#1915519 - 05/07/10 07:51 AM
Re: Chronic Wasting disease (CWD)
[Re: bowriter]
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BSK
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BSK-Explain what you mean by new disease? What time span defines "new disease"? I personally have known about it for over 40 years. I am convinced it has been around for well over 100 years. Does that make me "new"? 
CWD-like diseases have been around, especially in sheep and possibly in cattle, for much of recorded history. However, the disease jumping the species barrier to deer and elk makes it a "new" disease for those species (like avian flu jumping the species barrier to humans, as it did in 1918-19).
"New" diseases to a particular species occur fairly regularly on a biological time-frame (once or twice per century), but often these are current diseases that mutate to something new or are a disease in another species--sometime even a fairly benign disease--that jumps the species barrier and is highly dangerous to the new species (i.e. AIDS).
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#1915568 - 05/07/10 08:22 AM
Re: Chronic Wasting disease (CWD)
[Re: BSK]
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bowriter
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When Elizabeth first discivered the disease, she was convinced it had present in the wild for many years. It wasn't until we began penning elk and studying them that we became aware of it. There was no question the elk we were studying brought it in with them from the mountain.
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#1915683 - 05/07/10 09:42 AM
Re: Chronic Wasting disease (CWD)
[Re: bowriter]
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BSK
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When Elizabeth first discivered the disease, she was convinced it had present in the wild for many years. It wasn't until we began penning elk and studying them that we became aware of it. There was no question the elk we were studying brought it in with them from the mountain.
I used to believe CWD was probably a naturally occurring disease in cervids. However, the massive testing of wild populations, the documented spread of the disease, and the sudden cross-species development of CWD in mule deer in a penned facility that had held scrapie infected sheep makes it much more likely a "new" disease to elk and deer that is being spread across the country by the translocation of infected animals.
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"Know where you stand, and stand there" --Jesuit Father Daniel Berrigan
"There is no reasoning someone out of a position he has not reasoned himself into." --Clive James
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#1916319 - 05/07/10 06:30 PM
Re: Chronic Wasting disease (CWD)
[Re: BSK]
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bowriter
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No question that is how it id being spread. But how did it spread to moose and caribou? And when did they decide it was jumping a species barrier? I quit worrying about it a couple years ago and haven't really kept up with recent developments.
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#1916649 - 05/07/10 09:50 PM
Re: Chronic Wasting disease (CWD)
[Re: bowriter]
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spitndrum
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Bad Stuff
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#1916801 - 05/08/10 01:16 AM
Re: Chronic Wasting disease (CWD)
[Re: spitndrum]
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Locksley
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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-naïve 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.
http://www.sciencemag.org/cgi/content/abstract/sci;314/5796/133
The Host Range of Chronic Wasting Disease Is Altered on Passage in Ferrets
Jason C. Bartza, Richard F. Marsha, Debbie I. McKenziea and Judd M. Aiken1, a
a Department of Animal Health and Biomedical Sciences, University of Wisconsin, 1655 Linden Drive, Madison, Wisconsin, 53706
Received 5 June 1998; revised 17 July 1998; accepted 15 September 1998. Available online 6 April 2002.
Abstract
Chronic wasting disease (CWD), a member of the transmissible spongiform encephalopathies (TSEs), was first identified in captive mule and black-tail deer in 1967. Due to the failure to transmit CWD to rodents, we investigated the use of ferrets (Mustela putorius furo) as a small animal model of CWD. The inoculation of CWD into ferrets resulted in an incubation period of 17–21 months on primary passage that shortened to 5 months by the third ferret passage. The brain tissue of animals inoculated with ferret-passaged CWD exhibited spongiform degeneration and reactive astrocytosis. Western blot analysis of ferret-passaged CWD demonstrated the presence of PrP-res. Unlike mule deer CWD, ferret-passaged CWD was transmissible to Syrian golden hamsters (Mesocricetus auratus). Increasing the passage number of CWD in ferrets increased the pathogenicity of the agent for hamsters. This increase in host range of a field isolate on interspecies transmission emphasizes the need for caution when assessing the potential risk of transmission of TSEs, such as bovine spongiform encephalopathy, to new host species.
C. Gibbs
http://www.sciencedirect.com/science?_ob...c962a8f2eb6fab8
Prions in Skeletal Muscles of Deer
with Chronic Wasting Disease
Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J. Sigurdson,4‡
Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§
Prions are transmissible proteinaceous
agents of mammals that cause fatal neurodegenerative
diseases of the central nervous
system (CNS). The presence of infectivity
in skeletal muscle of experimentally infected
mice raised the possibility that dietary exposure
to prions might occur through meat consumption
(1). Chronic wasting disease (CWD), an
enigmatic and contagious prion disease of
North American cervids, is of particular concern.
The emergence of CWD in an increasingly
wide geographic area and the interspecies
transmission of bovine spongiform encephalopathy
(BSE) to humans as variant Creutzfeldt
Jakob disease (vCJD) have raised concerns
about zoonotic transmission of CWD.
To test whether skeletal muscle of diseased
cervids contained prion infectivity,
Tg(CerPrP) mice (2) expressing cervid prion
protein (CerPrP) were inoculated intracerebrally
with extracts prepared from the
semitendinosus/semimembranosus muscle
group of CWD-affected mule deer or from
CWD-negative deer. The availability of CNS
materials also allowed for direct comparisons
of prion infectivity in skeletal muscle and
brain. All skeletal muscle extracts from CWDaffected
deer induced progressive neurological
dysfunction in Tg(CerPrP) mice, with
mean incubation times ranging between 360
and È490 days, whereas the incubation times
of prions from the CNS ranged from È230 to
280 days (Table 1). For each inoculation
group, the diagnosis of prion disease was confirmed
by the presence of disease-associated,
protease-resistant PrP (PrPSc) in the brains of
multiple infected Tg(CerPrP) mice Esee (3) for
examples^. In contrast, skeletal muscle and
brain material from CWD-negative deer failed
to induce disease in Tg(CerPrP) mice (Table 1),
and PrPSc was not detected in the brains of
asymptomatic mice as late as 523 days after
inoculation (3).
http://www.cst.cmich.edu/users/gehri1tm/...0al.%202009.pdf
Chronic wasting disease (CWD) is perhaps the most enigmatic of the naturally occurring prion diseases. Although recognized as a transmissible spongiform encephalopathy (TSE) since the late 1970s (Williams and Young 1980, 1982), interest in and concern about CWD has only recently emerged. CWD most closely resembles scrapie in sheep in most respects, but recent media and public reaction to CWD has been more reminiscent of that afforded to bovine spongiform encephalopathy (BSE) less than a decade ago. Yet, with the exception of transmissible mink encephalopathy (TME), CWD is the rarest of the known animal TSEs: fewer than 1,000 cases have been diagnosed worldwide, and all but two of these occurred in North America. CWD is unique among the TSEs in that it affects free-living species (Spraker et al. 1997; Miller et al. 2000). The three natural host species for CWD, mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), and Rocky Mountain elk (Cervus elaphus nelsoni), are all in the family Cervidae and native to North America. Like scrapie, CWD is contagious: epidemics are self-sustaining in both captive and free-ranging cervid populations (Miller et al. 1998, 2000). The geographic extent of endemic CWD in free-ranging wildlife was initially thought to be quite limited and its natural rate of expansion slow; however, recent investigations have revealed that CWD has been inadvertently spread much more widely via market-driven movements of infected, farmed elk and deer. Both the ecological and economic consequences of CWD and its spread remain to be determined; moreover, public health implications remain a question of intense interest. Here, we review current understanding of CWD, its implications, and its management.
http://www.ncbi.nlm.nih.gov/pubmed/15148993
Introduction
The apparent transmission of bovine spongiform encephalopathy (BSE) to humans (Bruce et al., 1997; Hill et al., 1997) and other mammalian species emphasizes the importance of considering the potential for cross-species transmission of other animal transmissible spongiform encephalopathy (TSE) diseases. A high percentage (up to 15%) of free-ranging deer and elk in parts of north-eastern Colorado and south-eastern Wyoming are infected with chronic wasting disease (CWD) (Miller et al., 2000). CWD-infected cervids have also been identified in game farms in several other western US states. Although it appears that natural transmission of CWD between cervids is important in the maintenance of the CWD epidemic, the origin of CWD and the mode of transmission between wild animals are not understood. Furthermore, it is not clear whether the disease can be transmitted to humans who hunt and eat these animals or to domestic livestock whose range may overlap with infected cervids. The transmissibility of CWD to animals should be tested experimentally in vivo, but such tests will take years to complete because of the long incubation periods commonly encountered in interspecies TSE transmissions. Because of these problems, and the fact that CWD transmissibility cannot be tested directly in humans, we have sought alternative clues to the potential interspecies transmissibility of CWD.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC302048/
The PrP gene encodes the putative causative agent of the transmissible spongiform encephalopathies (TSEs), a heterogeneous group of fatal, neurodegenerative disorders including human Creutzfeldt–Jakob disease, bovine spongiform encephalopathy, ovine scrapie and chronic wasting disease (CWD) of North American deer and elk. Polymorphisms in the PrP gene are associated with variations in relative susceptibility, pathological lesion patterns, incubation times and clinical course of TSEs of humans, mice and sheep. Sequence analysis of the PrP gene from Rocky Mountain elk showed only one amino acid change (Met to Leu at cervid codon 132). Homozygosity for Met at the corresponding polymorphic site (Met to Val) in humans (human codon 129) predisposes exposed individuals to some forms of Creutzfeldt–Jakob disease. In this study, Rocky Mountain elk homozygous for PrP codon 132 Met were over-represented in both free- ranging and farm-raised CWD-affected elk when compared to unaffected control groups.
http://jgv.sgmjournals.org/cgi/content/abstract/80/10/2765
Edited by Locksley (05/08/10 02:04 AM)
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