TPWD Still Searching For CWD, Program Has Cost $1 Million
The door is closing on another deer season in Texas. Even those who hunt under Managed Lands Deer Permits are storing their guns, ending a season that opened way back in September.
This was a season in which much of the talk was about costs, the economy and the future, and about a quiet drought that resulted in below-average antler quality.
What wasn't discussed, and really hasn't been for several seasons, is Chronic Wasting Disease.
The Texas Parks and Wildlife Department has been on the lookout for CWD since 1999, and despite the testing of more than 20,000 pen-reared and wild deer in Texas, the disease has not been found.
First identified in Colorado in the 1960s, Chronic Wasting Disease was all the rage in the early portion of this decade. It is a fatal brain and nervous system disease. It attacks the brains of infected deer and elk and causes animals to become emaciated, display abnormal behavior, lose bodily functions and ultimately die. It has been found in wild populations in 10 states and in captive herds in 10 states, some being the same states, and two Canadian provinces.
KEEPING AN EYE OUT: The Texas Parks and Wildlife Department has continued their search for Chronic Wasting Disease. After more than 20,000 samples, CWD has not found it in Texas.
Kevin Schwausch, TPWD's deer disease program specialist, said the department has been taking samples statewide, and is currently working to fill in the gaps where samples have been limited. The department is currently waiting on the final results from this winter.
TPWD tests wild deer and some from private breeders that are tested through the U.S. Department of Agriculture. Other deer from private breeders are tested by the Texas Veterinary Medical Diagnostic Laboratory. Schwausch explained those samples are tested on a confidential basis, but notes that if a sample were to test positive that it would be reported to the Texas Animal Health Commission.
"CWD is one of those diseases that it is better to not have and keep looking for it than to have it and try to prevent it. We feel good about our surveillance. We will continue testing as long as we think it is necessary," Schwaush said.
The biologist said he believes the disease will eventually find its way into Texas, but it could be decades until it shows up.
Despite the fact CWD was identified 50 years ago, there is a lot that is still not known about the disease, and even some ongoing debate about its cause. There is also debate about what to do if CWD is found in the wild. Most of the states where it has been discovered have done nothing but attempt to monitor it. Wisconsin game officials took a different tact and attempted to kill every deer in an area covering almost 300 square miles.
Schwausch said there is no clear-cut plan about what would be done in Texas if a positive sample ever did appear. The odds are good, however, the state wouldn't attempt as drastic a measure as was the undertaking in Wisconsin.
If it is found in Texas, chances are it is going to be at one of the numerous deer breeding operations statewide. There are those who believe that is what the department hoped would have happened when testing began. It didn't, and now breeders are blocked from bringing deer into the state.
In the wild, CWD is probably going to be like Largemouth Bass Virus. It is going to be a disease that biologists can do nothing about other than watch it run its course. On the other hand, chances are it won't decimate a local deer population. It never has.
Is this the time TPWD pulls the plug on this program and put its efforts and money elsewhere?
The department has spent almost $1 million of hunters' money testing deer. It has received about a third of that back through a grant program from the USDA.
There are some biologists outside the department who have worked with CWD program who believe the department can stand down.
In contrast, a recent report funded by the Canadian Wildlife Federation says no. The report, "Both Sides of the Fence: A strategic Review of Chronic Wasting Management Costs and Benefits," suggests the emphasis, as being done in Texas, should be placed on surveillance, monitoring and additional research into the disease.
At the same time, the study notes that CWD doesn't pose a risk to other species of wildlife, livestock or humans.
Contact Outdoor Editor Steve Knight at 903-596-6277 or by e-mail at
outdoor@tylerpaper.com.
http://www.tylerpaper.com/article/20090301/SPORTS0202/903010366/-1/SPORTS03that's a drop in the bucket considering what the cost will be when a case is finally documented.
here is the past history of CWD testing in Texas. ...terry
##################### 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.usFOR 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.
http://www.wildlife.state.nm.us/publications/press_releases/documents/0624CWDandcatfish.pdfSEE MAP ;
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdfGreetings 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.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/implementation/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.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/detection/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
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/images/fig1AppendixA.pnghttp://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/appendix_a/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.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/appendix_b/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. A imal 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.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/appendix_c/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.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/appendix_d/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 ;
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/appendix_d1/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.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/appendix_e/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 o 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. o 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 o
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/ * 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.usActions 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.
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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.usDear 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.
Free-Ranging (Wild) Cervids
There have been no reported CWD infections of free-ranging susceptible cervids in Texas. Currently targeted surveillance of free-ranging cervids having clinical symptoms is ongoing in Texas with no positives identified. Additionally, sampling of hunter-killed animals was initiated statewide during the 2002-2003 deer hunting season and sampling will be continued for the next three to five years.
Historic Status
Some have speculated that CWD is "spontaneous" and may exist naturally at low levels, even in Texas. The Texas Wildlife Disease Project, a cooperative research project between TPWD and Texas A&M University (circa 1965-1975), was created to address two disease issues; a) low reproduction in Texas pronghorn and b) "circling disease" in white-tailed deer. One of the leading veterinary pathologists on this project was already suspicious that the etiology of "circling disease" was scrapie being transmitted from sheep to deer. During the project's existence, a total of 780 clinically affected animals (601 white-tailed deer, 7 mule deer, 2 elk, and 170 exotic deer and antelope) were collected. Tissues, including brain and lymph nodes, from the collected animals were examined for spongiform histological lesions, and all were found to be negative. Had CWD (a form of TSE, like scrapie) existed in Texas during this time frame, it is probable that these investigations would have detected these classic histological lesions, especially in clinically affected animals. It must be noted, however, that the current laboratory tests used to diagnose CWD were not available during the time the Wildlife Disease Project so it can not be stated with absolute certainty that CWD was not present.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/status/PLAN FOR MANAGEMENT OF THE DISEASE IN TEXAS
Diseases such as CWD tend to be managed more effectively when efforts are applied before or as the disease emerges, rather than after it becomes established. CWD is an emerging disease. The current number of known infections within private elk and deer breeding facilities varies markedly among states (and Canada) and is increasing steadily with continued and expanding surveillance and investigations. The geographic spread of CWD in free-ranging mule deer, white-tailed deer and elk is a concern. The recent discovery of CWD in free-ranging white-tailed deer in Wisconsin and Illinois, approximately 700 miles east of any previously known infection, and the discovery of several CWD positive mule deer in New Mexico, approximately 35 miles north of the Texas border were well out of the known boundaries of the disease.
The disease prevalence appears to be increasing in localized areas, although it is not clear whether this is due to increased incidence, or increased surveillance, reporting, and testing. Information from states with direct experience in managing CWD is being used for developing Texas plans as we learn from their experiences.
TPWD and TAHC are developing stepped up targeted and geographically-focused surveillance plans to monitor free-ranging deer for the presence of the disease and a rapid response plan to guide both TPWD and TAHC should CWD be detected in the State. TPWD and TAHC are also evaluating cervid management laws, rules, and policies for free ranging and scientific breeder permitted cervids under their authority to identify issues and potential weaknesses related to disease management. In these efforts, TPWD and TAHC will work with other agencies and organizations responsible for or are concerned about cervid disease management in an attempt to ensure comprehensive approaches to effective management of CWD risks (see Appendix C: Importation of Susceptible Cervids).
TAHC and TPWD have split jurisdictions and regulatory responsibilities, which creates challenges for both agencies (i.e., TAHC responsible for elk, TPWD responsible for white-tailed deer and mule deer). Both agencies will cooperate to resolve issues as they arise.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/plan/COMPONENTS OF THE PLAN
1. Education and information sharing with public, constituents, and other government agency personnel concerning CWD. 2. Ongoing targeted surveillance of clinical deer statewide (i.e., collecting and CWD- testing deer/elk exhibiting symptoms that may be consistent with CWD). 3. Development and implementation of a geographically-focused Monitoring Plan involving the sampling and CWD-testing of hunter-harvested deer. 4. TAHC Rules for Importation of Susceptible Cervids (Appendix C ). 5. Response Plan for CWD should it occur in Texas(Appendix D ). 6. TAHC rules for monitoring for CWD in breeding facilities (Appendix E ). 7. Media Response plan development in the possible event of a positive CWD occurrence (Appendix F ). 8. Advance education of relevant professionals such as resource agency personnel, private wildlife consultants, veterinarians, landowners, wildlife co-ops, taxidermists, and others
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/components/EDUCATION AND INFORMATION SHARING
TPWD/TAHC will help educate and share current information with the general public, constituent groups, and other government agency personnel. These efforts will include website updates, distribution of brochures, periodic news releases, public meetings, informational workshops, agency communications and reports. This information will include: 1) basic history and understanding of CWD; 2) its nationwide distribution, and status of knowledge of the disease (e.g., epidemiology, transmission, clinical signs, population effects); 3) other CWD related issues and concerns (e.g., carcass handling and meat consumption, transmission potential to humans and livestock, deer feeding); and 4) management and research actions being taken by TPWD and TAHC. Information may also be designed to focus on specific issues of importance to landowners, hunters, meat processors, taxidermists, deer feeders, veterinarians, rehabilitators, feed companies, feeder manufacturers and operators of captive deer and elk facilities.
Publication of technical findings of research in peer-reviewed journals and agency reports will be strongly encouraged. The more informed all agencies and the public (including hunters) become, the more effectively CWD risks will be managed in the future.
Informing and educating the public, constituents, TPWD and other agency personnel about CWD is essential. Development of informational brochures and leaflets for public and intra-/interagency distribution containing information about CWD being directed toward general public (including hunter) interests and concerns are a necessity. This information will be distributed as follows:
* Available at all TPWD offices statewide. * Carried by Wildlife Biologists, Game Wardens and Park Peace Officers. * Distributed to potential contact agencies and individuals. * Potential contact agencies/individuals (in alphabetical order) include: o Cooperative Extension Service o Exotic Wildlife Association o Federal Natural resource and land management agencies, NPS, USFWS and USFS o Governors Office, EOC o Military installations o Sportsmen Conservationists of Texas o Texas Ag. Council o Texas Agricultural Extension Service o Texas Animal Health Commission o Texas Chapter of the Wildlife Society o Texas Deer Association o Texas Department of Agriculture o Texas Game Warden Association o Texas Grain and Feed Association o Texas Farm Bureau o Texas Taxidermists Association o Texas Veterinary Medical Diagnostic Laboratory o Texas Veterinary Medical Association o Texas Wildlife Association o TSCRA (Texas and Southwestern Cattle Raisers Association) o TS&GRA o USDA/APHIS o Wildlife rehabilitators
Should CWD occur it could have a significant adverse economical impact upon landowners, local communities and landowners possessing deer held under authority of Scientific Breeder Permits and elk. Special emphasis would be directed toward informing all constituents that potentially could be affected by the discovery of CWD in the State. These efforts could be accomplished through the completion of a general news packet, video releases, TPWD/TAHC web sites, as well as television and radio news releases, as well as partner publications and information systems.
Informing and educating TPWD wildlife biologists and law enforcement personnel is also critical, as these individuals will generally be the first lines of information for the public and press. Internal distribution of relevant information in a timely manner will aid TPWD personnel in addressing any CWD concerns from the public or constituent groups. As information is gathered regarding testing or other pertinent data, TPWD should present this information as requested at interagency meetings and professional meetings/symposia. These data should additionally be published peer-reviewed journals or TPWD Technical Reports. In addition, advance education of relevant professionals such as other resource agency personnel, private wildlife consultants, veterinarians, landowners, wildlife co-ops, taxidermists, feed store personnel, and other similar professions who may be contacted by the public and press for comments should be invited to education workshops.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/education/ONGOING TARGETED SURVEILLANCE OF CLINICAL DEER STATEWIDE
Collecting CWD clinical-free-ranging cervids began in late summer 2002. The collection of clinical deer has been reported by researchers in other states to be particularly useful in detecting the presence/absence of CWD in local areas statewide. TPWD will continue testing clinical free-ranging deer for CWD as they are encountered. Federal funding through APHIS/USDA may be available and would provide for increased sampling during FY-04 sampling period and beyond.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/surveillance/Chronic Wasting Disease Testing
Submitting a Specimen for Testing
Texas Veterinary Medical Diagnostic Laboratory (TVMDL) will provide Immunohistochemistry (IHC) based testing for Chronic Wasting Disease (CWD), and screening for tuberculosis (TB) in cervids. These tests are available at the College Station and Amarillo Laboratories. Specimens required for testing are the obex of the brain, both retropharyngeal lymph nodes, and both tonsils. If both CWD and TB testing are requested, it is recommended that the entire head be shipped to the lab so each of those specimens can be identified and processed. Antlers should be removed from the head and the head, including a liberal amount of the soft tissue posterior to the pharynx, should be packed in multiple plastic bags to prevent leakage. A completed Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form
or a letter with the name, address and telephone number of the submitter should be enclosed in a separate plastic bag. Specimens must be chilled within 2 hours after kill and should remain chilled during transit. For optimum results, specimens should arrive at the lab within 24 hours after kill. Charges are as follows:
Charges for Chronic Wasting Disease Testing Note: There will be a $100.00 additional charge for carcass disposal if an entire carcass is submitted. Brain removal $10.00 IHC test for CWD $30.00 TB Screen $15.00 Head Disposal $15.00 Total $70.00
Payment by check or money order must be included with specimens for testing to be completed. Credit Cards are not accepted. Specimens submitted for both CWD and TB screening will require a pre-payment of $65.00 or $50.00 if CWD testing alone is requested. Submission of previously removed obexs must include a $30.00 payment for each test to be completed. Please call 979-845-3414 if you have questions on specimen submittal or charges.
Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form
The Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form media download (PDF 270.3 KB) should be printed and filled out prior to submitting a sample. See instructions above.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/testing/SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdf http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwd_flyer.pdfNO 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.usHello 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. P.O. Box 42 Bacliff, Texas USA 77518
CJD WATCH
http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htmCJD Watch message board
http://disc.server.com/Indices/167318.html-------- 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.usGreetings,
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
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-------- Original Message -------- Subject: CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS ? Date: Mon, 16 Aug 2004 15:09:58 -0500 From: "Terry S. Singeltary Sr." To: Bovine Spongiform Encephalopathy
Greetings List members,
as i stated in my previous email;
http://www.tahc.state.tx.us/news/pr/2004/2004Aug10_Anthrax_Confirmed.pdfCWD has not been detected in Texas,
SADLY, they have not tested enough from the total population to know if CWD is in Texas or not. time will tell though. IF they get serious about finding and documenting CWD in sufficient numbers here in TEXAS, sadly, i am afraid they will find it. ITs already at NM, Texas border, TSEs knows no borders. HOWEVER, with the recent finding of a CNS cow with high potential for BSE/TSE in TEXAS, with one high official over ruling another official that wanted it tested, with the high official winning out and the **** thing going to render without being tested, head spinal cord and all. THIS weighs heavy on the credibility of any surveillance for any TSE in TEXAS, and speaks a great deal for the over all surveillance of TSE in the USA...TSS
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
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdfNEXT, 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
http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.htmlNOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
http://www.tahc.state.tx.us/animal_health/diseases/cwd/CWD2003.gifEcoregions of TEXAS
http://www.tpwd.state.tx.us/images/tx-eco95.gifIF 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...
TSS
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http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=12;t=000426Archive Number 20050628.1827 Published Date 28-JUN-2005 Subject PRO/AH/EDR> Chronic wasting disease, cervids - USA (NM)
CHRONIC WASTING DISEASE, CERVIDS - USA (NEW MEXICO) *************************************************** A ProMED-mail post <
http://www.promedmail.org> ProMED-mail is a program of the International Society for Infectious Diseases <
http://www.isid.org>
Date: 24 Jun 2005 From: Terry S. Singeltary Sr. <
flounder9@verizon.net> Source: New Mexico Wildlife News, Mon, 27 Jun 2005 [edited] <
http://www.wildlife.state.nm.us/publications/press_releases/documents/0624CWDandcatfish.pdf>
2 Mule Deer Test Positive For Chronic Wasting Disease --------------------------------------------------- 2 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.
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 <
http://www.wildlife.state.nm.us/>
See map: <
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdf>
-- ProMED-mail <
promed@promedmail.org>
[Members are strongly encouraged to view the NM CWD map at the URL below. In 2004 they tested 997 deer, each shown. These recent deer are clustered with the others just to the east of Las Cruces in southern New Mexico. The absence of cases elsewhere in the state at this level of surveillance increases one's confidence in the reality of this specific high-risk area. The origin of their infection is still obscure.
The New Mexico CWD website is: <
http://www.wildlife.state.nm.us/conservation/disease/cwd/> <
http://www.wildlife.state.nm.us/conservation/disease/cwd/where_is_it.htm> Unfortunately, other than their admirable map, they have not been updated since 14 Jun 2004.
The site being close to Texas and to Mexico has spawned speculation, but as yet without foundation. In the past 3 years Texas has tested some 9103 deer out of a target population estimate of 3 917 926, all negative. For details of the Texas Chronic Wasting Management Plan, go to: <
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/#summary> or the Texas Animal Health Commission CWD website: <
http://www.tahc.state.tx.us/animal_health/diseases/cwd/cwd.shtml> - Mod.MHJ]
[see also: 2003 ---- Chronic wasting disease, cervids - USA (NM) (02) 20030217.0414 Chronic wasting disease, cervids - USA (NM) 20030207.0328 2002 ---- Chronic wasting disease, cervids - USA (New Mexico) (02) 20020620.4548 Chronic wasting disease, cervids - USA (New Mexico) 20020619.4535] ...............lm/mhj/pg/lm
*##########################################################* ************************************************************
http://www.promedmail.org/pls/otn/f?p=2400:1202:3479181492587080::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,29447Subject: 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.usFOR 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/ .
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http://www.wildlife.state.nm.us/publications/press_releases/documents/2006/0707CWD.htmSEE MAP NM
http://www.wildlife.state.nm.us/documents/cwdcontrolmap.pdfSEE SAMPLING MAP TEXAS
CWD Sampling Maps
Three Year Summary of Hunter-Kill CWD Sampling (as of August 31, 2005)
http://www.tahc.state.tx.us/animal_health/diseases/cwd/CWD_Sampling_Aug2005.pdfCWD 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.usFOR 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.
http://www.wildlife.state.nm.us/publications/press_releases/documents/0624CW Dandcatfish.pdf
SEE MAP ;
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdfSEEMS TO ME, TEXAS is not sampling enough along it's borders with NM ;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
http://www.tahc.state.tx.us/animal_health/diseases/cwd/CWD2003.gifEcoregions
TSS
http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=12;t=000488DOC] Texas Chronic Wasting Disease Management PlanFile Format: Microsoft Word - View as HTML As an alternative to mandatory testing the Texas Deer Association encouraged it's members and ..... New Mexico discovered CWD in a free-ranging mule deer on the White Sands Missile Range, Minnesota found CWD in a captive elk herd, ...
www.cwd-info.org/docs/Texas%20Chronic%20Wasting%20Disease%20Management%... - Similar pages
http://www.cwd-info.org/docs/Texas%20Chronic%20Wasting%20Disease%20Management%20Plan.doc- [DOC] Texas Chronic Wasting Disease Management PlanFile Format: Microsoft Word - View as HTML 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 ..... Options for CWD testing (i.e. ELISA test) within localities should a CWD-positive ...
www.cwd-info.org/docs/TexasPlan.doc - Similar pages - More results from
www.cwd-info.org » [PDF]
http://www.cwd-info.org/docs/TexasPlan.docInformation From The Texas Animal Health Commission Texas’ Chronic ...File Format: PDF/Adobe Acrobat - View as HTML
http://www.tahc.state.tx.us/news/pr/2002/702CWD.pdfExotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease (February 9) Mon, 09 Feb 2009 14:25:00 -0600
Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah's Ark Processors LLC.
Recall -- Firm Press Release FDA posts press releases and other notices of recalls and market withdrawals from the firms involved as a service to consumers, the media, and other interested parties. FDA does not endorse either the product or the company.
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease Contact: Exotic Meats USA 1-800-680-4375
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah's Ark Processors LLC.
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The Elk Tenderloin was sold from January 16 - 27, 2009. The Elk Tenderloins was packaged in individual vacuum packs weighing approximately 3 pounds each. A total of six packs of the Elk Tenderloins were sold to the public at the Exotic Meats USA retail store. Consumers who still have the Elk Tenderloins should return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX 78209. Customers with concerns or questions about the Voluntary Elk Recall can call 1-800-680-4375. The safety of our customer has always been and always will be our number one priority.
Exotic Meats USA requests that for those customers who have products with the production dates in question, do not consume or sell them and return them to the point of purchase. Customers should return the product to the vendor. The vendor should return it to the distributor and the distributor should work with the state to decide upon how best to dispose. If the consumer is disposing of the product he/she should consult with the local state EPA office.
#
http://www.fda.gov/oc/po/firmrecalls/exoticmeats02_09.htmlCross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain
Date: August 25, 2007 at 12:42 pm PST
our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.
http://www.jbc.org/snip...
Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs.
snip...
http://www.emboj.org/current.shtmlsnip
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htmFrom: TSS (216-119-163-189.ipset45.wt.net) Subject: CWD aka MAD DEER/ELK TO HUMANS ??? Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias" To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias" Sent: Monday, September 30, 2002 9:22 AM Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message----- From: Sent: Sunday, September 29, 2002 10:15 AM To: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask] Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
also,
A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed. Most serious because of rapid horizontal spread and higher prevalence than BSE in UK, up to 15% in some populations. Also may be a risk to humans - evidence that it is not dangerous to humans is thin.
http://www.tseandfoodsafety.org/activities/bse_conference_basel_april_02/2summarhttp://chronic-wasting-disease.blogspot.com/2008/08/cwd-stakeholder-advisory-group.htmlThe following paper published in the November issue of the Journal of Virology reports experimental transmission of Chronic Wasting Disease (CWD) prions to a primate species. The paper is entitled Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel Monkeys (_Saimiri sciureus_). The authors are: Richard F. Marsh (1) (Deceased), Anthony E. Kincaid (2), Richard A. Bessen (3), and Jason C. Bartz(4)*, at the Department of Animal Health and Biomedical Sciences, University of Wisconsin, Madison 53706(1), Department of Physical Therapy(2), Department of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska 68178(4), Department of Veterinary Molecular Biology, Montana State University, Bozeman, Montana 59718(3).
The Abstract reads as follows: "Chronic wasting disease (CWD) is an emerging prion disease of deer and elk. The risk of CWD transmission to humans following exposure to CWD-infected tissues is unknown. To assess the susceptibility of nonhuman primates to CWD, 2 squirrel monkeys were inoculated with brain tissue from a CWD-infected mule deer. The CWD-inoculated squirrel monkeys developed a progressive neurodegenerative disease and were euthanized at 31 and 34 months postinfection. Brain tissue from the CWD-infected squirrel monkeys contained the abnormal isoform of the prion protein, PrP-res, and displayed spongiform degeneration. This is the 1st reported transmission of CWD to primates."
http://apex.oracle.com/pls/otn/f?p=2400:1001:265605120839108489::::F2400_P1001_BACK_PAGE,F2400_P1001_ARCHIVE_NUMBER,F2400_P1001_USE_ARCHIVE:1202,20051108.3270,YP01.47 Quantifying the Species Barrier in Chronic Wasting Disease by a Novel invitro Conversion Assay
Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR11University of British Columbia, Brain Research Centre, Canada; 2PublicHealth Agencyof Canada, National Microbiology Laboratory, Canada; 3Animal DiseasesResearch Institute, Canada Food Inspection Agency, National ReferenceLaboratory forScrapie and CWD, Canada; 4Ontario Cancer Institute and Department of MedicalBiophysics, University of Toronto, Canada
Background: Chronic wasting disease (CWD) is a transmissible spongiformencephalopathy that can affect North American cervids (deer, elk, andmoose).Although the risk of CWD crossing the species barrier and causing humandisease is still unknown, however, definite bovine spongiform encephalopathy(BSE)transmission to humans as variant CJD (vCJD), it would seem prudent to limitthe exposure of humans to CWD.Aim: In view of the fact that BSE can be readily transmitted to non-bovidspecies, it is important to establish the species susceptibility range ofCWD.Methods: In vitro conversion system was performed by incubation of prionswith normal brain homogenates as described before, and protease K (PK)resistantPrP was determined by immunoblotting with 6H4 monoclonal prion antibody.Results: Our results demonstrate that PrPC from cervids (including moose)can be efficiently converted to a protease-resistant form by incubation withelkCWD prions, presumably due to sequence and structural similarities betweenthesespecies. Interestingly, hamster shows a high conversion ratio by PrPCWD.Moreover,partial denaturation of substrate PrPC can apparently overcome thestructuralbarriers between more distant species.Conclusions: Our work correctly predicted the transmission of CWD to a wildmoose.We find a species barrier for prion protein conversion between cervids andother species, however, this barrier might be overcome if the PrPC substratehasbeen partially denatured in a cellular environment. Such an environmentmightalso promote CWD transmission to non-cervid species, *** including humans. Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitroconversion than PrPC treated at physiological pH. This has implications forthe processby which the prion protein is converted in disease.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdfNorth American Cervids Harbor Two Distinct CWD Strains
Authors
Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin; Colorado State University.
Content
Despite the increasing geographic distribution and host range of CWD, little is known about the prion strain(s) responsible for distinct outbreaks of the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/· mice with 29 individual prion samples from various geographic locations in North America. Upon serial passage, intrastudy incubation periods consistently diverged and clustered into two main groups with means around 210 and 290 days, with corresponding differences in neuropathology. Prion strain designations were utilized to distinguish between the two groups: Type I CWD mice succumbed to disease in the 200 day range and displayed a symmetrical pattern of vacuolation and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300 days and displayed a strikingly different pattern characterized by large local accumulations of florid plaques distributed asymmetrically. Type II CWD bears a striking resemblance to unstable parental scrapie strains such as 87A which give rise to stable, short incubation period strains such as ME7 under certain passage conditions. In agreement, the only groups of CWD-inoculated mice with unwavering incubation periods were those with Type I CWD. Additionally, following endpoint titration of a CWD sample, Type I CWD could be recovered only at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice inoculated with all dilutions resulting in disease. Although strain properties are believed to be encoded in the tertiary structure of the infectious prion protein, we found no biochemical differences between Type I and Type II CWD. Our data confirm the co·existence of two distinct prion strains in CWD-infected cervids and suggest that Type II CWD is the parent strain of Type I CWD.
see page 29, and see other CWD studies ;
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdfA prion disease of cervids: Chronic wasting disease 2008Posted Jun 24 08 5:07pm 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
The recent discovery of chronic wasting disease in cervids (CWD) beyond the borders of Colorado and Wyoming, as far east as New York and including two Canadian Provinces, has led to the emergence of CWD as a prion disease of domestic and international importance. The apparent ease of horizontal transmission, potentially via environmental contamination or by prion-containing saliva, creates enormous challenges for disease management. Ongoing studies of CWD interspecies transmission by exposure of domestic and non-domestic species directly or using transgenic mice have shed light on species barriers. Transgenic mice expressing cervid PrP have also proven useful for assessing the genetic influences of Prnp polymorphisms on CWD susceptibility. Accumulating evidence of CWD pathogenesis indicates that the misfolded prion protein, PrPSc, seems to be widely disseminated in many nonneural organs, and CWD infectivity has been recently detected in blood. This review highlights recent research findings in this disease of free-ranging wildlife.
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3. CWD prion spread and target organs
Collectively, CWD pathogenesis studies have revealed extensive deposition of PrPSc in the central nervous system (CNS) and extraneural tissues (Fig. 1). The only other natural prion diseases that even approach this degree of systemic involvement are variant Creutzfeldt-Jakob disease (vCJD) in humans, sheep scrapie, and transmissible mink encephalopathy [22, 23, 30, 61, 62]. In mule deer, PrPSc is detectable in the retropharyngeal lymph node within only 6 weeks following an oral exposure [76]. In a further study of the kinetics of prion
1
http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html5
infection in mule deer, Fox et al. showed that PrPSc is widely distributed in lymphoid tissues by 3 months post-oral exposure when it is first detected in brain [17]. By 9 months, PrPSc was detected in the myenteric and submucosal plexi throughout the gastrointestinal tract and in the vagus nerve, and by 16 months, PrPSc deposits were detectable throughout the brain and spinal cord. The Prnp genotype seemed to impact the infection kinetics in that mule deer that were SF heterozygous at codon 225 showed a delay in PrPSc spread; PrPSc was not
detectable in the brain until 16 months post-inoculation which was 13 months later than the 225SS deer. Perhaps the 225F allele confers a dominant negative effect on the kinetics of this CWD strain, as has been described in sheep, where the 171R allele has been shown to have a dominant negative effect on prion susceptibility [20, 33]. CWD pathogenesis seems to vary between deer and elk: PrPSc levels have been found to be lower in lymphoid tissues of elk compared to deer [66]. In a report of 226 CWD-infected elk, 28 had no PrPSc in lymphoid tissues despite having PrPSc in brain [81]. In addition to lymphoid tissues, PrPSc or infectivity has been detected in other non-CNS tissues, including pancreas [17, 77], adrenal gland [17, 77], and skeletal muscle [2]. Recently PrPSc was described in cardiac muscle from 7 of 16 (44%) white-tailed deer and from 12 of 17 (71%) elk [35]. This is the first report of PrPSc in cardiac muscle in any TSE. The cellular and molecular mechanisms of systemic prion spread are under investigation in many laboratories. A recent report showed that blood from CWD-infected deer contained infectivity and could transmit prion disease via a blood transfusion [50]. This finding recapitulates indirect findings of blood infectivity in vCJD affected humans [61] and experimental transfusion studies of scrapie sick sheep [32], and indicates that prion transport
throughout the body may include the blood as a potential vehicle.
snip...
6. CWD strains among deer and elk
Prion strains, such as those seen in sheep scrapie, show distinct incubation periods in differentially susceptible inbred mice and lesions target discrete brain regions [11, 18, 19]. CWD in deer and elk has been considered a single disease entity, and western blot glycoform patterns of PrPSc are similar among deer and elk [67]. However, some new data indicate otherwise, suggesting that conformational variants, or strains, may exist. In a study by Raymond et al., Syrian golden hamsters were infected with mule deer or elk CWD, but with an incomplete attack rate; only 2 of 7 and 0 of 7 hamsters developed terminal disease, respectively. Indeed, second and third passage of the mule deer derived strain resulted in a short incubation period of only 85-89 days, whereas the elk-derived strain led to an incubation period of 408-544 days. Surprisingly, when mule deer CWD was first passaged in hamster PrP expressing transgenic mice and then into hamsters, a slowly replicating strain
with distinct clinical disease and PrPSc deposition patterns in brain ensued. Therefore two different strains could be passaged from a single mule deer CWD isolate, a rapid and a slowly replicating strain with differing disease phenotypes [70]. Alternatively, these strains could have been generated upon interspecies transmission [6].
We have also observed two strains arising from a single CWD-infected mule deer upon
passage in transgenic mice overexpressing murine PrP. Here, mice developed different
PrPSc aggregate morphologies in brain, either dense, congophilic plaques or fine, diffuse aggregates which could be selectively passaged [78]. LaFauci et al. have reported that elk PrP expressing transgenic mice developed phenotypically divergent diseases when inoculated with either mule deer or elk CWD, which was also suggestive of different strains [44]. In each of these studies, it is not clear whether mule deer and elk possess heterogeneous PrP aggregates (strain mixture), or whether the strains may have developed in the new host. However, Safar et al. have reported differing conformational characteristics for PrPSc from CWD-infected white-tailed deer and elk directly, using a conformation dependent immunoassay (CDI) [71], which supports the existence of CWD strains. The possible existence of CWD strains is perhaps not entirely surprising, considering that there are genetic Prnp differences among deer and elk that could influence PrPSc conformation [34, 36, 58].
7
7. Interspecies CWD transmission
Wild predators and scavengers are presumably feeding on CWD-infected carcasses.
Skeletal muscle has been shown to harbor CWD prion infectivity [2], underscoring that other species will almost certainly be exposed to CWD through feeding. However, CWD has not been successfully transmitted by oral inoculation to species outside of the cervid family, suggestive of a strong species barrier for heterologous PrP conversion. Ferrets (family Mustelidae) can be infected with deer CWD after intracerebral (ic) but not oral exposure [5, 80]. Raccoons resisted even ic infection for up to 2 years thus far [24]. Mountain lion (Puma concolor) susceptibility to experimental feeding of CWD prions is currently under investigation (M. Miller and L. Wolfe, personal communication).
Could wild rodents colonizing CWD- or scrapie-infected pastures serve as an environmental reservoir of prion infectivity? Interestingly, bank voles (Clethrionomys glareolus), are readily infected with CWD and sheep scrapie by intracerebral inoculation ([64]; U. Agrimi, unpublished data) and are considered as a potential reservoir for sheep scrapie [64]. Many vole species occur in North America [65, 83] and further research may determine whether voles enhance CWD or scrapie spread through environmental contamination.
Given that environmental contamination with CWD prions likely occurs [55], domestic
ruminants may be exposed to CWD through common grazing areas. However, sheep and
cattle appear to be poorly susceptible to mule deer CWD: ic inoculation with mule deer CWD succeeded to infect only 2 of 8 sheep [28]; likewise cattle have not been infected after cograzing with CWD-infected mule deer, or after a direct oral exposure (over 6 years) (M. Miller, personal communication). Even direct ic inoculation led to CWD infection in only 5 of 13 cattle (38%) after 2-5 years [26]. In contrast, cattle are highly susceptible to white-tailed deer CWD with 12 of 14 animals developing neurologic disease and PrPSc by only 22 months post-ic inoculation (+/-0.5 months) [29]. Further studies are planned to determine whether
cattle are susceptible to white-tailed deer prions after an oral exposure (J. Richt, personal communication). The differential susceptibility of cattle to CWD from mule deer versus whitetailed deer suggests that CWD strains exist, and that CWD may differentially cross species barriers depending on the strain. Nevertheless, to date, natural CWD infections have been detected only in cervids.
Is the converse true, are cervids susceptible to sheep scrapie? Only one study has been performed on cervid susceptibility to sheep scrapie by the ic route, and showed that 3 of 6 elk developed neurologic signs, spongiform encephalopathy and PrPSc in brain [25]. Further experiments to address this question may be interesting since sheep scrapie is considered a possible source for CWD in North America [89, 91].
8. Human susceptibility to CWD
Millions of North Americans hunt deer and elk (U.S. Department of the Interior, Census Bureau), and there is no doubt that people have been exposed to CWD through venison consumption, particularly in light of recent data showing CWD prions in muscle [2]. Human susceptibility to CWD or to other newly emerging animal TSE [9, 14] is still unclear, although we can be somewhat reassured in that there have been no large scale outbreaks of human TSE cases in Colorado and Wyoming, where CWD has existed for decades [51]. Up until approximately 10 years ago, autopsies were not performed on suspect human TSE cases in many states due to biosafety concerns, therefore the diagnosis of potential new TSE strains has been hampered. This indicates that clinical TSE diagnoses in humans were not confirmed, nor was any strain typing done to look for the appearance of potentially subtle or unusual pathological or biochemical phenotypes of a new TSE strain. Fortunately, the
autopsy rate for suspect cases is improving. At the National Prion Disease Pathology
Surveillance Center at Case Western Reserve University (Cleveland, Ohio), Creutzfeldt-Jakob disease (CJD) suspect cases are studied and classified by CJD subtype. Thus far,
8
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
however there have been no unusual or novel prion subtypes that might indicate the appearance of a new prion strain [7, 41]. Other indirect studies of human susceptibility to CWD also suggest that the risk is low. In biochemical conversion studies, Raymond et al. [68] showed that the efficiency of CWD to
convert recombinant human PrP into amyloid fibrils was low, but similar to that of both BSE and scrapie fibrils to do the same. These results suggest that there is a molecular incompatibility in the conversion of human PrPC by CWD, sheep scrapie, or BSE, and that cross species infections in humans may be rare events.
To determine whether common PrPSc strain features may link CWD and CJD, histopathology and the PrPSc biochemical characteristics from deer and elk were compared with that of humans with sporadic CJD (sCJD) cases that are methionine homozygous at codon 129 of the Prnp gene by Xie et al. [96], although strain features including histologic profile, target organs, and glycoform patterns will not necessarily remain the same upon crossing species barriers [6, 5, 8, 57]. The PrPSc form is cleaved by proteinase-K (PK) at different sites depending on the conformation of the protein and may aid determination of whether the PrPSc conformation is similar. By western blot (SDS-PAGE) of elk CWD, the unglycosylated
PK-resistant PrPSc migrated at 21 kDa, similar to sCJD (MM1 subtype) and the PK cleavage site was the same, occurring at residues 78 and 82 as assessed by N-terminal sequencing. Conformational stability was evaluated by measuring the PrPSc stability under partially denaturing conditions and also showed no significant difference between elk CWD and sCJD MM1 PrPSc. However, elk CWD and human sCJD MM1 strains exhibited distinct glycoform patterns by two dimensional gel electrophoresis, suggesting that the strains differed. Future studies may utilize luminescent conjugated polymers, which were recently shown to distinguish naturally- and experimentally-derived prion strains [79].
To study elk-human prion species barriers, Kong et al. inoculated elk CWD into transgenic mice expressing either human PrP or elk PrP. Whereas the elk PrP expressing mice developed disease after only 118-142 days post-inoculation, human PrP expressing mice (129M) did not develop any features of TSE after more than 657 or more than 756 days [41].
In accordance with these results, Tamgüney et al. also reported that human PrP
overexpressing mice were not susceptible to 9 CWD isolates from mule deer, white-tailed deer, and elk [84]. However, mice have a limited lifespan and further passages may be necessary to detect low levels of prion infectivity that may be present subclinically. Although indirect evidence is accumulating that there may be a robust species barrier for CWD transmission to humans, one report indicates nonhuman primate susceptibility to CWD. Intracerebral inoculation of squirrel monkeys (Saimiri sciureus) demonstrated a positive CWD transmission [49]. Among non-human primates, however, the Prnp sequence of the new world monkeys are the most distant from humans [72], and therefore may not indicate that human prion conversion would occur by CWD.
snip...
11. Disease control challenges posed by CWD
Evidence is building that indicates efficient horizontal transmission occurs in CWD, indeed a complicating aspect in disease control [91]. Potential transmission mechanisms range from spread via direct contact among animals to environmental exposure through grazing in areas contaminated by prion-infected secretions, excretions (saliva, urine, feces), tissues (placenta), or decomposed carcasses. Recently, in a breakthrough finding, saliva from CWD infected deer was shown to transmit prion disease [50]. An additional experiment by Miller and colleagues showed that CWD-infected carcasses allowed to decay naturally in confined pastures can lead to CWD infections in captive deer, demonstrating the potential for
environmental contamination to spread infection [55]. Modelling studies have provided further
10
support that environmental contamination is likely playing a significant role in transmitting CWD [56, 53]. Additionally, infectious prions have been demonstrated to bind soil particles and remain infectious to animals by both intracerebral and oral exposure routes [38, 37]. Prion infectivity has been recovered from soil more than two years after experimental exposure to prions, suggesting the soil may serve as a reservoir for CWD prions [75]. Taken together, these results indicate that there may even be multiple sources for CWD exposure, perhaps through direct contact and environmental routes.
Significant challenges to CWD eradication exist in free-ranging cervids. Infected deer and elk range over a broad geographic region, and even previously surmised geographic barriers such as the Continental Divide have proven passable by infected animals. Ridding the environment of CWD-contaminated soil or even CWD-infected carcasses is not possible.
Moreover, the available ante-mortem diagnostic tests for surveillance are laborious and impractical for large numbers of free-ranging animals [74, 88, 95]. Therefore for a wildlife manager, this disease is costly to survey and difficult to control.
12. Conclusion
CWD in cervids is efficiently transmitted, likely more than any other TSE in animals or humans. Therefore, it is unlikely that this TSE can be eradicated, but perhaps through an improved understanding of transmission routes, biological factors influencing pathogenesis, and the molecular basis of CWD prion conversion, a targeted strategy for interrupting disease spread may be developed.
Acknowledgements
I thank Drs. Michael Miller, Jason Bartz and Mathias Heikenwalder for critical review of the manuscript.
snip...see full text 19 pages ;
http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/aResearch Project: Strain Typing of Chronic Wasting Disease (Cwd) and Scrapie by Intracerebral Inoculation into Transgenic and Inbred Mouse Lines
Location: Animal Diseases Research
Project Number: 5348-32000-026-07
Project Type: Specific C/A
Start Date: Sep 28, 2007
End Date: Sep 27, 2012
Objective:
To identify and differentiate typical and atypical case samples of CWD and Scrapie by characterizing the biologic phenotype and pathologic profile of these agents when administered to susceptible lines of transgenic and inbred mice.
Approach:
Tissue samples from deer, elk, sheep and goats with Transmissible Spongiform Encephalopathy (TSE) will be administered to mice by intracerebral injection. Multiple tissue types will be included, such as samples of brain, lymph node, blood, urine, feces, antler velvet and muscle. Mouse models used as recipient hosts will include both preexisting and recently created transgenic and inbred mouse lines. Recipient mouse phenotype will be evaluated by measuring clinical response, population disease rate, incubation time, and pathologic profile within the central nervous system (CNS). Pathologic profile of CNS lesion foci is assessed by evaluating anatomic localization, spongiform change, astrocytic gliosis, and deposition of protease resistant prion protein. BSL-1; 9-4-06. Documents SCA with U. of WA.
http://www.ars.usda.gov/research/projects/projects.htm?accn_no=411895Research Project: Strain Typing of Chronic Wasting Disease (Cwd) and Scrapie by Intracerebral Inoculation into Transgenic and Inbred Mouse Lines
Location: Animal Diseases Research
2007 Annual Report
1a.Objectives (from AD-416)
To identify and differentiate typical and atypical case samples of CWD and Scrapie by characterizing the biologic phenotype and pathologic profile of these agents when administered to susceptible lines of transgenic and inbred mice.
1b.Approach (from AD-416)
Tissue samples from deer, elk, sheep and goats with Transmissible Spongiform Encephalopathy (TSE) will be administered to mice by intracerebral injection. Multiple tissue types will be included, such as samples of brain, lymph node, blood, urine, feces, antler velvet and muscle. Mouse models used as recipient hosts will include both preexisting and recently created transgenic and inbred mouse lines. Recipient mouse phenotype will be evaluated by measuring clinical response, population disease rate, incubation time, and pathologic profile within the central nervous system (CNS). Pathologic profile of CNS lesion foci is assessed by evaluating anatomic localization, spongiform change, astrocytic gliosis, and deposition of protease resistant prion protein. BSL-1; 9-4-06. Documents SCA with U. of WA.
3.Progress Report
This report serves to document research conducted under a specific cooperative agreement between ARS and the University of Washington. Additional details of research can be found in the report for the parent project 5348-32000-026-00D Transmissible Spongiform Encephalopathies: the role of genetics, strain variation, and environmental contamination in disease control. The purpose of this new SCA is to identify and differentiate typical and atypical case samples of CWD and scrapie by characterizing the biologic phenotype and pathologic profile of these agents when administered to susceptible lines of transgenic and inbred mice. There will be weekly interactions between the ADODR, ADRU scientists and University of Washington collaborators through personnel visits, conference calls and emails.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=411895&showpars=tChronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,? Michael W. Miller,? Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; ?University of Wyoming, Laramie, Wyoming, USA; ?Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA
Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
--------------------------------------------------------------------------------
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.
snip...full text ;
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htmVolume 12, Number 10-October 2006
Research
Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease
Samantha MaWhinney,* W. John Pape,? Jeri E. Forster,* C. Alan Anderson,?§ Patrick Bosque,?¶ and Michael W. Miller#
*University of Colorado at Denver and Health Sciences Center, Denver, Colorado, USA; ?Colorado Department of Public Health and Environment, Denver, Colorado, USA; ?University of Colorado School of Medicine, Denver, Colorado, USA; §Denver Veteran's Affairs Medical Center, Denver, Colorado, USA; ¶Denver Health Medical Center, Denver, Colorado, USA; and #Colorado Division of Wildlife, Fort Collins, Colorado, USA
Suggested citation for this article
The transmission of the prion disease bovine spongiform encephalopathy (BSE) to humans raises concern about chronic wasting disease (CWD), a prion disease of deer and elk. In 7 Colorado counties with high CWD prevalence, 75% of state hunting licenses are issued locally, which suggests that residents consume most regionally harvested game. We used Colorado death certificate data from 1979 through 2001 to evaluate rates of death from the human prion disease Creutzfeldt-Jakob disease (CJD). The relative risk (RR) of CJD for CWD-endemic county residents was not significantly increased (RR 0.81, 95% confidence interval [CI] 0.40-1.63), and the rate of CJD did not increase over time (5-year RR 0.92, 95% CI 0.73-1.16). In Colorado, human prion disease resulting from CWD exposure is rare or nonexistent. However, given uncertainties about the incubation period, exposure, and clinical presentation, the possibility that the CWD agent might cause human disease cannot be eliminated.
snip... full text ;
http://0-www.cdc.gov.mill1.sjlibrary.org/ncidod/EID/vol12no10/06-0019.htmfull text ;
http://chronic-wasting-disease.blogspot.com/2006_12_01_archive.htmlCWD
http://chronic-wasting-disease.blogspot.com/CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/Monitoring the occurrence of emerging forms of CJD
http://cjdusa.blogspot.com/Singeltary, Sr et al. JAMA.2001; 285: 733-734.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Since this article does not have an abstract, we have provided the first 150
words of the full text and any section headings.
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. FREE FULL
TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=1JOURNAL OF NEUROLOGY
MARCH 26, 2003
In light of the findings of Asante and Collinge et al, there
should be drastic measures to safeguard the medical and surgical arena
from sporadic CJDs and all human TSEs. I only ponder how many sporadic
CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535Saturday, January 24, 2009
Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report
http://bse-atypical.blogspot.com/2009/01/research-project-detection-of-tse.htmlSaturday, January 24, 2009 Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
2008 Annual Report
http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.htmlWednesday, January 28, 2009 TAFS1 Position Paper on Specified Risk Materials (January, 2009)
TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
(January 2009)
TAFS1 Position Paper on Specified Risk Materials
http://madcowspontaneousnot.blogspot.com/2009/01/tafs1-position-paper-on-specified-risk.htmlWednesday, January 28, 2009 TAFS1 Position Paper on BSE in small ruminants (January 2009)
http://scrapie-usa.blogspot.com/2009/01/tafs1-position-paper-on-bse-in-small.htmlMonday, September 1, 2008 RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [No. 00-072-1] September 1, 2008
http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.html-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr." <
flounder@wt.net>
To:
fdadockets@oc.fda.govGreetings FDA,
i would kindly like to comment on; Docket 03D-0186FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the_total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test toassure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthyones as well. it this is not done, they system will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.
4. THERE are and have been for some time many TSEs in theUSA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread theseTSE mad cow agents in the USA.
I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in theUSA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same mistakes...
references
snip...
Oral transmission and early lymphoid tropism of chronic wasting diseasePrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1Department of Pathology, College of Veterinary Medicine and BiomedicalSciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1Department of Veterinary Sciences, University of Wyoming, 1174 SnowyRange Road, University of Wyoming, Laramie, WY 82070, USA 2Colorado Division of Wildlife, Wildlife Research Center, 317 WestProspect Road, Fort Collins, CO 80526-2097, USA3Colorado State University Veterinary Diagnostic Laboratory, 300 WestDrake Road, Fort Collins, CO 80523-1671, USA4Animal Disease Research Unit, Agricultural Research Service, USDepartment of Agriculture, 337 Bustad Hall, Washington State University,Pullman, WA 99164-7030, USA5Author for correspondence: Edward Hoover.Fax +1 970 491 0523.
e-mailehoover@lamar.colostate.eduMuledeer fawns (Odocoileus hemionus) were inoculated orally with abrain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associatedl ymphoid tissues (one or more of the following: retropharyngeal lymphnode, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonalantibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.
snip...
These results indicate that mule deer fawns develop detectable PrPres after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoidtissues draining the oral and intestinal mucosa (i.e. there tropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileumand spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node.He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings supportoral exposure as a natural route of CWD infection in deer and supportoral inoculation as a reasonable exposure route for experimental studies of CWD.
snip...
http://vir.sgmjournals.org/cgi/content/full/80/10/2757===================================
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-LTo: BSE-L
8420-20.5% Antler DeveloperFor Deer and Game in the wildGuaranteed Analysis Ingredients / Products Feeding Directions
snip...
_animal protein_
http://www.surefed.com/deer.htmBODE'S GAME FEED SUPPLEMENT #400A RATION FOR DEERNET WEIGHT 50 POUNDS22.6 KG.
snip...
_animal protein_
http://www.bodefeed.com/prod7.htmIngredientsGrain Products, Plant Protein Products, Processed Grain By-Products,Forage Products, Roughage Products 15%, Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Pyosphate, Salt,Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, CholineChloride, Folic Acid, Menadione Soduim Bisulfite Complex, PyridoxineHydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, ZincOxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, DriedSacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,Artificial Flavors added.http://www.bodefeed.com/prod6.htm
===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER
Bode's #1 Game PelletsA RATION FOR DEERF3153GUARANTEED ANALYSISCrude Protein (Min) 16%Crude Fat (Min) 2.0%Crude Fiber (Max) 19%Calcium (Ca) (Min) 1.25%Calcium (Ca) (Max) 1.75%Phosphorus (P) (Min) 1.0%Salt (Min) .30%Salt (Max) .70%IngredientsGrain Products, Plant Protein Products, Processed Grain By-Products,Forage Products, Roughage Products, 15% Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt,Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, CholineChloride, Folic Acid, Menadione Sodium Bisulfite Complex, PyridoxineHydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, ZincOxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, DriedSaccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,Artificial Flavors added.FEEDING DIRECTIONSFeed as Creep Feed with Normal Diet
http://www.bodefeed.com/prod8.htmINGREDIENTS
Grain Products, Roughage Products (not more than 35%), Processed GrainBy-Products, Plant Protein Products, Forage Products,
__Animal Protein Products__,
L-Lysine, Calcium Carbonate, Salt, Monocalcium/DicalciumPhosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, BasicCopper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin ASupplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, CalciumLignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium BisulfiteComplex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate
DIRECTIONS FOR USE
Deer Builder Pellets is designed to be fed to deer under rangeconditions or deer that require higher levels of protein. Feed to deerduring gestation, fawning, lactation, antler growth and pre-rut, allphases which require a higher level of nutrition. Provide adequateamounts of good quality roughage and fresh water at all times.
http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html===================================================
DEPARTMENT OF HEALTH & HUMAN SERVICESPUBLIC HEALTH SERVICEFOOD AND DRUG ADMINISTRATIONApril 9, 2001 WARNING LETTER01-PHI-12CERTIFIED MAILRETURN RECEIPT REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145
PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23,2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattleor other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal.Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.The above is not intended to be an all-inclusive list of deviations fromthe regulations. As a manufacturer of materials intended for animalfeed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance withthe law. We have enclosed a copy of FDA's Small Entity Compliance Guideto assist you with complying with the regulation... blah, blah, blah...
http://www.fda.gov/foi/warning_letters/g1115d.pdf==================================
snip...end...full text ;
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 7 Terry S. Singeltary Sr. Vol #: 1
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 7 Terry S. Singeltary Sr. Vol #: 1
http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm01N-0423 Substances Prohibited from use in animal food/Feed Ruminant
APE 5 National Renderers Association, Inc. Vol#: 2
APE 6 Animal Protein Producers Industry Vol#: 2
APE 7 Darling International Inc. Vol#: 2
EMC 1 Terry S. Singeltary Sr. Vol#: 3
http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htmsnip...end
Tuesday, January 06, 2009
CWD Update 93 December 29, 2008
http://chronic-wasting-disease.blogspot.com/2009/01/cwd-update-93-december-29-2008.htmlTuesday, January 13, 2009
Antemortem detection of PrPCWD in preclinical, ranch-raised Rocky Mountain elk (Cervus elaphus nelsoni) by biopsy of the rectal mucosa Full Scientific Reports
http://chronic-wasting-disease.blogspot.com/2009/01/antemortem-detection-of-prpcwd-in.htmlSaturday, January 10, 2009
Chronic Wasting Disease Investigation Update Michigan December 18, 2008
http://chronic-wasting-disease.blogspot.com/2009/01/chronic-wasting-disease-investigation.htmlSunday, September 07, 2008
CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA
http://chronic-wasting-disease.blogspot.com/2008/09/cwd-live-test-and-political-aspects-or.html2008 CWD Laboratory Testing for Wild White-tailed Deer
http://www.michigan.gov/emergingdiseases/0,1607,7-186-25806-202922--,00.htmlWednesday, January 07, 2009
CWD to tighten taxidermy rules Hunters need to understand regulations
http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.htmlMonday, January 05, 2009
CWD, GAME FARMS, BAITING, AND POLITICS
http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.htmlThursday, December 25, 2008 Lions and Prions and Deer Demise
http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.htmlTuesday, January 06, 2009
CWD Update 93 December 29, 2008
http://chronic-wasting-disease.blogspot.com/2009/01/cwd-update-93-december-29-2008.htmlTuesday, September 09, 2008 CWD MICHIGAN UPDATE September 5, 2008
http://chronic-wasting-disease.blogspot.com/2008/09/cwd-michigan-update-september-5-2008.htmlMonday, August 25, 2008 CWD FIRST DOCUMENTED IN MICHIGAN
http://chronic-wasting-disease.blogspot.com/2008/08/cwd-first-documented-in-michigan.htmlSaturday, January 24, 2009
Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report
http://bse-atypical.blogspot.com/2009/01/research-project-detection-of-tse.htmlWednesday, February 04, 2009 Nebraska reports 22 cases of CWD in deer
http://chronic-wasting-disease.blogspot.com/2009/02/nebraska-reports-22-cases-of-cwd-in.htmlMonday, February 09, 2009
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD
http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.htmlFriday, February 20, 2009
Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease
snip...
Greetings,
Despite the expenditures of countless millions of dollars fighting CWD across North America, it has not been eradicated or contained to any significant extent, and continues to gain ground. As such, the ‘fence’ between the wild and farmed herds no longer exists, and regulations and policies of both government and non-government agencies regarding CWD need to be revisited in this light.<<<
CONSIDERING these factors then, in my opinion, the game farms should all be shut down for good, asap, on both sides of the border. ...
QUESTION and opinions welcome ;
IS a 'do nothing' ... 'don't look, don't tell policy', a good thing, or a bad thing for the management of CWD, just because of 'economic cost' ???
WE know how high some game farm infection rates are, so do we gamble with the wild $$$
kind regards,
Terry
Chronic wasting disease in a Wisconsin white-tailed deer farm 79% INFECTION RATE
http://chronic-wasting-disease.blogspot.com/2008/09/chronic-wasting-disease-in-wisconsin.htmlsnip...full text ;
Friday, February 20, 2009
Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease
http://chronic-wasting-disease.blogspot.com/2009/02/both-sides-of-fence-strategic-review-of.htmlTuesday, March 03, 2009
Kent County Private Cervid Facility Charged With Violation of Quarantine
http://chronic-wasting-disease.blogspot.com/2009/03/kent-county-private-cervid-facility.htmlTerry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Labels: CWD, ENVIRONMENT, GAME FARMS, sporadic CJD
