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Bull elk herd in winter. "Weve prepared an environmental assessment to help identify the choices the agency would have to make should CWD be discovered in Montanas wild deer or elk herds," said Tim Feldner, FWPs CWD plan coordinator. "Now it is time for the public to take a look at those potential actions and let us know which they think would be the most acceptable and effective." CWD has been detected in Wyoming, South Dakota, Utah, Colorado and Saskatchewan, among other states and provinces. No one is sure where CWD came from. It first showed up in the wild in 1981. Since then it has been found in wild herds or alternative livestock ranches, or game farms, in 12 states and two provinces. Since 1998, FWP has tested more than 7,000 wild elk or deer in Montana for CWD and has not yet found any evidence of the disease. CWD was diagnosed in 1999 in nine captive elk on an alternative livestock facility near Philipsburg. All the animals there were destroyed and the facility was quarantined. Montana voters passed an initiative the following year that prohibits transfer of existing game farm licenses, ends new licensing, and forbids shooting captive elk. "It appears from the way the disease has spread in the past several years in adjacent states, that it is highly likely CWD will appear here in wild deer and elk herds at some point," Feldner said. "Were preparing now to manage that situation as effectively as possible." Feldner said the CWD environmental assessment describes actions the agency might take if CWD is identified, the impact on wildlife populations and the related economic, agricultural, environmental and social issues. The plan makes recommendations on prevention, surveillance, management, public information and research. Management alternatives include reducing the number of deer or elk in the area where the disease is identified to reduce or stop its spread. A series of public meetings to discuss the environmental assessment will held from 7-9 p.m. at the following FWP regional offices: Aug. 16 Missoula 3201 Spurgin Rd. Aug. 23 Bozeman 1400 South 19th Aug. 25 Great Falls 4600 Giant Springs Rd. Sept. 1 Kalispell 490 N. Meridian Rd. Sept. 13 Billings 2300 Lake Elmo Dr. Sept. 14 Miles City Industrial Site W Sep. 15 Glasgow Rural Route 1-4210 Copies of the CWD environmental assessment are available at FWP regional and the headquarters office, on the FWP web site, under Public Notices, Chronic Wasting Disease Mgmt Plan-EA, or by calling 406-444-2452. The public may comment on the EA during the public meetings, or until Sept. 23 by email to gpayne@mt.gov . Those reviewing the document on the FWP web site may email comments from there, or comment by mail to: Montana Fish, Wildlife & Parks, Attn: Chronic Wasting Disease EA, 1420 East Sixth Ave., P.O. Box 200701, Helena, MT 59620-0701. http://fwp.state.mt.us/news/article_3778.aspx This environmental assessment (EA) evaluates potential effects on the human environment from actions proposed by the Montana Department of Fish, Wildlife & Parks intended to prevent and/or control Chronic Wasting Disease (CWD) in Montanas free-ranging deer and elk populations. Any actions taken, or any actions not taken per the no action alternative, have the potential to affect wildlife populations as well as the economic, agricultural, environmental and social issues directly tied to those wildlife populations. This document represents a coordinated effort using the best science currently available to state and federal agencies and their scientific staffs in the development of a CWD management plan for the state of Montana. Contact Information CHRONIC WASTING DISEASE MANAGEMENT PLAN FOR FREE RANGING WILDLIFE IN MONTANA AUGUST, 2005 Wildlife Division, Helena, MT 59620 TABLE OF CONTENTS Table of Contents
i List of Tables
iii List of Figures
.. iii Glossary
iv Introduction
1 Background
1 Chapter 1: Purpose of and Need for Action
7 1.1: Proposed action
7 1.2: Location
. 7 1.3: Need for the Action
7 1.4: Objectives of the Action
8 1.4.1 Objective #1
8 1.4.2. Objective #2
8 1.4.3. Objective #3
8 1.4.4. Objective #4
8 1.5: Decisions to be Made
8 1.6: History of the Planning and Scoping Process
8 1.7: Relationship to Other Plans and Goals
.. 9 1.8: Permits, Licenses, or other Authorizations Required
10 1.9: Issues
.. 10 1.9.1
10 1.9.2
13 Chapter 2: Alternatives
.. 15 2.1: Introduction
15 2.2: Description of the Alternatives
.. 15 2.2.1: Alternative I No Action
15 2.2.2: Alternative II Enhanced Surveillance
. 16 2.2.3: Alternative III Enhanced Prevention
.. 18 2.2.4: Alternative IV Control at 1%
.. 20 2.2.5: Alternative V Control at 0%
22 2.2.6: Alternative VI Aggressive Elimination
24 2.3: Process Used to Develop the Alternatives
. 26 2.4: Summary Comparison of the Activities of Each
27 Alternative, Predicted Achievement of Objectives, and Predicted Environmental Effects on Issue Resources Chapter 3: Affected Environment
34 3.1: Introduction
.. 34 3.2: Description of Relevant Affected Resources
34 3.2.1: Montanas Native Deer and Elk Populations.. 34 i 3.2.2: Wildlife Management Tools
.. 39 3.2.3: Wildlife and Montanas Economy
. 40 3.2.4: Human Health
41 3.2.5: Alternative Livestock
. 42 3.2.6: Disposal/Environmental Contamination
44 3.3: Other Regulatory Agencies
50 Chapter 4: Environmental Consequences
54 4.1: Introduction
54 4.2: Cumulative Impacts
54 4.3: Irreversible and Irretrievable Commitments
.. 55 4.4: Environmental Consequences of CWD on
55 Identified Issues 4.4.1: Effect on Montanas Wild Deer and Elk
55 4.4.2: Effect on Wildlife Management Tools
... 57 4.4.3: Effect on Montanas Economy
.. 58 4.4.4: Effect on the Alternative Livestock Industry.. 60 4.4.5: Effect on Human Health
. 62 4.4.6: Effect on Environmental Contamination and..62 Carcass Disposal 4.5: Predicted Environmental Impacts of Alternative II
.. 63 4.5.1: Biological Environment
. 64 4.5.2: Physical Environment
. 64 4.5.3: Socioeconomic Environment
.. 65 4.6: Predicted Environmental Impacts of Alternative III
.. 65 4.6.1: Biological Environment
. 65 4.6.2: Physical Environment
66 4.6.3: Socioeconomic Environment
. 67 4.7: Predicted Environmental Impacts of Alternative IV
. 67 4.7.1: Biological Environment
. 68 4.7.2: Physical Environment
. 69 4.7.3: Socioeconomic Environment
. 69 4.8: Predicted Environmental Impacts of Alternative V
.. 70 4.8.1: Biological Impacts
.. 70 4.8.2: Physical Impacts
. 71 4.8.3: Socioeconomic Impacts
.. 71 4.9: Predicted Environmental Impacts of Alternative VI
. 72 4.9.1: Biological Impacts
.. 72 4.9.2: Physical Impacts
72 4.9.3: Socioeconomic Impacts
.. 73 Chapter 5: List of Individuals Associated with the Project
74 Chapter 6: List of Persons and Agencies Consulted
75 Bibliography
. 76 Appendix 1: "Public Information Plan Chronic Wasting.
.. 79 Disease in Montana" Appendix 2: "Mule Deer Population Ecology and Chronic
87 Wasting Disease Study" ii LIST OF TABLES Table 1. 2.4.1. Summary Comparison of the Activities of Each Alternative
28 Table 2. 2.4.2 Summary Comparison of the Achievement of Project Objectives
. 30 Table 3. 2.4.3 Summary Comparison of Predicted Environmental Effects
31 Table 4. CWD Survey Result Totals for Montana from 1998 through 2004
39 LIST OF FIGURES Figure 1. Distribution of CWD in both captive and wild deer and elk populations as of 2004. (from CWD Alliance webpage, CWD-info.org)
4 Figure 2. 2004 Montana Mule Deer Distribution and Population Estimate
. 34 Figure 3. 2004 Montana White-tailed Deer Distribution and Population Estimate
35 Figure 4. 2004 Montana Elk Distribution and Population Estimate
.. 37 Figure 5. Model of Deer Herds with Chronic Wasting Disease (an average of 250 simulations)
.. 56 iii GLOSSARY Biopsy: Removal of tissue from a living body for microscopic examination to establish diagnosis. Cervid: Members of the cervidae family, which include deer, elk, moose, and caribou. Ecological niche: The area within a particular habitat occupied by an animal in which it interacts with other different species of animals and plants. Emigration: To leave one area to settle elsewhere. Endemic area: A geographical area where a disease has been present in the population for a period of time or has become established. Epizootic: A term used to describe a disease that attacks a large number of animals simultaneously. High-risk area: A geographical area identified as having a higher probability of finding CWD within its boundaries. Incubation period: The period of time between becoming infected with a disease causing organism or a prion and actually showing outward signs of the disease. Immigration: To enter and settle in a new region. Infective dose: The amount of infectious material required to establish an infection or disease in a susceptible animal. Morbidity: An unhealthy condition indicating that a disease is ongoing in an animal. Mortality: The frequency of number of deaths in proportion to a population. Offal: Waste parts of a butchered animal. Pathogen: An agent that causes a disease (bacterium, virus, prion, etc.) Pathogenesis: The development of a diseased or morbid condition. Generally refers to the mechanism by which a pathogen is able to affect the cells, organs, and organ systems of an animal eventually causing disease. Prevalence: The percentage of animals affected in a given population. iv Spongiform lesions: Microscopic "holes" appearing in the brain tissue that are characteristic of transmissible spongiform encephalopathies. Telemetry: The science and technology of automatic data measurement and transmission by radio from remote sources to a receiving station for analysis. Used in wildlife biology to locate and track animals that have been fitted with a device that sends out a radio signal. Ungulate: Hoofed animals such as horses, cattle, swine, deer, and sheep. Zoonotic: A term used to describe a disease that can be transmitted from animals to man. v CHRONIC WASTING DISEASE MANAGEMENT PLAN DRAFT ENVIRONMENTAL ASSESSMENT INTRODUCTION This environmental assessment (EA) evaluates potential effects on the human environment from actions proposed by the Montana Department of Fish, Wildlife & Parks intended to prevent and/or control Chronic Wasting Disease (CWD) in Montanas free-ranging deer and elk populations. Any actions taken, or any actions not taken per the "no action alternative," have the potential to affect wildlife populations as well as the economic, agricultural, environmental and social issues directly tied to those wildlife populations. This document represents a coordinated effort using the "best science" currently available to state and federal agencies and their scientific staffs in the development of a CWD management plan for the state of Montana. Although we can benefit from the experience gained in other states where actions have been taken to manage ongoing CWD problems, conclusions regarding the success of those actions are premature at this time. Almost all scientists and wildlife managers in states faced with ongoing CWD problems have agreed, however, that action must be taken to prevent and/or control CWD. To be passive in the fight against this disease can only result in decreased wildlife populations and decreased opportunities for the enjoyment of this valuable resource in the state of Montana. BACKGROUND Disease has been defined as a "deviation from the normal" for a functioning organism or their systems. Bacteria, viruses, rickettsia, parasites, and fungi, generally referred to as "pathogens", have historically caused transmissible diseases. A new concept in transmissible disease has emerged in the last 20 years proposing that a set of diseases called transmissible spongiform encephalopathies (TSEs) are not caused by "historical" pathogens, but by a protein referred to as a "prion." A prion lacks the genetic information (DNA or RNA) that all of the previously mentioned pathogens rely on for their infective nature. Although the "prion theory" has not enjoyed full acceptance in the scientific community, prions have been implicated in a number of diseases in a wide variety of mammalian species. These diseases include Kuru and Creutzfeldt-Jakob Disease (CJD) in humans, scrapie in sheep, bovine spongiform encephalopathy (BSE or mad cow disease) in cattle, transmissible mink encephalopathy in mink, feline spongiform encephalopathy in cats, and CWD in deer and elk. There is no cure for any of the TSEs - all of these diseases cause the eventual death of the affected animal. CWD was first identified as a fatal condition of unknown cause in captive deer at a Colorado wildlife research facility in the late 1960s. In 1978, that condition was linked to abnormalities found in the brains of the infected deer. Those abnormalities had a remarkable resemblance to what was observed in the brains of sheep infected with scrapie, a TSE disease that has afflicted sheep for centuries. This finding led scientists to conclude that the disease affecting the captive deer was a TSE. Field observations, proven later by experimental studies, indicate that CWD is transmissible from animal to animal, although 1 the exact method or natural route(s) of transmission remains unclear. Most researchers believe that transmission occurs when a susceptible animal is directly exposed to the urine, feces, or saliva of an infected animal. Transmission of CWD has also been shown to occur through exposure of non-infected animals either to pastures contaminated as long as two years earlier by infected animals or by exposure to decomposed carcasses of animals that have died of CWD. The role played by environmental contamination in the natural transmission of CWD is presently being evaluated. What is known is that the prion protein is very difficult to destroy and that normal inactivating agents such as alcohol, UV light, heat, and oxidizing agents normally effective in destroying bacteria, virus, etc. are much less effective in destroying the prions. Because of this, prions may remain in the environment for much longer than the classical pathogens. CWD was first recognized as a disease in a free ranging elk in Colorado in 1981 and in Wyoming in 1985. By 1990, CWD had been found in free ranging mule and white-tailed deer in both states. Although the disease seemed to remain relatively localized for two to three decades within northeastern Colorado and southeastern Wyoming, appearance of CWD in captive game farm elk in Saskatchewan in 1996 preceded findings in game farms in South Dakota, Colorado, Oklahoma, Montana, Nebraska, Kansas, Wisconsin, Minnesota, New York, and in the province of Alberta. The movement of captive deer and elk by the game farm industry has been implicated in the spread of CWD to both captive cervids and free ranging cervids in other states. Increased surveillance efforts for CWD by many states may also have added to the known geographical distribution of CWD in the United States outside the original endemic area. In addition to Colorado and Wyoming, CWD has now been detected in free ranging deer or elk populations in Nebraska, South Dakota, Wisconsin, Illinois, Utah, New Mexico, New York, and in the province of Saskatchewan. The minimum incubation period prior to the observation of clinical signs in animals experimentally infected with CWD is 15 months; incubation periods are variable and may exceed 25 months in deer and 34 months in elk (Williams et al. 2002a). The time course to observation of clinical signs, however, appears to be inversely related to the infective dose, so experimental data probably underestimates the incubation periods seen in natural infections (Williams et al. 2002b). Clinical signs in infected animals include weight loss, increased drinking, increased salivation and drooling, lowered head, drooping ears, and behavioral changes. Because these clinical signs mimic those seen in animals affected by other diseases, the only way to accurately diagnose CWD in deer and elk is by direct examination of either a section of the brain (obex) or of specific lymph nodes (lymph nodes of choice for diagnosis are retropharyngeal lymph nodes) from the affected animal. Previously, positive CWD diagnosis was accomplished by either microscopic examination of the collected tissues for evidence of characteristic "spongiform lesions" or by a technique employing specialized staining of the tissues called immunohistochemistry (IHC). Recent advances in diagnostic techniques, including development of an enzyme- linked immunosorbent assay (ELISA) for diagnosis of CWD, have decreased both the cost of performing the test and the time required to provide results. These advances in testing methodology and efficiency have come at a time when more states across the U.S have 2 either experienced CWD in their wildlife populations or have become concerned about its possible presence resulting in dramatically expanded surveillance programs for CWD. There is a good deal of work going on in the United States and around the world focused on the development of a diagnostic test for CWD and other TSEs. The goal of that work is to develop a diagnostic test that can be performed on a sample that can be collected from a live animal. Recently, a Canadian company announced progress in the development of a test that detects a specific protein in the blood of mammals that may indicate, among other things, infection with a TSE. CWD remained limited in distribution to Colorado and Wyoming for 20-30 years. Although it was a new disease and of interest to researchers, effects on the deer and elk populations were thought to be minimal and there was little concern regarding public health or environmental issues. Experience with another TSE in the United Kingdom, however, brought international attention to the prion diseases when BSE (mad cow disease) was associated with a condition in humans called variant Creutzfeldt-Jakob disease (vCJD). Although sporadic CJD has occurred in the human population at a rate of approximately 1 per one million people for at least the last century, vCJD was suddenly implicated as a disease that was transmitted to humans from BSE infected cattle. Whereas sporadic CJD did not seem to be transmissible person-to-person and generally affected individuals 50 years or older, vCJD affected a younger population, seemed to be transmitted through eating contaminated meat from BSE affected cattle, and caused some distinguishing diagnostic characteristics in its victims allowing differentiation from sporadic CJD. As of December 1, 2003, a total of 153 cases of vCJD had been reported in the world: 143 from the United Kingdom, six from France, and one each from Canada, Ireland, Italy, and the United States (note: the Canadian, Irish, and U.S. cases were reported in persons who resided in the United Kingdom during a key exposure period of the U.K. population to the BSE agent) (Center for Disease Control, 2004). Concern over direct transmission of TSE diseases from other animal species to humans suddenly became a public issue. Public concern over the potential connection between mad cow disease and vCJD surfaced just as the distribution of CWD in deer and elk was increasing in the United States. To date, there have been no cases of human prion disease that have been associated with CWD. Because of differing experiences seen with two more common animal TSEs, BSE and scrapie, there is a lingering uncertainty about assessing any potential risk that CWD may pose to humans (Williams et al. 2002a). Scrapie, a TSE disease-affecting sheep, has been found in sheep populations in many countries for at least 200 years. Although there is a long history of human exposure to the scrapie infective agent (prion) through handling sheep and consuming sheep tissues, including brain, there is no evidence that this exposure presents a risk to human health. In contrast, BSE, as discussed, has been implicated in the deaths of 153 humans due to vCJD. In the absence of complete information on risk, and in light of similarities between animal and human TSEs, public health officials and wildlife management professionals recommend that hunters, meat processors and taxidermists handling deer and elk carcasses from areas where CWD has been diagnosed should take measures to avoid exposure to the CWD agent and to other known zoonotic pathogens. Boning game meat is recommended as an effective way to reduce the potential for 3 exposure. It is also recommended that hunters not consume the brain, spinal cord, eyes, spleen, tonsils, or lymph nodes from harvested deer and elk, particularly those harvested from areas where CWD has been identified in the free ranging populations. These precautionary measures should serve as a "firewall" to further reduce any human risk from CWD. ... snip...full text 96 pages http://fwp.state.mt.us/publicnotices/download.aspx?id=e12cc040-ded8-42cb-8e19-549b108f870a http://fwp.state.mt.us/publicnotices/notice_892.aspx Ermias D. Belay,*Comments Suggested citation for this article: Belay ED, Maddox RA, Williams ------------------------------------------------------------------------ Chronic wasting disease (CWD) of deer and elk is endemic in a FULL TEXT http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm CWD DOES TRANSMIT TO PRIMATE, COWS AND SHEEP, TSS Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC. Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of PMID: 6997404 Xavier Bosch My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost 49-year-old Singeltary is one of a number of people who have remained Singeltary was greatly demoralised at the few attempts to monitor the Until recently, CWD was thought to be confined to the wild in a small To date, experimental studies have proven that the CWD agent can be Part of the problem seems to stem from the US surveillance system. CJD Although in November last year the US Food and Drug Administration Getting data on TSEs in the USA from the government is like pulling Norman Foster, director of the Cognitive Disorders Clinic at the Ali Samii, a neurologist at Seattle VA Medical Center who recently CDC spokesman Ermias Belay says that the CDC will not be investigating http://infection.thelancet.com/journal/vol3/iss8/full/laid.3.8.newsdesk.26517.1 Introduction 1. The Food Standards Agency asked SEAC to consider the possible public and animal health implications of chronic wasting disease (CWD), in particular the level of risk posed to consumers of meat from infected animals. The committee also considered the possibility that BSE may be present in UK deer. Background 2. CWD has emerged as an endemic transmissible spongiform encephalopathy (TSE) in certain captive and free-ranging species of cervid (deer) in some areas of North America. The disease is characterised by weight loss and behavioural changes in infected animals, usually over a period of weeks or months leading to death. CWD has not been found in the UK or elsewhere in Europe. No definitive or suspected cases of transmission of CWD to humans have been reported. 3. SEAC considered a review of the published, and some unpublished, research on CWD, together with surveillance data on TSEs in European cervids and information on UK cervid populations (1). Origins 4. The origins of CWD are unknown. On the basis of epidemiological data, it is highly improbable that CWD originated from the recycling of mammalian protein in processed feed. It has been suggested that CWD may have arisen from transmission and adaptation of scrapie from sheep to cervids, as a result of a spontaneous change of endogenous prion protein (PrP) to an abnormal disease-associated form, or from an unknown source. 5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis are lacking. Host range 6. The known natural hosts for CWD are mule deer (Odocoileus hemionus hemionus), black-tailed deer (Odocoileus hemionus columbianus), white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk (Cervus elaphus nelsoni). The prevalence and geographical distribution of CWD in these species appears to be increasing in North America in a manner which is unlikely to be due simply to increased surveillance. 7. There are no direct data relating to the transmissibility of CWD to UK cervid species. However, comparison of a limited number of PrP codons indicates some homology in the endogenous PrP gene of European and North American cervid species. Thus, the possibility that UK cervids may be susceptible to CWD cannot be excluded, in particular red deer (Cervus elaphus elaphus) which are closely related to elk. 8. There is no evidence to suggest that CWD is present in UK cervids. However, because surveillance in the UK is very limited, a low level prevalence of CWD cannot be ruled out. The committee endorsed the opinion of the European Food Safety Authority on CWD surveillance in the European Union (2004) . 9. Transmission studies using parenteral routes of administration to cattle, sheep and a single goat, together with data from in vitro PrP conversion experiments, suggest that a significant barrier to CWD transmission to these species may exist. No transmission has been evident so far in an on-going oral transmission study in cattle after six years. Furthermore, no signs of infection have been observed from monitoring of cattle co-habiting areas with infected cervids, or in cattle, sheep or goats in close contact with infected cervids in research facilities. Thus, although the data are limited, there is currently no evidence to suggest that CWD can be transmitted naturally to cows, sheep or goats, and it is likely that there is a strong species barrier to such transmission. Routes of transmission 10. Epidemiological data indicate that lateral transmission between infected and susceptible cervids occurring naturally is sufficiently effective to maintain epidemics in both captive and free-living populations. There is good evidence from studies of cervids inhabiting paddocks previously inhabited by infected animals or contaminated with infected carcases, that CWD can be transmitted laterally between animals via the environment. The precise mechanism of transmission is unclear. It is possible that the infectious agent is shed in the saliva, faeces or urine or as a result of decomposition of infected carcases and transferred to other cervids grazing the contaminated areas. It is also possible that some maternal transmission occurs. 11. There have also been suggestions that the lateral transmission of CWD may be influenced by environmental factors. Pathogenesis 12. Information on the pathogenesis of CWD is limited. The data show that, following oral challenge, PrPCWD is first detected in the oral and gut-associated lymphoid tissues before spreading more widely within the lymphoid system and then to the brain. Involvement of the retropharyngeal lymph nodes or tonsils in the pathogenesis may not occur in some elk. At the microscopic level, the nature and distribution of the tissue lesions are similar to those found for scrapie. The available data suggest the pathogenesis of CWD is similar to scrapie. BSE in UK deer 13. Both captive and free-ranging cervids in the UK may have been exposed to contaminated feed prior to the reinforced mammalian meat and bone meal ban instituted in 1996. A study to look at the potential susceptibility of red deer to BSE has shown no signs of transmission of the disease by the oral route, but it is at a very preliminary stage. Although a theoretical possibility exists, there is no evidence from the very limited surveillance data to suggest that BSE is present in the UK cervid population. Human health implications 14. Epidemiological data on possible CWD infection of humans are very limited. The possibility that clinical symptoms of CWD in humans differ from those of Creutzfeldt-Jakob Disease (CJD) cannot be excluded. There is no significant difference between the prevalence of CJD in CWD endemic areas and other areas of the world. However, because CJD surveillance in the USA is relatively recent, not all CJD cases may have been identified. Additionally, detection of a small increase in prevalence of such a rare disease is very difficult. Investigation of six cases of prion disease in young people (< 30 years of age) in the USA found no definite causal link with consumption of venison from known CWD endemic areas. The disease characteristics in these cases were indistinguishable from sporadic CJD or Gerstmann-Strδussler-Scheinker syndrome. Likewise, in a study of three hunters (> 54 years of age) diagnosed with sporadic CJD, no link with consumption of venison from CWD endemic areas was found. No causal link was found in an investigation of three men with neurological illnesses who were known to partake in wild game feasts. Only one of these subjects was found to have a prion disease and this was also indistinguishable from sporadic CJD. 15. Preliminary results from transmission experiments in transgenic mice expressing human PrP suggest the presence of a significant species barrier to transmission of CWD to humans. However, these findings must be interpreted with caution as they may not accurately predict the human situation. Data from in vitro experiments on conversion of human PrP by disease-associated forms of PrP, including PrPCWD, are equivocal. 16. The committee concluded there is no evidence of transmission of CWD to humans from consumption of venison, and that there may be significant barriers to transmission. Nevertheless, as the data are extremely limited a risk cannot be ruled out should CWD enter UK herds. Conclusions 17. There is no evidence that CWD (or BSE) is present in the UK cervid population. However, because only limited surveillance is conducted in the cervid population, a low level prevalence of CWD cannot be ruled out. It is recommended that further surveillance of TSEs in UK cervids is conducted. 18. There is no evidence of transmission of CWD to humans from consumption of meat from infected cervids. Although epidemiological and experimental data on potential transmission of CWD are extremely limited, they suggest that there may be a significant species barrier. It would be helpful if further studies were available assessing the potential species barrier for transmission to humans. 19. Although limited, there is no evidence CWD can be transmitted to cattle, sheep or goats by natural means. 20. In summary, it appears that CWD currently poses relatively little risk to human health, or to the health of cattle, sheep or goats in the UK. Nevertheless, as a risk cannot be excluded a watching brief should be maintained. 10:00 Chronic Wasting Disease in UK deer Alan Harvey (FSA).Wildlife Information Network. 85/2*(pdf) http://www.seac.gov.uk/papers/tsesdeer-%20final.pdf Annex 1 (pdf) http://www.seac.gov.uk/papers/cwdiseaseannex1.pdf Annex 2 (pdf): http://europa.eu.int/comm/food/fs/sc/ssc/out324_en.pdf Annex 3 (incl. appendices) (pdf) http://www.seac.gov.uk/papers/munrodeerrptannex3.pdf Annex 4 (pdf) http://www.seac.gov.uk/papers/deersurvannex4.pdf Annex 5 (pdf): ALL of these false reassurances we have heard time and time again, and ALL have been proven wrong. AS with the BSE TO HUMANS AND BSE to GOAT. IT was always it never happend under natural conditions, just in the lab, so not to worry. NOW WE HAVE TO WORRY; http://www.jarvm.com/articles/Vol2Iss1/DEBOSSCHERE.htm http://www.pnas.org/cgi/content/full/041490898v1 CWD TRANSMITS TO PRIMATES, COWS AND SHEEP, TRANSMISSION STUDIES HAVE NEVER BEEN DONE ON HUMANS...TSS Evidence For CWD/Mad Cow/TSEs In Confidence - Perceptions of unconventional slow virus diseases Transmission Studies http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf Greetings 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; AvailabilitySeveral 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 feedban of 8/4/97. this partial and voluntary feed ban of some ruminantmaterials being fed back to cattle is terribly flawed. without the_total_ and _mandatory_ ban of all ruminant materials being fedback 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 recentfindings of deer fawns being infected with CWD, how many couldpossibly 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 infectivityin the rump or ass muscle. wether it be low or high, accumulationwill 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 unidentifiedTSE in USA cattle. all this has been proven, but the TSE in USAcattle has been totally ignored for decades. i will document thisdata below in my references.5. UNTIL we ban all ruminant by-products from being fed backto ALL ruminants, until we rapid TSE test (not only deer/elk) butcattle in sufficient numbers to find (1 million rapid TSE test inUSA cattle annually for 5 years), any partial measures such as theones proposed while ignoring sub-clinical TSEs and not rapid TSEtesting cattle, not closing down feed mills that continue to violate theFDA's BSE feed regulation (21 CFR 589.2000) and not makingfreely available those violations, will only continue to spread theseTSE mad cow agents in the USA. I am curious what we willcall a phenotype in a species that is mixed with who knowshow many strains of scrapie, who knows what strain or how manystrains of TSE in USA cattle, and the CWD in deer and elk (notelling how many strains there), but all of this has been renderedfor animal feeds in the USA for decades. it will get interesting oncesomeone 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 mustbe issued to every family of a victim of TSE. only checking deathcertificates 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 makethe same mistakes... REFERENCES snip... Department of Pathology, College of Veterinary Medicine and Biomedical Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail Mule deer fawns (Odocoileus hemionus) were inoculated orally with a snip... These results indicate that mule deer fawns develop detectable PrP res snip... http://vir.sgmjournals.org/cgi/content/full/80/10/2757 snip... April 9, 2001 WARNING LETTER 01-PHI-12 Brian J. Raymond, Owner Tel: 215-597-4390 Dear Mr. Raymond: Food and Drug Administration Investigator Gregory E. Beichner conducted Our investigation found failure to label your In addition, we note that you are using approximately 140 pounds of The above is not intended to be an all-inclusive list of deviations from http://www.fda.gov/foi/warning_letters/g1115d.pdf From: TSS () Jean E. Jewell1, Mary M. Conner2, Lisa L. Wolfe3, Michael W. Miller3 and Elizabeth S. Williams1, 1 Department of Veterinary Sciences, University of Wyoming, Wyoming State Veterinary Laboratory, 1174 Snowy Range Road, Laramie, WY 82070, USA The prion protein (PrP) gene was characterized in 1482 free-ranging mule deer (Odocoileus hemionus) from Wyoming and Colorado. Using DNA sequences from 363 deer, dimorphisms at codons 20 (aspartate/glycine) and 225 [serine (S)/phenylalanine (F)] were found; silent changes occurred at codons 131 (tyrosine) and 247 (isoleucine). The remaining samples were surveyed for codon 225 genotype and all were characterized for chronic wasting disease (CWD) infection status. A total of 112 deer with the genotype 225SF or FF were found, of which one was CWD-positive; 1370 were 225SS, with 289 positive for CWD. Among CWD-negative deer, the frequency of 225SF/FF genotypes was 9·3 % but among CWD-positive deer it was only 0·3 %. For all samples combined, CWD status was not independent of codon 225 genotype (P<0·0001). The odds that a deer of the 225SS genotype was CWD-infected were 30 times greater (95 % confidence intervals=4213) than for a 225SF deer. The proportion of 225SF animals in sampled subpopulations varied from 0 to 18 %; the CWD prevalence varied from 0 to 25 %. However, no relationship was observed between genotype frequency and CWD prevalence in different areas. The PrP sequences of experimentally infected mule deer were analysed from pre-existing projects and 10 animals were found with 225SF genotypes, all of which were positive for CWD. Data available from some of these animals suggest that the 225SF genotype could be associated with longer incubation periods in CWD infection compared with the 225SS genotype. Published online ahead of print on 27 May 2005 as DOI 10.1099/vir.0.81077-0. Deceased 29 December 2004. Authors Hamir, Amirali http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=166311 HELLO Tim Feldner, please don't be to complacent on the real potential of CWD transmission to humans. they said this about BSE of cattle to humans, as now documented nvCJD. but this is only one strain. we now have BASE in cattle that seems to be very similar to some of the sporadic CJDs; Medical Sciences Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini Ά, Salvatore Monaco ||, and Maria Caramelli * *Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ΆIstituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003) Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease. C.C. and G.Z. contributed equally to this work. ||To whom correspondence should be addressed. E-mail: salvatore.monaco@mail.univr.it. www.pnas.org/cgi/doi/10.1073/pnas.0305777101 http://www.pnas.org/cgi/content/abstract/0305777101v1 WITH all the many documented TSEs in many different species in the USA. WITH all rendered and fed back to animals for human and animal consumption for decades. WITH the fact already proven that USA SCRAPIE TO USA CATTLE does NOT produce UK BSE, but something different; http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf SCRAPIE to humans, why not; http://www.bseinquiry.gov.uk/files/yb/1976/10/12002001.pdf THE findings from Corinne Ida Lasmιzas*, [dagger] , Jean-Guy Fournier*, Hermann Boe*, Domνnνque Marcι*, Franηois Lamoury*, Nicolas Kopp [Dagger ] , Jean-Jacques Hauw§, James IronsideΆ, Moira Bruce [||] , Dominique Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible http://www.pnas.org/cgi/content/full/041490898v1 HOW MANY of the sporadic CJDs in the USA are of animal origin, either directly or indirectly via 2nd, or 3rd passage via the medical or surgical arena and OR blood transfusion ??? HOW many of the sporadic CJDs i.e. 85%+ of all _documented_ cases, how many of these are truely sporadic/spontaneous without any route or source, if one believes in spontaneous TSE at all ??? Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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