Missouri Comment time running out on deer farming regs (AUDIO)
Missouri Comment time running out on deer farming regs (AUDIO)
August 13, 2014 By Bob Priddy
Tomorrow is the deadline for Missourians to comment on the Conservation
Department’s new regulations for farmers who want to raise deer. But an
important political decision could make the regulations moot.
The legislature will consider next month whether to override the Governor’s
veto of a bill transferring regulation of deer farming from the Conservation
Department to the Agriculture Department. Conservation says it’s not assuming
the veto will stand as it solicits comments about new regulations that requires
fences deer can’t jump over, improved record-keeping when the deer are shipped,
and mandatory testing for chronic wasting disease for deer that die in
captivity.
Department deputy director Tim Ripperger says testing is needed “to get a
better handle” on Chronic Wasting Disease, which attacks the animal’s nervous
system and is always fatal, in captivity and in the wild. “We did find it in a
facility in north-central Missouri and the wild herd where we found it has been
…within two miles of that captive facility,” he says.
He’s not saying the disease originated in the captive facility. But halting
the spread of the disease is so important that the new rules ban captive deer
operations within 25 miles of places where CWD has been found.
The regulations also ban the importation of live white-tailed deer, mule
deer, and their hybrids from other states being in captive cervid operations.
The rules require fences that deer can’t jump over and space between double
fences to keep outside deer from touching noses with impounded deer. It bans
captive deer operations with 25 miles of any place where CWD has been
confirmed.
Comments should be sent to the Secretary of State’s office by tomorrow
although the department will keep taking them for a while longer.
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM ***
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets? ***
Monday, July 07, 2014
Governor Nixon Hosting Press Conference to “Act” on Captive Deer
Legislation in Missouri
Tuesday, July 08, 2014
Missouri Gov. Nixon vetoes two bills defining captive deer as livestock
Saturday, August 02, 2014
*** Structural effects of PrP polymorphisms on intra- and inter-species
prion transmission
In contrast, the scrapie prions used in the deer transmission studies of
Greenlee and colleagues were isolated from a sheep encoding A136, ***raising the
possibility that deer may be susceptible to multiple scrapie strains.
snip...
Significance
The unpredictable recurrences of prion epidemics, their incurable
lethality, and the capacity of animal prions to infect humans, provide
significant motivation to ascertain the parameters governing disease
transmission. The unprecedented spread, and uncertain zoonotic potential of
chronic wasting disease (CWD), a contagious epidemic among deer, elk, and other
cervids, is of particular concern. Here we demonstrate that naturally occurring
primary structural differences in cervid PrPs differentially impact the
efficiency of intra- and interspecies prion transmission. Our results not only
deliver new information about the role of primary structural variation on prion
susceptibility, but also provide functional support to a mechanism in which
plasticity of a tertiary structural epitope governs prion protein conversion and
intra- and inter-species susceptibility to prions.-
snip...
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
TSS
posted by Terry S. Singeltary Sr. at
1:36 PM
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