New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.
WHAT'S THE FINAL CWD TSE PRION TALLY FOR CWD POSITIVES IN 2017?
WHAT'S THE TOTAL CWD TSE PRION COUNT TO DATE?
WHERE ARE THE MAPS?
Texas and New Mexico both played Russian Roulette, OR Prion Poker with Chronic Wasting Disease CWD TSE Prion aka mad cow disease in cervid, and both states lost. ...terry
MEMORANDUM
DEPARTMENT OF GAME & FISH
T0: Whom it may concern
FROM: New Mexico Department of Game and Fish
DATE: 22 January 2018
RE: Suspension of live Cervid importation
As of today, the director of New Mexico Department of Game and Fish is suspending all importation into New Mexico of live animals from the deer family (Cervidae.) Director’s authority to take this action is specified in 17-1-14, 17-1-26 and 17-3-32 NMSA 1978 as well as 19.35.7.10.B NMAC.
Chronic Wasting Disease (CWD) continues to expand and be detected in areas where CWD has not previously been known to exist. New detections have become common within the United States, including states in the intermountain west and southwest. New occurrences of CWD seem to be associated with game farms or from expansion of the known range of CWD through disease transmission. This expansion of CWD across North America and the importation of live animals from outside the state poses an elevated risk to New Mexico’s wild cervid populations.
CWD has not been detected in any of New Mexico's game parks, however, CWD has been detected in free ranging deer and elk in the Organ and Sacramento Mountains. New Mexico Department of Game and Fish management of CWD includes actions to prevent new introductions of CWD and reduce the risk of expansion of the known range of the disease. The suspension of importations (per 19.35.7.10.B NMAC) of live cervids into New Mexico will reduce the risk of human caused spread and/or introduction of CWD.
Alexandra Sandoval
STILL WAITING FOR 2017 CWD POSITIVE SAMPLE RESULTS UPDATE???
Chronic Wasting Disease Rules Apply to Units 19, 28 and 34
It is unlawful to transport deer, elk or their parts taken from any chronic wasting disease (CWD) control area designated by the Director of the New Mexico Department of Game and Fish. e exceptions are:
• Meat that is cut and wrapped either privately or commercially within the control area.
• Quarters or other portions of meat with no part of the head or spinal column attached.
• Meat that has been boned out.
• Hides with no heads attached.
• Clean skull plates with antlers attached.
• Antlers with no meat or tissue attached.
• Finished heads mounted by a taxidermist within the control area.
You may not remove the whole head and spinal column from the CWD control area. You must keep proof of sex with all big-game species until transported to where it will be consumed or placed in cold storage.
New Mexico 19.35.7.10.B NMAC
http://www.wildlife.state.nm.us/home/nmdgf-site-search/#gsc.tab=0&gsc.q=Cwd&gsc.sort=date&gsc.page=1
THURSDAY, NOVEMBER 02, 2017
New Mexico Chronic Wasting Disease CWD Figures 2016 - 2017 Update ???
THURSDAY, SEPTEMBER 22, 2016
New Mexico CWD confirmed in 5 McGregor Range deer during the 2015-16 hunting season
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
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas
SUNDAY, OCTOBER 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009
CHRONIC WASTING DISEASE CWD TSE PRION HISTORY TEXAS AND NEW MEXICO
2001 - 2002
Subject: Texas Borders Reopened for Importing Black-Tailed Deer & Elk New Entry Regulations in Effect $ CWD TESTING STATISTICS ?
Date: Fri, 6 Sep 2002 17:18:16 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
NEWS RELEASE
Texas Animal Health Commission
Box l2966 * Austin, Texas 78711 * (800) 550-8242 * FAX (512) 719-0719
Linda Logan, DVM, PhD * Executive Director
For info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710, or ceverett@tahc.state.tx.us
snip...
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
To: flounder@wt.net
CC: mcoats@tahc.state.tx.us
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
Captive Cervids
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.
snip...
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
CWD TEXAS TAHC OLD FILE HISTORY
updated from some of my old files. ...
Subject: CWD SURVEILLANCE STATISTICS TEXAS (total testing figures less than 50 in two years)
Date: Sun, 25 Aug 2002 21:06:49 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
greetings list members,
here are some figures on CWD testing in TEXAS...TSS
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.
xxxxxxx
Texas Animal Health Commission
(personal communication...TSS)
Austin 8 news
snip...
"There's about 4 million deer in the state of Texas, and as a resource I think we need to be doing as much as we can to look for these diseases," said Doug Humphreys with Texas Parks and Wildlife. "Right now Texas is clear. We haven't found any, but that doesn't mean we don't look."
With approximately 4 million animals, Texas has the largest population of white-tailed deer in the nation. In addition, about 19,000 white-tailed deer and 17,000 elk are being held in private facilities. To know if CWD is present in captive herds, TPWD and Texas Animal Health Commission are working with breeders to monitor their herds.
How is it spread?
It is not known exactly how CWD is spread. It is believed that the agent responsible for the disease may be spread both directly (animal to animal contact) and indirectly (soil or other surface to animal). It is thought that the most common mode of transmission from an infected animal is via saliva, feces, and urine.
some surveillance?
beyond the _potential_ methods of transmissions above, why, not a single word of SRM of various TSE species in feed as a source?
it's a known fact they have been feeding the deer/elk the same stuff as cows here in USA.
and the oral route has been documented of CWD to mule deer fawns in lab studies.
not to say that other _potential_ transmission mechanisms are possible, but why over look the obvious?
TSS
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
From: Ken Waldrup, DVM, PhD (host25-207.tahc.state.tx.us)
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border)
Date: December 15, 2003 at 3:43 pm PST
In Reply to: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border) posted by TSS on December 12, 2003 at 2:15 pm:
Dear sirs:
With regard to your comment about Texas NOT looking for CWD along the New Mexico border, it is painfully obvious that you do not know or understand the natural distribution of mule deer out there or the rights of the land owners in this state.
As of 15 December 2003, a total of 42 deer had been sampled from what we call "Trans-Pecos", beyond the Pecos River.
Mule deer are very widely dispersed through this area, sometimes at densities of one animal per 6 square miles.
The Texas Parks and Wildlife Department does not have the legal authority to trepass on private property to collect deer.
Some landowners are cooperative.
Some are not.
Franklin State Park is at the very tip of Texas, and deer from the park have been tested (all negative).
One of the single largest land owners along the border is the National Park Service.
Deer and elk from the Guadalupe Peak National Park cannot be collected with federal permission.
The sampling throughout the state is based on the deer populations by eco-region and is dictated by the availability of funds.
I am concerned about your insinuation that CWD is a human health risk.
We are at a stand-off - you have no proof that it is and I have no definitive proof that it isn't.
However I would say that the inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern (i.e. no evidence of an increased incidence of human brain disorders within the CWD "endemic" areas of these states).
From my professional interactions with the Texas Parks and Wildlife Department, I can definitely say that they want to do a thorough and sound survey throughout the state, not willy-nilly "look here, look there".
There are limitations of manpower, finances and, in some places, deer populations.
I would congratulate TPWD for doing the best job with the limitations at hand rather than trying to browbeat them when you obviously do not understand the ecology of West Texas.
Thank you for your consideration.
======================
From: TSS (216-119-139-126.ipset19.wt.net)
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border)
Date: December 16, 2003 at 11:03 am PST
In Reply to: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border) posted by Ken Waldrup, DVM, PhD on December 15, 2003 at 3:43 pm:
HEllo Dr. Waldrup,
thank you for your comments and time to come to this board.
Ken Waldrup, DVM, PhD states;
> it is painfully obvious that you do not know or understand the natural distribution of mule deer out there or the rights of the land owners in this state...
TSS states;
I am concerned about all deer/elk not just mule deer, and the rights of land owners (in the case with human/animal TSEs) well i am not sure of the correct terminology, but when the States deer/elk/cattle/sheep/humans are at risk, there should be no rights for land owners in this case.
the state should have the right to test those animals.
there are too many folks out there that are just plain ignorant about this agent.
with an agent such as this, you cannot let landowners (and i am one) dictate human/animal health, especially when you cannot regulate the movement of such animals...
Ken Waldrup, DVM, PhD states;
> Deer and elk from the Guadalupe Peak National Park cannot be collected with federal permission.
TSS states;
I do not understand this? so there is no recourse of action even if every deer/elk was contaminated with CWD in this area (hypothetical)?
Ken Waldrup, DVM, PhD states;
> I am concerned about your insinuation that CWD is a human health risk. We are at a stand-off - you have no proof that it is and I have no definitive proof that it isn't. However I would say that the inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern (i.e. no evidence of an increased incidence of human brain disorders within the CWD "endemic" areas of these states)...
TSS states;
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...end...TSS
===============================
2005
SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
NO update on CWD testing in Texas, New Mexico that i could find. I have inquired about it though, no reply yet...
-------- Original Message --------
Subject: CWD testing to date TEXAS ?
Date: Mon, 09 May 2005 12:26:20 –0500
From: "Terry S. Singeltary Sr."
To: kristen.everett@tpwd.state.tx.us
Hello Mrs. Everett,
I am most curious about the current status on CWD testing in Texas. could you please tell me what the current and past testing figures are to date and what geographical locations these tests have been in. good bust on the illegal deer trapping case. keep up the good work there.........
thank you, with kindest regards,
Terry S. Singeltary Sr. Bacliff, Texas USA 77518
-------- Original Message --------
Subject: CWD testing in New Mexico
Date: Mon, 09 May 2005 14:39:18 –0500
From: "Terry S. Singeltary Sr."
To: ispa@state.nm.us
Greetings,
I am most curious of the current and past CWD testing in New Mexico, and there geographical locations...
thank you,
Terry S. Singeltary SR. CJD Watch
#################### https://lists.aegee.org/bse-l.html ####################
From: TSS Subject: CWD 3 NEW CASES SOUTHERN NEW MEXICO Date: July 10, 2006 at 8:51 am PST
New Mexico Department of Game and Fish Media contact: Dan Williams, (505) 476-8004 Public contact: (505) 476-8000 dan.williams@state.nm.us
FOR IMMEDIATE RELEASE, JULY 7, 2006:
3 SOUTHERN NEW MEXICO DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
SANTA FE – Three deer in southern New Mexico have tested positive for chronic wasting disease, bringing the total number of confirmed CWD-infected deer in the state to 15 since the first infected deer was discovered in 2002.
The Department received test results Wednesday from the state Veterinary Diagnostic Services laboratory in Albuquerque that two wild deer captured near the White Sands Missile Range headquarters east of Las Cruces had tested positive for chronic wasting disease. A third wild deer captured in the small community of Timberon in the southern Sacramento Mountains also tested positive for the disease.
The discoveries of the infected deer were part of the Department's ongoing efforts to monitor the disease, which to date has been confined to the southern Sacramento Mountains southeast of Cloudcroft and areas surrounding the Organ Mountains near Las Cruces. Two wild elk from the southern Sacramento Mountains tested positive for the disease in December 2005.
Chronic wasting disease is a fatal neurological illness that afflicts deer, elk and moose. There is no evidence of CWD being transmitted to humans or livestock. The disease causes animals to become emaciated, display abnormal behavior and lose control of bodily functions. To date, it has been found in captive and wild deer, elk and moose in eight states and two Canadian provinces.
For more information about CWD in New Mexico and how hunters can assist in research and prevention, please visit the New Mexico Department of Game and Fish Web site, www.wildlife.state.nm.us . More information about CWD also can be found on the Chronic Wasting Disease Alliance site at www.cwd-info.org/ .
###
SEE MAP NM
SEE SAMPLING MAP TEXAS
CWD Sampling Maps
Three Year Summary of Hunter-Kill CWD Sampling (as of August 31, 2005)
CWD Sampling Maps
Three Year Summary of Hunter-Kill CWD Sampling (as of August 31, 2005)
USDA CWD Maps
March 2006 — Current Distribution of CWD
TAHC CWD Monitoring Program Information
CWD Sample Submission and Costs
2006 Factsheet For Producers Enrolling in the Complete Herd Monitoring Program
USDA CWD Maps
March 2006 — Current Distribution of CWD
TAHC CWD Monitoring Program Information
CWD Sample Submission and Costs
2006 Factsheet For Producers Enrolling in the Complete Herd Monitoring Program
----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Monday, June 27, 2005 6:51 PM
Subject: CWD TWO NEW CASES NEAR WHITE SANDS MISSLE RANGE NEW MEXICO
##################### Bovine Spongiform Encephalopathy #####################
From: TSS Subject: CWD TWO NEW CASES NEAR WHITE SANDS MISSLE RANGE NEW MEXICO Date: June 27, 2005 at 4:43 pm PST
New Mexico Department of Game and Fish
Contact: Dan Williams, (505) 476-8004
dan.williams@state.nm.us
FOR IMMEDIATE RELEASE, JUNE 24, 2005:
TWO MULE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
ANGLER LANDS STATE RECORD BLUE CATFISH AT ELEPHANT BUTTE LAKE
TWO MULE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
SANTA FE – Two mule deer captured in the Organ Mountains as part of an ongoing research project near White Sands Missile Range have tested positive for chronic wasting disease (CWD), a fatal neurological disease that attacks the brains of infected deer and elk, the Department of Game and Fish announced.
The number of confirmed CWD cases in New Mexico now stands at 11 since 2002, when the disease was first confirmed in a deer found near the eastern foothills of the Organ Mountains. All 11 CWD-infected deer were found in the same general area of southern New Mexico. The origin of the disease in New Mexico remains unknown.
The carcasses of the infected deer will be incinerated, said Kerry Mower, the Department’s lead wildlife disease biologist.
Chronic wasting disease causes animals to become emaciated, display abnormal behavior, lose bodily functions and die. The disease has been found in wild deer and elk, and in captive deer and elk, in eight states and two Canadian provinces. There currently is no evidence of CWD being transmitted to humans or livestock.
Mower said the most recent CWD-positive deer showed no obvious physical signs of having the disease. They were captured in April 2005 and tested as part of a 3-year-old research project studying deer population dynamics in southern New Mexico. More than 140 deer have been captured alive and tested for the study, in which researchers hope to find the cause of a 10-year decline in the area deer population. Study participants include the Department of Game and Fish, the U.S. Army at White Sands Missile Range and Fort Bliss, Bureau of Land Management, U.S. Geological Survey at New Mexico State University, and San Andres National Wildlife Refuge.
Hunters can assist the Department in its CWD research and prevention efforts by bringing their fresh, legally harvested deer or elk head to an area office, where officers will remove the brain stem for testing. Participants will be eligible for drawings for an oryx hunt on White Sands Missile Range and a trophy elk hunt on the Valle Vidal.
For more information about the drawing and chronic wasting disease, visit the Department web site at www.wildlife.state.nm.us.
SEE MAP ;
Greetings list members,
I am deeply concerned with these CWD mad deer so close to the Texas border.
WHAT keeps them from crossing the border to Texas ???
IF these illegal aliens can so easily cross our borders, why not these infected deer?
maybe we should get these minute men to start watching for mad deer coming in to Texas from New Mexico.
I mentioned my concerns several other times before;
-------- Original Message --------
Subject: Current status of CWD testing in Texas
Date: Tue, 10 May 2005 09:09:47 -0500
From: "kschwaus"
To: Mr. Singeltary,
I was asked to provide you with the following information. If you have any other questions regarding CWD sampling in Texas, please do not hesitate to give me a call. My office number is below.
Below I have included a chart showing CWD samples that have been tested since the fall of 2002 through the present at the eco-region level. The second chart shows the totals on a given year. The unknown location samples come from private individuals sending in samples directly to the Texas Veterinary Medical Diagnostic Lab (TVMDL). Due to the confidentiality laws that the TVMDL operates under, they are unable to provide TPWD with the location of those samples.
Region
Population Estimate
Sampling from Fall 2002 to Present
Pineywoods
502,521
975
Gulf Prairie
90,664
441
Post Oak Savannah
291,119
1146
Black Land Prairies
54,505
153
Cross Timbers
441,031
1015
Edwards Plateau
1,608,390
1618
South Texas Plains
500,183
1253
Rolling Plains
231,358
352
High Plains
49,981
81
Trans Pecos
148,174
173
Unknown Location
1,896
Total
3,917,926
9,103
Samples Collected By
2002-03
2003-04
2004-Present
TPWD
1,722
2,955
2,540
Private (unknown location)
326
608
952
Total
2,048
3,563
3,492
Thank you,
Kevin Schwausch
Big Game Program Specialist
Texas Parks & Wildlife Department
PO Box 1394
Burnet, TX 78611
512-756-4476
===============================
I would like to thank Kevin and TPWD for there prompt reply with updated data.
I am still concerned about the Texas, New Mexico border and New Mexico's apparent lack of CWD testing updates. Makes one wonder about there CWD testing program. NO report/reply back from New Mexico about there CWD testing update yet. ...
TSS
===================
-------- Original Message --------
Subject: CWD SURVEILLANCE TEXAS UPDATE (kinda)
Date: Mon, 9 May 2005 14:52:48 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@aegee.org
##################### Bovine Spongiform Encephalopathy #####################
IMPLEMENTATION OF A GEOGRAPHICALLY FOCUSED CWD SURVEILLANCE PROGRAM FOR FREE-RANGING CERVIDS
A geographically-focused free-ranging cervid Monitoring Program was implemented during the fall 2002 deer-hunting season. Brain stem samples from hunter-killed deer will be obtained from TPWD Wildlife Management Areas (WMA), State Parks, and where otherwise available with hunter and/or landowner permission, from deer taken on private land. Volume 1, Sixth Edition of United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services, Regulatory Statistics (Appendix D1) indicates that 148 samples is sufficient to detect disease at two per-cent prevalence, regardless of the population size. Therefore the goal is to acquire 148 samples from each of the State's ten ecoregions provided adequate sampling distribution is achieved across each ecoregion. The five year 2002 -2006, goal is to cumulatively collect 459 samples from each of the ten ecoregions. The cumulative sample would be used statistically to detect CWD at one per-cent prevalence level with 99 per-cent confidence. However, funding from APHIS/USDA could provide the necessary funds for sampling at the one per-cent prevalence level each year. TAHC conducted a risk assessment of counties where deer and elk have been imported and where high densities of free-ranging deer occur. The assessment was conducted for USDA funding consideration. The risk assessment was based on limited number of criteria. Since CWD could potentially occur anywhere in Texas, monitoring efforts would be focused to achieve a stratified sampling scheme across each ecoregion of the State.
Confidentiality laws restrict the type of data TPWD personnel can collect as it relates to a specific parcel of land. Therefore, personnel will ensure that no property specific information is collected (i.e. ranch name or exact location) without the landowner's written permission. The following are guidelines for data and sample collection distributed to TPWD personnel prior to sample collection:
1. A Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form must be submitted with brain stem samples.
2. The most important items to be filled out are the TPWD employee name, address and phone number, and "Patient/Deer ID". County of Kill can be recorded on the bottom of the form, but DO NOT report any information that identifies the specific parcel of land.
3. The "Patient/Deer ID" number MUST BE specific to the field data sheet the employee is using to record data.
4. Specific CWD field data sheets will not be provided, as current field data sheets (i.e. Age/Weight Antler Data Sheets, Hunter Check Station Data Sheets, etc.) will be appropriate in most cases. Field staff may produce their own CWD data sheet if necessary.
5. The field data sheet must contain:
1. Employee Name
2. Sample Number (same as Patient/Deer ID on TVMDL Accession Form
3. Sample Date
4. Deer Age
5. Deer Sex
6. County of Kill
7. Hunter Name
8. Hunting License Number
9. Ranch name or tract name/location ONLY with landowner permission.
6. Should a CWD positive be detected, TAHC will use hunter contact information to conduct CWD investigation under their regulatory authority.
7. Make sure the container containing the brain stem sample is legibly identified with the sample number, deer age and sex, county of kill and date. Although the sample number is all that is needed, additional information will help resolve any problems should batches of samples be combined.
8. Should a landowner retain deer heads for our sampling purposes, remind the landowner to issue the hunters a proof of sex document as provided for in TAHC 65.10 (c). In addition, a Wildlife resource document (PWD 905) must accompany the head until the carcass reaches a final destination and finally processed.
9. Samples MAY NOT be taken from legally harvested deer without the hunter's consent.
ACTIONS SHOULD A CWD POSITIVE BE DETECTED
Should sampling detect a CWD positive animal, TAHC and TPWD would activate the Media Response Plan (Appendix F).
TAHC and TPWD would immediately begin review of the information at hand and determine the action to be taken within the Response Plan (Appendix C.)
The first action should be to inform landowners adjacent to the property containing the CWD positive and hold a meeting with advisory committees and affected landowner to discuss plans for secondary sampling. Planning for secondary sampling, investigating movements of deer into and away from property for further actions would then be the next step. The secondary sampling is critical for determining distribution and prevalence of the disease.
As distribution and prevalence is being determined, information review and discussions with TPWD advisory committees (e.g., Private Lands Advisory Board, Hunting Advisory Committee, White-tailed Deer Advisory Committee etc.) and landowners would take place in order to determine the appropriate management action to be taken.
APPENDIX A: Results of CWD Sampling
Sampling and testing results for CWD from June, 2002 to April 1, 2003 are presented below:
Sampling and testing results for CWD from June, 2002 to April 1, 2003 TPWD TAHC Private Sector 1349 CWD Negative Deer 335 CWD Negative Deer 336 CWD Negative Deer 23 CWD Negative Exotics No Exotics No Exotics 1372 Total 335 Total 336 Total
The Grand Total of all samples collected and known 4/1/03 is 2043 of which 2020 deer and 23 exotics were found CWD negative. Samples were collected from 143 of 254 counties in Texas, and seven counties had 50 or more samples collected. Five ecoregions had 160 or more samples collected (150 samples from each ecoregion was the goal). The geographic distribution of sampling is currently not considered adequate for determining whether or not CWD exists in Texas (see map pg. 15). The goal is to improve upon distribution of samples collected within ecoregions and within counties. The goal of 2003-2004 and the next three to five years, is to collect 5000 samples (500 from each ecoregion) each sample year. The increased sampling is to have a 99 per-cent confidence level in detecting CWD if only one per-cent of the population is infected. Long-term surveillance sampling for CWD is required, as little is known about the incubation and infectious periods of the disease.
fig1AppendixA (18K)
SEE MAP OF TEXAS CWD TESTING
APPENDIX B: Chronic Wasting Disease - Status of Current Knowledge
Occurrence and Distribution
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy, which is a disease that alters the structure of the brain, in a way that resembles a sponge-like appearance and texture. Much is not known about CWD, including its origin, exact mode of transmission, and the causative or etiological agent. The source of CWD may be related in some way to scrapie in domestic sheep; it may "represent a spontaneous, naturally occurring" form of this disease in cervids thought to be caused by a "low virus infection." A more plausible theory is that CWD is caused by a point mutation of a membrane-bound protein resulting in accumulations of proteinase-resistant proteins called "prions" in the brain (medulla oblongata), tonsils (in deer only), and lymphoid tissue.
The only known long-term distribution of CWD in free-ranging susceptible cervids includes two contiguous local areas in northeastern Colorado and southeastern Wyoming. Up to 15% and less than 1% prevalence were reported for mule deer and elk, respectively, in certain management units. Two cases of CWD occurred in mule deer in the southwestern corner of the panhandle of Nebraska, which is close to the endemic area of Colorado and Wyoming. Both of these latter animals were close enough to have originated from the endemic area. More recently, CWD was diagnosed in deer in Nebraska within and outside a fenced pasture of a captive operation where elk were diagnosed with the disease. Infections in captive elk also have been documented in Colorado, Wyoming, Montana, Oklahoma, South Dakota, and Kansas. In early 2002, CWD was detected in free-ranging white-tailed deer in South Dakota and Wisconsin, later the disease was found in breeder pens in northern Wisconsin. Cases of CWD have been documented in captive elk and free ranging mule deer in Saskatchewan and Ontario as well. New Mexico discovered CWD in a free-ranging mule deer on the White Sands Missile Range, Minnesota found CWD in a captive elk herd, Illinois detected CWD in a free-ranging white-tailed deer and an infected white-tailed deer was found in a breeding facility in Alberta.
Incubation, Transmission, and Clinical Course of CWD
Incubation time, that time from infection to appearance of clinical signs, typically is less than 2 years (18-24 months). However, incubation time can be variable and ranges up to 36 months. The exact mode of transmission of CWD is unknown; however, circumstantial and experimental data indicate horizontal (or lateral) transmission in captive susceptible cervids, either by direct animal-to-animal contact or by environmental contamination. For susceptible cervids, the routes of transmission are presumed to be by exposure to saliva, urine, feces, or placental tissue, with infection occurring through the alimentary canal (mouth/nose - esophagus - stomach - intestines). If this transmission mode is confirmed for free-ranging deer or elk, it could potentially exacerbate the risk of infection. In contrast to outbreaks of mad cow disease, where exposure to animal protein-contaminated feed was documented, this has not been the case for captive or wild cervids infected with CWD. Presently, feed contamination is not considered a likely underlying transmission mechanism. Whereas, the importance of maternal transmission (mother to fetus or nursing young) as a mode of scrapie transmission in domestic sheep has at least been debated, its importance relative to CWD persistence in captive and wild cervid herds has been contraindicated thus far by current reports. Although the route of agent shedding from infected individuals is presently unknown, it is believed that the rate of agent shedding may very well increase as the disease progresses. Thus far, evidence also indicates that there is no difference between males and females or across age classes in susceptibility to CWD.
Importantly, natural transmission of TSEs (i.e., BSE, CWD) between domesticated bovines (i.e., cattle, bison), sheep and cervids has not been documented. Deer, domestic cattle and sheep have been experimentally inoculated with brain tissue containing (PrP(res)) from CWD - infected mule deer, and 2 years later, only the deer have become infected with CWD. However, healthy deer have been inoculated with brain tissue from scrapie-infected sheep, and the deer developed spongiform encephalopathy.
The clinical course of CWD is about 12 months. That is, once clinical signs are apparent, cervids rarely survive more than 12 months. Chronic wasting disease is a progressive, fatal disease, with no vaccine to prevent the disease or treatment for reversing the disease (recovery), and there is no evidence of immunity. There has been no effective, practical ante mortem (live-animal) test for diagnosis until recently; a live-test for deer (not elk) involving tonsil biopsy and immunohistochemical analysis for (PrR (res)) accumulation has demonstrated promise, and may be more sensitive than the post-mortem analysis of the obex of the medulla oblongata in the brain. The practicality of this test remains to be decided.
Clinical Signs of CWD
All signs or symptoms of CWD do not occur in all cases, and many of these signs are symptoms of other diseases and conditions as well. Further, the occurrence and severity of symptoms will depend in part on the stage (early versus advanced) of the disease. Below is a comprehensive list of the clinical signs of CWD: (1) loss of fear of humans; (2) nervousness or hyper-excitability; (3) teeth-grinding; (4) ataxia or loss of coordination; (5) notable weakness; (6) intractability; (7) inability to stand; (8) rough dull hair coat; (9) excessive salivation; (10) flaccid, hypotonia of the facial muscles; (11) drooping of the head and ears; (12) excessive thirst (polydipsia); (13) excessive urination (polyuria); (14) esophageal hypotonia and dilation, difficulty swallowing, and regurgitating ruminal fluid and ingesta; and (15) severe emaciation and dehydration.
It is important to note that while some primary symptoms may be directly related to CWD, others may be secondary, more of a consequence of the deteriorating body condition (emaciation) and related physiology (e.g., pneumonia, abscesses, enteritis, or internal parasitism that may often cause emaciation).
Pathological Signs of CWD
Pathological signs of the disease include: (1) emaciation associated with absence or serous atrophy of subcutaneous and visceral adipose tissue or fat, and yellow gelatinous bone marrow; (2) sub acute to chronic bronchopneumonia; (3) digestive tract (abomasal or omasal) ulcers; (4) enlarged adrenal glands; (5) watery or frothy rumen contents; and (6) histological lesions. These lesions have primarily and most consistently been observed in the brain and spinal cord. (7) Immunohistochemistry (IHC) is very sensitive and specific to CWD and is typically used to confirm diagnoses by measuring accumulations of proteinase-resistant prion protein (PrP(res)) in brain tissues (specifically in the obex of the medulla oblongata) of infected deer and elk. This prion protein is indistinguishable from the scrapie-associated prion protein (PrP(Sc)) found in brain tissues of domestic sheep infected with scrapie, but other differences have been noted. (PrP(res)) has not been detected in uninfected cervids. This test can detect CWD infection before lesions are observable; however, IHC (+) results are not detected until at least three months after infection. Lesions do not always accompany (PrP(res)) accumulation and IHC (+) results. (8) Scrapie associated fibrils (SAFs) have been observed by electron microscopy in the brain tissue of infected cervids, but not in uninfected cervids. (9) Generally, blood (whole blood and serum) and urine profiles have remained within the normal range, with the exception that certain characteristics have reflected the emaciated condition of the infected animals. Low specific gravity of the urine, is the one urine characteristic that may be directly related to CWD, specifically to degenerative encephalopathic changes in the hypothalamus. The hypothalamus is important in regulating anti diuretic hormone, which influences concentrations of urinary electrolytes (e.g., Na) and osmolality.
APPENDIX C: Importation of Susceptible Cervids
On March 20, 2002, the Texas Animal Health Commission, and Texas Parks and Wildlife Commission issued separate orders to prohibit the entry of all elk, white-tailed deer, black-tailed deer, and mule deer into Texas.
On August 25, 2002, Texas Animal Health Commission adopted entry requirements for black-tailed deer, elk, or other cervid species determined to be susceptible to CWD. All mule deer and white-tailed deer held under authority of Scientific Breeder Permits are also required to obtain a purchase permit and, in some cases, a transport permit from Texas Parks and Wildlife Department in order to enter the state. All requests for entry must be made in writing and accompanied with the information necessary to support import qualification of the animal(s). Requests for entry and supporting documentation should be received by the TAHC at least 10 working days prior to the proposed entry date. The processing of the application can be expedited by assuring that all of the necessary documentation has been provided and that the necessary staff is available for review. The application must be accompanied by an owner's statement stating that to his/her knowledge the animals (or donor animals) to be imported have never come in contact with equipment or resided on a premise where CWD was ever diagnosed.
Entry Requirements: The applicant must identify the herd of origin and the herd of destination on both the permit application and the certificate of veterinary inspection. The susceptible cervid(s) to be imported into this state, shall be identified to their herd of origin by a minimum of two official/approved unique identifiers to include, but not limited to, legible tattoo, USDA approved ear tag, breed registration or other state approved permanent identification methods. If a microchip is used for identification, the owner shall provide the necessary reader. A certificate of veterinary inspection completed by an accredited veterinarian shall accompany the shipment. Additionally, the herd of origin must meet the following criteria:
1. In states where there is a state approved CWD monitoring program which meets the requirements provided in Section D of Appendix C (below) and where CWD has not been identified in a susceptible species, then all elk, white-tailed deer, mule deer, and black-tailed deer to be imported must originate from a herd that has been in a state-approved complete herd certification program for a minimum of three years (or current federal standards).
2. From states which do not have a CWD monitoring program which meets the standards provided in Section D of Appendix C (below) and where CWD has not been identified in a susceptible species, then all elk, white-tailed deer, mule deer, and black-tailed deer shall originate from herds that have complete herd records, including, but not limited to, complete and detailed herd inventories, records of deaths, laboratory results, and sales and purchase receipts, for a minimum of five years. Complete documents which support this type of status shall be submitted with the permit application.
3. In states where CWD has been identified in a susceptible species, then elk, white-tailed deer, mule deer, and black-tailed deer (or other susceptible species) to be imported must originate from a herd that has been in a state-approved complete herd monitoring program, as provided in Section D of Appendix C (below) for a minimum of five years.
4. A state-approved chronic wasting disease monitoring program must be certified by the Texas State Veterinarian as meeting the following minimum standards: 1. In states where CWD has been found in free-ranging wildlife, the state program shall have perimeter fencing requirements adequate to prevent ingress, egress or contact with susceptible cervids.
2. Surveillance based on testing of susceptible cervid deaths over 16 months of age is required of all herds within a complete herd monitoring program. Surveillance sampling at commercial slaughter and at shooter operations should be at least 10 percent of the number slaughtered annually.
3. A good quality sampling program where state and federal officials have the authority to adjust herd status if poor quality samples, particularly samples that are from the wrong portion of the brain, are routinely submitted from a premise. Laboratory analysis of the brain stem by United States Department of Agriculture (USDA) approved lab is recognized as the current standard for CWD diagnosis. Other laboratory analyses may be accepted as validated or accepted by USDA/Animal and Plant Health Inspection Service (APHIS).
4. Physical herd inventory with annual verification reconciling animals and identification with records by an accredited veterinarian or state or federal personnel is required. Inventory is to include a cross check of all animal identifications with the herd inventory and specific information on the disposition of all animals not present.
5. Premise locations must be specifically identified by GIS or detailed description during the initial herd inventory.
6. Herd additions are allowed from herds with equal or greater time in an approved state CWD monitoring program with no negative impact on the certification status of the receiving herd. If herd additions are acquired from a herd with a later date of enrollment, the receiving herd reverts to the enrollment date of the sending herd. If a herd participating in the monitoring program acquires animals from a non-participating herd, the receiving herd must start over with new enrollment date based upon the date of acquisition of the animal(s). If a new herd begins with animals of a given status, that status will be retained by the new herd, based upon the lowest status of the animals received. Animals of different status which are commingled during marketing or transport will revert to the lowest status.
7. Elk, white-tailed deer, mule deer and black-tailed deer will only be allowed to enter the state of Texas if the state of origin lists CWD as a reportable disease and imposes an immediate quarantine on a herd and/or premise when a CWD positive animal is disclosed.
8. Animal health officials in the state of origin must have access to herd records for the appropriate number of years (three to five), including records of deaths and causes of death.
9. Section D also addresses entry requirements as they pertain to tuberculosis testing. However, these requirements are not included as a part of the Texas Chronic Wasting Disease Management Plan.
At the November 2002 meeting the TPWD Commission adopted regulations, to suspend the ban on importation of mule deer and white-tailed deer and provide for importation under TAHC requirements. Additionally, the TPW Commission adopted changes to Trap, Transportation, and Transplant rules, which will require a sample of deer to be tested for CWD on any property serving as a trap site for relocated deer. The rule sets forth the minimum sample size, requires the sample to be tested 100% negative by the Texas Veterinary Medical Diagnostic Laboratory and stipulates that all deer transported be uniquely marked with an ear tattoo prior to release.
APPENDIX D: Response Plan for CWD If Detected
1. If the Texas Veterinary Medical Diagnostic Laboratory reports a CWD positive test, the suspect sample will be immediately shipped to USDA Laboratory at Ames, Iowa for conformation of positive finding. The time between initial suspect finding and Ames Lab confirmation will be used to mobilize staff and groups for response plan initiation.
2. The confirmation notice of a positive would come through the USDA Veterinary Services Office in Austin, and USDA/VS personnel would be part of the response effort.
3. Governor's Office will be notified of the finding, as well as Commission members of both TAHC and TPWD. 4. CWD Media Response Plan will be activated (Appendix F).
5. Source location of CWD positive concerns:
1. The source location of the CWD positive animal and information about the area, landowners (to contact for cooperative discussions on further sampling, review of management plans), and the deer density within a 4-8 mile radius will be determined.
2. Should the source location of the CWD positive be in a Scientific Breeder facility or pen, TAHC will inform and work cooperatively with the landowner. TAHC may elect to monitor the herd with special conditions (i.e. double-fencing) or negotiate indemnification (cap established at $3000.00 for prime breeding animals) for eradication of the herd.
6. GIS locations and mapping for sampling will be utilized.
7. TAHC and TPWD will inform and work cooperatively with landowners and with landowner permission in the sample area that may be affected.
8. TAHC would determine sampling requirements. Sample numbers and the size of the area to be sampled will be determined based upon population numbers and the statistically-based numbers required for detecting CWD at a 2% prevalence level from "Regulatory Statistics Volume 1, Sixth Edition" (See Appendix D1). The numbers of animals to be sampled (projected at 150) would be collected throughout an area from 64-1056 square miles and not from a single property unless it is as large as the sample area around a positive. A square mile is 640 acres, in areas where the herd density is 1 deer per 5 acres an area of 64 square miles should contain 8192 deer (128 deer per section) and less than 3 deer per section will be sampled. In areas where the herd density is 1 deer per 200 acres an area of 1056 square miles should contain 3379 deer (3.2 deer section) a deer per 7 sections would be sampled. This sampling is not designed to reduce the population below viability.
9. Sampling will be conducted at no cost to the landowner in a cooperative manner to detect additional CWD positives, and sampling around any additional positive finds, to determine direction of spread, prevalence of the disease and to determine distribution. Additional samples would be taken surrounding any new positive to determine direction, but re-sampling again in an area previously sampled would not be necessary.
10. Simultaneously with the sampling, a joint investigation into movement of deer into or out of area will be conducted.
11. Identify geologic features or barriers, which may be used to limit population distribution, will be determined.
12. After distribution is determined, reasonable, responsible, and rational management strategies will be determined in association with landowners and applied as situations dictate following sampling activities, to include monitoring at appropriate intervals, herd reduction as a possible strategy, and eradication of local populations in limited appropriate circumstances. Strategies for possible treatments will also be discussed and reviewed with the TTT/MLDP Task Force/ White-tailed Deer Advisory Committee and the Private Lands Advisory Board.
13. TPWD will collect and take samples from cervids and transport sample to Texas Veterinary Medical Diagnostic Laboratory for analysis.
14. Options for CWD testing (i.e. ELISA test) within localities should a CWD-positive be detected will be considered and evaluated. The purpose would be to ensure reliable test results in a timely manner within the local area providing little interruption to hunting and recreation in the area.
15. TPWD must be prepared to make budget and personnel adjustments for the sampling.
APPENDIX D1
United States Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services
REGULATORY STATISTICS
Volume 1
Sixth Edition
June 1983
By Victor C. Beal, Jr.
Table 2 - NUMBER NEEDED TO TEST TO BE 95% CONFIDENT THAT THE DISEASE WILL BE DETECTED IF PRESENT AT OR ABOVE FIVE LEVELS OF INCIDENCE OR CONTAMINATION
SEE FUZZY MATH BELOW ;
APPENDIX E: TAHC Rules for Monitoring CWD
Participating herds must have adequate perimeter fencing to prevent ingress and egress of cervids. Collection and submission of appropriate samples from all cases of mortality in animals over 16 months of age will accomplish surveillance in participating herds. Exemptions are provided for animals consigned to commercial slaughter operations with state or federal meat inspection. An annual inventory in participating herds shall be verified by a TAHC, USDA or accredited veterinarian. All animals over one year of age shall be identified with an official ear tag or other approved identification device. All animals less than one year of age shall be officially identified on a change of ownership.
Herd status designation shall be assigned on the basis of the number of years of participation provided that CWD is not confirmed in the herd:
1. Level A - One full year of participation.
2. Level B - Two to three years of participation.
3. Level C - Four to five years of participation.
4. Level D - Six years or more of participation.
Additions to Complete Monitored Herd:
1. Additions may originate from herds of equal or higher status with no change in the status of the receiving herd.
2. Additions may originate from herds of lower status with the receiving herd acquiring the lower status of the herd(s) involved.
APPENDIX F: Media Response Plan
A deer tissue sample tests positive for CWD in Texas, then the TPWD and TAHC officials have only a few hours to manage communication before news reaches the public section.
Prior to Trigger Event, these items are complete and ready to go:
* Step-by-Step Media Response Plan
* Shell of news release announcing CWD find-Draft pending response plan protocols being developed between TPWD and TAHC.
* Identify news media spokespersons with TPWD and TAHC in Austin
TAHC: (512) 719-0700. Media Contact: Carla Everett.
Spokespersons: Dr. Ken Waldrup, Dr. Max Coates, Dr. Linda Logan, Dr. Dan Baca, and Dr. Terry Conger.
TPWD: (512) 389-8900. Media Contact: Steve Lightfoot. Spokespersons: Robert L. Cook, Ron George, Clayton Wolf, and Doug Humphreys
* Web site for news media and general public on CWD. Listings on site include:
* FAQ/Q&A sheet with basic facts on CWD
* Names/contact info for local/regional experts who can speak about CWD in various regions of Texas.
* Streaming video of CWD educational video on Web for general public.
* Downloadable radio PSAs.
* High-resolution photos and video of animals with CWD.
Actions Needed:
* Gain a clear understanding of Texas operational plan for handling CWD outbreak, including likely sequence of events from initial find to confirmation, and approve policies concerning quarantines, stoppage of intrastate animal movement, and designation of infection zone for monitoring, sampling protocols and possible depopulation plan.
* Effective communication planning hinges on our through understanding of state's plan for dealing with a CWD outbreak.
* Obtain concurrence with media response plan from TAHC and TPWD.
* Make final these above-listed information instruments.
Trigger Event
Notification that a suspected case of CWD exists in Texas.
Notify media contacts at TAHC and TPWD.
* TAHC - Carla Everett, (512) 719-0700 or (800) 550-8242. ceverett@tahc.state.tx.us
* TPWD - Steve Lightfoot, (512) 389-4701 or (512) 565-3680. steve.lightfoot@tpwd.state.tx.us
Actions Needed:
* TAHC and TPWD confirm contacts and alternates, e-mail addresses, cell phone numbers and office and home phone numbers provided to Carla Everett and/or Steve Lightfoot for compilation, coordination and distribution to agency leadership and involved personnel from other entities.
* News release distributed to media, agency(s) personnel and commissioners, affected stakeholder groups and constituents.
* News conference called, depending on level of media response.
------------------------------------------------------------------------
2006
----- Original Message -----
From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET
To: BSE-L@aegee.org
Sent: Saturday, December 23, 2006 1:47 PM
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???
Date: December 23, 2006 at 11:25 am PST
Greetings BSE-L members,
i never know if i am going crazy or just more of the same BSe.
several years ago i brought up the fact to the TAHC that CWD was literally at the Texas borders and that the sample size for cwd testing was no where near enough in the location of that zone bordering NM.
well, i just wrote them another letter questioning this again on Dec. 14, 2006 (see below) and showed them two different pdf maps, one referencing this url, which both worked just fine then.
since then, i have NOT received a letter from them answering my question, and the url for the map i used as reference is no longer working?
i had reference this map several times from the hunter-kill cwd sampling as of 31 August 2005 pdf which NO longer works now???
but here are those figures for that zone bordering NM, for those that were questioning the url.
the testing samples elsewhere across Texas where much much more than that figure in the zone bordering NM where CWD has been documented bordering TEXAS, near the White Sands Missile Range.
SO, why was the Texas hunter-kill cwd sampling as of 31 August 2005 document removed from the internet???
you know, this reminds me of the infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al documented it, when the TAHC accidentally started ramping up for the announcement on there web site, then removed it (see history at bottom).
i am not screaming conspiracy here, but confusious is confused again on the ciphering there using for geographical distribution of cwd tissue sample size survey, IF they are serious about finding CWD in TEXAS.
common sense would tell you if cwd is 35 miles from the border, you would not run across state and have your larger samples there, and least samples 35 miles from where is what found..........daaa..........TSS
THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare to the other sample locations ;
TPWD has been conducting surveys of hunter-kill animals since 2002 and has collected more than 7300 samples (as of 31 August 2005). In total, there have been over 9400 samples, both hunter-kill and private samples, tested in Texas to date, and no positives have been found.
SO, out of a total of 9,400 samples taken for CWD surveillance in TEXAS since 2002 of both hunter-kill and private kill, ONLY 191 samples have been taken in the most likely place one would find CWD i.e. the border where CWD has been documented at TEXAS and New Mexico
latest map NM cwd old data
CWD in New Mexico ;
What is the Department doing to prevent the spread of CWD?
Chronic wasting disease (CWD) was recently detected in a mule deer from Unit 34. Until 2005, CWD had only been found in Unit 19. With this discovery, the Department will increase its surveillance of deer and elk harvested in Units 29, 30 and 34.
Lymph nodes and/or brain stems from every harvested deer and brain stems from all elk taken in Unit 34 will be sampled.
snip...
CWD SURVEILLANCE TEXAS
SNIP...SEE FULL TEXT ;
2011 – 2012
Friday, October 28, 2011
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
I kindly submit the following ;
2017-2018
WEDNESDAY, JANUARY 24, 2018
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE
2017 7/6/17 Breeder Deer Medina Facility #5 White-tailed Deer M 4
2017 9/13/17 Breeder Deer Uvalde Facility #3 White-tailed Deer F 5
2017 10/6/17 Release Site Medina Facility #3 Elk F 4
2017 10/6/17 Breeder Deer Uvalde Facility #3 White-tailed Deer F 1
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer M 7
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 9
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 9
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 6
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer M 4
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4
2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4
2017 10/25/17 Breeder Deer Medina Facility #5 White-tailed Deer F 3
2017 11/27/17 Breeder Release Site Medina Facility #4 White-tailed Deer M 4.5
2017 11/29/17 Breeder Release Site Medina Facility #3 White-tailed Deer M 4.5
2017 12/18/17 Free Range El Paso Mule Deer M 5.5
2017 12/22/17 Free Range Hartley Mule Deer M 2.5
2017 12/22/17 Free Range Hartley Mule Deer M 4.5
2017 12/29/17 Free Range Hartley White-tailed Deer M 2.5
2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 3.5
2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 3.5
2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 6.5
2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 5.5
2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 4.5
2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 4.5
2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 8.5
2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 3.5
2017 1/8/18 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 5.5
2017 1/8/18 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 4.5
snip...see more here, you will have to hit the EXPAND button and go page by page to get all CWD postives;
WEDNESDAY, JANUARY 24, 2018
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play, a lesson on how political and corporate science helps spread a deadly disease
TEXAS HISTORY OF CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW TYPE DISEASE
MONDAY, FEBRUARY 05, 2018
Nebraska Chronic Wasting Disease CWD TSE Prion 2017 Survey Confirms 203 Positives From 1,807 Deer Sampled
FRIDAY, JANUARY 26, 2018
WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE
SATURDAY, FEBRUARY 03, 2018
Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018
TUESDAY, JANUARY 30, 2018
Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)
THURSDAY, JANUARY 25, 2018
Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY
SATURDAY, JANUARY 20, 2018
Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed
WEDNESDAY, JANUARY 24, 2018
Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date
TUESDAY, JANUARY 23, 2018
Iowa Preliminary CWD TSE Prion Minimal Low Testing Reports 2 Confirmed With 5 Suspects To Date for 2017 Season
Iowa Supreme Court rules law allows quarantine of CWD deer, not land
This is very, very concerning imo.
IF this ruling is upheld as such ;
''The Iowa Supreme Court upheld the district court ruling — saying the law gives the DNR only the authority to quarantine the deer — not the land. The ruling says if the Iowa Legislature wants to expand the quarantine powers as suggested by the DNR, then it is free to do so.''
IF a 'precedent' is set as such, by the Legislature not intervening to expand quarantine powers to the DNR for CWD TSE Prion, and the precedent is set as such that the cervid industry and land there from, once contaminated with the CWD TSE Prion, are free to repopulate, sell the land, etc, imo, this will blow the lid off any containment efforts of this damn disease CWD TSE Prion. The Iowa Supreme Court did not just pass the cwd buck down the road, the Supreme Court of Iowa just threw the whole state of Iowa under the bus at 100 MPH. all those healthy deer, while the litigation was going on, well, they were incubating the cwd tse prion, loading up the land even more, and in the end, 79.8% of those healthy looking deer had CWD TSE Prion. what about the exposure to the other species that come across that land, and then off to some other land? this makes no sense to me, if this is set in stone and the Legislation does not stop it, and stop if fast, any containment of the cwd tse prion will be futile, imo...terry
FRIDAY, JUNE 16, 2017
Iowa Supreme Court rules law allows quarantine of CWD deer, not land
FRIDAY, NOVEMBER 24, 2017
Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors
January 14, 2018
Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases
Michigan UPDATE, see also ;
Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan
Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources
Jan. 30, 2018
Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.
January 14, 2018
Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer
MONDAY, JANUARY 29, 2018
Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161
MONDAY, JANUARY 29, 2018
North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2
TUESDAY, DECEMBER 12, 2017
*** Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017 ***
(zoonosis and environmental risk factors towards the bottom, after state by state reports)
MONDAY, MARCH 13, 2017
CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017
SATURDAY, JANUARY 14, 2017
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017
FRIDAY, DECEMBER 15, 2017
Canada CFIA updating its national CWD TSE PRION efforts to eradicate disease farmed cervid NOT successful December 14, 2017
TUESDAY, DECEMBER 12, 2017
Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017
TUESDAY, DECEMBER 12, 2017
SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017
TUESDAY, DECEMBER 12, 2017
Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017
Tuesday, December 12, 2017
Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology
TUESDAY, JANUARY 30, 2018
Chronic Wasting Disease A Time Bomb For Agriculture?
WOW, i am shocked, this came from the PORK farm journal...nice article!
CWD TO PIGS
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
WEDNESDAY, APRIL 05, 2017
*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***
cattle are highly susceptible to white-tailed deer CWD and mule deer CWD
***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.
SNIP...
price of prion poker goes up for cwd to cattle;
Monday, April 04, 2016
*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***
*** 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.
MONDAY, JUNE 12, 2017
Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
MONDAY, SEPTEMBER 25, 2017
Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis
FRIDAY, NOVEMBER 24, 2017
Brain Tanning Hides and CWD Transmissible Spongiform Encephalopathy TSE Prion Disease Risk Factors Warning
SUNDAY, AUGUST 06, 2017
USA Chronic Wasting Disease CWD TSE Prion Emergency Response Plan Singeltary et al
ZOONOSIS OF TSE PRION DISEASE
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
R. BRADLEY
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
Volume 23, Number 9—September 2017
Research Letter Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion
***Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
* Strongly consider having the deer or elk tested for CWD before you eat the meat.
* If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals.
* If your animal tests positive for CWD, do not eat meat from that animal.
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
SATURDAY, JANUARY 27, 2018
CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE.
THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$
BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.
SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.
SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.
SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
CDC CWD TSE PRION UPDATE USA JANUARY 2018 MAP
CDC CWD TSE PRION UPDATE USA JANUARY 2018
As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk.
CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand.
Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd.
As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids.
Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018
snip...
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** WDA 2016 NEW YORK ***
We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans;and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
the tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
URINE
SUNDAY, JULY 16, 2017
*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***
Discussion
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
*** DOCUMENT ID: APHIS-2006-0118-0411
FRIDAY, NOVEMBER 24, 2017
Norwegian Food Safety Authority makes changes to measures to limit the spread of disease Skrantesjuke (CWD) in deer wildlife
TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION
*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip...
http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf
snip...
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip...
http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf
Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;
Some unofficial information from a source on the inside looking out -
Confidential!!!!
As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
Some unofficial information from a source on the inside looking out -
Confidential!!!!
As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
MONDAY, JANUARY 29, 2018
Assessment of Chronic Wasting Disease Prion Shedding in Deer Saliva with Occupancy Modeling
SATURDAY, FEBRUARY 03, 2018
Dehydration of prions on environmentally relevant surfaces protects them from inactivation by freezing and thawing
SATURDAY, JANUARY 27, 2018
CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor:
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Terry S. Singeltary Sr.
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