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.
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.-
*** 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.