Persistence of the bovine spongiform encephalopathy infectious agent in
sewage
Carlos Maluquer de Motesa, 1, Juan-Carlos Espinosab, Ana Estebanb, Miquel
Calvoc, Rosina Gironesa, Juan MarÃa Torresb, ,
a Department of Microbiology, University of Barcelona, Diagonal 643, 08028
Barcelona, Spain b Centro de Investigacion en Sanidad Animal, CISA-INIA,
Carretera Algete-El Casar s/n, Valdeolmos, 28130 Madrid, Spain c Department of
Statistics, University of Barcelona, Diagonal 643, 08028 Barcelona, Spain
Received 12 December 2011. Revised 28 May 2012. Accepted 18 June 2012. Available
online 7 July 2012. http://dx.doi.org/10.1016/j.envres.2012.06.010,
How to Cite or Link Using DOI
Abstract Horizontal transmission of prion diseases through the environment
represents a considerable concern. Prions are extremely resistant to
inactivation and are thought to enter the environment after burial of animal
mortalities or through biosolids from wastewater treatment plants. In addition,
deposition of prions in the environment through biological fluids and/or faeces
has been proved in the last years. Little is known about the behaviour of prion
infectivity in the environment. In this study, the persistence of BSE infectious
agent in sewage has been assessed by both PrPRes immunoblotting and mouse
bioassay in a long-term incubation study. Results indicated that no PrPRes was
detected after 150 day of incubation and consistent with this, a statistical
regression model estimated 2-logs decay in 151 day. In contrast, no reduction in
infectivity was observed during this period. Similarly, BSE infectivity remained
unaltered after incubation in PBS for 265 day, whereas PrPRes levels dropped
progressively over the length of the study. These results indicate that in
sewage and PBS, prion infectivity persists longer and with different dynamics
than its commonly used marker PrPRes. Thus, mathematical models computed on the
basis of PrPRes detection were unable to predict inactivation of prion
infectivity. It is also reasonable to assume that conventional wastewater
treatments with low retention times could have a very limited impact on prion
infectivity. This data is essential for the development of accurate risk
assessment analysis for BSE and other prion diseases in the environment.
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Highlights ► Persistence of BSE agent over 265 day as environmental
contaminant in sewage. ► Progressive decay in PrPRes detection: 150 day in
sewage needed for 2 logs reduction. ► Conversely, no infectivity decay after 150
day in sewage. ► Inactivation dynamics of PrPRes and infectivity in sewage are
different. ► Prediction models based on BSE PrPRes fail to predict BSE
infectivity decay in sewage.
Abbreviations BSE, bovine spongiform encephalopathy; CWD, chronic wasting
disease; TSE, transmissible spongiform encephalopathies; PrPc, cellular prion
protein; PrPSc, scrapie-associated prion protein; PrPRes, protease-resistant
prion protein Keywords Prions; BSE; PrPRes; Infectivity; Sewage;
Environment
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Figures and tables from this article:
Fig. 1. Detection of PrPRes in sewage and PBS contaminated with BSE.
Aliquots of each sample were collected and concentrated on the indicated day.
After proteinase K treatment, PrPRes was detected by IB.
Fig. 2. Prediction models computed for the PrPRes decay over time. (A)
Linear regression curve on the logarithm of the densitometry data obtained for
the BSE PrPRes immunoreactive bands observed by IB after incubation in PBS. (B)
Linear (blue line) and quadratic (red line) regression curve on the logarithm of
the densitometry data obtained after incubation in sewage. (C) Quadratic
regression curve on the densitometry data obtained after incubation in sewage.
RDU, relative densitometry units. (For interpretation of the references to color
in this figure legend, the reader is referred to the web version of this
article).
Fig. 3. Statistical analysis of the infectivity data obtained after
incubation of BSE in either sewage or PBS for 0, 45, 150 and 265 day. Log-rank
tests with the Benjamini and Hochberg's correction were carried out for all
incubation times (*p<0.05). Data are expressed as means±standard deviation.
Fig. 4. Statistical analysis of the infectivity data obtained after
inoculation of serial dilutions of the BSE inoculum used in this study in
BoPrP-Tg110 transgenic mice. Log-rank tests with the Benjamini and Hochberg's
correction were carried out for all incubation times (*p<0.05). Data are
expressed as means±standard deviation.
Table 1. Infectivity of samples contaminated with BSE and incubated in
sewage or PBS for the indicated lengths of time. Data indicates mean survival
time±standard deviation.
Table 2. Infectivity of serial dilutions of the BSE inoculum used in this
study. Data indicates mean survival time±standard deviation.
COMERCIAL IN CONFIDENCE
SPREADING OF UNPROCESSED BLOOD ON LAND
Friday, June 29, 2012
Highly Efficient Prion Transmission by Blood Transfusion
Saturday, January 24, 2009
Research Project: Detection of TSE Agents in Livestock, Wildlife,
Agricultural Products, and the Environment Location: 2008 Annual Report Research
Project: Detection of Transmissible Spongiform Encephalopathy Agents in
Livestock, Wildlife, Agricultural Products, and the Environment Location:
Foodborne Contaminants Research
2008 Annual Report
1a.Objectives (from AD-416) We will develop highly sensitive diagnostic
tests to detect transmissible spongiform encephalopathy (TSE) in livestock and
wildlife animal species prior to the onset of clinical disease. We will also
develop tests to confirm the presence or absence of TSE disease agents in
ingredients of animal origin and decontaminated environments.
1b.Approach (from AD-416) The threat of BSE continues to affect export
economics for US meat. Meanwhile scrapie continues to influence sheep profits
and herd biosecurity, and CWD is spreading throughout North America. Thus U.S.
animal industry stakeholders have identified detection of the TSE infectious
agent (prions) as a priority biosecurity research issue essential for prevention
of TSE diseases. We will build on our previous successes using mass spectrometry
(MS) for high-sensitivity and specificity in detection of PrPsc as a marker for
TSE infectivity in blood using a hamster scrapie model. We will also develop a
novel PrP-null mouse strain and related myeloma cell culture system for
production of monoclonal antibodies (MAb), which may be specific for PrPsc. We
will then choose MS or MAb and validate our novel diagnostic for preclinical
diagnosis of scrapie in sheep blood. Whereas MS and MAb methods rely on
dissolved samples, contamination of agricultural products and environmental
surfaces is associated with solid samples. So we will produce a cell culture
based assay for TSE infectivity that is surface-adsorbed. After using the
relatively convenient hamster model for early development, we will validate this
technology for detection of scrapie in sheep brain on meat-and-bone meal and
stainless steel. Replacing 5325-32000-007-00D (3/19/2008).
3.Progress Report At this point in the Project, in general, we are
completing preliminary studies using our relatively convenient hamster and mouse
models, and are starting to work with more agriculturally relevant sheep and
deer tissues. We are finding the cervid tissues quite different from rodent
tissues, in their requirements for sample workup (e.g., amount and quality of
lipid and fiber) and in their expression of TSE infectivity and presence of
markers. OSQR required us to establish a new collaboration with a reputable cell
biologist, to assist with our cell-based scrapie assay. We now have a new MTA
with Dr. Charles Weissmann (Scripps), under which we are sharing cell lines and
laboratory protocols. We have completed one part of our speed congenics project
to develop PrP-null (disease-resistant) mice for use in antibody generation.
After conceiving a new procedure for immunogen enrichment, we performed
experimental vaccination of these animals in our facilities. This project
relates to NP103 Component 8: Prevention and control of transmissible spongiform
encephalopathies. Problem statement 9A: Scrapie; 9B Chronic Wasting Disease
(CWD); and 9C: Bovine Spongiform Encephalopathy (BSE).
4.Accomplishments 1. Proteinase K-free method for preparation of samples
facilitates TSE blood assay.
The most widely used and regulatory approved methods for detection of
Transmissible Spongiform Encephalopathy (TSE) contain a step in which the sample
is subjected to digestion by a very strong enzyme, proteinase K, which degrades
almost all proteins in the sample except for an Infectious isoform of the normal
cellular prion protein, a prion (PrPsc). Although PrPsc has served well as a
marker for brain disease, infectivity in the blood is mostly not proteinase K
resistant. The proteinase K-free technique developed by ARS scientists in the
Foodborne Contaminants Research Unit in Albany, CA will allow scientists to
detect infectivity in blood. These efforts will lead to diagnostic tests that
will save farmers and ranchers money and resources by allowing them to identify
infected animals prior to purchase, sale or slaughter, and keep TSE-infected
animals out of the US food supply. This accomplishment addresses NP103 Component
8: Prevention and Control of Transmissible Spongiform Encephalopathies; Problem
Statement 9A: Scrapie; 9B: Chronic Wasting Disease (CWD); and 9C: Bovine
Spongiform Encephalopathy (BSE).
2. Demonstrated conversion of a non-infectious normal cellular prion
protein (PrP) into disease isoform in cell culture.
Although Transmissible Spongiform Encephalopathy (TSE) infectivity can be
detected using animal models and mass spectroscopy, a cell culture system offers
increased speed and throughput. ARS scientists in the Foodborne Contaminants
Research Unit in Albany, CA developed conditions for growth and infection of
existing cell cultures and cultures expressing transgenic PrP genes, observing
conversion to the disease-associated PrPsc isoform. This method will be further
developed to detect infectivity that is adsorbed onto surfaces, such as
stainless steel and soil. These efforts will lead to diagnostic tests that will
save farmers and ranchers money and resources by allowing them to identify
infected areas and equipment before these areas or items can infect their
animals. This accomplishment addresses NP103 Component 8: Prevention and Control
of Transmissible Spongiform Encephalopathies; Problem Statement 9A: Scrapie; 9B:
Chronic Wasting Disease (CWD); and 9C: Bovine Spongiform Encephalopathy
(BSE).
5.Significant Activities that Support Special Target Populations
None.
6.Technology Transfer Number of New Commercial Licenses Executed 1
Review Publications Bruederle, C.E., Hnasko, R.M., Kraemer, T., Garcia,
R.A., Haas, M.J., Marmer, W.N., Carter, J.M. 2008. Prion infected Meat-and-Bone
Meal is still infectious after biodiesel production. PLoS Pathogens. Available:
Onisko, B.C., Chen, N., Napoli, J. 2008. The Nuclear Transcription Factor
RAR Associates with Neuronal RNA Granules and Suppresses Translation. Journal of
Biological Chemistry. 283(30):20841-20847.
Sajnani, G., Pastrana, M.A., Dynin, I.A., Onisko, B.C., Requena, J.R. 2008.
Insights on scrapie prion protein (prpsc) structure obtained by limited
proteolysis and mass spectrometry. Journal of Molecular Biology.
382(2008):88-98.
FY2006: Tests for prion contamination in soil and water will be developed.
Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after
Persistence in Soil over Years
Bjoern Seidel1#*, Achim Thomzig2#, Anne Buschmann3#, Martin H. Groschup3,
Rainer Peters1, Michael Beekes2, Konstantin Terytze4
1 Fraunhofer Institute for Molecular Biology und Applied Ecology (IME),
Schmallenberg, Germany, 2 P24 -Transmissible Spongiform Encephalopathies, Robert
Koch-Institut, Berlin, Germany, 3 Institute for Novel and Emerging Infectious
Diseases, Friedrich-Loeffler-Institut, Insel Riems, Germany, 4 German Federal
Environmental Agency (Umweltbundesamt, UBA), Dessau, Germany
Abstract The persistence of infectious biomolecules in soil constitutes a
substantial challenge. This holds particularly true with respect to prions, the
causative agents of transmissible spongiform encephalopathies (TSEs) such as
scrapie, bovine spongiform encephalopathy (BSE), or chronic wasting disease
(CWD). Various studies have indicated that prions are able to persist in soil
for years without losing their pathogenic activity. Dissemination of prions into
the environment can occur from several sources, e.g., infectious placenta or
amniotic fluid of sheep. Furthermore, environmental contamination by saliva,
excrements or non-sterilized agricultural organic fertilizer is conceivable.
Natural transmission of scrapie in the field seems to occur via the alimentary
tract in the majority of cases, and scrapie-free sheep flocks can become
infected on pastures where outbreaks of scrapie had been observed before. These
findings point to a sustained contagion in the environment, and notably the
soil. By using outdoor lysimeters, we simulated a contamination of standard soil
with hamster-adapted 263K scrapie prions, and analyzed the presence and
biological activity of the soil-associated PrPSc and infectivity by Western
blotting and hamster bioassay, respectively. Our results showed that 263K
scrapie agent can persist in soil at least over 29 months. Strikingly, not only
the contaminated soil itself retained high levels of infectivity, as evidenced
by oral administration to Syrian hamsters, but also feeding of aqueous soil
extracts was able to induce disease in the reporter animals. We could also
demonstrate that PrPSc in soil, extracted after 21 months, provides a
catalytically active seed in the protein misfolding cyclic amplification (PMCA)
reaction. PMCA opens therefore a perspective for considerably improving the
detectability of prions in soil samples from the field.
Prions Adhere to Soil Minerals and Remain Infectious
Christopher J. Johnson1,2, Kristen E. Phillips3, Peter T. Schramm3, Debbie
McKenzie2, Judd M. Aiken1,2, Joel A. Pedersen3,4*
1 Program in Cellular and Molecular Biology, University of Wisconsin
Madison, Madison, Wisconsin, United States of America, 2 Department of Animal
Health and Biomedical Sciences, School of Veterinary Medicine, University of
Wisconsin Madison, Madison, Wisconsin, United States of America, 3 Molecular and
Environmental Toxicology Center, University of Wisconsin Madison, Madison,
Wisconsin, United States of America, 4 Department of Soil Science, University of
Wisconsin Madison, Madison, Wisconsin, United States of America
Abstract An unidentified environmental reservoir of infectivity contributes
to the natural transmission of prion diseases (transmissible spongiform
encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter
soil environments via shedding from diseased animals and decomposition of
infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of
disposal has resulted in unintentional introduction of prions into subsurface
environments. We examined the potential for soil to serve as a TSE reservoir by
studying the interaction of the disease-associated prion protein (PrPSc) with
common soil minerals. In this study, we demonstrated substantial PrPSc
adsorption to two clay minerals, quartz, and four whole soil samples. We
quantified the PrPSc-binding capacities of each mineral. Furthermore, we
observed that PrPSc desorbed from montmorillonite clay was cleaved at an
N-terminal site and the interaction between PrPSc and Mte was strong, making
desorption of the protein difficult. Despite cleavage and avid binding, PrPSc
bound to Mte remained infectious. Results from our study suggest that PrPSc
released into soil environments may be preserved in a bioavailable form,
perpetuating prion disease epizootics and exposing other species to the
infectious agent.
Synopsis Transmissible spongiform encephalopathies (TSEs) are a group of
incurable diseases likely caused by a misfolded form of the prion protein
(PrPSc). TSEs include scrapie in sheep, bovine spongiform encephalopathy (“mad
cow” disease) in cattle, chronic wasting disease (CWD) in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and CWD 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, because PrPSc likely
enters soil environments through urinary or alimentary shedding and
decomposition of infected animals. In this manuscript, the authors test the
potential for soil to serve as a reservoir for PrPSc and TSE infectivity. They
demonstrate that PrPSc binds to a variety of soil minerals and to whole soils.
They also quantitate the levels of protein binding to three common soil minerals
and show that the interaction of PrPSc with montmorillonite, a common clay
mineral, is remarkably strong. PrPSc bound to Mte remained infectious to
laboratory animals, suggesting that soil can serve as a reservoir of TSE
infectivity.
Direct Detection of Soil-Bound Prions
Sacha Genovesi1, Liviana Leita2, Paolo Sequi3, Igino Andrighetto4, M. Catia
Sorgato1,5, Alessandro Bertoli1*
1 Dipartimento di Chimica Biologica, Università di Padova, Padova, Italy, 2
Istituto Sperimentale per la Nutrizione delle Piante, Gorizia, Italy, 3 Istituto
Sperimentale per la Nutrizione delle Piante, Roma, Italy, 4 Istituto
Zooprofilattico Sperimentale delle Venezie, Legnaro, Italy, 5 CNR Istituto di
Neuroscienze, Padova, Italy
Abstract Scrapie and chronic wasting disease are contagious prion diseases
affecting sheep and cervids, respectively. Studies have indicated that
horizontal transmission is important in sustaining these epidemics, and that
environmental contamination plays an important role in this. In the perspective
of detecting prions in soil samples from the field by more direct methods than
animal-based bioassays, we have developed a novel immuno-based approach that
visualises in situ the major component (PrPSc) of prions sorbed onto
agricultural soil particles. Importantly, the protocol needs no extraction of
the protein from soil. Using a cell-based assay of infectivity, we also report
that samples of agricultural soil, or quartz sand, acquire prion infectivity
after exposure to whole brain homogenates from prion-infected mice. Our data
provide further support to the notion that prion-exposed soils retain
infectivity, as recently determined in Syrian hamsters intracerebrally or orally
challanged with contaminated soils. The cell approach of the potential
infectivity of contaminated soil is faster and cheaper than classical
animal-based bioassays. Although it suffers from limitations, e.g. it can
currently test only a few mouse prion strains, the cell model can nevertheless
be applied in its present form to understand how soil composition influences
infectivity, and to test prion-inactivating procedures.
now, something i have pondered long about, with the atypical BSE in Texas
and Alabama, where, as far as i know, those farms WERE NOT quarantined for 5
years due to an atypical TSE. HOWEVER, the farms of the atypical scrapie from
where the mad sheep of mad river valley occurred, these farms were quarantined.
...
----- Original Message -----
From: Terry S. Singeltary Sr.
To:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000169/!x-usc:mailto:Boyd.Rutherford@usda.gov
Sent: Sunday, February 25, 2007 12:35 PM
Subject: FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP
Greetings USDA,
I respectfully request the final results of the mouse bio-assays test that
were to have supposedly began 2+ years late, 5 years ago, on the imported sheep
from Belgium ?
WHAT happened to the test results and MOUSE BIO-ASSAYS of those imported
sheep from Belgium that were confiscated and slaughtered from the Faillace's,
what sort of TSE did these animals have ?
WERE they atypical scrapie, BSE, and or typical scrapie ?
HOW much longer will you refuse to give us this information ? and for what
reason ?
WHY is it that the Farm of the Mad Sheep of Mad River Valley were
quarantined for 5 years, but none of these farms from Texas and Alabama with
Atypical TSE in the Bovine, they have not been quarantined for 5 years,why not,
with the real risk of BSE to sheep, whom is to say this was not BSE ?
snip...
full text ;
Monday, September 1, 2008
RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL
T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [No. 00-072-1]
September 1, 2008
Greetings again BSE-L members,
I had a pleasant surprise this past Saturday. I got an unexpected package
from O.I.G. on my old F.O.I.A. request, of the final test results of the
infamous mad sheep of mad river valley. IF you all remember, back on Thu, 24 Apr
2008 15:00:20 -0500 I wrote ;
snip...full text ;
i remember a few years back ???
PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL
that a study showed the prion uptake in a tomato plant, not that this would
surprise me ;
56. Members considered that there is no evidence that crops grown on the
land which received composted excreta from BSE-challenged animals pose a TSE
risk to humans or animals. One member suggested that, as some of these animals
are orally challenged with high doses of BSE-infected materials, and the
distribution of infectivity in the digestive system is not completely
understood, it might be premature to conclude that there is no infective agent
in the manure. Furthermore, an unpublished study had indicated low level
absorption of PrP from soil by tomato plants although it should be noted that
this study had not been repeated. Details of this work would be sent to the SEAC
Secretary. Dr Matthews explained that most of the manure from animals challenged
with high doses of BSE had already been composted and used for coppicing.
Members agreed that the risks from disposal of residual manure from experimental
animals would be much less than historic risks of on farm contamination from
naturally infected animals at the height of the BSE epidemic.
SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester
Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE
BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences &
Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s
Hospital London and William Harvey Hospital Ashford April 1999
snip...
88. Natural decay: Infectivity persists for a long time in the environment.
A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep,
after they had grazed on land which had previously been grazed by
scrapie-infected sheep, even though the land had lain fallow for three years
before the healthy sheep were introduced. Brown also quoted an early experiment
of his own (1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later near where
the material had been placed. 89. Potential environmental routes of infection:
Brown discusses the various possible scenarios, including surface or subsurface
deposits of TSE-contaminated material, which would lead to a build-up of
long-lasting infectivity. Birds feeding on animal remains (such as gulls
visiting landfill sites) could disperse infectivity. Other animals could become
vectors if they later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface water
channels, by effluents and discarded solid wastes from treatment plants. A
reasonable conclusion is that there is a potential for human infection to result
from environmental contamination by BSE-infected tissue residues. The potential
cannot be quantified because of the huge numbers of uncertainties and
assumptions that attend each stage of the disposal process". These comments,
from a long established authority on TSEs, closely echo my own statements which
were based on a recent examination of all the evidence. 90. Susceptibility: It
is likely that transmissibility of the disease to humans in vivo is probably
low, because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no definitive data
are available.
91. Recommendations for disposal procedures: Brown recommends that material
which is actually or potentially contaminated by BSE should be: 1) exposed to
caustic soda; 2) thoroughly incinerated under carefully inspected conditions;
and 3) that any residue should be buried in landfill, to a depth which would
minimise any subsequent animal or human exposure, in areas that would not
intersect with any potable water-table source.
92. This review and recommendations from Brown have particular importance.
Brown is one of the world's foremost authorities on TSEs and is a senior
researcher in the US National Institutes of Health (NIH). It is notable that
such a respected authority is forthright in acknowledging the existence of
potential risks, and in identifying the appropriate measures necessary to
safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M
Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will,
"Geographical distribution of variant CJD in the UK (excluding Northern
Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD
(variant CJD) might live closer to rendering factories than would be expected by
chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were
studied. The incubation period of vCJD is not known but by analogy with other
human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure
to rendering products, such exposure might plausibly have occurred 8-10 years
before the onset of symptoms. The authors were able to obtain the addresses of
all rendering plants in the UK which were in production in 1988. For each case
of vCJD, the distance from the place of residence on 1st January 1998 to the
nearest rendering plant was calculated
snip...
Infectivity surviving ashing to 600*C is (in my opinion) degradable but
infective. based on Bown & Gajdusek, (1991), landfill and burial may be
assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years.
CJD-infected brain-tissue remained infectious after storing at room-temperature
for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable
after at least 30 months of desiccation (Wilson et al, 1950). and pastures that
had been grazed by scrapie-infected sheep still appeared to be contaminated with
scrapie agent three years after they were last occupied by sheep (Palsson,
1979).
PAUL BROWN SCRAPIE SOIL TEST
snip...
please see full text ;
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Friday, February 25, 2011
Soil clay content underlies prion infection odds
PRION 2010
International Prion Congress: From agent to disease September 8–11, 2010
Salzburg, Austria
snip...
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
2009 CWD SYMPOSIUM UTAH
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic
Area
65
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic
Area
Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal
Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and
M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of
Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort
Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services,
United States Department of Agriculture, Fort Collins, Colorado, 80521, USA
3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA
4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory,
University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology,
Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging,
University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author-
tracy.a.nichols@aphis.usda.gov
Chronic wasting disease (CWD) is the only known transmissible spongiform
encephalopathy affecting free-ranging wildlife. Experimental and epidemiological
data indicate that CWD can be transmitted horizontally and via blood and saliva,
although the exact mode of natural transmission remains unknown. Substantial
evidence suggests that prions can persist in the environment, implicating it as
a potential prion reservoir and transmission vehicle. CWD- positive animals can
contribute to environmental prion load via biological materials including
saliva, blood, urine and feces, shedding several times their body weight in
possibly infectious excreta in their lifetime, as well as through decomposing
carcasses. Sensitivity limitations of conventional assays hamper evaluation of
environmental prion loads in water. Here we show the ability of serial protein
misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions
in spiked water samples at a 1:1 x106 , and protease-resistant prions in
environmental and municipal-processing water samples from a CWD endemic area.
Detection of CWD prions correlated with increased total organic carbon in water
runoff from melting winter snowpack. These data suggest prolonged persistence
and accumulation of prions in the environment that may promote CWD
transmission.
snip...
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.
snip...end...full text at ;
Wednesday, June 27, 2012
First US BSE Case Since 2006 Underscores Need for Vigilance
Neurology Today 21 June 2012
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Monday, June 11, 2012
another atypical Nor-98 Scrapie case documented in Canada for 2012
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
layperson
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518