Saturday, March 15, 2014

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.




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( 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. ...








Current as of: 2014-02-28

Domestic cervid herds confirmed to be infected with CWD in Canada in 2014
Date confirmed Location
Animal type infected
February 3




Current as of: 2013-12-31

Domestic cervid herds confirmed to be infected with CWD in Canada in 2013
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

Domestic cervid herds confirmed to be infected with CWD in Canada in 2012
Date confirmed Location Animal type infected
June 11 Saskatchewan Elk
April 26 Saskatchewan Elk





Current as of: 2011-12-31

Domestic cervid herds confirmed to be infected with CWD in Canada in 2011
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.

Number of domestic cervid herds in Canada
 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.




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.





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="">



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.




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




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.




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.




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).




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.




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.




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.






> Baiting for deer ... what do you think?


Monday, January 05, 2009






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





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





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




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.




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


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