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MARQUETTE SAUK COLUMBIA DODGE WASHINGTON OZAUKEE MILWAUKEE WAUKESHA JEFFERSON DANE KENOSHA RACINE WALWORTH ROCK GREEN LAFAYETTE WISCONSIN ILLINOIS JO DAVIESS STEPHENSON CARROLL OGLE WINNEBAGO BOONE DE KALB KANE MCHENRY LAKE IOWA GRANT RICHLAND CRAWFORD VERNON JUNEAU ADAMS CWD Positive Location Herd Reduction Zone Disease Eradication Zone C W D Chronic Wasting Disease UPDATE from the Wisconsin Department of Natural Resources March 2005 Wisconsin is wrapping up its third season of CWD management. Once again landowners and hunters gave generously of their time and talents to help manage CWD in the state. We at the Department of Natural Resources (DNR) are so grateful for this help. Strides are being made in managing the disease but more work still needs to be done. We are committed to eradicating CWD in Wisconsin. It is going to be a long-term process, and a process that will continue to rely on support and involvement from people like you. Surveillance continues to be a priority in CWD management as we develop a clear picture of the geographic extent and prevalence of the disease. For the 2004-05 deer season, we concentrated disease surveillance efforts in and around the two DEZs, southeastern Wisconsin, and in areas of CWDpositive game farms. Over 18,000 deer have been sampled so far this season. As of February 15, 2005, we have received news of 99 positive deer. A few positives were discovered outside of the established DEZs. These outlying positives will be taken into consideration when deciding on CWD management plans for next season. Thanks to those who brought their deer to a DNR collection station for CWD sampling! Data to date suggests that the western DEZ and eastern DEZ are separate disease events. Analysis of the geo- Locations of CWD-Positive Deer in Wisconsin and Illinois Wisconsin data updated 2/15/2005; Illinois data updated 12/1/2004 Researchers believe that the two areas of infection—one in the Dane-Iowa county area and the other along the Wisconsin/Illinois border—may represent two separate infection areas. Continued on p. 2 graphic distribution of the western DEZ outbreak shows that the pattern of positives is not random, but is tightly clustered. Although the western DEZ is over 1,300-square miles in size, more than 80 percent of the positive deer are in a 126-square mile area bounded by Spring Green, Mazomanie, Black Earth, Mount Horeb, and Ridgeway. Within this area of concentrated disease, there is a core of highest prevalence. A few sections within this core had as high as 8 to For more information on chronic wasting disease, please visit dnr.wi.gov Click on "Chronic Wasting Disease in Wisconsin." 2 Chronic Wasting Disease Update 12 percent of adult deer testing positive for CWD. The eastern DEZ cases appear to be adjacent to an outbreak in northeastern Illinois where currently 75 CWD-positive deer have been found since 2002. Surveillance data to date indicates a more scattered pattern of disease distribution in northern Illinois and southeast Wisconsin, rather than the tight pattern of disease distribution in the western DEZ. (See map on front page for locations of CWD-positive deer.) In addition to surveillance, herd reduction remains a key component of CWD management. For the 2004-05 season, we continued to ask hunters to take as many deer off the landscape as possible in an effort to drastically reduce the herd size, and ultimately control the spread of CWD. We heard from many hunters that they wanted to help reduce the herd, but taking more deer than can be used goes against their hunting ethic. To address the issue we funded a program where hunters could donate DEZ deer to a food pantry. Over 1,800 deer have been donated by hunters to the food pantry program. We also worked with Valley of the Kings large-cat sanctuary in Sharon, WI, to send hundreds of deer carcasses not appropriate for the food pantry to be used as lion food. Both options were well received by hunters. Please take the time to read the rest of this newsletter for more updates on CWD in Wisconsin. Additionally, more CWD information, including the most up to date CWD surveillance results, is available online at dnr.wi.gov. Thank you once again for your interest and help in managing CWD in Wisconsin! Alan Crossley CWD Project Leader Farmed Cervid Update The Department of Agriculture, Trade, and Consumer Protection (DATCP) regulates farm-raised deer and elk in Wisconsin. There are approximately 720 registered deer and elk farms in the state containing about 30,500 animals. The discovery of CWD in Wisconsin has led to major changes in the regulation of these farmed deer and elk. Regulations include: . It is no longer legal to accept orphaned or injured deer from the wild into farms or to fence in property and capture wild deer. . Cervid farms must be enrolled in the CWD monitoring program to sell live animals. The CWD monitoring program requires an initial herd census with offi cial individual animal identifi cation and annual reports accounting for where every animal on the farm came from or went in the past year. About 550 herds are enrolled in the monitoring program. . All farms, whether enrolled in the monitoring program or not must CWD test every deer or elk that is 16 months or older that dies or goes to slaughter. More than 10,000 farm-raised deer and elk have been tested. . Importation of deer and elk into Wisconsin requires a permit from the State Veterinarian, a certifi cate of veterinary inspection, proof that they are free of TB and brucellosis, offi cial identifi cation numbers on the animals, and documentation that they come from a herd with no evidence of CWD in the past fi ve years. This last requirement amounts to a temporary moratorium on many deer and elk imports because most states did not begin surveillance until recently. . Deer and elk farms are required to meet fencing standards. Producers are required to report escapes within 48 hours. The DNR has authority to kill escaped farm-raised animals if they are not immediately recaptured. As of January 2005, 27 farmraised white-tailed deer and one elk have tested positive for CWD on seven farms. The latest was a white-tailed deer on a Crawford County farm. The herd was enrolled in the CWD monitoring program. The 19-month-old buck was tested for CWD after it died from respiratory causes. Additionally, 20 herds are under quarantine because they contain animals that may have been exposed to CWD. In some cases, animals were bought from herds later found to be infected with CWD while others are within Wisconsin’s wild deer CWD zones and may have been exposed to infected free-ranging deer. For more information on CWD relating to farmed deer, please visit DATCP’s Web site at datcp.wi.gov CWD Update, Continued from p. 2 Chronic Wasting Disease Update 3 Research Research studies include topics such as: . Deer dispersal, social behavior, and mortality; . Disease ecology, including genetic resistance of deer to the disease; . Comparing Wisconsin CWD strains to those found on other parts of the continent; . Spatial patterns and prevalence of CWD in southwest and southeast Wisconsin; . Transmission mechanisms, including the effects of baiting and feeding and between does and fawns before they are born; . Dynamics of CWD prions in the soil; . Susceptibility of other species, such as cattle and scavengers, to CWD; . Possible risks to human health, including primate studies and comparison of deer and human prion genetic and molecular structures; A comprehensive interagency CWD research plan was developed in 2002 to determine what was currently known about CWD, CWD control strategies, and what key information was needed to manage the disease in Wisconsin. Compared to many other diseases, relatively little was known about CWD and effectiveness of control strategies. Research priorities were identifi ed in fi ve broad areas to increase knowledge: disease ecology, deer ecology, human ecology, diagnostics, and human health implications of CWD. Because of the need to implement the disease control program quickly, an adaptive management approach integrating research and management activities was identifi ed as a key component of the CWD control strategy. By taking this "learn-and-adapt" management approach, we are able to incorporate research and surveillance fi ndings into management strategies as the information becomes available. In 2004, a total of 34 CWD research studies were underway in Wisconsin. Another 12 studies were underway in other states with which we are collaborating by providing data and/or tissue samples. These studies are being conducted and funded by many partners such as University of Wisconsin and the USGS National Wildlife Health Center. Coordination of these studies is being done by an interagency team to insure research is focused on high priority needs for managing CWD in Wisconsin, to promote collaboration among scientists, to facilitate data sharing, and to promote joint problem solving. . Attitudes, behavior, and desires of hunters and landowners in relation to CWD; . Analysis of deer removal efforts in southwest Wisconsin and changes in deer population size; . Computer modeling to evaluate alternate management strategies; . Better diagnostic tools for detecting the disease; . Development of techniques to detect CWD prion in the environment. Information from these projects is being used to evaluate the effectiveness of disease control activities and in making management decisions about future control strategies. Research on diagnostic tests for CWD has already resulted in the adoption of screening tests that signifi cantly shorten the time required to notify most hunters of the status of their deer. The following accounts give highlights from a few of the CWD research efforts. 4 Chronic Wasting Disease Update The Risk of CWD Transmission with Baiting and Feeding Michael Samuel, Ph.D. and Abbey Thompson USGS Cooperative Wildlife Research Unit University of Wisconsin-Madison Tim VanDeelen, Ph.D University of Wisconsin - Madison Chris Yahnke University of Wisconsin-Stevens Point In this study the research team is evaluating the role of supplemental feeding in the direct and indirect transmission of diseases like CWD in white-tailed deer. They are using various feeding techniques (trough, pile and spread) and varying amounts of corn at four supplemental feed stations and two monitored natural feeding areas within the fenced Sandhill Wildlife Demonstration Area in Babcock, Wisconsin. Disease transmission rates are being estimated through comparison of deer use, contact rates, and fecal contamination at supplemental feeding sites. Cameras are also being used to capture information on deer use and interactions occurring at supplemental feeding sites and natural feeding areas. Biology and wildlife students at the University of Wisconsin–Stevens Point have been doing their part to quantify CWD transmission risks associated with baiting and feeding deer. They compared 2.5-gallon versus 10-gallon bait sites and piling the bait versus spreading the bait over a larger area. Using motion-sensing digital cameras, the students, led by senior Casey Wilke, found a signifi cantly higher incidence of close deer-to-deer contact at bait sites where the bait was piled relative to sites where bait was broadcast. Deer densities increased at all bait sites relative to control sites where only natural forage was available The Dynamics of CWD Prions in Soil Joel Pedersen, Ph.D. University of Wisconsin–Madison Dr. Pedersen is trying to understand what happens to CWD prions in soil. This is important to understanding the risks for environmental transmission to deer and also to developing practical and safe disposal practices. Researchers are currently looking at the persistence of prions and the movement of prions through different types of soil. They have found that clay soils adsorb disease prions at a much higher rate than sandy soils. Researchers are using animal models to estimate how long prions persist in the soil and if infectivity declines over time. They will also be exploring what happens to prions in landfi ll and wastewater systems. Genetic Resistance to CWD in White-tailed Deer Judd Aiken, Ph.D. School of Veterinary Science University of Wisconsin–Madison Researchers are investigating whether there is genetic CWD resistance in deer by comparing CWD-infected and non-infected wild deer. Conclusions indicate that there is variability in prion proteins among Wisconsin deer and that at least 95 percent of Wisconsin deer have genotypes known to be genetically susceptible to CWD. These results suggest that virtually all Wisconsin deer are susceptible to CWD and would not be genetically resistant to the disease. Chronic Wasting Disease Update 5 Human Dimensions Research Jordan Petchenik, M.S. Wisconsin Department of Natural Resources Human dimensions researchers surveyed hunters statewide in 2002, DEZ hunters in 2003 and landowners in the DEZ in 2004 to determine attitudes towards CWD management, hunting behavior in response to CWD, their assessment of health risks, and likelihood of future hunting participation. Landowners and hunters are key components to CWD management. Their feelings and attitudes are very important to understand and should be carefully considered in making management and communication decisions. Wisconsin also is a participant in an eight-state study of hunters’ responses to CWD. The Western Association of Fish and Wildlife Agencies is organizing the study which will allow comparison across states with an emphasis on learning how CWD has affected, if at all, hunting experiences, and how future hunts may be affected if conditions changed or CWD spread to new areas. 2003 Report on Hunter Effort and Attitudes Robert Holsman, Ph.D. and Ryan D. Meinerz University of Wisconsin–Stevens Point In an effort to better understand hunter behavior in the western DEZ, UW-Stevens Point researchers Holsman and Meinerz mailed diary cards over a three month period to 2,000 hunters in southern Wisconsin to measure the amount of time they spent in the fi eld. The project is funded by the DNR and UW-Stevens Point. It is an effort to be responsive to hunter opinions and is one part of the DNR’s learn-and-adapt disease management plan. The preliminary results show that most gun deer hunters in the western DEZ give the DNR a "B" or better grade in their handling of the management, despite the sacrifi ces hunters have been asked to make to help eliminate the disease. Survey results also show widespread support for the baiting and feeding bans. These preliminary results provide baseline data by which to compare this and future fall gun deer hunts. The study will track over the next few years how hunter attitudes vary as agency management does or does not change within the DEZs. The second year of the study is well underway, collecting and analyzing information related to signifi cant social and psychological variables that predict public concern about CWD and support of control strategies put in place by the DNR. Human Prion Disease Surveillance James Kazmierczak, DVM Department of Health and Family Services Creutzfeldt-Jakob disease (CJD) is a TSE that affects humans. First described in the 1920s, CJD occurs sporadically worldwide at a rate of about one case per million population. The Wisconsin Division of Public Health maintains an ongoing surveillance for CJD, consisting of case-reporting by neurologists and hospital infection control practitioners, as well as reviews of death certifi cates. Suspected cases are investigated, and whenever possible, are confi rmed by autopsy. From 1997 to date, there have been 17 autopsy-confi rmed cases and 20 possible/probable cases reported through this surveillance. All of the confi rmed cases are consistent with the sporadic or familial form of CJD, and do not have the characteristics of variant CJD, the form of the disease seen in Europe associated with bovine spongiform encephalopathy ("mad cow disease"). The average annual incidence of reported CJD in Wisconsin, including confi rmed, probable, and possible cases, is approximately one per million. PRINTED ON RECYCLED PAPER Department of Natural Resources Bureau of Wildlife Managment 101 S. Webster Street PO Box 7921 Madison, WI 53707-7921 Presorted Standard U.S. Postage Paid Madison, WI Permit 906 Are You Getting More than One Newsletter? If you receive more than one of these newsletters each month, please clip off the labels from each of the newsletters and send them back to us so we can remove doubles from our mailing list: CWD Information, Wisconsin DNR WM/6, PO Box 7921, Madison, WI 53707. For more information on CWD visit the following Web sites: dnr.wi.gov and click on "Chronic Wasting Disease in Wisconsin," and http://wildlife.wisc. edu/coop/CWD/CWD_ Introduction.html or call the DNR’s toll-free CWD information line 1-877-WISC CWD or 1-877-947-2293 between 8 A.M.–4 P.M. Monday–Friday What should I do if I observe or harvest a deer that I suspect might have CWD? Call the local DNR offi ce right away. The DNR will make every effort to collect samples from the possibly affected deer for CWD testing. Wisconsin State Agency Contacts Department of Natural Resources Bureau of Wildlife Management 608-266-8204 Department of Agriculture, Trade and Consumer Protection Offi ce of Outreach and Policy/Animal Health and Safety Issues 608-224-5130 datcp.wi.gov keyword: chronic wasting disease Department of Health and Family Services 608-267-7321 dhfs.wi.gov/healthtips/BCD/ creutzfeldt.htm The Wisconsin Department of Natural Re sourc es pro vides equal opportunity in its employment, pro- grams, services and func tions under an Affi rmative Action Plan. If you have any questions, please write to Equal Opportunity Offi ce, Department of the Interior, Wash ing ton, D.C. 20240. This publication is available in alternate format (large print, Braille, audio tape, etc.) upon request. Please call 608-266- 8204 for more information. http://www.dnr.state.wi.us/org/land/wildlife/whealth/issues/cwd/pubs/05_03_news.pdf Transcript Does CWD pose a threat to human health? James Kazmierczak, Epidemiologist, Wisconsin Department of Health Hi, I'm Jim Kazmierczak. I'm with the state division of public health. The single issue that I am going to try to address today is the issue of whether chronic wasting disease poses any risk to human health. As you probably already heard earlier in the presentation, chronic wasting disease belongs to a family of related diseases called transmissible spongiform encephalopathies, or TSE's for short. These diseases are related in the sense that they're all caused by this infectious protein that we call a prion, and also they're related in the fact affected the all present the same sort of clinical disease as a result of the type of lesions that they produce in the brain. We know that different diseases in this family called TSE's, affect different species. For instance, we have disease called scrapie that affects sheep and goats. We have a particular kind of prion that affects mink. We have the bovine spongiform encephalopathy that's been in the news a lot, the Mad Cow Disease that affects obviously bovines. We have chronic wasting disease that affects deer and elk. And actually humans have their own unique type of spongiform encephalopathy. That disease is called Creutzfeldt-Jakob Disease, or CJD. This is the disease of humans that is similar, it's in the same group or family, as the other TSE's that we just mentioned. I want to talk a bit about Creutzfeldt-Jakob Disease in humans. I feel I need to cover this because first of all, it's logical to assume that any prion disease that may in fact across the species barrier to humans, will result in a similar type of disease as Creutzfeldt-Jakob Disease. Also, you're going to need to know a little bit about Creutzfeldt-Jakob Disease and in order to understand some of the points I'll make when I talk about the potential risk of chronic wasting disease to humans. Creutzfeldt-Jakob Disease is a nasty disease. It produces progressive dementia, confusion, lack of coordination, and eventually death. This is an invariably fatal disease, and it usually kills its victims within twelve months of onset. The incubation period of this disease-- that is, the time between when one becomes exposed to the infectious protein, and when one actually develops symptoms, can be very variable, and it can range from between 15 months to over 20 years. So it can have an extraordinarily long incubation period. As far as how Creutzfeldt-Jakob Disease is diagnosed in humans, the first thing you need to know is that there is no test that can be applied to show that someone is in the incubation phase of CJD. It's not until clinical signs appear that the disease can start to be diagnosed, and at that point the diagnosis is based on clinical signs and symptoms, laboratory tests, electroencephalogram patterns, and the definitive diagnosis is then made by actually looking at sections of the brain microscopically either with a brain biopsy or with a post-mortem examination. I'm going to add another wrinkle to this. We've been looking at CJD or Creutzfeldt-Jakob Disease until now as a single entity-- when in fact one could split CJD into two different forms. The first is what we call classic Creutzfeldt-Jakob Disease. This form of the disease has been known to occur for at least 70 years, and it was probably occurring long before that. So this is not a new disease. It affects primarily older people. The vast majority of people to do get this disease are over the age of 65, and it affects people worldwide at a rate of approximately one case per million people. And that rate holds true here in the United States, including in Wisconsin. How does one acquire this classic form of Creutzfeldt-Jakob Disease? In many cases it's just not known with certainty; although there are some mechanisms that are well-known. The majority of cases do appear to occur spontaneously for no apparent reason. There are, however, a percentage of cases that apparently are familial; in other words, there is a family history of this, so there is a genetic component to a certain percentage of these cases, and interviewing patient families we can find a family history of this. It is also possible to acquire CJD through certain medical procedures; procedures that involve the transfer of tissues or tissue extracts from an infected patient (although obviously it's unknown to the medical providers at the time that the person was infected). But it can be transmitted, for instance, to people who receive pituitary extract; or certain brain covering tissue that is used for transplants. The infectious agent can be transmitted from the sick individuals to the well individuals by these sorts of medical procedures. And finally there's a small number of people who actually have developed this from ingestion. You may think that's an odd way of acquiring it, but this was discovered upon study of a Creutzfeldt-Jakob-like disease among some New Guinea tribesmen back several decades ago. At that time they were still practicing some ritualistic cannibalistic practices, and that's how we know the disease can also be transmitted by ingestion. So that's sort of a summary of the classic form of Creutzfeldt-Jakob Disease. Again this is the form of disease has been known to occur for decades, and has been occurring worldwide at a rate of approximately one per million people. Now, what's new on the scene is a form of the disease called new variant Creutzfeldt-Jakob Disease, or new variant CJD. This form of the disease was first seen in England only about six years ago, and it is still limited to the United Kingdom and some European countries. It has not been found in the United States. New variant CJD is quite similar to the classic form that we've just finished talking, about it does tend to occur in younger people-- people with an average age in their thirties, actually-- and it differs in some ways-- subtly, though-- from the classic CJD in clinical signs. For instance, a neurologist would normally be able to differentiate on a clinical basis and some laboratory work, whether one has the classic form, or one has this new variant form of CJD. There's also enough difference in the microscopic appearance of brain tissue, so the bottom line is that the two types of disease-- the classic and the new variant forms-- can be differentiated. So why has this new variant of Creutzfeldt-Jakob Disease appeared on the scene, seemingly of nowhere? Well, most of you probably know that during the 1980s there was an epidemic of bovine spongiform encephalopathy (better known as Mad Cow Disease) that occurred in Great Britain. It certainly got tons of media coverage at the time. Hundreds of thousands of cattle at that time were infected, many of which eventually found their way into the human food chain. The best evidence suggests that the prion that causes the bovine encephalopathy somehow managed to jump the species barrier and affect humans. Apparently when this prion did manage to infect a different species (in other words did manage to get in to humans), it produced a different clinical picture than the classic form of CJD. By now you're probably wondering, "So what?" Now that we know the background about this disease form in humans, let's go back to the original question about the potential for chronic wasting disease to affect human beings. First of all, as far as we know there's never been the case of new variant Creutzfeldt-Jakob Disease here in this country-- and people have looked. The Centers for Disease Control began looking for the new variant form of Creutzfeldt-Jakob Disease several years ago. What they're doing is looking at people with compatible symptoms to Creutzfeldt-Jakob Disease who are under the age of 55. If you recall, I said that this disease tends to occur mostly in younger people, so onset at a young age would be a tip-off that we may be seeing this new variant form of Creutzfeldt-Jakob Disease. The other bit of information that is somewhat reassuring as far as looking at the human health potential of chronic wasting disease, is that the classic form of CJD which does occur in this country, does not occur at any increased rates in the states out west that have had chronic wasting disease in their deer and elk herd for decades. Those states are not seeing any increase in Creutzfeldt-Jakob Disease, compared to states that don't have this disease in their deer herds. Furthermore, both the World Health Organization and the Centers for Disease Control state that there's no scientific evidence to prove any sort of link between chronic wasting disease and any human health affects. And finally, researchers have never been able to demonstrate infectivity of muscle tissue, whether that's from CWD infected deer or elk, or BSE infected cattle, they've never been able to show that muscle tissues actually is infective as far as transmitting this disease. So those are all fairly reassuring points, but-- as we mentioned earlier it appears that at least once in the past, a prion disease has been able to jump the species barrier and affect humans. This is what happened in Great Britain with the Mad Cow problem. And in a study that was just recently published, mice that were injected with a strain of the prion protein that was actually adapted to grow in rodents, they found that when they infected these mice they were actually able to transfer the infection by way of their skeletal muscle. So at least under these laboratory conditions, skeletal muscle can be infectious in those circumstances. Whether that's truely relatable to what happens in the real world, frankly we just aren't sure. So can one say with certainty that chronic wasting disease will never cause human disease? Unfortunately, not. None of us has a crystal ball, and its actually very difficult, as you might expect, to be able to prove a negative-- to prove that CWD will never affect humans. I do think that if there is any risk-- and I said if-- it's likely to be quite low, based on the fact that first of all chronic wasting disease has never been known to affect humans, and also based on what we know about the epidemic of BSE in England and the new variant form of CJD in humans there. Here we are about a decade and a half after the outbreak in cattle, and even today there's only approximately 120 cases in all of Europe of the new variant Creutzfeldt-Jakob Disease. So that's fairly reassuring. I do wish I could quantify this risk in some way and try to put it in some perspective-- like perhaps comparing it to, say, the risk of cigarette smoking or the risk of drinking and driving. But it's impossible to try to quantify an event that's never occurred-- and again, CWD has never been known to result in human illness. As far as anyone knows, this is strictly a disease of deer and elk. Finally, the question is, "Is it safe to eat venison from deer that are harvested from this area?" Even though there is no evidence that CWD has ever caused human disease, because of the uncertainty about how it's transmitted, experts in the World Health Organization do advise that no part of any deer or elk that's known to be infected with CWD, be consumed by people. It also suggests that people avoid consuming certain tissues of any deer or elk-- and that would include tissues like brain, spinal cord, eyes, spleen, tonsils and lymph nodes-- because that's where the prion tends to congregate, in those tissues. So although the World Health Organization does state that there's never been any scientific evidence to demonstrate that CWD can cause illness in humans, they do recommend not eating any venison from known infected deer. So are they hedging their bets? Well, sure they are-- even though the scientific evidence so far does not indicate a risk, no one can give you that absolute guarantee of future safety. The best that I could do is to try to accurately convey to you what's known about the potential risk, and then let each person decide how comfortable he or she is with that small degree of uncertainty about the safety of venison. Unfortunately there just are no easy answers. http://dnr.wi.gov/org/land/wildlife/whealth/issues/CWD/video/jktranscript.pdf Perspective Chronic Wasting Disease and Potential Transmission to Humans 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... Conclusions Acknowledgments snip... http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm Current Neurology and Neuroscience Reports 2002, 2:488-495 Published 1 November 2002 Abstract Ongoing endemics and epidemics of prion disease afflict several species of ruminants regularly consumed by humans. Bovine spongiform encephalopathy (BSE) is epidemic in British cattle, and is now found in the cattle of more than 20 countries. A large, and apparently growing, epidemic of chronic wasting disease plagues deer and elk in North America. Finally, scrapie has been endemic in the sheep of most countries for many decades. It was once assumed that humans were not susceptible to these ruminant forms of prion disease, but an outbreak of a new form of Creutzfeldt-Jakob disease (CJD) among young Britons, almost certainly due to dietary exposure to BSE-contaminated beef, has disproved this supposition. Although all prion diseases share the same fundamental pathologic mechanism, transmission between species is sometimes inefficient. The basis of this "species barrier" is incompletely understood, but interspecies differences in the amino acid sequence of the prion protein and the strain of prions involved play critical roles. Reliable experimental models for determining the resistance of humans to animal prion diseases do not yet exist. It is possible that animal to human transmission of prion disease may manifest as CJD with unusual characteristics, but this is not necessarily the case. In the absence of a reliable means for determining the susceptibility of humans to animal prion disease, measures to minimize human exposure to animal prions should be emphasized. http://www.biomedcentral.com/1528-4042/2/488/abstract -------- Original Message -------- Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability 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... full text; 2003D-0186 TSS
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