Resistance of Soil-Bound Prions to Rumen Digestion
Resistance of Soil-Bound Prions to Rumen Digestion
Samuel E. Saunders1¤, 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
Abstract
Before prion uptake and infection can occur in the lower gastrointestinal
system, ingested prions are subjected to anaerobic digestion in the rumen of
cervids and bovids. The susceptibility of soil-bound prions to rumen digestion
has not been evaluated previously. In this study, prions from infectious brain
homogenates as well as prions bound to a range of soils and soil minerals were
subjected to in vitro rumen digestion, and changes in PrP levels were measured
via western blot. Binding to clay appeared to protect noninfectious hamster PrPc
from complete digestion, while both unbound and soil-bound infectious PrPSc
proved highly resistant to rumen digestion. In addition, no change in
intracerebral incubation period was observed following active rumen digestion of
unbound hamster HY TME prions and HY TME prions bound to a silty clay loam soil.
These results demonstrate that both unbound and soil-bound prions readily
survive rumen digestion without a reduction in infectivity, further supporting
the potential for soil-mediated transmission of chronic wasting disease (CWD)
and scrapie in the environment.
Citation: Saunders SE, Bartelt-Hunt SL, Bartz JC (2012) Resistance of
Soil-Bound Prions to Rumen Digestion. PLoS ONE 7(8): e44051.
doi:10.1371/journal.pone.0044051
Editor: Jiyan Ma, Ohio State University, United States of America
Received: June 7, 2012; Accepted: July 27, 2012; Published: August 24,
2012
Copyright: © 2012 Saunders et al. This is an open-access article
distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided
the original author and source are credited.
Funding: This work was supported by National Science Foundation
(CBET-1149242) and the National Center for Research Resources (P20 RR0115635-6,
C06 RR17417-01 and G200RR024001). The funders had no role in study design, data
collection and analysis, decision to publish or preparation of the
manuscript.
Competing interests: The authors have declared that no competing interests
exist.
* E-mail: sbartelt2@unl.edu
¤Current address: Stanford Law School, Stanford, California, United States
of America
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Implications for Environmental Prion Transmission To initiate infection via
absorption across the lower gastrointestinal epithelium, orally ingested prions
must survive passage through the rumen [8]–[10]. Previous studies have observed
varied PrPSc resistance to in vitro rumen digestion [9], [18], [20]. We observed
that active in vitro rumen digestion did not reduce PrPSc abundance (Figure 1),
and consistent with the previous work of Scherbel et al. [19], unbound prion
infectivity was not reduced following rumen digestion (Table 2). Moreover, our
results demonstrate that PrPSc sorption to soil does not reduce prion resistance
to rumen digestion. However, since both unbound and soil-bound prions were
resistant to rumen digestion, we cannot conclude that soil sorption increases
prion resistance to gut degradation, only that it does not decrease it.
Nevertheless, the resistance of soil-bound prions to rumen digestion supports
the efficacy of soil-mediated prion transmission (prion-soil sorption and
subsequent ingestion or inhalation by a naïve host) [21] as a natural mechanism
of CWD and scrapie transmission.
We did observe variance in PrPSc resistance to digestion with respect to
soil type, where, in contrast to the other soils and minerals, PrPSc levels
bound to sand and sandy loam soil were reduced following digestion (Figure 1D
and 1E). Variance in prion-soil interactions of this kind could lead to spatial
variance in prion disease incidence based on local soil-type [21]. However,
preliminary protein misfolding cyclic amplification (PMCA) experiments [27]
indicate the replication efficiency of prions subjected to active digestion
while bound to sand or SiO2 is not significantly different than unbound prions
(data not shown). Based on the established relationship between PMCA replication
efficiency and infectious titer [24], [27], these results suggest the SCL soil
bioassay results are typical of the other soils and soil minerals used. Still,
bioassay of other soils is needed to definitively evaluate soil-type variance in
digestion resistance.
A number of factors must be considered in extending the present results.
First, the results were obtained using in vitro digestion, which is a simulation
of in vivo processes with limitations [30], [35]. We used standard in vitro
methods, consistent with previous prion digestion studies, although the limited
amount of prion-infected brain homogenate available necessitated using small
(0.2 ml) tubes, which may have contributed to the observed variance. Second,
prion resistance to digestion may vary with prion strain and species [23], [33].
As noted above, our preliminary work with other prion strains and species
suggests broad prion resistance to rumen digestion, but these results would need
to be confirmed with additional studies. Third, rumen digestion can vary with
host species and diet, with the latter appearing more significant than the
former [38]. Studies have reported similar in vitro digestion (as measured by
parameters such as gas production and substrate utilization) when using rumen
fluid contents from sheep and cows [39], [40], sheep and goats [41], and sheep
and red deer [42] when animals were fed the same diet. Variance in the diet of
the cows used to collect rumen fluid (23–66% grain) did not observably affect
the immunoblot results of this study (data not shown), suggesting that diet is
not a significant factor and that our results are applicable across a wide range
of diets and species (cervids, sheep, goats, and cattle). However, an extensive
study of the effect of diet was not conducted. Moreover, dairy cow diets are
notably different than free-ranging deer diets, and deer diets vary seasonally
as well as geographically, which can affect rumen digestion [43].
Finally, unbound and soil-bound prions surviving rumen passage will be
exposed to stomach and intestinal digestion before uptake. These two processes
are less complex than rumen digestion, and previous results indicate unbound
prions are resistant to both [8], [9], [44]. Still, the effect of soil sorption
on prion resistance to lower gastrointestinal digestion has yet to be
investigated. Moreover, while passage through the rumen and lower
gastrointestinal tract may not digest PrPSc, it may alter PrPSc uptake
efficiency, which would not be detected by immunoblot or intracerebral bioassay.
Thus, study of soil-bound prions in, for example, the gut-loop system employed
by Dagleish and Jeffery [8], [9] would be of interest in further evaluating the
efficacy of soil-mediated prion transmission.
April/May/June 2012; © 2012 Landes Bioscience
PO-033: Replication efficiency of soil-bound prions varies with soil type
Shannon Bartelt-Hunt,1 Samuel Saunders,1 Ronald Shikiya,2 Katie
Langenfeld,2 Jason Bartz2 1University of Nebraska-Lincoln; Omaha, NE USA;
2Creighton University; Omaha, NE USA
Prion sorption to soil is thought to play an important role in the
transmission of scrapie and chronic wasting disease (CWD) via the environment.
Sorption of PrP to soil and soil minerals is influenced by the strain and
species of PrPSc and by soil characteristics. However, the ability of soil-bound
prions to convert PrPc to PrPSc under these wide-ranging conditions remains
poorly understood. We developed a semiquantitative protein misfolding cyclic
amplification (PMCA) protocol to evaluate replication efficiency of soil-bound
prions. Binding of the hyper (HY) strain of transmissible mink encephalopathy
(TME) (hamster) prions to a silty clay loam soil yielded a greater-than-1-log
decrease in PMCA replication efficiency with a corresponding 1.3-log reduction
in titer. The increased binding of PrPSc to soil over time corresponded with a
decrease in PMCA replication efficiency. The PMCA efficiency of bound prions
varied with soil type, where prions bound to clay and organic surfaces exhibited
significantly lower replication efficiencies while prions bound to sand
exhibited no apparent difference in replication efficiency compared to unbound
controls. PMCA results from hamster and CWD agent-infected elk prions yielded
similar findings. Given that PrPSc adsorption affinity varies with soil type,
the overall balance between prion adsorption affinity and replication efficiency
for the dominant soil types of an area may be a significant determinant in the
environmental transmission of prion diseases.
PO-248: TSE infectivity survives burial for five years with little
reduction in titer
Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and
R(D)SVS; University of Edinburgh; Edinburgh, UK
BSE infected animals, BSE-contaminated materials and other sources of TSE
(prion) infection, such as carcasses from scrapie infected sheep, CWD infected
deer and cadavers of individuals infected with CJD may all end up in the
environment through burial or other methods of disposal. They may continue to
act as a reservoir of TSE infectivity if cattle or other susceptible animals
were to be exposed to these sources in the future. In order to address these
concerns, we performed two large scale demonstration experiments under field
conditions which were designed to mimic some of the ways by which TSE infected
materials may have been disposed of. The project examined the fate of TSE
infectivity over a period of five years in two scenarios; when the infectivity
was contained within bovine heads and when the infectivity was buried without
any containment. Two soil types were compared: a sandy loam and a clay loam. We
used the 301V TSE strain which was derived by serial passage of BSE in VM
mice.
TSE infectivity was recovered from all the heads exhumed annually for five
years from both types of soil, with little reduction in the amount of
infectivity throughout the period of the experiment. Small amounts of
infectivity were found in the soil immediately surrounding the heads, but not in
samples remote from them. Similarly there was no evidence of significant lateral
movement of infectivity from the buried bolus. However large amounts of TSE
infectivity were recovered at the site of burial of both boluses. There was
limited vertical upward movement of infectivity from the bolus buried in clay
soil and downward movement from the bolus buried in sandy soil.
Now that these experiments are completed we conclude that TSE infectivity
is likely to survive burial for long periods of time with minimal loss of
infectivity and restricted movement from the site of burial. These experiments
emphasize that the environment is a viable reservoir for retaining large
quantities of TSE infectivity, and reinforce the importance of risk assessment
when disposing of this type of infectious material.
PRION 2011
Envt.16: Soil Properties as a Factor in CWD Spread in Western Canada
Alsu Kuznetsova,† Tariq Siddique and Judd Aiken
University of Alberta; Edmonton, AB Canada†Presenting author; Email: alsu@ualberta.ca
Soil can serve as a stable reservoir for infectious prion proteins (PrPSc).
Soils are diverse and complex, varying in clay, silt, sand and organic
components. We have shown that PrPSc binds clay minerals avidly, an interaction
that considerably enhances prion infectivity. Conversely quartz sand bound PrPSc
less avidly. These studies would suggest that soils with lower clay and higher
sand content bind prions less avidly and do not enhance infectivity to the same
level as clay-rich soils. We hypothesize that clay content of a soil plays an
integral role in the spread of CWD. In this study, we present the soil
properties in the western Canada. Soils of the CWD-region generally are similar
in texture, clay mineralogy and soil organic matter content. In total these
soils can be characterized as clay loamy, montmorillonite (smectite) with 6–10 %
organic carbon. The major soils in the CWD-region are Chernozems, present in 60%
of total area. These soils have a humic horizon in which organic matter has
accumulated (1–17% organic C). Solonetzic soils are also common to Alberta and
Saskatchewan. We suggest that the greatest risk of CWD spread in western Canada
is restricted 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.
Envt.28:
High Survival Rates of TSE Infectivity Buried in Two Soil
Types Allister J. Smith The Roslin Insitute; Roslin, UK Email: allister.smith@roslin.ed.ac.uk
Two field experiments nearing completion are investigating the migration
and/or persistence of TSE infectivity in the soil environment, either buried
within bovine heads or buried without containment. In the first experiment five
pairs of bovine heads, spiked with mouse-passaged BSE (301V) macerate, were
buried within lysimeters containing either clay or sandy soil. A pair of
unspiked bovine heads was also buried to act as controls. Pairs of heads have
been exhumed annually during which a corer is used to take soil samples above,
surrounding and below the head. Any brain material within the head is recovered
during dissection. The soil samples have undergone protein extraction, and the
extracts along with the brain material have been assayed for infectivity by
bioassay in VM mice. Bioassay results from the first experiment show that for
all four years most of the intracranial brain samples have been positive for TSE
infectivity in both the clay and sandy soil. There is little change in the
survival curves between years 1 and 4 indicating little reduction in the amounts
of infectivity over time. There has been very limited infectivity found in
samples surrounding the heads buried in the sandy soil, but infectivity has been
found in the soil samples surrounding the clay heads and the levels increase
slightly from years one to four, presumably as the heads have decomposed. In a
parallel experiment a bolus of infectivity (301V) was placed in the centre of
two large lysimeters, containing either clay or sandy soil. Over the course of
four years, core samples have been taken at eight time points, on the vertical
and at 3 distances from the centre. These samples have been assayed for
infectivity and to date only one sample from the sandy soil has produced
pathological evidence of TSE disease in one mouse. In order to ascertain whether
any of the bolus remained at the end of the experiment, we collected a much
larger central core (d = 16 cm) and extracted samples for bioassay,
concentrating on the core portions that correlated to the original bolus
location. The samples from these core portions caused disease in a high
proportion of mice (bioassay still in progress), with apparently higher
infectivity levels in the clay soil, so far. This result indicates that there
has been very little migration of TSE infectivity without containment in either
clay or sandy soil and that there has been little reduction in titre with time.
Envt.29:
Time-Dependent Decline in PrPTSE Desorption from Soil
Particles Christen B. Smith,1,† Clarissa J. Booth,2 Kartik Kumar2 and Joel
A. Pedersen1–3 1Environmental Chemistry and Technology Program; 2Molecular and
Environmental Toxicology Center; 3Department of Soil Science, University of
Wisconsin; Madison, WI USA †Presenting author, Email: cmbell@wisc.edu
Environmental routes of transmission are implicated in epizootics of sheep
scrapie and chronic wasting disease in deer, elk, and moose. Strong evidence
suggests that soil may serve as an environmental reservoir of prions, which can
persist in the environment for years. The disease-associated form of the prion
protein (PrPTSE) readily attaches to soil particle surfaces. Prior studies
reported reduced PrPTSE recovery from experimentally spiked soils after longer
contact times, which in some cases has been interpreted as degradation of
PrPTSE. Here, we investigate PrPTSE desorption from sterilized and untreated
soil particles as a function of protein-soil contact time. Soil particles were
sterilized by autoclaving or g-irradiation. Desorption of PrPTSE from whole
soils, montmorillonite clay, and quartz sand was analyzed by immunoblotting
following 1-, 7-, and 14-day contact times. We found that PrPTSE recovery from
both sterile and untreated soil samples declined significantly with contact time
suggesting the strengthening of protein-particle interactions over time.
Recovery of PrPTSE from whole soils declined to a larger extent than did that
from montmorillonite and quartz sand possibly reflecting t he contribution of
particle-associated natural organic matter to the mechanisms of PrPTSE
attachment. The influence of PrPTSE-soil particle attachment on oral disease
transmission warrants investigation.
www.landesbioscience.com PRION
PO-031: Aerosol transmission of chronic wasting disease to white-tailed
deer
Nathaniel Denkers,1 Jeanette Hayes-Klug,1 Kelly Anderson,1 Sally Dahmes,2
David Osborn,3 Karl Miller,3 Robert Warren,3 Candace Mathiason,1 Edward
Hoover1
1Colorado State University; Fort Collins, CO USA; 2WASCO Inc.; Monroe, GA
USA; 3Warnell School of Forestry and Natural Resources, University of Georgia;
Athens, GA USA
Purpose. A signature feature of chronic wasting disease (CWD) is its
efficient lateral transmission in nature, almost surely by mucosal exposure. Our
previous studies employing Tg(cerPrP) mice determined that CWD can be
transmitted to a susceptible host by aerosol exposure, a route with relatively
little investigation. The present study was designed to determine whether CWD is
transmissible by aerosol to a native cervid host, white-tailed deer.
Materials and Methods. Nine white-tailed deer were exposed to two (2)
aerosol doses of a 5% w/v CWD+ (n = 6) or CWD- (n = 3) brain homogenate,
delivered via the nasal passages using a customized aerosol apparatus. At
3-month intervals post inoculation (mpi), tonsil and recto-anal
mucosa-associated lymphoid tissue (RAMALT) biopsies were collected and assayed
for CWD infection by protein misfolding cyclic amplification (PMCA), western
blotting (WB), and immunohistochemistry (IHC).
Results. At 3 mpi and 6 mpi, tonsil and RAMALT biopsies were collected from
5 of the 6 CWD + aerosol-exposed deer. Three of the 5 (60%) tested positive for
CWD by PMCA but not IHC or western blot analysis at 3 mpi. By 6 mpi, 5 of 5
(100%) were tonsil and/or RAMALT biopsy positive by at least two of the three
assays. Biopsies were collected from all CWD+ aerosol-exposed deer at 9 mpi,
with 6 of 6 (100%) tonsil and/ or RAMALT positive by western blot or IHC. At 10
mpi 3 of the 6 prion-exposed deer have developed early clinical signs of CWD
infection (hyperphagia, polydypsia, wide leg stance and head/neck
dorsi-flexion). All sham-inoculated deer are showing no clinical signs and have
remained CWD negative as assessed by all three assays. Interestingly, the prion
dose delivered to the deer by aerosol-exposure is estimated to be 20-fold lower
than the historical oral dose that has resulted in detectable CWD infection at 6
or 12 mpi.
Conclusions. This study documents the first aerosol transmission of CWD in
deer. These results further infer that aerosolized prions facilitate CWD
transmission with greater efficiency than does oral exposure to a larger prion
dose. Thus exposure via the respiratory mucosa may be significant in the facile
spread of CWD in deer and perhaps in prion transmission overall.
PO-073: Multiple routes of prion transepithelial transport in the nasal
cavity following inhalation
Anthony Kincaid, Shawn Feilmann, Melissa Clouse, Albert Lorenzo, Jason
Bartz
Creighton University; Omaha, NE USA
Introduction. Inhalation of either prion-infected brain homogenate or
aerosolized prions has been shown to cause disease, and in the case of
inhalation of infected brain homogenate, the nasal route of infection has been
shown to be 10–100 times more efficient than the oral route. The cell types
involved in the in vivo transport of prions across the nasal cavity epithelium
have not been determined. M cells in the follicular associated epithelium have
been shown to mediate transcellular transport of prions in vitro and in the gut
of experimentally infected mice. We tested the hypothesis that M-cell mediated
transport was responsible for prion entry across nasal cavity epithelium
following inhalation. Materials and Methods. Hamsters were inoculated
extranasally with 50 or 100ul of infected (n = 31) or mock-infected (n = 13)
brain homogenate. Control animals were inoculated with buffer (n = 4) or were
untreated (n = 5). Following survival periods ranging from 15 to 180 min,
animals were perfused, skulls were decalcified and nasal cavities were embedded
in paraffin. Tissue sections were cut and processed immunohistochemically for
glial fibrillary acidic protein to identify brain homogenate, or for the
disease-associated form of the prion protein. Tissue sections not further than
112 um apart through the entire extent of the nasal cavity were analyzed using
light microscopy; photomicrographs were obtained wherever inoculum was observed
on the surface of, within, or deep to the nasal mucosa for each animal. Results.
Infected or uninfected brain homogenate was identified within the nasal cavities
of animals at all time points and was seen crossing the nasal cavity epithelium
within minutes of inoculation; the transepithelial transport of brain homogenate
continued for up to 3 h after inoculation. Infected or uninfected brain
homogenate was seen adhering to, or located within, M cells at all time points.
However, larger volumes of infected or uninfected brain homogenate were
identified crossing between cells of the olfactory and respiratory epithelia in
multiple locations. In addition, infected or uninfected brain homogenate was
identified within the lumen of lymphatic vessels in the lamina propria beneath
the nasal mucosa at all time points. Conclusion. Transepithelial transport of
prions across nasal cavity mucosa begins within minutes of inhalation and can
continue for up to 3 h. While M cells appear to transport prions across the
follicular associated epithelium, larger amounts of prions are transported
between the cells of the respiratory and olfactory epithelia, where they
immediately enter the lymphatic vessels in the lamina propria. Thus, inhaled
prions can be spread via lymph draining the nasal cavity and have access to
somatic and autonomic nerves in the lamina propria of the nasal cavity. The
increased efficiency of the nasal cavity route of infection compared with the
oral route may be due to the rapid and prolonged transport of prions between
cells of the respiratory and olfactory epithelia.
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease
in the United States
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Soil clay content underlies prion infection odds
W. David Walter 1 , * , Daniel P. Walsh 2 , * , Matthew L. Farnsworth 3 ,
Dana L. Winkelman 1 & Michael W. Miller 2
1 United States Department of the Interior, United States Geological
Survey, Colorado Cooperative Fish and Wildlife Research Unit , Fort Collins ,
Colorado
80523-1484, USA. 2 Colorado Division of Wildlife, Wildlife Research Center,
Fort Collins, Colorado 80526-2097, USA. 3 United States Department
of Agriculture, Animal and Plant Health Inspection Services, Veterinary
Services, Centers for Epidemiology and Animal Health , Fort Collins ,
Colorado
80526-8117 , USA . * These authors contributed equally to this work.
Correspondence and requests for materials should be addressed to M.W.M.
(email: mike.miller@state.co.us ) .
Received 6 Sep 2010 | Accepted 19 Jan 2011 | Published 15 Feb 2011 DOI:
10.1038/ncomms1203
Environmental factors — especially soil properties — have been suggested as
potentially important in the transmission of infectious prion diseases. Because
binding to montmorillonite (an aluminosilicate clay mineral) or clay-enriched
soils had been shown to enhance experimental prion transmissibility, we
hypothesized that prion transmission among mule deer might also be enhanced in
ranges with relatively high soil clay content. In this study, we report apparent
influences of soil clay content on the odds of prion infection in free-ranging
deer. Analysis of data from prion-infected deer herds in northern Colorado, USA,
revealed that a 1 % increase in the clay-sized particle content in soils within
the approximate home range of an individual deer increased its odds of infection
by up to 8.9 % . Our findings suggest that soil clay content and related
environmental properties deserve greater attention in assessing risks of prion
disease outbreaks and prospects for their control in both natural and production
settings.
snip....
The capacity of clay minerals and clay-laden soils to capture and enhance
infectivity of shed or deposited prions 19,20,25 – 27 and the common tendency of
ruminants to ingest soil both deliberately and incidentally in the course of
foraging and grooming 12,44,45 provide an elegantly simple hypothetical
mechanism for indirect prion transmission, as follows: infected individuals
propagate infectious prions in mucosa-associated lymphoid tissues and shed
prions into ingesta and saliva; ingested and environmental soil microparticles
with a high phyllosilicate (especially smectite) content bind to, sequester and
enhance infectivity of prions both before and after leaving the host;
microparticle-bound prions are incorporated into surface soil; susceptible
individuals consume contaminated soil and some become infected. (Also see
Supplementary Figure S1 .) This mechanism may underlie the apparent importance
of indirect transmission in explaining observed patterns of prion infection
among captive mule deer 10,11 , and perhaps among sheep 3,4,6,7 . In light of
these and others ’ findings, soil clay content and related environmental
properties deserve greater attention in assessing local and regional risks of
prion disease outbreaks and prospects for their control in natural and
production settings.
Friday, February 25, 2011
Soil clay content underlies prion infection odds
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
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
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 ;
Volume 18, Number 3—March 2012
Synopsis
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
Samuel E. Saunders1, Shannon L. Bartelt-Hunt, and Jason C. Bartz Author
affiliations: University of Nebraska-Lincoln, Omaha, Nebraska, USA (S.E.
Saunders, S.L. Bartelt-Hunt); Creighton University, Omaha (J.C. Bartz)
snip...
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B). Except in South Korea, CWD has not been
detected outside North America. In most locations reporting CWD cases in
free-ranging animals, the disease continues to emerge in wider geographic areas,
and prevalence appears to be increasing in many disease-endemic areas. Areas of
Wyoming now have an apparent CWD prevalence of near 50% in mule deer, and
prevalence in areas of Colorado and Wisconsin is <15 0="0" 10="10" 5="5" according="according" adult="adult" age="age" agencies.="agencies." and="and" appear="appear" areas="areas" between="between" but="but" cwd="cwd" data="data" deer.="deer." deer="deer" div="div" elk="elk" factors="factors" for="for" from="from" gene="gene" genetic="genetic" highest="highest" however="however" in="in" include="include" influence="influence" influences="influences" is="is" known="known" less="less" lower="lower" male="male" many="many" obtained="obtained" of="of" parts="parts" polymorphisms="polymorphisms" prevalence="prevalence" provincial="provincial" prp="prp" reaches="reaches" remain="remain" remains="remains" reports="reports" risk="risk" scrapie.="scrapie." sex="sex" show="show" state="state" strong="strong" susceptibility="susceptibility" than="than" the="the" to="to" understood="understood" wildlife="wildlife" wyoming.="wyoming.">
snip...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5). In addition, CWD-infected deer are
selectively preyed upon by mountain lions (5), and may also be more vulnerable
to vehicle collisions (10).
snip...
Conclusions
Much remains unknown about prion diseases and CWD in particular, especially
about CWD strains (which may have varied zoonotic potentials) and the long-term
effects of CWD on cervid ecosystems. CWD prevalence and geographic range appear
likely to continue to increase. Moreover, the disease is inevitably fatal, and
no effective therapeutic measures are presently available. As such, it would
seem wise to continue research and surveillance of CWD to elucidate the details
of its transmission, pathogenesis, and continued emergence in cervid populations
in hopes that strategies for mitigating its negative effects on humans and
cervid ecosystems can be identified.
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE CWD
2012
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
Despite the five year premise plan and site decontamination, The WI DNR has
concerns over the bioavailability of infectious prions at this site to wild
white-tail deer should these fences be removed. Current research indicates that
prions can persist in soil for a minimum of 3 years.
However, Georgsson et al. (2006) concluded that prions that produced
scrapie disease in sheep remained bioavailable and infectious for at least 16
years in natural Icelandic environments, most likely in contaminated soil.
Additionally, the authors reported that from 1978-2004, scrapie recurred on
33 sheep farms, of which 9 recurrences occurred 14-21 years after initial
culling and subsequent restocking efforts; these findings further emphasize the
effect of environmental contamination on sustaining TSE infectivity and that
long-term persistence of prions in soils may be substantially greater than
previously thought
SNIP...SEE FULL TEXT ;
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Friday, July 20, 2012
CWD found for first time in Iowa at hunting preserve
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
LANCET INFECTIOUS DISEASE JOURNAL
Volume 3, Number 8 01 August 2003
Previous
Next
Newsdesk
Tracking spongiform encephalopathies in North America
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 disease
(CJD). So he decided to gather hundreds of documents on transmissible spongiform
encephalopathies (TSE) and realised that if Britons could get variant CJD from
bovine spongiform encephalopathy (BSE), Americans might get a similar disorder
from chronic wasting disease (CWD)the relative of mad cow disease seen among
deer and elk in the USA. Although his feverish search did not lead him to the
smoking gun linking CWD to a similar disease in North American people, it did
uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the
occurrence of CJD and CWD in the USA. Only a few states have made CJD
reportable. Human and animal TSEs should be reportable nationwide and
internationally, he complained in a letter to the Journal of the American
Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue
to expect us to still believe that the 85% plus of all CJD cases which are
sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small
region in Colorado. But since early 2002, it has been reported in other areas,
including Wisconsin, South Dakota, and the Canadian province of Saskatchewan.
Indeed, the occurrence of CWD in states that were not endemic previously
increased concern about a widespread outbreak and possible transmission to
people and cattle.
To date, experimental studies have proven that the CWD agent can be
transmitted to cattle by intracerebral inoculation and that it can cross the
mucous membranes of the digestive tract to initiate infection in lymphoid tissue
before invasion of the central nervous system. Yet the plausibility of CWD
spreading to people has remained elusive.
Getting data on TSEs in the USA from the government is like pulling teeth,
Singeltary argues. You get it when they want you to have it, and only what they
want you to have.
SNIP...FULL TEXT ;
TSS
posted by Terry S. Singeltary Sr. at
4:19 PM
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