>but under the federal regulations the standard provides merely that the fencing must be adequate to prevent ingress or egress of cervids and the commission is modifying agency requirements to meet that standard by removing the eight foot requirement.
and they call this sound science $$$
IF there are no restrictions on fencing heights, this CWD program in Texas is a failure before it ever get’s started. you cannot let the wolf guard the henhouse, and this is what the TAHC/USDA have done with captive shooting pens and regulations there from here in the great state of Texas. this in essence confirms what I said all along, that the USDA et al have no intentions of monitoring or capturing all the cervid escapees from cwd index herds of captive shooting pens and the folks that cater to them, and the by-products there from that potentially carry the CWD TSE prion agent. this was absolutely insane to remove the fencing height regulations by the USDA. political science as usual coming out of the USDA et al. the USDA have given up on trying to manage any TSE prion disease, and for this reason, I would advise (my honest opinion), that any other state that is seriously trying to eradicate, manage, control, cwd in the wild herds, and to protect the wild herds (if there are any states left out there that want to protect there wild cervid herds), this change of regulations in Texas with CWD regulations that now will maintain NO regulations on fencing heights, would be like playing Russian Rullett with CWD. this is asking CWD to cross into Texas, but TAHC et al did that back in 2002, where I told them that CWD was in the Trans Pecos region, and that they were not testing nearly enough for CWD there in 2002 (see emails at the bottom), but imagine what would have happened if TAHC would have gotten serious about CWD in cervids back then. Texas has not a clue about CWD in captive shooting pens, farms, and ranches in Texas. ...
Physical Capabilities When attempting to exclude or contain an animal, its size, intelligence, and physical ability must be considered (Fitzwater 1972). In most cases, a 2.4-m fence design will exclude nonstressed deer on level ground (Fitzwater 1972, Falk et al. 1978, Duffy et al. 1988); however, running, stressed deer are capable of making this jump (Arnold and Verme 1963, Sauer 1984). This suggests that a 3.0-m wire-mesh fence may be more appropriate in rough terrain where slope may decrease the overall effective height of a fence or complete exclusion is required (Kaneene et al. 2002).
Deer are not only adept at jumping barriers but are likely to maneuver through or under poorly constructed fences (Feldhamer et al. 1986). Openings in fences that appear small enough to impede deer may actually be large enough for a motivated deer. A 25-cm gap at the bottom of a fence provides adequate passage for an adult white-tailed deer (Falk et al. 1978, Palmer et al. 1985, Feldhamer et al. 1986). Ward (1982) reported that a 15-cm gap under a fence was enough to allow passage of mule deer and Feldhamer et al. (1986) documented deer in Pennsylvania passing through openings as narrow as 19 cm.
Deer Feeding Behavior
Behavior that deer exhibit while feeding include tolerating bad taste or smells, colored strobe lights, sirens and loud noises. A motivated deer can jump up to 12 feet vertically or 30 feet horizontally, but not high and far at the same time. Deer are more likely to jump fences in woodland than in grasslands. They learn to pull off bud caps. They can crawl through holes as small as 7.5 inches in diameter.
one example ;
> There were 26 reported escape incidents so far this year, this amounted to 20 actual confirmed escape incidents because 3 were previously reported, 2 were confirmed as wild deer, and 1 incident was not confirmed.
Wisconsin Conservation Congress CWD Committee Notes recorded by Secretary- Tony Grabski, Iowa County Delegate From the meeting at Mead Wildlife Area Visitor Center Milladore, WI Saturday, August 7, 2010, 9:30 AM
C. & D. Captive Cervid and Law Enforcement Update (11:10 AM)- Warden Pete Dunn gave the captive cervid farm update. There were 26 reported escape incidents so far this year, this amounted to 20 actual confirmed escape incidents because 3 were previously reported, 2 were confirmed as wild deer, and 1 incident was not confirmed. Approximately 30% of these escapes were caused by gates being left open and the other 70% resulted from bad fencing or fence related issues. The 20 actual confirmed escape incidents amounted to 77 total animals. 50 of the escaped animals were recovered or killed and 27 were not recovered and remain unaccounted for. Last year the CWD Committee passed a resolution to require double gates, but this has not gone into effect yet. Questions were raised by the committee about double fencing requirements? Pete responded that double fencing has not been practical or accepted by the industry. The DNR has the authority to do fence inspections. ? If a fence fails to pass the inspection the fencing certificate can be revoked and the farmer can be issued a citation. This year three citations and one warning have been issued for escapes.
see the rest of the shooting pens escapees, some from CWD index herds. ...tss
see about breaches of fences and shooting pens here ;
Wednesday, August 21, 2013
IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
Wednesday, September 04, 2013
***cwd - cervid captive livestock escapes, loose and on the run in the wild...
LIKE I said before, in my opinion, the only reason that the shooting pen owners want the USDA et al as stewards of that industry, it’s the lack of oversight by the USDA to regulate them properly, thus, CWD will spread further. this is just another fine example of just that $$$
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Monday, June 24, 2013
The Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry Following its Discovery
Tuesday, June 11, 2013
CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013
6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Thursday, August 08, 2013
Characterization of the first case of naturally occurring chronic wasting disease in a captive red deer (Cervus elaphus) in North America
Thursday, July 11, 2013
The New Hornographers: The Fight Over the Future of Texas Deer, Captive shooting pens, and the CWD TSE prion disease
Friday, September 27, 2013
***Uptake of Prions into Plants
Tuesday, September 17, 2013
Mother to Offspring Transmission of Transmissible Spongiform Encephalopathy TSE prion disease
Sunday, September 01, 2013
hunting over gut piles and CWD TSE prion disease
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
Monday, August 8, 2011
Susceptibility of Domestic Cats to CWD Infection
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012
Sunday, August 25, 2013
Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
NOW, let’s take a look at what the science is saying on the risk factors of human TSE prion disease from CWD prion disease of cervids.
first, from the cdc/nih et al prion gods, and what they said on human cwd potential, and what that might look like ;
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ??
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ??
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Sent: Sunday, September 29, 2002 10:15 AM
To: firstname.lastname@example.org; email@example.com; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
full text ;
Monday, February 09, 2009
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain
Date: August 25, 2007 at 12:42 pm PST
our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
CWD TO HUMAN RISK FACTORS PRION2013
PRION2013 CONGRESSIONAL ABSTRACTS
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong
Case Western Reserve University; Cleveland, OH USA
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1
1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.
Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.
Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.
Invited.16: Studies of chronic wasting disease transmission in cervid and non-cervid species
Edward A, Hoover,1 Candace K. Mathiason,1 Davin M. Henderson,1 Nicholas J. Haley,1 Davis M. Seelig,1 Nathaniel D. Denkers,1 Amy V. Nalls,1 Mark D. Zabe,1 Glenn C. Telling,1 Fernando Goni2 and Thomas Wisniewski,2
1Prion Research Center; Colorado State University; Fort Collins, CO USA; 2New York University School of Medicine; New York, NY USA
How and why some misfolded proteins become horizontally transmitted agents and occasionally cross species barriers are issues fundamental to understanding prion disease. Chronic wasting disease (CWD) of cervids is perhaps a prototype of horizontal prion transmission, encompassing efficient mucosal uptake, lymphoid amplification, neuroinvasion, peripheralization, and dissemination via mucosal excretion. Efficient mucosal transmission of CWD in deer has been demonstrated by oral, nasal, aerosol, and indirect contact exposure. In addition, other studies (Mathiason CK, et al.) reported at the symposium support a significant role for pre- and/or postnatal transmission of CWD from doe to offspring. Accumulating, yet still incomplete, evidence also suggests that the period of relatively covert CWD infection may be longer than originally thought. Given the above, minimally invasive sensitive assays based on body fluids from live animals would aid substantially in understanding the biology of CWD. We have been applying seeded realtirne quaking-induced amplification of recombinant PrP substrates (i.e., RT-QuIC methodology) to: (1) investigate antemortem CWD detection, and (2) model PrP-based species barriers and trans-species adaptation-topics we previously explored using sPMCA and in vivo bioassays. At this symposium, we report sensitive and specific detection CWD prions in saliva, urine, blood (Mathiason lab), and rectal and pharyngeal lymph node samples (Haley NJ, et al.) from pre-symptomatic and symptomatic experimentally and naturally exposed deer. Other ongoing studies are employing RT-QuIC methodology to model amplification barriers among CWD, FSE, BSE, and CJD prions using cervine, feline, bovine, human, and promiscuous rPrP substrates and the above species prion seeds, cellular co-factors, and transgenic mice. Finally, in collaboration with the Wisniewski laboratory, we are conducting of experimental CWD vaccination studies in deer employing oral administration of an attenuated Salmonella vector expressing cervid PrP epitopes.
AD.06: Detecting prions in the brain and blood of TSE-infected deer and hamsters
Alan Elder,1 Davin Henderson,1 Anca Selariu,1 Amy Nalls,1 Byron Caughey,2 Richard Bessen,1 Jason Bartz3 and Candace Mathiason1
1Colorado State University; Fort Collins, CO USA; 2NIH Rocky Mountain Laboratories; Hamilton, MT USA; 3Creighton University; Omaha, NE USA
While large quantities of protease resistant prion protein (PrPres) can be demonstrated by western blot or IHC in lymphoid biopsies or post-mortem brain tissues harvested from prion-infected animals, these conventional assays are less reliable as means to detect the small quantities of prions thought to be present in bodily fluids or associated with early and asymptomatic phases of TSE disease. The Real Time-Quaking Induced Conversion (RT-QuIC) assay is capable of detecting prions at concentrations below the level of sensitivity of conventional assays and provides a real-time fluorescent readout negating the use of proteases. We have made modifications to the RT-QuIC assay to utilize it for the detection of PrPres in brain and blood harvested from various species infected with prions. In this study, we analyzed CWD-infected deer and CWD/TME-infected hamster whole blood to determine the effect of:
(1) various anticoagulants,
(2) freezing and
(3) NaPTA precipitation.
Brain tissue and blood collected from naive deer and hamsters served as negative controls.
We were able to demonstrate amplifiable prions in
(1) brain and blood samples harvested from CWD/TME-infected animals,
(2) heparinized blood,
(3) frozen vs. fresh blood and
(4) NaPTA treated samples.
The RT-QuIC assay is able to detect PrPres in various species of animals and shows promise as an antemortem diagnostic tool for blood-borne TSEs.
Sunday, July 21, 2013
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?
sCJDMM1-2 should be considered as a separate entity at this time.
All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.
*** 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.
Thursday, July 04, 2013
New TAHC Movement Requirements for Species Susceptible to Chronic Wasting Disease (CWD)
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Thursday, March 29, 2012
TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT CALLING KETTLE BLACK
TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING;
Subject: CWD testing in Texas
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
Dear Dr. Singletary,
In Fiscal Year 2001, seven deer from Texas were tested by the National Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer). During these two years, an additional six elk and one white-tailed deer were tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least eight other white-tailed deer have been tested at TVMDL. One elk has been tested at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke of the Texas Parks and Wildlife Department also has records of 601 clinically ill white-tailed deer which were necropsied at Texas A&M during the late 1960's and early 1970's, and no spongiform encepalopathies were noted.
Thank you for your consideration.
Ken Waldrup, DVM, PhD Texas Animal Health Commission
TEXAS CWD STATUS
There have been no reported CWD infections of captive elk or deer in Texas. There is currently no mandatory surveillance program for susceptible cervids kept on game farms, although, there has been voluntary surveillance since 1999, which requires owners of participating herds to maintain an annual herd inventory and submit samples for all mortalities of animals over 16 months of age.
SO, i thought i would just see where these Ecoregions were, and just how the CWD testing was distributed. YOU would think that with the cluster of CWD bordering TEXAS at the WPMR in NM, you would have thought this would be where the major CWD testing samples were to have been taken? wrong! let's have a look at the sample testing. here is map of CWD in NM WPMR bordering TEXAS;
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to
> know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...
snip...see full text ;
SEE UPDATED REPORTS AND MORE HERE ;
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILS FROM TEXAS BORDER
kind regards, terry
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 firstname.lastname@example.org