# Deer-scent ban aims to prevent wasting disease



## Hamilton Reef (Jan 20, 2000)

Deer-scent ban aims to prevent wasting disease

http://www.hfxnews.ca/index.cfm?sid=25012&sc=89

04/25/07 BETH JOHNSTON

Nova Scotia hunters will have to leave their deer pee at home.

In an effort to stop the contagious, lethal Chronic Wasting Disease from hitting Nova Scotia deer and elk, the Department of Natural Resources is banning the use of deer scents that contain bodily fluid.

Chronic wasting disease - a transmissible neurological disease of deer and elk-is a very serious problem in Western Canada and parts of the United States, said Natural Resources wildlife director Barry Sabean.

"We don't have it and we don't want it," he said.

CWD, which is similar to mad cow disease in cattle, produces small lesions in brains of infected animals. Affected animals rapidly lose weight and act strangely before death.

The disease has been diagnosed in commercial game farms in several states and provinces where the products originate. There are no regulations on the imported scents, which hunters can purchase at WalMart and Canadian Tire.

Hunters often soak cotton balls in the urine from a doe in heat to attract bucks.

Hunter Roger Lewis said the ban makes perfect sense.

"I don't think there's going to be a huge uproar about it," he said, adding hunters have been ahead of the government on the CWD issue.

"Most of the hunters in the know will support it, I'd bet you my last dollar that's where the idea (to ban the product) came from."

Hunters are still free to use deer scents of apple or acorn.


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## answerguy8 (Oct 15, 2001)

Never thought of the dangers of deer pee. You might want to sell your stock in any company that makes that.


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## jimmy johans (Feb 19, 2007)

extensive tests have been done looking for cause of transmission of CWD. Deer pee never even a factor although it has been looked at.


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## WAUB-MUKWA (Dec 13, 2003)

Make your own synthetic pee.
1/2 part 12-12-12 fertilizer
1 part ammonia
1 part salt
4 parts water

instant pee


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## sadocf1 (Mar 10, 2002)

Terry posted this thread 4/27/07- there were 323 views


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## One Eye (Sep 10, 2000)

sadocf1 said:


> Terry posted this thread 4/27/07- there were 323 views


That's because the majority of hunters in this state could care less about CWD since it is "not in their backyard". It is scary what it will take to get their attention.

Dan


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## William H Bonney (Jan 14, 2003)

This should make deer hunting real easy in Canada now. Instead of planting yourself over a baitpile,, just park yourself right next to the "restrooms",, they gotta go sometime.  


Seriously,, this is one of the more absurd things I've heard. If CWD was linked to deer pee,, don't you think CWD would be EVERYWHERE by now and would literally be NO WAY to stop it.


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## Airoh (Jan 19, 2000)

William H Bonney said:


> This should make deer hunting real easy in Canada now. Instead of planting yourself over a baitpile,, just park yourself right next to the "restrooms",, they gotta go sometime.
> 
> 
> Seriously,, this is one of the more absurd things I've heard. If CWD was linked to deer pee,, don't you think CWD would be EVERYWHERE by now and would literally be NO WAY to stop it.


CWD "IS" spreading everywhere as we speak. 
And there is as of right now... NO WAY to stop it.

This disease is hurdling many hundreds of miles across the US and the common link is a game farm nearby when it shows up.


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## terry (Sep 13, 2002)

DEER URINE ALERT
CWD prions can be shed in the urine of infected deer. Commercial deer lures are commonly formulated from urine collected from captive deer. If that captive herd becomes infected with CWD, this disease could conceivably be spread to wild deer when hunters apply deer lures to vegetation or the ground.

Since commercial deer lures are not currently tested for CWD prions, deer hunters everywhere should take the following precautions.

Do not place urine-based deer lures on your boots or clothing where they can contact the ground. 
Do not place urine-based deer lures directly on the ground or on vegetation within reach of deer. 
A safer alternative is to place the lure on a cotton ball and hang it out of reach where air currents can circulate the odor to deer.


http://www.samcef.org/cwdalert100705.htm


Date: 6 May 2002
From: ProMED-mail <[email protected]
Source: National Post [edited]
<http://www.nationalpost.com/news/national/story.html?f=/stories/20020506/13
3605.html>


Canada: Deer hunters could be spreading lethal germs
Illness related to mad cow disease, experts say
--------------------------------------------------------
CALGARY - Hunters may be unwittingly spreading Chronic Wasting Disease (CWD)
by using deer scents made from the urine of infected animals in game farms,
some scientists and hunting advocates fear.

The packaged scents, spread on the ground by hunters to lure quarry, could
contain prions, the resilient agent scientists blame for CWD, an illness
related to mad cow disease that is associated with animals in fenced game
farms.

Although the link between deer scents and CWD has not been studied, several
experts say there is a "theoretical risk" that CWD could be spread by the
deer attractants.

Rob Miskosky, editor of Alberta Outdoorsmen, says some game farmers are
packaging deer scents to diversify in an industry tainted by outbreaks of
CWD and reeling from bans on shooting captive animals and collapsed Asian
markets for elk antler velvet. One consortium of Alberta game farmers is
constructing a facility capable of collecting 1000 ounces of urine a day
from deer.

Norm Moore, a game farmer and industry spokesman, dismisses the concerns,
saying the industry is strictly monitored for disease. "We have an
identification and tracking system that is second to none in agriculture,"
he said.

Although packaged scents are not tested for safety, Mr. Moore says health
precautions undertaken by game ranchers make it unlikely any disease would
be associated with the packaged urine. "I don't think there are any
regulations specifically for that product, but [game farm] herds would have
to be on the normal health program or they couldn't have the animals," Mr.
Moore said.

Darrel Rowledge, director of the advocacy group Alliance for Public
Wildlife, says it is astonishing such products, which have been used by
hunters for decades, are released into the marketplace untested. Hunters
spread the scents, made from a combination of urine and feces, on their
boots and clothing and on trees, branches, rock, grasses and the ground.

Mr. Miskosky, writing in the current edition of Alberta Outdoorsmen, says
scientific journals confirm TSE prions, the mutant protein causing CWD, have
been found in urine long before the disease is detected in animals and could
remain viable in soil for years. Destroying the prions requires incineration
of an infected animal in temperatures higher than 600 Celsius.

The Canadian Food Inspection Agency (CFIA) is investigating 1 case of CWD in
Alberta. Dr. George Luterbach, a CFIA veterinarian, said all 72 animals on
the infected farm will be destroyed and a compensation package is being
worked out with the rancher. In Saskatchewan, about 8000 elk from game farms
were destroyed last year after an outbreak of the disease, which was
confirmed in more than 200 animals.

The cost to federal taxpayers of controlling the Saskatchewan outbreak has
been estimated by one animal rights group at $60 million [Canadian],
including compensation to the affected game farmers.

Dr. Luterbach said the agency is also waiting for lab test results on 12
animals from the infected Alberta farm that were sold to other game
ranchers. If the tests come back positive, it is likely all the animals on
the other farms will also be destroyed, he said.

The game farming industry says it is unfairly blamed for CWD. Mr. Moore says
the disease started in the wild in Colorado, spread into a zoo and was then
passed into captive herds when a stricken zoo animal was sold to a game
farm, where it spread among the contained herd. The industry's stringent
testing makes it a lightning rod for CWD because its detection system is
unmatched by public wildlife administrators, he said.

Game farmers sell the meat of wild game such as deer and elk -- which is low
in fat and cholesterol -- to restaurants.

--
ProMED-mail
<[email protected]>

[There are tests that clearly detect prions in urine. So although this is a
theoretical risk, it stands to reason the scents utilizing feces and urine
may be able to spread the disease. There is research indicating prions may
be in saliva, and survive the gastrointestinal track, which suggests
credibility for prions in feces. This may be a theoretical risk at the
moment, but it clearly points to an area where research is lacking. -
Mod.TG]




Subject: Infectious Prions in the Saliva and Blood of Deer with Chronic
Wasting Disease
Date: October 5, 2006 at 1:45 pm PST


Infectious Prions in the Saliva

and Blood of Deer with Chronic

Wasting Disease


Candace K. Mathiason,1 Jenny G. Powers,3 Sallie J. Dahmes,4 David A.
Osborn,5 Karl V. Miller,5

Robert J. Warren,5 Gary L. Mason,1 Sheila A. Hays,1 Jeanette Hayes-Klug,1
Davis M. Seelig,1

Margaret A. Wild,3 Lisa L. Wolfe,6 Terry R. Spraker,1,2 Michael W. Miller,6
Christina J. Sigurdson,1

Glenn C. Telling,7 Edward A. Hoover1*


A critical concern in the transmission of prion diseases, including chronic
wasting disease (CWD)

of cervids, is the potential presence of prions in body fluids. To address
this issue directly, we

exposed cohorts of CWD-nai¨ve deer to saliva, blood, or urine and feces from
CWD-positive deer.

We found infectious prions capable of transmitting CWD in saliva (by the
oral route) and in blood

(by transfusion). The results help to explain the facile transmission of CWD
among cervids and

prompt caution concerning contact with body fluids in prion infections.


SNIP...


Deer cohorts 1 (blood), 2 (saliva), and 3

(urine and feces) were electively euthanized at

18 months pi to permit whole-body examination

for PrPCWD. The greatest scrutiny was directed

toward those tissues previously established

to have highest frequency of PrPCWD deposition

in infected deer and generally regarded

as the most sensitive indicators of infection-

medulla oblongata and other brainstem regions,

tonsil, and retropharyngeal lymph node. We

found unequivocal evidence of PrPCWD in brain

and lymphoid tissue of all six tonsil biopsy-

positive deer in cohorts 1 (blood) and 2 (saliva),

whereas all deer in cohorts 3 and 5 were negative

for PrPCWD in all tissues (Table 2 and

Figs. 1 and 2).

The transmission of CWD by a single blood

transfusion from two symptomatic and one

asymptomatic CWDþ donor is important in at

least three contexts: (i) It reinforces that no tissue

from CWD-infected cervids can be considered

free of prion infectivity; (ii) it poses the

possibility of hematogenous spread of CWD,

such as through insects; and (iii) it provides a

basis for seeking in vitro assays sufficiently

sensitive to demonstrate PrPCWD or alternate

prion protein conformers in blood-one of the

grails of prion biology and epidemiology.

The identification of blood-borne prion

transmission has been sought before with mixed

results (9-11). Bovine spongiform encephalopathy

and scrapie have been transmitted to naBve

sheep through the transfer of 500 ml of blood

or buffy coat white blood cells from infected

sheep (12, 13). In addition, limited but compelling

evidence argues for the transmission of variant

Creutzfeldt-Jakob disease (vCJD) through blood

from asymptomatic donors (14-16). Even in

sporadic CJD, PrPres has been found in periph-

eral organs of some patients (17). The present

work helps establish that prion diseases can be

transmitted through blood.

The presence of infectious CWD prions in

saliva may explain the facile transmission of

CWD. Cervid-to-cervid interactions (SOM text),

especially in high density and captive situations,

would be expected to facilitate salivary crosscontact

(11, 18, 19). Salivary dissemination of

prions may not be limited to CWD. Proteaseresistant

prion protein has been demonstrated in

the oral mucosa, taste buds, lingual epithelium,

vomeronasal organ, and olfactory mucosa of

hamsters infected with transmissible mink

encephalopathy (19) and ferrets infected with

CWD (20). Although no instance of CWD

transmission to humans has been detected, the

present results emphasize the prudence of using

impervious gloves during contact with saliva or

blood of cervids that may be CWD-infected.

Environmental contamination by excreta

from infected cervids has traditionally seemed

the most plausible explanation for the dissemination

of CWD (21). However, we could not

detect PrPCWD in cohort 3 deer inoculated repeatedly

with urine and feces from CWDþ deer and examined up to 18 months pi (Table
2).

There are several reasons to view this negative

finding cautiously, including small sample size,

elective preclinical termination, and potential

variation in individual susceptibility that may

be associated with the 96 G/S polymorphism in

the PRNP gene (7, 22). Although no genotype

of white-tailed deer is resistant to CWD infection,

PRNP genotypes S/S or G/S at codon 96

appear to have reduced susceptibility manifest

by longer survival (7). Both deer in cohort 3

(urine and feces) were subsequently shown to

be of the PRNP 96 G/S genotype. Thus, it is

possible, although we think unlikely, that these

deer had a prolonged incubation period (918

months pi) before the amplification of PrPCWD

became detectable in tissues. Recent studies

have shown that PrPres is poorly preserved

after incubation with intestinal or fecal content

(23, 24). Further research using cervid and surrogate

cervid PrP transgenic mice (25) are indicated

to continue to address the presence of

infectious CWD prions in excreta of CWDþ deer and to provide a more
substantial basis for

reconsideration of the assumption that excreta

are the chief vehicle for CWDdissemination and

transmission.

The results reported here provide a plausible

basis for the efficient transmission of CWD in

nature. We demonstrate that blood and saliva in

particular are able to transmit CWD to naBve deer

and produce incubation periods consistent with

those observed in naturally acquired infections

(3, 26). The time from exposure to first detection

of PrPCWD by tonsil biopsy was variable-as

short as 3 months but as long as 18 months (likely

underestimates due to sampling frequency).

The results also reinforce a cautious view of the

exposure risk presented by body fluids, excreta,

and all tissues from CWDþ cervids. ...



SNIP...END


http://www.sciencemag.org/cgi/content/abstract/314/5796/133


Research

Environmental Sources of Prion Transmission in Mule Deer
Michael W. Miller,* Elizabeth S. Williams, N. Thompson Hobbs, and Lisa L. Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; University of Wyoming, Laramie, Wyoming, USA; and Colorado State University, Fort Collins, Colorado, USA

Suggested citation for this article: Miller MW, Williams ES, Hobbs NT, Wolfe LL. Environmental sources of prion transmission in mule deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm


--------------------------------------------------------------------------------

Whether transmission of the chronic wasting disease (CWD) prion among cervids requires direct interaction with infected animals has been unclear. We report that CWD can be transmitted to susceptible animals indirectly, from environments contaminated by excreta or decomposed carcasses. Under experimental conditions, mule deer (Odocoileus hemionus) became infected in two of three paddocks containing naturally infected deer, in two of three paddocks where infected deer carcasses had decomposed in situ &#8776;1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier. Indirect transmission and environmental persistence of infectious prions will complicate efforts to control CWD and perhaps other animal prion diseases.

http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm


Perspective

Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams, Michael W. Miller, Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; University of Wyoming, Laramie, Wyoming, USA; Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


--------------------------------------------------------------------------------

Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.

snip...

Conclusions
The lack of evidence of a link between CWD transmission and unusual cases of CJD, despite several epidemiologic investigations, and the absence of an increase in CJD incidence in Colorado and Wyoming suggest that the risk, if any, of transmission of CWD to humans is low. Although the in vitro studies indicating inefficient conversion of human prion protein by CWD-associated prions raise the possibility of low-level transmission of CWD to humans, no human cases of prion disease with strong evidence of a link with CWD have been identified. However, the transmission of BSE to humans and the resulting vCJD indicate that, provided sufficient exposure, the species barrier may not completely protect humans from animal prion diseases. Because CWD has occurred in a limited geographic area for decades, an adequate number of people may not have been exposed to the CWD agent to result in a clinically recognizable human disease. The level and frequency of human exposure to the CWD agent may increase with the spread of CWD in the United States. Because the number of studies seeking evidence for CWD transmission to humans is limited, more epidemiologic and laboratory studies should be conducted to monitor the possibility of such transmissions. Studies involving transgenic mice expressing human and cervid prion protein are in progress to further assess the potential for the CWD agent to cause human disease. Epidemiologic studies have also been initiated to identify human cases of prion disease among persons with an increased risk for exposure to potentially CWD-infected deer or elk meat (47). If such cases are identified, laboratory data showing similarities of the etiologic agent to that of the CWD agent would strengthen the conclusion for a causal link. Surveillance for human prion diseases, particularly in areas where CWD has been detected, remains important to effectively monitor the possible transmission of CWD to humans. Because of the long incubation period associated with prion diseases, convincing negative results from epidemiologic and experimental laboratory studies would likely require years of follow-up. In the meantime, to minimize the risk for exposure to the CWD agent, hunters should consult with their state wildlife agencies to identify areas where CWD occurs and continue to follow advice provided by public health and wildlife agencies. Hunters should avoid eating meat from deer and elk that look sick or test positive for CWD. They should wear gloves when field-dressing carcasses, bone-out the meat from the animal, and minimize handling of brain and spinal cord tissues. As a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified.

Acknowledgments

http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


TSS


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## FREEPOP (Apr 11, 2002)

I had thought about this and even discussed it on here. I haven't used the stuff in years and now i have a better reason not too. The ultimate cost is too great and I'd rather error on the side of caution. CWD is scary stuff, once it's in the ground, it there and animals reintroduced will get it. Think about it in those terms, and then when humans start contacting it in large amounts :yikes:


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## sadocf1 (Mar 10, 2002)

It has been demonstrated that the causitive agent for CWD is found in the saliva and urine of CWD diseased cervids. We can assume that the agent is present in the blood as that is the only way it can be present in urine. A certain amount of blood remains in de-boned venison from states and provinces where CWD is found in the wild. Here in Michigan perhaps as concerned hunters we should require a negative CWD test of hunter killed cervid carcasses (or parts) imported from states or provinces where CWD is found in the wild.


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## FREEPOP (Apr 11, 2002)

sadoc1, did they ever figure out what happened in Colorado? (I never did see or hear the determination)

For those not in the know, the deer that had CWD in an enclosure where euthanized. Then the pen was sterilized and new deer put in. THe new deer got CWD also. The was concern about it being in the soil and/or other hypothosis.


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## terry (Sep 13, 2002)

a new study out on scrapie in soil with disturbing outcome ;


Subject: Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route
after Persistence in Soil over Years
Date: May 16, 2007 at 10:01 am PST

PLoS ONE. 2007; 2(5): e435.
Published online 2007 May 9. doi: 10.1371/journal.pone.0000435.
Copyright Seidel 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.

Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after
Persistence in Soil over Years

Bjoern Seidel,#1* Achim Thomzig,#2 Anne Buschmann,#3 Martin H. Groschup,3
Rainer Peters,1 Michael Beekes,2 and Konstantin Terytze4
1Fraunhofer Institute for Molecular Biology und Applied Ecology (IME),
Schmallenberg, Germany
2P24 -Transmissible Spongiform Encephalopathies, Robert Koch-Institut,
Berlin, Germany
3Institute for Novel and Emerging Infectious Diseases,
Friedrich-Loeffler-Institut, Insel Riems, Germany
4German Federal Environmental Agency (Umweltbundesamt, UBA), Dessau, Germany
Joseph El Khoury, Academic Editor
Massachusetts General Hospital & Harvard Medical School, United States of
America
#Contributed equally.
* To whom correspondence should be addressed. E-mail:
[email protected]
Conceived and designed the experiments: MB AT MG AB BS RP KT. Performed the
experiments: AT AB BS RP. Analyzed the data: MB AT MG AB BS RP KT.
Contributed reagents/materials/analysis tools: MB AT. Wrote the paper: MB AT
MG AB BS KT.
Received March 21, 2007; Accepted April 18, 2007.


Abstract

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.



snip...


Discussion


The results of this research project show for the first time that
the scrapie strain 263K remains persistent in soil over a period of at least
29 months and remains highly infectious after oral application to Syrian
hamsters. It has to be pointed out that the key results of our time-course
study on the fate of PrPSc in soil have been validated, in part by examining
blinded samples, at independent laboratories.

Only a few studies have addressed the question of a persistence of prions in
soil so far [24][26], [47], and the results from these studies are in
principle in accordance with our observations. A pioneering study was
published by Brown and Gajdusek in 1991 [24] showing that an aqueous extract
from scrapie-contaminated soil remains infectious even after an incubation
period of three years as confirmed by hamster bioassay. However, the
infectivity studies were conducted by intracerebral injection and not by
oral application. Furthermore, the PrPSc concentration was not analyzed in
this study, so that no data are available about the proteins absorption
behavior to soil particles and about the corresponding degradation kinetics.
Most recently, PrPSc has been shown to bind to soil minerals [25] but only
short-time incubation experiments of maximal one week were conducted and,
again, bioassays were performed by the intracerebral route.

In this study we show by Western blotting a strong decrease in the amount of
extractable PrPSc over an incubation period of 29 months in soil. It is not
yet clear whether this decrease resulted from a molecular degradation of
PrPSc or a tighter binding to soil particles. Stronger binding of molecules
to soil particles with increasing incubation time is a well-known phenomenon
in soil chemistry  the so called aging  and influences bioavailability
and re-mobilization significantly [48], [49].

Upon feeding hamsters with scrapie contaminated soil which had been
incubated for over two years in outdoor lysimeters all animals developed
terminal scrapie after relatively short incubation times (162 dpi). In other
studies it has been well established that pure 10% (w/v) brain homogenates
from 263K scrapie hamsters cause terminal scrapie in perorally challenged
hamsters after mean incubation times of about 155165 days with an attack
rate of 100% [50][53]. This indicates that scrapie-contaminated soil may
represent a potential TSE hazard for ruminants in the environment. While a
considerable excretion of infectivity has to be assumed for scrapie or BSE
infected sheep and CWD infected deer [40], [43], [54], it is generally
acknowledged that the potential environmental contamination risk represented
by BSE infected cattle is marginal, if at all present [41], [42]. On the
other hand, the burial of bovine carcasses [44] might have accidentally led
to a spill of BSE prions into the environment. Furthermore, the fact that
even feeding of aqueous extracts from scrapie-contaminated soil induced a
terminal scrapie infection in four hamsters so far suggests that surface
water or groundwater from pastures of scrapie-affected flocks may provide a
potential source of scrapie infectivity.

However, the relevance of the results obtained in this study for the field
situation should be interpreted with some caution, since only one soil type
was used and only a limited number of animals were challenged in the
bioassay. Therefore, other soil types and a larger number of animals have to
be tested in future studies to allow for a robust risk assessment.
Furthermore the exact binding properties and degradation kinetics of PrPSc
should be subject to further research. In addition, all published studies
addressing the persistence of prion infectivity in soil were performed with
scrapie prions while TSE agents causing BSE and especially CWD have not been
analyzed so far.

An intensified monitoring of PrPSc (and possibly also prion infectivity) in
the soil appears mandatory for a more precise assessment of the risks
emanating for humans and animals from prions in the environment. As shown in
this report, PrPSc extracted from soil can be used as a catalytically active
seed in the protein misfolding cyclic amplification (PMCA) reaction. This
opens a promising perspective for considerably improving the detectability
of prions in the environment.


snip...

for anyone interested in the full text of this article ;


http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1855989#pone.0000435-Prusiner1


http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&blobtype=pdf&artid=1855989


TSS


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## terry (Sep 13, 2002)

J. Virol. doi:10.1128/JVI.00635-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.


EFFICIENT IN VITRO AMPLIFICATION OF CHRONIC WASTING DISEASE PrPRES 

Timothy D. Kurt, Matthew R. Perrott, Carol J. Wilusz, Jeffrey Wilusz, Surachai Supattapone, Glenn C. Telling, Mark D. Zabel, and Edward A. Hoover* 
Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University; Department of Biochemistry, Dartmouth Medical School, Department of Molecular Biology and Genetics, University of Kentucky



* To whom correspondence should be addressed. Email: [email protected]. 


Abstract 


Chronic wasting disease (CWD) of cervids is associated with conversion of the normal cervid prion protein, PrPC, to a protease-resistant conformer, PrPCWD. Here we report use of both non-denaturing amplification and protein-misfolding cyclic amplification (PMCA) to amplify PrPCWD in vitro. Normal brain from deer, transgenic mice [Tg(cerPrP)1536] expressing cervid PrPC, and ferrets supported amplification. PMCA using Tg(cerPrP)1536 normal brain as PrPC substrate produced amplification of >6.5 x 109-fold after six rounds. Highly efficient in vitro amplification of PrPCWD is a significant step toward detection of PrPCWD in body fluids or excreta of CWD-susceptible species.

http://jvi.asm.org/cgi/content/abstract/JVI.00635-07v1?papetoc


TSS


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## FREEPOP (Apr 11, 2002)

Thanks Terry, a wealth of info.


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## terry (Sep 13, 2002)

FREEPOP said:


> sadoc1, did they ever figure out what happened in Colorado? (I never did see or hear the determination)
> 
> For those not in the know, the deer that had CWD in an enclosure where euthanized. Then the pen was sterilized and new deer put in. THe new deer got CWD also. The was concern about it being in the soil and/or other hypothosis.




Epidemiology of Chronic Wasting Disease in Captive White-Tailed
and Mule Deer
Michael W. Miller1,3 and Margaret A. Wild1,2 1 Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, Colorado 80526-2097, USA; 2 Current address: National Park Service, Biological
Resource Management Division, 1201 Oak Ridge Drive, Suite 200, Fort Collins, Colorado 80525, USA; 3 Corresponding
author (email: [email protected])
ABSTRACT: The natural occurrence of chronic
wasting disease (CWD) in a 1993 cohort of captive
white-tailed deer (Odocoileus virginianus)
afforded the opportunity to describe epidemic
dynamics in this species and to compare dynamics
with those seen in contemporary cohorts
of captive mule deer (O. hemionus) also
infected with CWD. The overall incidence of
clinical CWD in white-tailed deer was 82%
(nine of 11) among individuals that survived
.15 mo. Affected white-tailed deer died or
were killed because of terminal CWD at age
4976 mo (x¯559.6 mo, SE53.9 mo). Epidemic
dynamics of CWD in captive white-tailed deer
were similar to dynamics in mule deer cohorts.
Incidence of clinical CWD was 57% (4/7)
among hand-raised (HR) and 67% (4/6) among
dam-raised (DR) mule deer; affected HR mule
deer succumbed at 64286 mo of age (x¯572
mo; SE55 mo), and affected DR mule deer
died at age 3158 mo (x¯541.3 mo; SE56.1
mo). Sustained horizontal transmission of
CWD most plausibly explained epidemic dynamics,
but the original source of exposures
could not be determined. Apparent differences
in mean age at CWD-caused death among
these cohorts may be attributable to differences
in the timing or intensity of exposure to CWD,
and these factors appear to be more likely to
influence epidemic dynamics than species differences.
It follows that CWD epidemic dynamics
in sympatric, free-ranging white-tailed
and mule deer sharing habitats in western
North American ranges also may be similar.


snip...


Captive mule deer held in what is now
the FWRF had been infected with CWD
since at least the late 1960s (Williams and
Young, 1992). After attempting to eradicate
CWD from the FWRF in 1985 by
killing all captive mule deer and elk and
cleaning the facility (Williams and Young,
1992; Miller et al., 1998), a new mule deer
research herd was started in 1990 with
nine animals (Miller and Williams, 2003).
This founder herd was augmented by natural
births and orphan fawns. Founders
and orphans were accepted only from outside
areas where CWD was known to be
endemic. Despite extensive preventive
measures, a case of CWD was diagnosed
in 1994 in a FWRF-born female from the
1991 cohort. This represented the beginning
of another CWD epidemic in captive
mule deer (Fig. 1), 8.5 yr after the last
infected deer had lived at FWRF.
White-tailed deer had not been held at
the FWRF site before 1993. In MayJune
1993, 12 newborn white-tailed deer fawns
were captured by hand from the Rocky
Mountain Arsenal National Wildlife Refuge,
a fenced enclosure where surveys
conducted since 1993 have revealed no evidence
of CWD in resident deer populations
(Creekmore et al., 1999; Miller et al.,
2000; Miller and Williams, 2003; M. W.
Miller, unpubl.). After capture, fawns were
transported to FWRF. There, they were
held in dedicated rearing pens on the facilitys
east side, away from adult cervids.
Fawns were fed canned evaporated milk,
a pelleted feed, and alfalfa hay, using wellestablished
rearing protocols (Wild and
Miller, 1991). Eleven of 12 fawns (six females,
two males, and three castrated
males) survived until weaning, at which
time they were moved to a new paddock
(W) on the facilitys west side (Fig. 2A).
This new paddock, which had an electri-
fied perimeter fence, was in proximity to
other new deer paddocks and to older
paddocks but had not previously held deer
or elk. Weaned deer were maintained on
pelleted feed, alfalfa hay, and natural veg
etation consisting of forbs and grasses;
their diet was free from animal-derived
protein. Once they were sexually mature
(.12 mo old), the two males were moved
into an adjacent paddock (A) during November
February each year, to prevent
breeding with females; this adjacent paddock
housed intact and castrated male
mule deer year round. Aside from occasional
research-related movements to handling
and weighing facilities and isolation
pens, female and castrated male whitetailed
deer resided in their primary paddock
throughout their respective lives.
Clinical signs suggestive of CWD
(weight loss, inattentiveness, and mild depression)
were first recorded in one male
and one castrated male white-tailed deer
in May 1997. By late June, both deer were
showing signs of end-stage CWD (emaciation,
pronounced behavioral changes,
ataxia, and ptyalism; Fig. 3), and both were
killed on 8 July. The other male began
showing clinical signs in late June; his condition
deteriorated rapidly, and he was
killed on 23 July after exhibiting an acute
onset of neurological signs, including opisthotonos.
A fourth deer, a female, was
found dead on 27 July after several days
of heavy rain and flooding at the FWRF;
CWD was diagnosed postmortem. In retrospect,
early signs of CWD (particularly
social isolation) had been present in this
fourth animal for ;1 mo. Four additional
deer were killed during end-stage CWD 9,
11, 23, and 26 mo after the index cases
(Fig. 4). By October 1999, because only
three white-tailed deer remained in the
herd, and one was showing signs of CWD,
the surviving deer were killed.
Chronic wasting disease was confirmed
in all nine clinical cases via histopathology
and immunohistochemistry (IHC), using
methods described elsewhere (Williams
and Young, 1993; Spraker et al., 1997;
Miller et al., 2000). Accumulations of
CWD-specific protease-resistant prion
protein (PrPCWD) were detected in multiple
sections of brain (particularly the medulla
oblongata, sectioned at the obex), in
tonsil, retropharyngeal lymph node, and
mesenteric lymph node tissues, and in
Peyers patches. Histological lesions of
spongiform encephalopathy described by
pathologists who evaluated these cases
were indistinguishable from those described
in free-ranging white-tailed deer
(Spraker et al., 1997; Williams and Miller,
2002); plaques composed of PrPCWD were
relatively consistent among these cases ....


PLEASE SEE FULL TEXT ;

http://wildlife.state.co.us/NR/rdonlyres/C82EB818-90C6-4D85-897E-9CE279546CCB/0/JWDEpiCWD.pdf


(13) CHRONIC WASTING DISEASE IN ELK (CERVUS ELAPHUS NELSONI)
HELD IN A CWD ENDEMIC FACILITY.
ELIZABETH S. WILLIAMS, Department of Veterinary Sciences, University of
Wyoming, Laramie, WY 82070; WALTER E. COOK, HANK EDWARDS, TERRY
KREEGER, Wyoming Game and Fish Department, Research Laboratory, Laramie, WY
82071; and SCOTT SMITH, Wyoming Game and Fish Department, Pinedale, WY
82941.
Fifty-seven female elk calves were captured on the National Elk Refuge, Teton County,
Wyoming in February, 1995 and transported to the Sybille Wildlife Research and
Conservation Education Unit near Wheatland, Wyoming. Chronic wasting disease
(CWD) is endemic in deer and elk in this facility. Chronic wasting disease has never been
diagnosed in the Jackson Herd and tests of over 700 harvested adult elk have been
negative. The elk calves were involved in a study of the efficacy of Brucella abortus
strain RB51 vaccine; 33 were vaccinated by hand or ballistic implant. They were held in
groups according to vaccination status in paddocks that had been used to house cervids
for many years. These elk were not known to have had direct contact with elk or deer
with CWD, though fence-line contact was possible. Between 19 and 28 months after
moving into the facility, five elk developed clinical CWD. These animals had spongiform
encephalopathy and were positive for accumulation of PrPres in the brain by
immunohistochemistry. As part of the vaccination trial protocol, the remaining elk were
necropsied 27 to 31 months after moving to Sybille. Three of these elk had spongiform
encephalopathy and were positive for PrP by immunohistochemistry and an additional
three elk were positive by immunohistochemistry alone. Of the 54 elk that lived for 1
year or more after introduction into the research facility, 11 (20%) developed clinical or
subclinical CWD within 31 months. Exposure to the CWD prion apparently was only
from environmental sources or possible fence- line contact with affected cervids.


======================================


(14) MECHANISMS FOR CHRONIC WASTING DISEASE TRANSMISSION:
CLUES FROM INFORMATION-BASED COMPARISON OF COMPETING
TRANSMISSION MODELS.
MICHAEL W. MILLER, Colorado Division of Wildlife, Wildlife Research Center, Ft.
Collins, CO.
Chronic wasting disease (CWD), a transmissible spongifom encephalopathy (TSE),
occurs naturally in both captive and free-ranging deer (Odocoileus spp.) and elk (Cervus
elaphus nelsoni). Although CWD is clearly a transmissible disease, mechanisms
underlying its natural transmission remain undescribed. I used information-based model
selection methods to compare four models for CWD transmission in mule deer (O.
hemionus): maternal (dam-offspring) transmission; direct (lateral) transmission without
latency; direct transmission with latency; and indirect (environmental) transmission with
latency. Cumulative numbers of CWD cases forecast by each model were compared to an
epidemic curve from a naturally-infected captive mule deer herd (n = 84 individuals)
maintained by the Colorado Division of Wildlife between June 1992 and May 2000. I
constrained parameter ranges and obtained maximum likelihood estimates of relevant
parameters, then compared performance of respective models using Akaike's information
criterion adjusted for small sample size (AICc). Of the models compared, the indirect
transmission with latency model was strongly supported by epidemic data from captive
mule deer (wr = 0.883). The direct transmission with latency model was only marginally
supported by observed data (DAICc = 4.05, wr = 0.117), and the other two models
enjoyed essentially no support from the data (wr * 3*10-7). Based on these findings,
there appears to be a strong possibility that indirect transmission of CWD via
contaminated environments occurs. It follows that indirect transmission should be
considered in developing disease management strategies for both captive and freeranging
cervids.





http://www.wildlifedisease.org/Documents/Proceedings/Wyoming_00.pdf


TSS


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## sadocf1 (Mar 10, 2002)

Here in the TBIZ of N.E Michigan's lower penninsula baiting and feeding of our wild deer has been banned ?? Baiting and feeding continues unabated.
Hunters will continue to use every available method or resource (LEGAL OR ILLEGAL) to prove that they are smarter than their quarry. We are only human. Our DNR is of course aware of the baiting and feeding and writes a few citations, mostly on state land. When the TB Eradication Program fails to show the desired effects they can point to the private land owners and hunt clubs where these banns are largely ignored and say "it's not our fault"
If and when CWD is found in our wild deer, the deer farmers will recieve the credit for its introduction, not the hunters who bring back deer elk carcasses (or parts) from CWD infected states and provinces


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## sadocf1 (Mar 10, 2002)

TB or should we say the fuss about XDRTB has all but dominated the news media for the past 3 weeks. On the Internet the Center for Disease Control and Prevention, CDC, provides us with the whole story in all the gory details.However, altho great concern for the health of the other airline passengers is shown by all the TB xperts one would expect that his bride would be the one to be more likely to contract the disease as she certainly would be subject to more exposure.
This is, of course, mycobacterium Tuberculosis, the human type. Others are the avian and bovine types of TB, found in our cattle and wildlife.
One third of the human population, 2,000,000 people ,are infected with latent non-infectious TB. 10 %, 200,000 may become diseased, capable of spreading the infection. TB is perhaps one of the oldest of diseases, and it will be with us for a long, long time. We now have XDR TB We have no live animal test for TB. We have no effective vaccine for TB, human or animal. Our USDA/MDA TB Eradication Program is 90 years old. When Bovine TB was found in our states cattle,(8 YEARS AGO) the USDA APHIS VS administrator assured us that Bovine TB would be eradicated from the United States in 2 years


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## s&a smolen (Feb 20, 2005)

Ok I have some questions? Bovine. tincture's. What about the animals that make the urine? In a state like Michigan .Ok Go on post some one's half -study.Not in Michigan we can't even agree on baiting.


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