Potential role of soil properties in the spread of CWD in western Canada
Potential role of soil properties in the spread of CWD in western
Canada
Alsu Kuznetsova*, Debbie McKenzie, Pamela Banser, Tariq Siddique, Judd M.
AikenView affiliations
Submitted 16 Dec 2013
Revised 26 Feb 2014
Accepted 7 Mar 2014
Published Online 11 Mar 2014 Abstract
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 CWD-endemic 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
Chronic wasting disease (CWO) is a fatal prion disease affecting free range
white-tailed deer, mule deer, elk and moose as well as farmed cervids. It first
appeared in North America in the western USA in the 1960s. Over the past
decades, the geographic range has expanded. In Canada CWD was initially
identified in a captive elk and, subsequently, in free-ranging mule deer in
Saskatchewan in 2000. The first free-ranging case of CWD in Alberta was
identified in mule deer in 2005. in white-tailed deer in 2007; a CWD-infected
moose was identified in Alberta in 2012(http://esrd.alberta.ca/fish-wildlife/wildlife-diseases/chronic-wasting-disease/).
CWD has not been identified in Manitoba; however, southwestern regions of that
province are clearly at risk. Spread of CWD further north jeopardizes caribou
herds and may trigger a new wave of prion disease among this cervid species.
Prion protein (PrP) of Caribou (Rangifer tarandus spp.) has an identical amino
acid sequence as the common allele of mule deer and white-tailed deer.1 Recent
transmission studies have demonstrated the ability of CWD to transmit to
reindeer by the oral route.2 The Woodland (R.T. caribou) and Barren ground (R.t.
caribou) caribou range extends south to central parts of Alberta, Saskatchewan
and Manitoba3 (Fig. 1). The physical distance between caribou and the
CWD-endemic region appears to be the sole factor currently limiting the exposure
and transmission of CWD to caribou herds.
The routes of CWD transmission remain unclear. CWD is a contagious prion
diease, the infectious agent is released in various body fluids including
saliva, feces, blood and urine.4 Although the majority of studies suggest an
oral route of exposure to be responsible for environmental transmission,5 there
is also evidence for intranasal and aerosol transmission6,7 as contributing
factors. In all transmission routes, soils can serve as a stable reservoir of
prion diseases (transmissible spongiform encephalopathies, TSEs). Prions bound
to soil particles Can remain infectious in the soils for many years.8,9
Therefore, soil properties are an important factor for PrPTSE preservation and
transmission in the environment.10-13 Analysis of soil-prion interactions and
the impact on infectivity is a complicated task because soils are multicomponent
systems consisting of mineral particles (clay. silt, sand); soil organic matter
(humic, fulvic acids and humin); humus or/and Fe-Mn film and cutans interacting
with mineral particles. The enormous complexity of soils indicates a need to
examine a variety of soils and their separated compounds (mineral and organic)
to identify the ability of prions to bind the soil, what the effect of binding
is on infectivity and what components of soil bind prions. ...
snip...
Current as of:
2014-02-28
| Date confirmed | Location |
Animal type infected
|
|---|---|---|
|
February 3
|
Saskatchewan
|
Elk
|
Current
as of: 2013-12-31
| Date confirmed | Location | Animal type infected |
|---|---|---|
| November 13 | Saskatchewan | Deer and Elk |
| April 8 | Saskatchewan | Deer |
| February 18 | Saskatchewan | Deer |
| January 30 | Saskatchewan | Deer |
Current
as of: 2012-12-31
| Date confirmed | Location | Animal type infected |
|---|---|---|
| June 11 | Saskatchewan | Elk |
| April 26 | Saskatchewan | Elk |
Current
as of: 2011-12-31
| Date confirmed | Location | Animal type infected |
|---|---|---|
| November 22 | Saskatchewan | Deer |
| May 15 | Saskatchewan | Elk |
| January 19 | Saskatchewan | Deer |
| January 4 | Saskatchewan | Deer |
Herds infected with Chronic Wasting Disease in Canada since 1996
The following table lists the number of domestic cervid
herds in Canada confirmed to be infected with chronic wasting disease (CWD)
since 1996.
| Year | Number of herds confirmed with CWD |
|---|---|
| 2012 | 2 |
| 2011 | 4 |
| 2010 | 5 |
| 2009 | 2 |
| 2008 | 4 |
| 2007 | 6 |
| 2006 | 2 |
| 2005 | 0 |
| 2004 | 1 |
| 2003 | 1 |
| 2002 | 3 |
| 2001 | 21 |
| 2000 | 15 |
| 1999 | 0 |
| 1998 | 1 |
| 1997 | 0 |
| 1996 | 1 |
| Total | 66 |
Lichens Unexpected anti-prion agents?
Cynthia M. Rodriguez,1,2 James P. Bennett1,3 and Christopher J. Johnson1,*
1USGS National Wildlife Health Center; 2Department of Bacteriology and
3Department of Botany; University of Wisconsin; Madison, WI USA
The prion diseases sheep scrapie and cervid chronic wasting disease are
transmitted, in part, via an environmental reservoir of infectivity; prions
released from infected animals persist in the environment and can cause disease
years later. Central to controlling disease transmission is the identification
of methods capable of inactivating these agents on the landscape. We have found
that certain lichens, common, ubiquitous, symbiotic organisms, possess a serine
protease capable of degrading prion protein (PrP) from prion-infected animals.
The protease functions against a range of prion strains from various hosts and
reduces levels of abnormal PrP by at least two logs. We have now tested more
than twenty lichen species from several geographical locations and from various
taxa and found that approximately half of these species degrade PrP. Critical
next steps include examining the effect of lichens on prion infectivity and
cloning the protease responsible for PrP degradation. The impact of lichens on
prions in the environment remains unknown. We speculate that lichens could have
the potential to degrade prions when they are shed from infected animals onto
lichens or into environments where lichens are abundant. In addition, lichens
are frequently consumed by cervids and many other animals and the effect of
dietary lichens on prion disease transmission should also be considered.
snip...
The consumption of lichens by wildlife species, and especially cervids, is
well known. For example, in arctic climates lichens minimally constitute 60% of
the winter diet of caribou.30 While the diets of cervids in other climates are
highly variable, lichens are desirable, and in some cases preferred,
browse.31,32 The effect of lichen consumption on CWD transmission is unknown,
but should lichen proteases promote degradation of CWD prions in the
gastrointestinal tract, lichen consumption could affect both direct and indirect
transmission of disease by reducing the infectious dose to which the host is
exposed. It is unclear if lichen proteases would remain active following
consumption. Endogenous protease inhibitors secreted by the host may inactivate
lichen proteolytic activity in the digestive tract. Similarly, gastrointestinal
and rumen microbes, low gastric pH and digestive enzymes all contribute to the
breakdown of ingested protein and may degrade lichen proteases prior their
contact with prions. Limited evidence, however, indicates poor protein
bioavailability in ruminants fed on lichens,33 suggesting protease activity
might be preserved in distal portions of the digestive system. Clearly, further
experimental trials are needed to assess what effect, if any, lichens may have
on CWD transmission. Our results suggest, however, that the effects of lichens
on TSEs are worth consideration.
PPo8-13:
Degradation of Pathogenic Prion Protein and Prion Infectivity by
Lichens
Christopher J. Johnson,1 James P. Bennett,1 Steven M. Biro,1,2 Cynthia M.
Rodriguez,1,2 Richard A. Bessen3 and Tonie E. Rocke1
1USGS National Wildlife Health Center; 2Department of Bacteriology;
University of Wisconsin, Madison; 3Department of Veterinary Molecular Biology;
Montana State University; Bozeman, MT USA
Key words: prion, lichen, bioassay, protease, degradation
Few biological systems have been identified that degrade the transmissible
spongiform encephalopathy (TSE)-associated form of the prion protein (PrPTSE)
and TSE infectivity. Stability of the TSE agent allows scrapie and chronic
wasting disease agents to persist in the environment and cause disease for
years. Naturally-occurring or engineered processes that reduce infectivity in
the environment could aid in limiting environmental TSE transmission. We have
previously identified that species of at least three lichens, unusual, symbiotic
organisms formed from a fungus and photosynthetic partner, contain a serine
protease capable of degrading PrPTSE under gentle conditions. We tested the
hypothesis that lichen extracts from these three species reduce TSE infectivity
by treating infected brain homogenate with extracts and examining infectivity in
mice. We found lichen extracts diminished TSE infectious titer by factors of 100
to 1,000 and that reductions in infectivity were not well-correlated with the
extent of PrPTSE degradation observed by immunoblotting. For example, treatment
of brain homogenate with Cladonia rangiferina extract caused <100-fold activity="" after="" agents.="" also="" and="" anti-prion="" but="" characterization="" cladonia="" closely="" clusters="" comparison="" data="" decrease="" degradation="" degrade="" div="" do="" extract="" favors="" focus="" fold="" for="" forms="" genera="" has="" immunoreactivity="" in="" indicate="" infectious="" infectivity="" known="" lichen="" more="" necessarily="" not="" of="" on="" or="" our="" phylogeny="" prion-degrading="" protease="" prp="" prptse.="" prptse="" reduction="" related="" remaining="" rendered="" searches="" some="" species-specificity="" species="" suggesting="" that="" the="" those="" to="" treatment="" uninfectious="" usnea="" was="" which="" with="" within="" yielded="">
PPo8-20:
The Anti-prion Activity of Soil Organic Compounds Humic and Fulvic
Acids
Joanna Narkiewicz,1,2 Ai H.N. Tran,1 Gabriele Giachin,1 Liviana Leita2 and
Giuseppe Legname1, 1Neurobiology Sector; Scuola Internazionale Superiore di
Studi Avanzati; International School for Advanced Studies; Bonomea, Trieste
Italy; 2Agricultural Research Council (CRA); Research Centre for Soil-Plant
System; Trieste, Gorizia Italy
A notable feature of prion diseases, as scrapie in sheep and chronic
wasting disease in mule deer and elk, is horizontal transmission between grazing
animals, suggesting that contaminated environment may contribute significantly
to disease transmission. Increasing evidence suggests that soil may present
natural reservoir of prion infectivity. Recent studies have shown that prions
may persist in contaminated soil and remain infectious for years. As the
mechanism of prion retention and persistence in soil is unknown, it is necessary
to understand which soil components may interact with prions and thus contribute
to disease transmission. Several reports indicate that prion have potential to
interact with soil minerals, however the contribution of soil organic fraction
in adsorption to prions has been neglected. Here, we present strong evidence for
soil humic substances (HS) interaction with prions. We show that two HS,
classified as humic and fulvic acids, interact with recombinant prion proteins
in vitro. Moreover, we show that both HS possess anti-prion activity, both in
vivo and in vitro. Both compounds induced elimination of PrPSc from chronically
scrapie-infected GT1 mouse hypothalamic cells (ScGT1) in a dose-dependent
manner. ScGT1 cells treatment with HS at concentration of 20mg/mL eliminated
more than 95% of PrPSc and did not affect cell viability. Moreover, both HS
induced inhibition of prion fibril formation in vitro, as determined by
thioflavin T assay. Our results suggest that HS may contribute significantly to
prion inactivation in natural soil environments.
PPo8-21:
Detection of PrPCWD in Rocky Mountain Elk Feces Using Protein Misfolding
Cyclic Amplification
Bruce E Pulford,1 Terry Spraker,1 Jenny Powers,2 Margaret Wild2 and Mark D.
Zabel1 1Department of Microbiology; Immunology and Pathology; College of
Veterinary Medicine and Biomedical Sciences; Colorado State University;
2Biological Resource Management Division; United States National Park Service;
CO, USA
Key words: CWD, feces, PMCA, elk
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy
affecting cervids, including mule and white-tailed deer (Odocoileus hemionus and
virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi). The
method of CWD transmission between hosts is unclear, though there is evidence
that feces excreted by infected animals may play a role. Recently, CWD prions
was detected in feces using bioassays in cervidized mice, which took many months
to produce results. In this study, we use a more rapid procedure, protein
misfolding cyclic amplification (PMCA), to test elk feces for the presence of
PK-resistant cervid PrP (PrPCWD). Feces were collected from symptomatic and
asymptomatic elk in several northern Colorado locations, homogenized, mixed with
normal brain homogenate from Tg5037 mice (expressing cervid PrP) and subjected
to up to 9 rounds of PMCA (1 round = 40 secs sonication/30 mins at 70% maximum
power, 24 hours). Western blots were used to detect PrPCWD using BAR-224
anti-PrP antibody. Rectal and CNS tissue from the elk were IHC-labeled and
examined for the presence of PrPCWD. Fecal samples from symptomatic and
asymptomatic elk that tested positive by IHC showed characteristic PrPCWD bands
on western blots following PMCA. In addition, PMCA detected PrPCWD in 25% of
fecal samples from IHC-negative animals. These data suggest that PMCA may (1)
prove useful as a non-invasive method to supplement or even replace IHC testing
of cervids for CWD, and (2) identify additional asymptomatic carriers of CWD,
the prevalence of which may be underestimated using IHC.
Saturday, March 10, 2012
CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein
feed CUSTOM MADE for deer and elk
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
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...
> Baiting for deer ... what do you think?
Monday, January 05, 2009
CWD, GAME FARMS, BAITING, AND POLITICS
Elk and Deer Use of Mineral Licks: Implications for Disease Transmission
Results from the mineral analyses combined with camera data revealed that
visitation was highest at sodium-rich mineral licks. Mineral licks may play a
role in disease transmission by acting as sites of increased interaction as well
as reservoirs for deposition, accumulation, and ingestion of disease agents.
Friday, October 26, 2012
CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT
PRODUCTS, BAITING, AND MINERAL LICKS
Sunday, September 01, 2013
hunting over gut piles and CWD TSE prion disease
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Tuesday, March 11, 2014
Science and Technology Committee Oral evidence: Blood, tissue and organ
screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD
Actually, it is nearer 2 per million per year of the population will
develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about
1 in 30,000. So that has not really changed. When people talk about 1 per
million, often they interpret that as thinking it is incredibly rare. They think
they have a 1-in-a-million chance of developing this disease. You haven’t.
You’ve got about a 1-in-30,000 chance of developing it.
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
*** DOCUMENT ID: APHIS-2006-0118-0411
Sunday, March 09, 2014
ACA Council Reviews Comment Period Procedure, Border Closings, Iowa Legal
Case, & Committee Recommendations
Sunday, March 09, 2014
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic
Wasting Disease in Domestic Cats
Science and Technology Committee Oral evidence: Blood, tissue and organ
screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD
Science and Technology Committee
Oral evidence: Blood, tissue and organ screening, HC 990 Wednesday 5 March
2014
Ordered by the House of Commons to be published on 5 March 2014.
Written evidence from witnesses:
– Prometic BioSciences Ltd
– Terumo BCT
– Prionics AG
– DuPont Chemicals and Fluoroproducts
Watch the meeting
Members present: Andrew Miller (Chair); Jim Dowd; David Heath; Stephen
Metcalfe; David Morris; Stephen Mosley; Pamela Nash; Sarah Newton; Graham
Stringer; David Tredinnick
snip...
Professor Collinge: I think there is some misunderstanding there. The
apparent incidence of sporadic CJD is increasing. There are about a hundred new
cases a year at the moment, and that has gone up substantially from the start of
surveillance. That is thought, principally, to reflect better diagnosis of the
disease, although that may not be all the explanation. It is possible, and we
can talk about that, that some of that may be BSE-related. However, I think that
the specific confusion there is that people talk about sporadic CJD occurring at
1 per million. That is not your individual risk. Your risk is 1 per million
every year. Actually, it is nearer 2 per million per year of the population will
develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about
1 in 30,000. So that has not really changed. When people talk about 1 per
million, often they interpret that as thinking it is incredibly rare. They think
they have a 1-in-a-million chance of developing this disease. You haven’t.
You’ve got about a 1-in-30,000 chance of developing it.
snip...
Tuesday, March 11, 2014
Science and Technology Committee Oral evidence: Blood, tissue and organ
screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD
Actually, it is nearer 2 per million per year of the population will
develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about
1 in 30,000. So that has not really changed. When people talk about 1 per
million, often they interpret that as thinking it is incredibly rare. They think
they have a 1-in-a-million chance of developing this disease. You haven’t.
You’ve got about a 1-in-30,000 chance of developing it.
kind regards, terry
posted by Terry S. Singeltary Sr. at
7:08 PM
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