Fields Amended with Untreated Biological Soil Amendments
of Animal Origin; Request for Comments, Scientific Data, and Information
MY comment as follows,
There has been proven documented risk for Untreated Biological Soil
Amendments of Animal Origin and risk of transmitting Transmissible Spongiform
Encephalopathy TSE Prion disease aka mad cow type disease such as the typical
and atypical Bovine Spongiform Encephalopathy strains, typical and atypical
Scrapie strains, typical and atypical Chronic Wasting Disease CWD strains, and
even the Transmissible Mink Encephalopathy TME Prion disease.
Science has shown that infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces thereby leading to
transmission by direct contact and environmental contamination.
Ingestion of prion contaminated 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.
Plants can uptake prions from contaminated soil and transport them to
different parts of the plant tissue (stem and leaves) [please see data from Soto
et al Prion2015 Conference below in Science reference data].
Also, Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area is very concerning.
Science has shown that soil plays a role in the spreading and transmission
of the CWD and Scrapie TSE prion agent.
For these reason and more (see reference materials) I urge the FDA to stop
this practice of Untreated Biological Soil Amendments of Animal Origin,
including blood, for use on our produce grown in fields, for the following
reasons ;
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.
SNIP...
***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 prion contaminated 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.
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
Hoover, Edward Arthur Colorado State University-Fort Collins, Fort Collins,
CO, United States
ABSTRACT Chronic wasting disease (CWD) of deer and elk is an emerging
highly transmissible prion disease now recognized in 18 States, 2 Canadian
provinces, and Korea.
***We have shown that Infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces, and in the tissues
generating those body fluids and excreta, thereby leading to facile transmission
by direct contact and environmental contamination.
***We have also shown that CWD can infect some non-cervid species, thus the
potential risk CWD represents to domestic animal species and to humans remains
unknown.
SNIP...
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an
emergent highly transmissible prion disease now recognized throughout the USA as
well as in Canada and Korea. We have shown that infected deer harbor and shed
high levels of infectious prions in saliva, blood, urine, and feces thereby
leading to transmission by direct contact and environmental contamination. In
that our studies have also shown that CWD can infect some non-cervid species,
the potential risk CWD may represents to domestic animal species and humans
remains unknown. The increasing parallels in the development of major human
neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and
prion diseases add relevance to CWD as a model of a transmissible protein
misfolding disease. Understanding how infectious misfolded proteins (prions) are
generated and transmitted will aid in interrupting, treating, and managing the
risks associated with these agents and the diseases they cause.
Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of
Prion Infection
A. Christy Wyckoff1, 2 n1 , Nathan Galloway3 n1 , Crystal Meyerett-Reid1 ,
Jenny Powers4 , Terry Spraker1 , Ryan J. Monello4 , Bruce Pulford1 , Margaret
Wild4 , Michael Antolin3 , Kurt VerCauteren2 […] & Mark Zabel
Infected animals shed prions into the environment through saliva, feces,
urine and even antler velvet15,20,21,22,23,24. Studies have successfully
transmitted PrPCWD through a single dose of urine or feces from animals
displaying signs of CWD, indicating that at the time of clinical disease
sufficient prions are shed to result in an infectious dose24,25. However, at
what stage(s) of disease animals shed prions into the environment remains
unclear. If shedding occurs early in disease, a sub-clinical animal may not only
shed prions into the environment, increasing the infectious reservoir, but may
also transmit CWD horizontally to their associates.
Short Communication
Early detection of chronic wasting disease prions in urine of
pre-symptomatic deer by real-time quaking-induced conversion assay
Volume 7, Issue 3 May/June 2013
Pages 253 – 258
Keywords: RT-QuIC, chronic wasting disease, diagnosis, feces, prion,
surveillance, urine
Authors: Theodore R. John, Hermann M. Schätzl and Sabine Gilch
Theodore R. John Department of Veterinary Sciences; University of Wyoming;
Laramie, WY USA
Hermann M. Schätzl Department of Veterinary Sciences; University of
Wyoming; Laramie, WY USA; Department of Molecular Biology; University of
Wyoming; Laramie, WY USA; Faculty of Veterinary Medicine; Department of
Comparative Biology and Experimental Medicine; University of Calgary; Calgary,
AB Canada
Sabine Gilch Corresponding author: sgilch@ucalgary.ca Department of
Veterinary Sciences; University of Wyoming; Laramie, WY USA; Faculty of
Veterinary Medicine; Department of Ecosystem and Public Health; University of
Calgary; Calgary, AB Canada
Abstract:
Chronic wasting disease (CWD) is a prion disease of captive and
free-ranging deer (Odocoileus spp), elk (Cervus elaphus nelsonii) and moose
(Alces alces shirasi). Unlike in most other prion diseases, in CWD prions are
shed in urine and feces, which most likely contributes to the horizontal
transmission within and between cervid species. To date, CWD ante-mortem
diagnosis is only possible by immunohistochemical detection of protease
resistant prion protein (PrPSc) in tonsil or recto-anal mucosa-associated
lymphoid tissue (RAMALT) biopsies, which requires anesthesia of animals. We
report on detection of CWD prions in urine collected from pre-symptomatic deer
and in fecal extracts by using real time quaking-induced conversion (RT-QuIC).
This assay can be useful for non-invasive pre-symptomatic diagnosis and
surveillance of CWD.
Received: February 7, 2013; Accepted: March 24, 2013; Published Online:
April 10, 2013
snip...
Introduction
Chronic wasting disease (CWD) is to date the most contagious prion disease
and affects captive and free-ranging elk, deer and moose in North America.1,2
The disease is caused by the accumulation of an abnormally folded isoform of the
cellular prion protein PrPC, denominated PrPSc.3,4 CWD is the cervid equivalent
of bovine spongiform encephalopathy (BSE), scrapie in sheep and goat5 or
Creutzfeldt-Jakob disease (CJD) in humans.6 Although transmission studies of CWD
prions to humanized transgenic mice or non-human primates suggest a strong
species barrier,7-9 recent in vitro studies have demonstrated that human PrP can
be converted by CWD prions into PrPSc upon adaptation.10 Therefore, a potential
for zoonotic transmission, as exemplified by BSE,11 cannot be completely
excluded.
A huge body of evidence suggests that CWD can be efficiently transmitted
horizontally within and between cervid species,12 which may be the reason for
geographical spread and increase in case numbers. Horizontal transmission is
explained by the rather unusual peripheral distribution of prions in CWD
affected animals and the high susceptibility to the disease by oral
infection.13,14 Unlike in most other prion diseases, CWD prions can be found in
a wide variety of tissues, such as skeletal and cardiac muscle15,16 or kidney,17
in addition to the lymphoreticular system and blood.18 Furthermore, they are
shed in significant amounts in saliva,18,19 urine19 or feces,20 which enables
oral infection of animals by foraging on contaminated pastures.
In addition, it has been demonstrated that prions can persist in soil21 and
that water in endemic areas can contain CWDassociated PrPSc.22
snip...
We demonstrate that CWD prions are detectable in urine of orally infected
deer prior to the onset of clinical symptoms. Furthermore, we show that fecal
extracts can be used as a seed in RT-QuIC assays. Thereby, we were able to
detect CWD prions in fecal extracts collected at later stages of the disease.
This study provides the first evidence that RT-QuIC can be successfully used for
the preclinical diagnosis of CWD in specimens that are available by non-invasive
methods.
snip...
In summary, we demonstrate that CWD prions can be detected by RT-QuIC in
urine of orally infected white-tailed deer and mule deer at a pre-symptomatic
stage of the disease.
snip...
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable
neurological diseases likely caused by a misfolded form of the prion protein.
TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’
disease) in cattle, chronic wasting disease in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are
unique among TSEs because they can be transmitted between animals, and the
disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
see ;
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.
Introduction ...snip...end
Research Article
Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted
Infectivity from Complex Solutions (BASICS)
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 x Published: March 4, 2013 DOI:
10.1371/journal.pone.0058630
Abstract Prions, the infectious agent of scrapie, chronic wasting disease
and other transmissible spongiform encephalopathies, are misfolded proteins that
are highly stable and resistant to degradation. Prions are known to associate
with clay and other soil components, enhancing their persistence and
surprisingly, transmissibility. Currently, few detection and quantification
methods exist for prions in soil, hindering an understanding of prion
persistence and infectivity in the environment. Variability in apparent
infectious titers of prions when bound to soil has complicated attempts to
quantify the binding capacity of soil for prion infectivity. Here, we quantify
the prion adsorption capacity of whole, sandy loam soil (SLS) typically found in
CWD endemic areas in Colorado; and purified montmorillonite clay (Mte),
previously shown to bind prions, by BioAssay of Subtracted Infectivity in
Complex Solutions (BASICS). We incubated prion positive 10% brain homogenate
from terminally sick mice infected with the Rocky Mountain Lab strain of
mouse-adapted prions (RML) with 10% SLS or Mte. After 24 hours samples were
centrifuged five minutes at 200×g and soil-free supernatant was intracerebrally
inoculated into prion susceptible indicator mice. We used the number of days
post inoculation to clinical disease to calculate the infectious titer remaining
in the supernatant, which we subtracted from the starting titer to determine the
infectious prion binding capacity of SLS and Mte. BASICS indicated SLS bound and
removed ≥ 95% of infectivity. Mte bound and removed lethal doses (99.98%) of
prions from inocula, effectively preventing disease in the mice. Our data reveal
significant prion-binding capacity of soil and the utility of BASICS to estimate
prion loads and investigate persistence and decomposition in the environment.
Additionally, since Mte successfully rescued the mice from prion disease, Mte
might be used for remediation and decontamination protocols.
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 CWDcontaminated
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 population and the risk of
transmission to other species is not known.
Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of
Prion Infection A. Christy Wyckoff1, 2 n1 , Nathan Galloway3 n1 , Crystal
Meyerett-Reid1 , Jenny Powers4 , Terry Spraker1 , Ryan J. Monello4 , Bruce
Pulford1 , Margaret Wild4 , Michael Antolin3 , Kurt VerCauteren2 […] & Mark
Zabel1 - Show fewer authors Scientific Reports 5, Article number: 8358 (2015)
doi:10.1038/srep08358 Download Citation
Molecular ecology Proteins Statistics Received: 27 June 2014 Accepted: 19
January 2015 Published 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.
Introduction
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
SUMMARY
Prions are the protein-based infectious agents responsible for prion
diseases. Environmental prion contamination has been implicated in disease
transmission. Here, we analyzed the binding and retention of infectious prion
protein (PrPSc) to plants. Small quantities of PrPSc contained in diluted brain
homogenate or in excretory materials (urine and feces) can bind to wheat grass
roots and leaves. Wild-type hamsters were efficiently infected by ingestion of
prion-contaminated plants. The prion-plant interaction occurs with prions from
diverse origins, including chronic wasting disease. Furthermore, leaves
contaminated by spraying with a prion-containing preparation retained PrPSc for
several weeks in the living plant. Finally, plants can uptake prions from
contaminated soil and transport them to aerial parts of the plant (stem and
leaves). These findings demonstrate that plants can efficiently bind infectious
prions and act as carriers of infectivity, suggesting a possible role of
environmental prion contamination in the horizontal transmission of the disease.
INTRODUCTION
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** 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.
COMERCIAL IN CONFIDENCE
SPREADING OF UNPROCESSED BLOOD ON LAND
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
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...
Survival of scrapie virus after 3 years
interment P Brown x P Brown Search for articles by this author
Correspondence Correspondence to Dr Paul Brown. , PhD correspondence x P Brown
Search for articles by this author Correspondence Correspondence to Dr Paul
Brown. , D.C Gajdusek x D.C Gajdusek Search for articles by this author , MD
Laboratory of CNS Studies, National Institute of Neurological Disorders and
Stroke, National Institutes of Health, Bethesda, Maryland 20892, U.S.A.
PAUL BROWN SCRAPIE SOIL TEST
Paul Brown, known and respected TSE scientist, former TSE expert for the
CDC said he had ''absolutely no confidence in USDA tests before one year ago'',
and this was on March 15, 2006 ;
"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the National
Institutes of Health's Laboratory for Central Nervous System Studies and an
expert on mad cow-like diseases, told United Press International. "The question
was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before one
year ago" because of the agency's reluctance to retest the Texas cow that
initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul
Brown is Senior Research Scientist in the Laboratory of Central Nervous System
... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy detailed
critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ;
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
Wednesday, March 2, 2016
RANCHO He did not know that they were placing healthy cow heads next to
suspect carcasses BSE TSE Prion
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations
of deposition via transport processes affecting soil particles, including
entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several
years. Significant interest remains in developing methods that could be applied
to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests
that serine proteases and the microbial consortia in stimulated soils and
compost may partially degrade PrPTSE. Transition metal oxides in soil (viz.
manganese oxide) may also mediate prion inactivation. Overall, the effect of
prion attachment to soil particles on its persistence in the environment is not
well understood, and additional study is needed to determine its implications on
the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding,
inferring a durable environmental reservoir, and an efficient mechanism for
indirect horizontal CWD transmission.
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al.,
2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
see page 176 of 201 pages...tss
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
***so 20 cases of atypical BSE in France, compared to the remaining 40
cases in the remaining 12 Countries, divided by the remaining 12 Countries,
about 3+ cases per country, besides Frances 20 cases. you cannot explain this
away with any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5,
2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR
FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
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.
”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.
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***Our 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.
================
==========================================
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain
location and PrPsc by PMCA only, how many cases have we missed?
***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.
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
*** Needless conflict ***
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
Published online 16 May 2012
Terry S. Singeltary Sr. said:
I kindly wish to submit the following please ;
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures
ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
***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.
Tuesday, December 16, 2014
*** Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. ***The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. ***These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
see more here ;
***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.***
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation
Friday, August 14, 2015
Carcass Management During a Mass Animal Health Emergency Draft Programmatic
Environmental Impact Statement—August 2015
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
”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.
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
AND THEY MEANT IT $$$
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission ***
Subject: CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14,
2015
UNITED STATES OF AMERICA
National Prion Disease Pathology Surveillance Center Cases Examined1
(August 25, 2015)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier
56 35 31 4 0 0
1997 113 68 59 9 0 0
1998 89 53 45 7 1 0
1999 121 73 65 7 1 0
2000 144 101 89 12 0 0
2001 210 118 110 8 0 0
2002 242 144 125 17 2 0
2003 257 159 138 21 0 0
2004 314 180 162 17 0 13
2005 328 179 157 21 1 0
2006 369 182 163 17 0 24
2007 370 206 187 19 0 0
2008 387 223 207 16 0 0
2009 399 233 212 20 1 0
2010 403 247 218 29 0 0
2011 393 239 216 23 0 0
2012 409 241 218 23 0 0
2013 416 257 222 34 1 0
2014 355 210 187 21 0 15
2015 237 137 118 8 0 0 TOTAL 56126 32857 2929 3338 7 4
1 Listed based on the year of death or, if not available, on year of
referral;
2 Cases with suspected prion disease for which brain tissue was submitted;
3 Disease acquired in the United Kingdom;
4 Disease acquired in the United Kingdom in one case and in Saudi Arabia in
the other;
5 Disease possibly acquired in a Middle Eastern or Eastern European
country;
6 Includes 28 cases in which the diagnosis is pending, and 19 inconclusive
cases;
7 Includes 12 (11 from 2015) cases with type determination pending in which
the diagnosis of vCJD has been excluded. The sporadic cases include 2853 cases
of sporadic Creutzfeldt-Jakob disease (sCJD), 54 cases of Variably
Protease-Sensitive Prionopathy (VPSPr) and 22 cases of sporadic Fatal Insomnia
(sFI).
8 Total Excludes 194 familial blood only cases.
Rev 8/26/2015
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in
June 2014 confirmed as home grown case
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in
Texas
Updated: October 7, 2014
CDC and the Texas Department of State Health Services (DSHS) have completed
the investigation of the recently reported fourth vCJD case in the United
States. It confirmed that the case was in a US citizen born outside the Americas
and indicated that the patient's exposure to the BSE/vCJD agent most likely
occurred before he moved to the United States; the patient had resided in
Kuwait, Russia and Lebanon. The completed investigation did not support the
patient's having had extended travel to European countries, including the United
Kingdom, or travel to Saudi Arabia. The specific overseas country where this
patient’s infection occurred is less clear largely because the investigation did
not definitely link him to a country where other known vCJD cases likely had
been infected.
>>>the patient had resided in Kuwait, Russia and Lebanon.
>>>The completed investigation did not support the patient's
having had extended travel to European countries, including the United Kingdom,
or travel to Saudi Arabia.
NOW we all know why the state of Texas or the CDC did not want to report
this case, because it was a home grown case of nvCJD right here in Texas...tss
Monday, June 02, 2014
Confirmed Variant CJD Case in Texas
Sunday, November 23, 2014
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in
June 2014 confirmed as USA case NOT European
Monday, November 3, 2014
USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014
National Prion Disease Pathology Surveillance Center Cases Examined1
(October 7, 2014)
***6 Includes 11 cases in which the diagnosis is pending, and 19
inconclusive cases;
***7 Includes 12 (11 from 2014) cases with type determination pending in
which the diagnosis of vCJD has been excluded.
***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob
disease (sCJD),
***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)
***and 21 cases of sporadic Fatal Insomnia (sFI).
Sunday, December 14, 2014
ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report
Sunday, August 11, 2013
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html
Risk.21
Monday, February 24, 2014
Sporadic Fatal Insomnia in an Adolescent
Friday, January 10, 2014
*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial
type prion disease, what it ???
>>> We concluded that VPSPr is transmissible; thus, it is an
authentic prion disease.
Sunday, November 23, 2014
Transmission Characteristics of Variably Protease-Sensitive Prionopathy
* We concluded that VPSPr is transmissible; thus, it is an authentic prion
disease.
Monday, November 3, 2014
The prion protein protease sensitivity, stability and seeding activity in
variably protease sensitive prionopathy brain tissue suggests molecular overlaps
with sporadic Creutzfeldt-Jakob disease
WHAT about the sporadic CJD TSE proteins ?
WE now know that some cases of sporadic CJD are linked to atypical BSE and
atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all
it’s sub-types $$$
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic
Creutzfeldt-Jakob Disease ***
07 02:27 AM
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-? pathology and cerebral
amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
*** I would kindly like to comment on the Nature Paper, the Lancet reply,
and the newspaper articles.
snip...see full text ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
SINGELTARY PEER REVIEW
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America. Now scientists in France have stumbled across new
evidence that adds weight to the campaigners' fears. To their complete surprise,
the researchers found that one strain of scrapie causes the same brain damage in
mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb...
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
Terry S. Singeltary Sr. flounder9@verizon.net
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