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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...
https://www.landesbioscience.com/journals/prion/article/28467/
https://www.landesbioscience.com/image_preview/journals/prion/2013PRION0109R.pdf
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
Saskatchewan
Elk
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/herds-infected-in-2014/eng/1394241838168/1394241839137
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
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/herds-infected-in-2013/eng/1360392113136/1363113991692
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
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/premises-infected-in-2012/eng/1336665765046/1367781979389
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
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/herds-infected-in-2011/eng/1330174719293/1330175566539
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
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/herds-infected-since-1996/eng/1330183608172/1330187238506
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.
https://www.landesbioscience.com/journals/prion/RodriguezPRI6-1.pdf
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.
snip...see full text and more here ;
Saturday, March 15, 2014
Potential role of soil properties in the spread of CWD in western Canada
http://chronic-wasting-disease.blogspot.com/2014/03/potential-role-of-soil-properties-in.html
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...
https://www.landesbioscience.com/journals/prion/article/28467/
https://www.landesbioscience.com/image_preview/journals/prion/2013PRION0109R.pdf
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
Saskatchewan
Elk
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/herds-infected-in-2014/eng/1394241838168/1394241839137
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
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/herds-infected-in-2013/eng/1360392113136/1363113991692
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
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/premises-infected-in-2012/eng/1336665765046/1367781979389
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
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/herds-infected-in-2011/eng/1330174719293/1330175566539
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
http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/herds-infected-since-1996/eng/1330183608172/1330187238506
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.
https://www.landesbioscience.com/journals/prion/RodriguezPRI6-1.pdf
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.
snip...see full text and more here ;
Saturday, March 15, 2014
Potential role of soil properties in the spread of CWD in western Canada
http://chronic-wasting-disease.blogspot.com/2014/03/potential-role-of-soil-properties-in.html
I will admit that I do skim thru Terry's stuff and read what looks to cover questions I have about this f'd up disease. It's gonna show up more and more here in Iowa, no doubt, and I like to read what they have observed so far. I have a doe skull in my freezer to try the "meateater" guy, Steve Rinella's recipe of cooking a deer head in a campfire pit in the hot coals, wrapped up. Sounds risky in a CWD area with the brain, eyes and spinal cord, huh?? I suppose in an area with cwd, you would only want to bone out your meat??