# Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long .....



## terry (Sep 13, 2002)

-------------------- [email protected] --------------------


Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer



Nicholas J. Haley1, Candace K. Mathiason1, Mark D. Zabel1, Glenn C. Telling2, Edward A. Hoover1*

1 Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, United States of America, 2 Department of Molecular Biology and Genetics, University of Kentucky, Lexington, Kentucky, United States of America

Abstract Top Background Chronic wasting disease (CWD) of cervids is a prion disease distinguished by high levels of transmissibility, wherein bodily fluids and excretions are thought to play an important role. Using cervid bioassay and established CWD detection methods, we have previously identified infectious prions in saliva and blood but not urine or feces of CWD+ donors. More recently, we identified very low concentrations of CWD prions in urine of deer by cervid PrP transgenic (Tg[CerPrP]) mouse bioassay and serial protein misfolding cyclic amplification (sPMCA). This finding led us to examine further our initial cervid bioassay experiments using sPMCA.

Objectives We sought to investigate whether conventional test-negative deer, previously exposed orally to urine and feces from CWD+ sources, may be harboring low level CWD infection not evident in the 19 month observation period. We further attempted to determine the peripheral PrPCWD distribution in these animals.

Methods Various neural and lymphoid tissues from conventional test-negative deer were reanalyzed for CWD prions by sPMCA and cervid transgenic mouse bioassay in parallel with appropriate tissue-matched positive and negative controls.

Results PrPCWD was detected in the tissues of orally exposed deer by both sPMCA and Tg[CerPrP] mouse bioassay; each assay revealed very low levels of CWD prions previously undetectable by western blot, ELISA, or IHC. Serial PMCA analysis of individual tissues identified that obex alone was positive in 4 of 5 urine/feces exposed deer. PrPCWD was amplified from both lymphoid and neural tissues of positive control deer but not from identical tissues of negative control deer.

Discussion Detection of subclinical infection in deer orally exposed to urine and feces (1) suggests that a prolonged subclinical state can exist, necessitating observation periods in excess of two years to detect CWD infection, and (2) illustrates the sensitive and specific application of sPMCA in the diagnosis of low-level prion infection. Based on these results, it is possible that low doses of prions, e.g. following oral exposure to urine and saliva of CWD-infected deer, bypass significant amplification in the LRS, perhaps utilizing a neural conduit between the alimentary tract and CNS, as has been demonstrated in some other prion diseases.

Citation: Haley NJ, Mathiason CK, Zabel MD, Telling GC, Hoover EA (2009) Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer. PLoS ONE 4(11): e7990. doi:10.1371/journal.pone.0007990

Editor: Jiyan Ma, Ohio State University, United States of America

Received: September 29, 2009; Accepted: October 29, 2009; Published: November 24, 2009

Copyright: © 2009 Haley 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 NIH/NCRR Ruth L. Kirschstein Institutional T32 R07072-03 and NIH/NIAID NO1-AI-25491-02 (EAH, GCT). 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: [email protected]



SNIP...


In summary, we provide evidence for the presence of infectious prions in the brains of conventional prion-assay-negative deer orally exposed 19 months earlier to urine and feces from CWD-infected donor deer. This apparent low level of prion infection was amplified by sPMCA, confirmed by Tg[CerPrP] mouse bioassay, and detected only in the obex region of the brain. These results demonstrate the potential for CWD prion transmission via urine and/or feces, and highlight the application of more sensitive assays such as sPMCA in identification of CWD infection, pathogenesis, and prevalence.




http://www.plosone.org/article/info:doi/10.1371/journal.pone.0007990



Tuesday, June 16, 2009 

Infectious Prions in Pre-Clinical Deer and Transmission of Chronic Wasting Disease Solely by Environmental Exposure


http://chronic-wasting-disease.blogspot.com/2009/06/infectious-prions-in-pre-clinical-deer.html


Molecular Model of Prion Transmission to Humans

Michael Jones, Darren Wight, Rona Barron, Martin Jeffrey, Jean Manson, Christopher Prowse, James W. Ironside, and Mark W. Head

To assess interspecies barriers to transmission of transmissible spongiform encephalopathies (TSEs), we investigated the ability of disease-associated prion proteins (PrPd) to initiate conversion of the human normal cellular form of prion protein of the 3 major PRNP polymorphic variants in vitro. Protein misfolding cyclic amplification showed that conformation of PrPd partly determines host susceptibility.

snip...

Conclusions

Our results are best appreciated in terms of the molecular interaction between seed PrPd and substrate PrPC, specifi cally the species-specific amino acid sequence and PRNP polymorphic status of PrPC and PrPd and the PrPd conformers involved (Table). Regardless of the seed PrP amino acid sequence, the PrPd conformers associated with bovine BSE, ovine BSE, and human vCJD were amplified in the humanized mouse substrate and displayed similar PRNP-129 genotype preferences (PRNP-129MM >PRNP- 129MV >PRNP-129VV). In contrast, the PrPd conformer associated with the ovine scrapie strain, although sharing the same PrP amino acid sequence as the PrPd in ovine BSE, could not be amplified in any of the PRNP humanized mouse substrates but could be amplifi ed in a sheep brain substrate. These observations are consistent with conformation of a TSE agent's PrPd (rather than solely its amino acid sequence) having a role in determining the susceptibility of a host's PrPC to conversion. They similarly suggest that these molecular factors could in turn have a powerful influence on disease susceptibility and incubation time.

To date, all clinical cases of vCJD have occurred in persons with the PRNP-129MM genotype, as might be predicted from the effi ciency of amplification of BSE-related PrPd shown here. Extrapolating from these results, one would predict that the next genotypic group most likely to show susceptibility to the BSE agent would be heterozygous (MV) at codon 129 of the PRNP gene, as previously suggested from the corresponding in vivo transmission studies (14).

In the wake of BSE epidemics in the United Kingdom and elsewhere, enhanced surveillance has identified apparently new TSEs (15), raising concerns regarding animal and human health. PMCA with suitable substrate sources could provide a rapid way to estimate the molecular component of transmission barriers for particular TSE agents between species, including humans. These estimates could thus indicate whether, like classical scrapie, the agents rep- resent little risk for human health or whether, like classical BSE, they represent cause for concern.

http://www.cdc.gov/eid/content/15/12/pdfs/2013.pdf



see more here ;



Saturday, December 05, 2009

Molecular Model of Prion Transmission to Humans 

http://creutzfeldt-jakob-disease.blogspot.com/2009/12/molecular-model-of-prion-transmission.html



TSS


Sunday, December 06, 2009 

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer


http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html





Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area
Posted by Terry S. Singeltary Sr. on December 4, 2009 at 11:42am 



65

Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area

Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- [email protected]

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 ;



http://www.landesbioscience.com/journals/prion/article/NicholsPRION...





http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf




http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html




http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html




TSS


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## e. fairbanks (Dec 6, 2007)

Keep that stuff coming Terry 
Altho this discovery shoots holes in my opinion that only hunter killed deer/elk (OR PARTS THEREOF) from states and provinces where CWD IS PRESENT IN THE WILD THAT TEST NEGATIVE FOR CWD SHOULD BE IMPORTED INTO MICHIGAN, IT INDICATES THAT WE SHOULD BAN THE IMPORT OF ANY HUNTER KILLED DEER/ELK OR PARTS FROM THESE STATES AND PROVINCES.
IF WE REALLY WANT TO PREVENT THE INTRODUCTION OF CWD IN OUR WILD DEER. DO THE OPINIONS EXPRESSED ON THIS FORUM CONCUR ???


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## 6inchtrack (Sep 29, 2008)

> 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.


Guys
If the burial site is tested and confirmed (the ground water)... I'll eat my hat and switch sides and join you.


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## Direwolfe (Sep 11, 2007)

This also supports the bait ban as a method to limit the spread of CWD. We will not know if CWD is in an area for perhaps many years after it is introduced due to "negative" tests that miss these subclinical CWD infected deer that can spread CWD. While many others precautions should be taken, banning baiting proactively makes sense.


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## ridgewalker (Jun 24, 2008)

Where does this report mention baiting? Does the banning of baiting stop the deer from removing wastes from their bodies? Will deer stop yarding up because baiting is banned? Will they stop checking scrapes during rut because baiting is banned? Will they stop licking each other, feeding their young, licking them clean, or completing the rutting process? I think not. What this report implies is that once cwd is in the environment it is there to stay. It also implies that the only way to keep it out is to keep out material from diseased deer. That will only happen by banning interstate traffic of deer and deer parts(that may contain prions). That is a far different issue from baiting.


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## Michihunter (Jan 8, 2003)

Direwolfe said:


> This also supports the bait ban as a method to limit the spread of CWD. We will not know if CWD is in an area for perhaps many years after it is introduced due to "negative" tests that miss these subclinical CWD infected deer that can spread CWD. While many others precautions should be taken, banning baiting proactively makes sense.


What this in fact implies is that a baiting ban has no significant value to preventing CWD transmission IF it can be sustained in water. That source of sustenance is a lot more widespread and the exposure to it is certainly more available than any baitpile would ever hope to be. Reducing population is about the only chance of decreasing transmission risk and unfortunately, one tool to assist in that endeavor has been removed from the hunters arsenal.


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## LarryA (Jun 16, 2004)

Those are interesting articles, but you should know that one or two studies prove nothing. That is not the manner that the Scientific Method is designed to work. Typically a decent study will point to more questions than answers. The long and short of it unless you are familiar with the procedures in a study it is difficult at best to make any assumptions on the validity of the science.

I have always thought the greatest threat to the spread of disease in cervids is more prone to winter yarding behavior over many other typical sources. Think about it for a moment ... in winter yards the chances of body secretion exposure is much greater than any other time. More deer are jammed into a smaller area than at any other time.


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## terry (Sep 13, 2002)

Greetings,

WE can debate this issue until cwd has your state completely infected, or not. You can stand by and do nothing, you can go at it half @ss, or you can do every thing that will help eradicate CWD. Baiting, helps the spreading of CWD, that's the bottom line. It congregates deer in large numbers in a single location (in a given area), the deer get use to this food plot, and they come back in more numbers, thus, this _artificial_ food plot becomes a petre dish for CWD. Yes, there are natural baiting habitats that will do the same thing as artificial baiting plots, but the question is, do you want to be part of the problem, or do you want to be part of the solution? (NOT to mention the other mode of transmission of CWD by BAIT that is of animal base protein). Baiting is but a small part of a much greater problem, where solutions are hard to come by, to date. All the rules and regulations in the world might not stop CWD once it is established in the environment. Michigan, to date, has dodged the fallout of CWD being _documented_ in the free range deer herds. You would think that everyone would be on the same page in trying to stop that from happening, and the baiting ban is but a small price to pay in doing just that. I don't see what the problem is, unless you are the ones selling the bait, or, you just don't know how to hunt, and or just too lazy too, and cannot make a kill without an artificial means to help you do that. just my opinion. But, if a bait ban has one chance in hell to stop the spreading of CWD, or to evening just slow it down, or to prevent it from being established in the wild in your state, I would support a baiting ban.


Role of baiting and feeding in transmission of CWD


http://wildlife.wisc.edu/coop/CWD/abbey's web stuff/Abbey_Page2.htm


http://wildlife.wisc.edu/coop/CWD/abbey..pdf


IMPACT: 2008-01-01 TO 2008-12-31 Our results demonstrate a connection between spatial patterns of CWD spread in Wisconsin and deer gene flow. In addition, we also evaluated whether some landscape features such as highways and rivers would be a barrier to disease spread. Work on diseases affecting scavenging mammals continues to show that native wildlife species may be infected by disease agents that also affect agricultural interests. Six species of scavenging mammals and and 8 speices of birds were found to consume deer carcasses, which may contain infectious prions. Most frequent scavengers included crows, raccoons, possums, and turkey vultures. We tested more than 800 native scavenging mammals and found no evidence that CWD or other TSEs were present. We found that feeding and baiting of deer can increase the risk of disease transmission by both direct contact and through environmental sources.

PUBLICATION INFORMATION: 2008-01-01 TO 2008-12-31 Blanchong, J. A., M. D. Samuel, K. T. Scribner, B. V. Weckworth, J. A. Langenberg, and K. Filcek. 2008. Landscape genetics and the spatial distribution of chronic wasting disease. Biology Letters 4: 130-133.


http://www.reeis.usda.gov/web/crisprojectpages/199117.html


February 14, 2003

Chronic Wasting Disease and the Science in support of the Ban on Baiting and Feeding Deer.

Timothy R. Van Deelen Ph.D. Wisconsin DNR

Research 

Summary Reliable science provides support for a ban of baiting and feeding of white-tailed deer to reduce disease risks for Chronic Wasting Disease (CWD). Peer-reviewed research papers published in reputable scientific journals indicate the following: 
 CWD is transmitted laterally (live diseased deer infect other deer) 
 Deer can get CWD by ingesting something contaminated with the disease prion 
 CWD prions may be shed in feces and saliva 
 Disease course and symptoms indicate high potential for transmission where deer are concentrated 
 Evidence from captive situations indicates that deer can get CWD from highly contaminated environments. 

 Baiting and Feeding causes unnatural concentration of deer 

 Reduction of contact through a ban on baiting and feeding is likely very important to eradicating or containing a CWD outbreak. 

 Baiting and feeding continues to put Wisconsins deer herd at risk to other serious diseases In addition, experts in CWD, wildlife disease and deer nutrition support bans on baiting and feeding as part of a comprehensive strategy to prevent and/or manage CWD. Under a baiting and feeding ban, disease outbreaks are more likely to be smaller in scale and more apt to be contained or eliminated. With the long CWD incubation period and other factors that make discovery of a new outbreak difficult, an outbreak that is already widespread when detected because of baiting and feeding may not be able to be contained or eliminated. This document provides details and explicit links to the supporting science.


SNIP...

Chronic Wasting Disease and the Science behind the Ban on Baiting and Feeding Deer.



 Baiting and Feeding causes unnatural concentration of deer

People use baiting and feeding to concentrate deer for enhanced hunter opportunity or viewing. In northern deer, seasonal concentration in deeryards is a well-known phenomenon (Blouch 1984). However, the potential for close animal-to-animal contact over a feed pile is fundamentally different than the contact yarded deer experience while foraging on natural food. In deeryards, deer eat a variety of woody browse plants and arboreal lichens (Blouch 1984) scattered across a large area. In terms of biomass and nutrition, the best source of browse and lichens may be litter-fall rather than live plant material growing in the understory (Ditchkoff and Servello 1998). Food sources in deeryards (litter and understory plants) are widely distributed over a large area and they are not replaced. Moreover, browse is typically held aloft on the plant stem such that fecal contamination is less likely. Foraging by wintering deer is an optimization process. Energy gains associated with eating need to be balanced against energy costs associated with travel and exposure (Moen 1976). Yarded deer with little or no access to supplemental food maintain relatively large overlapping home ranges (e.g. 110 acres in Minnesota [Nelson and Mech 1981], 480 acres in Michigan [Van Deelen 1995], 318 acres in Quebec [Lesage et al. 2000]) suggesting that foraging widely on a diffuse food source is normal. Garner (2001) monitored 160 radio-collared deer for 2 fall/winter periods in northern Michigan and documented their behavior over feeding sites using both telemetry and direct observations. He demonstrated that, relative to natural forage, supplemental feeding caused reduced home range sizes, increased overlap of home ranges in space and time and dramatic concentrations of activity around feeding sites.

 Reduction of contact through a ban on baiting and feeding is likely very important to eradicating or containing a CWD outbreak.

Epidemiological models fit to real-world data on CWD outbreaks in mule deer predict that local extinction of infected deer populations is likely (Gross and Miller 2001). The predicted outcomes of these models are highly sensitive to input estimates of the amount of contact between infected and susceptible deer meaning that small reductions in contact rates can dramatically reduce the rate at which prevalence changes during an epidemic (Gross and Miller 2001). Garner (2001) demonstrated that baiting and feeding was associated with deer concentration, extensive face-to-face contacts, and increasing overlap of deer home ranges. White-tailed deer have contacts from social and grooming behaviors apart from contact over baiting and feeding sites (Marchinton and Hirth 1984) but social groups of whitetails tend to be small during most of the year (4 to 6 individuals, Hawkins and Klimstra 1970). Whitetail physiology and behavior are adapted to selective foraging on nutritious plants (Putman 1988). Moreover, social groups tend to exclude one another by using different areas or by using shared areas at different times (Mathews 1989, Porter et al. 1991). Concentration of deer activity over feeding sites increase both direct and indirect contact between groups by increasing home range and core area overlap and by increasing the amount of time that unrelated deer feed in close proximity to each other (Garner 2001).

5

Eliminating these contacts has added significance because CWD is a uniquely difficult disease to manage and study. There is no treatment and no vaccine. Moreover CWD is difficult to track in a population because of long incubation periods, subtle early clinical sign, a resistant infectious agent, potential for environmental contamination and incomplete understanding of transmission mechanisms. These characteristics make prevention critically important (Williams et al. 2002).


http://dnr.wi.gov/org/land/wildlife/Whealth/issues/Cwd/doc/cwdscsu.pdf


Journal of Wildlife Management 72(2):416-421. 2008 doi: 10.2193/2006-543

Alternative Feeding Strategies and Potential Disease Transmission in Wisconsin White-Tailed Deer Abbey K. Thompsona, Michael D. Samuelb,1, Timothy R. Van Deelenc

aDepartment of Wildlife Ecology, 1630 Linden Drive, University of Wisconsin, Madison, WI 53706, USA

bUnited States Geological Survey, Wisconsin Cooperative Wildlife Research Unit, 1630 Linden Drive, University of Wisconsin, Madison, WI 53706, USA

cDepartment of Wildlife Ecology, 1630 Linden Drive, University of Wisconsin, Madison, WI 53706, USA

1 E-mail: [email protected]

Abstract

We conducted experimental feeding using 3 feeding methods (pile, spread, trough) and 2 quantities (rationed, ad libitum) of shelled corn to compare deer activity and behavior with control sites and evaluate potential direct and indirect transmission of infectious disease in white-tailed deer (Odocoileus virginianus) in central Wisconsin, USA. Deer use was higher at 2 of the feeding sites than at natural feeding areas (P = 0.02). Deer spent a higher proportion of time (P < 0.01) feeding at pile (49%) and spread (61%) treatments than at natural feeding areas (36%). We found higher deer use for rationed than ad libitum feeding quantities and feeding intensity was greatest at rationed piles and lowest at ad libitum spreads. We also observed closer pairwise distances (=0.3 m) among deer when corn was provided in a trough relative to spread (P = 0.03). Supplemental feeding poses risks for both direct and indirect disease transmission due to higher deer concentration and more intensive use relative to control areas. Concentrated feeding and contact among deer at feeding sites can also increase risk for disease transmission. Our results indicated that restrictions on feeding quantity would not mitigate the potential for disease transmission. None of the feeding strategies we evaluated substantially reduced the potential risk for disease transmission and banning supplemental feeding to reduce transmission is warranted.

Keywords: baiting, chronic wasting disease, disease transmission, fecal pellets, Odocoileus virginianus, supplemental feeding, white-tailed deer


http://www.bioone.org/doi/abs/10.2193/2006-543?cookieSet=1&journalCode=wild




I see NO conspiracy here, just common sense. ...TSS



Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer


http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html


Monday, January 05, 2009

CWD, GAME FARMS, BAITING, AND POLITICS


http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html


Thursday, August 28, 2008 cwd, feeding, and baiting piles

http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html



AS THE CROW FLIES, SO DOES CWD


Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html


Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/07/deer-carcass-decomposition-and.html


TSS


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## Direwolfe (Sep 11, 2007)

"Where does this report mention baiting? Does the banning of baiting stop the deer from removing wastes from their bodies? Will deer stop yarding up because baiting is banned? Will they stop checking scrapes during rut because baiting is banned? Will they stop licking each other, feeding their young, licking them clean, or completing the rutting process? I think not. What this report implies is that once cwd is in the environment it is there to stay. It also implies that the only way to keep it out is to keep out material from diseased deer. That will only happen by banning interstate traffic of deer and deer parts(that may contain prions). That is a far different issue from baiting." 

Once again, reading comprehension takes a hit! "While many others precautions should be taken..." Yes we need to also keep deer parts out, lower populations, etc. What this report shows is that we may not know of its presence in an area until long after it arrives. Thus all those who argue we can institute a baiting ban after we detect it in an area will cause us to lose out on one of many control strategies.


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## .480 (Feb 21, 2006)

If we ban bait, then Food Plots and these little watering holes that people are digging on the edges of their food plots must be gone too.

It gets sooooooo sickening listening to all of the "stop the baiting" but food plots and watering holes are just fine garbage.

If you are going to only address baiting and leave out food plots and watering holes then you might be that little boy with his finger stuck in the leaking dam.


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## Direwolfe (Sep 11, 2007)

"If we ban bait, then Food Plots and these little watering holes that people are digging on the edges of their food plots must be gone too."

I'm not disagreeing with that. Several measures should be taken, e.g. ban deer by-products such as deer urine based scents. The food plot industry and its advocates should study whether they pose an increased risk of disease transmission. Their argument that they don't pose a problem because the deer are spread out are just that, an argument. I haven't seen test results either way. With a normally infectious agent such as a bacteria they have a good argument - spread out the bacteria and its less likely to result in a threshhold dose before it degrades. With a much longer lasting prion that doesn't seem to be the case.

Latest CO report I read had an item where an inspection of three bucks hanging at someones' home includes 2 very nice and intact bucks from a CWD positive state. Not deboned as per regs. They were apparently confiscated for disease testing. Let's put a whopping fine on that activity. You want to take your hunting money out of state? That's fine but don't bring that state's hunting problems back to Michigan.

Let's also find some way to get the captive cervid industry to comply with..... etc., etc. The list continues.


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## Munsterlndr (Oct 16, 2004)

Direwolfe said:


> The food plot industry and its advocates should study whether they pose an increased risk of disease transmission. Their argument that they don't pose a problem because the deer are spread out are just that, an argument. I haven't seen test results either way. With a normally infectious agent such as a bacteria they have a good argument - spread out the bacteria and its less likely to result in a threshhold dose before it degrades. With a much longer lasting prion that doesn't seem to be the case.


If you or anyone else had any lingering doubts about the capacity of food plots to concentrate deer in a manner where the potential for deer coming into contact with soil or food that as been potentially contaminated with prion-containing urine, saliva or fecal matter, please take a look at this video. This was shot in one of my late season food plots this fall. What you are seeing are hoof prints left by deer feeding in this plot. Keep in mind that this is located in a relatively low density area of the NLP where our density is somewhere in the 15 DPSM range. Imagine the increase in concentration in an area that had 50-100 dpsm. 

Banning baiting or food plots for that matter, is simply plugging a couple of holes in a **** that has sprung dozens of leaks. The potential for it having a substantive impact on limiting the spread of disease is almost nil as long as agricultural fields provide a source of contact for free ranging deer. If CWD is found in the free ranging herd, the ONLY method that will have the slightest impact on limiting the spread of the disease is massive depopulation in the immediate vicinity of the index sample. I'm talking a scorched earth, thermonuclear approach that eradicates deer within 10 or 15 sq. miles of where the sick deer is found. Anything short of that is merely going to delay the inevitable and in that event we might as well just learn to live with the disease until more research on Prions gives us better tools to work with. 

[ame=http://s219.photobucket.com/albums/cc112/Munsterlndr/food%20plots/?action=view&current=P1080864.flv]







[/ame]


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## Direwolfe (Sep 11, 2007)

Munster,

Thank God you didn't post all of the usual pictures! I feel like I'm in Clockwork Orange being forced to view pictures of half-eaten sugar beets! I better log out before Pinefarm reposts pictures of feces-encrusted carrots.


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## Munsterlndr (Oct 16, 2004)

Direwolfe said:


> Munster,
> 
> Thank God you didn't post all of the usual pictures! I feel like I'm in Clockwork Orange being forced to view pictures of half-eaten sugar beets! I better log out before Pinefarm reposts pictures of feces-encrusted carrots.


:lol: You should feel special, that's the first time I posted that video, I've been saving it for the right thread! :lol:


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## e. fairbanks (Dec 6, 2007)

This thread "Detection of Sub-Clinical CWD Infection in Test-Negative Deer" soon ended up in a waterhole with baiting and food plots.
Re. Direwolfe post-3 bucks hanging at "someones " home, 2 intact carcasses from CWD+ state. We assume they were hunter killed. If they came from a game farm they are "livestock" and are not illegal. IF THEY WERE HUNTER KILLED IN THE WILD THE "SOMEONE" WHO BROUGHT THEM INTO MICHIGAN IS GUILTY OF VIOLATING THE FEDERAL LACEY ACT AND CAN BE FINED $5000 AND A YEAR IN JAIL.
WE HAVE NOT HAD THE PRIVILEGE OF ANY INFORMATION REGARDING PROSECUTION OF HUNTERS WHO HAVE ILLEGALY BROUGHT BACK DEER/ELK CARCASSES FROM CWD POSITIVE STATES. IT IS A DEEP DARK SECRET.


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## Direwolfe (Sep 11, 2007)

"-3 bucks hanging at "someones " home, 2 intact carcasses from CWD+ state. We assume they were hunter killed. If they came from a game farm they are "livestock" and are not illegal."

From the DNR report I believe they were sporting hunting tags from the other state, not livestock. See the rest of my post above. They were confiscated for testing. If you want more info read the DNR CO's report for end of November.


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## terry (Sep 13, 2002)

O.11.1

Prions in feces of asymptomatic deer

Gültekin Tamgüney1,2, Michael W. Miller3, Lisa L. Wolfe3, Tracey M. Sirochman3, David V. Glidden4, Christina Palmer 1, Azucena Lemus5, Stephen J. DeArmond5, Stanley B. Prusiner1,2

1Institute for Neurodegenerative Diseases, University of California, San Francisco, USA; 2Department of Neurology, University of California, San Francisco, USA; 3Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, USA; 4Department of Epidemiology and Biostatistics, University of California, San Francisco, USA; 5Department of Pathology, University of California, San Francisco, USA

Background: Chronic wasting disease (CWD) of several species in the deer family and scrapie of sheep are infectious prion diseases that are transmitted naturally within affected host populations. Even though several potential sources of infectivity have been identified in secretions and excretions from symptomatic animals, the biological importance of these sources in sustaining epidemics remains unclear.

Objective/Methods: Feces from mule deer (Odocoileus hemionus) were periodically collected before and after oral inoculation with CWD prions until the deer developed clinical signs of CWD. Fecal samples were irradiated and intracerebrally inoculated into transgenic mice overexpressing cervid PrP.

Results: We report that asymptomatic CWD-infected mule deer excrete CWD prions in their feces long before they develop clinical signs of prion disease. Intracerebral inoculation of irradiated deer feces into transgenic mice overexpressing cervid PrP revealed infectivity in 14 of 15 fecal samples collected from 5 deer at 711 months before the onset of neurological disease. Even though prion concentrations in deer feces were much lower than those in brain tissue from the same deer collected at the disease terminus, the estimated total infectious dose excreted in feces by an infected deer over the disease course may approximate the total contained in brain tissue.

Discussion: Fecal prion excretion over long periods of time by infected deer provides a likely natural mechanism that may explain the high incidence and efficient horizontal transmission of CWD within deer herds, as well as prion transmission among susceptible cervid species.

Selected by the scientific committee from the submitted abstracts

P.4.27

Minor oral lesions facilitate CWD infection

Nathaniel Denkers1, Glenn Telling2, Edward Hoover1 1Colorado State University, USA; 2University of Kentucky, USA

Background: While the exact mechanisms of chronic wasting disease (CWD) prion transmission, entry, and trafficking remain incompletely elucidated, transmission by exposure of the oral and/or nasal mucous membranes seems certain. As part of foraging, cervids likely experience minor lesions in the oral mucous membranes; these could have impact on susceptibility to prion entry and subsequent infection.

Objectives: To explore this potential co-factor, we used cervid PrP transgenic mice to assess whether or not micro-abrasions to the tongue may enhance susceptibility to oral CWD infection. Methods: Two sets of FVB mice transgenically expressing the normal cervid PrPC protein [Tg(cerPrP) mice], with or without abrasions on the lingual mucosa, were inoculated orally with 10µl of a 10% w/v brain homogenate from either CWD-positive or negative deer. Abrasions were created by lightly scratching the dorsal lingual epithelium with a 30g needle. Cohorts were sacrificed at 1, 2, 12, 52, 78, and 104 weeks post inoculation (pi) or when signs of neurologic disease were observed. Tongue, lymphoid tissue, and the brain were assessed by western blotting and immunohistochemistry to detect the CWD abnormal prion protein (PrPCWD).

Results: Between 296 and 430 dpi, 8 of the 9 CWD-inoculated mice with lingual lesions developed clinical signs of neurologic dysfunction mandating euthanasia. The brains of all 8 mice were positive by western blot and immunohistochemistry for PrPCWD. Conversely, all mice without oral lesions remain asymptomatic at >450 dpi. No evidence of PrPCWD was detected in any Tg(cerPrP) mice examined at any of the preterminal time points.

Discussion: Micro-abrasions to the lingual surface substantially facilitate CWD transmission, suggesting a co-factor that may be significant in foraging cervids or other species. Earlier post-inoculation sampling intervals (1 and 4 hours) are in progress in an attempt to determine when and where PrPCWD might be detectable after oral mucosal exposure.

P.4.26

Aerosol and intranasal transmission of CWD

Nathaniel Denkers1, Glenn Telling2, Edward Hoover1 1Colorado State University, USA; 2University of Kentucky, USA

Background: Little is known regarding the potential risk posed by aerosolized prions. Chronic wasting disease (CWD) prions are present in saliva and urine of infected animals and it is clearly established that CWD is transmitted horizontally, almost surely by mucosal exposure. However, the potential transmissibility of CWD by aerosol or nasal routes is not known.

Objectives: The present study was therefore designed to determine whether CWD prions are transmissible by these routes of exposure using the cervid PrP transgenic mouse model of CWD infection.

Methods: FVB mice transgenically expressing the normal cervid PrPC protein [Tg(cerPrP) mice] were exposed to CWD prions by either nose-only exposure to an aerosol generated by nebulizing 0.5 ml of a 5% w/v CWD+ brain homogenate or 10µl of a 10% w/v CWD+ brain homogenate by dropwise instillation into the nostrils. Mice were monitored for signs of clinical disease for up to 755 days post inoculation (dpi). Nasal mucosa, vomeronasal organ, lymphoid tissue, and the brain were assessed for PrPCWD by western blotting and immunohistochemistry.

Results: Six of 7 aerosol-exposed Tg(cerPrP) mice developed clinical signs of neurologic dysfunction between 411 and 749 dpi mandating euthanasia. In all symptomatic mice CWD infection was confirmed by histopathologic lesions and detection of PrPCWD within the brain. Two of 9 IN-inoculated Tg(cerPrP) mice also developed TSE between 417 and 755 dpi, again confirmed by PrPCWD detection within the brain. No evidence of PrPCWD was detected in any Tg(cerPrP) mice examined at any of the pre-terminal time points.

Discussion: CWD is transmissible by aerosol as well as intranasal exposure¯potentially implicating exposure via the respiratory system in CWD and potentially other prion diseases. Studies examining very early post-inoculation sampling intervals (1 and 4 hours) are in progress in an attempt to determine initial prion targeting and entry portals.

Transmission and Pathogenesis 115

POSTERS



http://www.prion2009.com/



http://chronic-wasting-disease.blogspot.com/



TSS


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## Michihunter (Jan 8, 2003)

Terry- By chance has anyone tested to find out if the prion can attach itself to vegetation through it's root system? In other words "soak up" the prion and make vegetation itself a potential vector?


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## terry (Sep 13, 2002)

Michihunter said:


> Terry- By chance has anyone tested to find out if the prion can attach itself to vegetation through it's root system? In other words "soak up" the prion and make vegetation itself a potential vector?




there are not many studies that I am aware of, that confirms this. there is one controversial study that brings up questions. sadly, that's all we have had over the past 20 years is more questions than answers. they suspect something, debate if for decades in hopes people will forget, and or until it comes around and finally bites them in the butt. then it's too late, everything is exposed. ...see study below ;



bse tomato seac

i remember a few years back ???

SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the open session of the 91st meeting held on 24th February 2006

56. Members considered that there is no evidence that crops grown on the land which received composted excreta from BSE-challenged animals pose a TSE risk to humans or animals. One member suggested that, as some of these animals are orally challenged with high doses of BSE-infected materials, and the distribution of infectivity in the digestive system is not completely understood, it might be premature to conclude that there is no infective agent in the manure. Furthermore, an unpublished study had indicated low level absorption of PrP from soil by tomato plants although it should be noted that this study had not been repeated. Details of this work would be sent to the SEAC Secretary. Dr Matthews explained that most of the manure from animals challenged with high doses of BSE had already been composted and used for coppicing. Members agreed that the risks from disposal of residual manure from experimental animals would be much less than historic risks of on farm contamination from naturally infected animals at the height of the BSE epidemic.

http://www.seac.gov.uk/minutes/final91.pdf

http://bse-atypical.blogspot.com/2009/01/research-project-detection-of-tse.html

Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer

http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html

Synopsis Transmissible spongiform encephalopathies (TSEs) are a group of incurable diseases likely caused by a misfolded form of the prion protein (PrPSc). TSEs include scrapie in sheep, bovine spongiform encephalopathy ("mad cow" disease) in cattle, chronic wasting disease (CWD) in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and CWD are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity, because PrPSc likely enters soil environments through urinary or alimentary shedding and decomposition of infected animals. In this manuscript, the authors test the potential for soil to serve as a reservoir for PrPSc and TSE infectivity. They demonstrate that PrPSc binds to a variety of soil minerals and to whole soils. They also quantitate the levels of protein binding to three common soil minerals and show that the interaction of PrPSc with montmorillonite, a common clay mineral, is remarkably strong. PrPSc bound to Mte remained infectious to laboratory animals, suggesting that soil can serve as a reservoir of TSE infectivity.

http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.0020032

The cell approach of the potential infectivity of contaminated soil is faster and cheaper than classical animal-based bioassays. Although it suffers from limitations, e.g. it can currently test only a few mouse prion strains, the cell model can nevertheless be applied in its present form to understand how soil composition influences infectivity, and to test prion-inactivating procedures.

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0001069

Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles

Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie McKenzie2, Judd M. Aiken1,2* 1 Program in Cellular and Molecular Biology, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 2 Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 3 Department of Soil Science and Molecular and Environmental Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 4 Biostatistics and Medical Informatics, University of Wisconsin Medical School, Madison, Wisconsin, United States of America

Soil may serve as an environmental reservoir for prion infectivity and contribute to the horizontal transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. Here, we assess the oral infectivity of Mte- and soil-bound prions. We establish that prions bound to Mte are orally bioavailable, and that, unexpectedly, binding to Mte significantly enhances disease penetrance and reduces the incubation period relative to unbound agent. Cox proportional hazards modeling revealed that across the doses of TSE agent tested, Mte increased the effective infectious titer by a factor of 680 relative to unbound agent. Oral exposure to Mte-associated prions led to TSE development in experimental animals even at doses too low to produce clinical symptoms in the absence of the mineral. We tested the oral infectivity of prions bound to three whole soils differing in texture, mineralogy, and organic carbon content and found soil-bound prions to be orally infectious. Two of the three soils increased oral transmission of disease, and the infectivity of agent bound to the third organic carbon-rich soil was equivalent to that of unbound agent. Enhanced transmissibility of soil-bound prions may explain the environmental spread of some TSEs despite the presumably low levels shed into the environment. Association of prions with inorganic microparticles represents a novel means by which their oral transmission is enhanced relative to unbound agent.

Citation: Johnson CJ, Pedersen JA, Chappell RJ, McKenzie D, Aiken JM (2007) Oral transmissibility of prion disease is enhanced by binding to soil particles. PLoS Pathog 3(7): e93. doi:10.1371/journal.ppat.0030093

http://www.aphis.usda.gov/emergency_response/downloads/tools/johnson et al prions in soil.pdf

Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years The persistence of infectious biomolecules in soil constitutes a substantial challenge. This holds particularly true with respect to prions, the causative agents of transmissible spongiform encephalopathies (TSEs) such as scrapie, bovine spongiform encephalopathy (BSE), or chronic wasting disease (CWD). Various studies have indicated that prions are able to persist in soil for years without losing their pathogenic activity. Dissemination of prions into the environment can occur from several sources, e.g., infectious placenta or amniotic fluid of sheep. Furthermore, environmental contamination by saliva, excrements or non-sterilized agricultural organic fertilizer is conceivable. Natural transmission of scrapie in the field seems to occur via the alimentary tract in the majority of cases, and scrapie-free sheep flocks can become infected on pastures where outbreaks of scrapie had been observed before. These findings point to a sustained contagion in the environment, and notably the soil. By using outdoor lysimeters, we simulated a contamination of standard soil with hamster-adapted 263K scrapie prions, and analyzed the presence and biological activity of the soil-associated PrPSc and infectivity by Western blotting and hamster bioassay, respectively. Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.

Article Metrics Related Content Comments: 0 Formal Correction: This article has been formally corrected to address the following errors.

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Abstract Introduction Results Discussion Materials and Methods Acknowledgments Author Contributions References Bjoern Seidel1#*, Achim Thomzig2#, Anne Buschmann3#, Martin H. Groschup3, Rainer Peters1, Michael Beekes2, Konstantin Terytze4

1 Fraunhofer Institute for Molecular Biology und Applied Ecology (IME), Schmallenberg, Germany, 2 P24 -Transmissible Spongiform Encephalopathies, Robert Koch-Institut, Berlin, Germany, 3 Institute for Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Insel Riems, Germany, 4 German Federal Environmental Agency (Umweltbundesamt, UBA), Dessau, Germany

Abstract Top The persistence of infectious biomolecules in soil constitutes a substantial challenge. This holds particularly true with respect to prions, the causative agents of transmissible spongiform encephalopathies (TSEs) such as scrapie, bovine spongiform encephalopathy (BSE), or chronic wasting disease (CWD). Various studies have indicated that prions are able to persist in soil for years without losing their pathogenic activity. Dissemination of prions into the environment can occur from several sources, e.g., infectious placenta or amniotic fluid of sheep. Furthermore, environmental contamination by saliva, excrements or non-sterilized agricultural organic fertilizer is conceivable. Natural transmission of scrapie in the field seems to occur via the alimentary tract in the majority of cases, and scrapie-free sheep flocks can become infected on pastures where outbreaks of scrapie had been observed before. These findings point to a sustained contagion in the environment, and notably the soil. By using outdoor lysimeters, we simulated a contamination of standard soil with hamster-adapted 263K scrapie prions, and analyzed the presence and biological activity of the soil-associated PrPSc and infectivity by Western blotting and hamster bioassay, respectively. Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.

http://www.plosone.org/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000435

also see ;

http://chronic-wasting-disease.blogspot.com/2009_01_01_archive.html

http://chronic-wasting-disease.blogspot.com/



kind regards,
terry


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## Michihunter (Jan 8, 2003)

So can I understand this as to say that it hasn't been tested thoroughly enough to base a conclusion on that possibility? I find that to be preposterous if that's the case. One would think that due to the nature of the prion itself being in a protein state that it would have been exhaustedly tested to ensure that it does/doesn't infect vegetation and indirectly the wildlife that consumes it.


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## e. fairbanks (Dec 6, 2007)

Colorado State Awarded $2.5 Million NSF Grant to Study Prevalence and Spread of CWD-Sept. 9, 2009
http://www.cwd-info.org/index.php/fuseaction/news.detail.ID/67f401d29cd6f3411c29acf
"In this NSF funded project, CSU scientists will model the impact of CWD on deer populations in an effort to better understand dynamics of transmission"


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