Carcass Transportation Regulations in the United States and Canada

cwd_mapDownload the full Chronic Wasting Disease and Cervidae Regulations in North America. [PDF]

Download a quick reference map of Rules Governing Interstate Transport of High-risk White-tailed Deer Carcass Parts [PDF].

The number one objective in the management of CWD is to prevent its spread into new areas. One theoretical mode of disease transmission is via infected carcasses. Therefore, in an effort to minimize the risk of disease spread, a number of states have adopted regulations affecting the transportation of hunter-harvested deer and elk.

Since the suspected infective agent (prion) is concentrated in the brain, spinal cord and lymph glands, the most common regulation is the prohibition of the importation of whole carcasses harvested from CWD areas. Some states, like Colorado, also have established regulations addressing the transport of deer and elk out of CWD areas. Generally, states that have adopted carcass transportation regulations do not allow the importation of any brain or spinal column tissue and allow transport of only the following:

  • Meat that is cut and wrapped (either commercially or privately).
  • Quarters or other portions of meat with no part of the spinal column or head attached.
  • Meat that has been boned out.
  • Hides with no heads attached.
  • Clean (no meat or tissue attached) skull plates with antlers attached.
  • Antlers with no meat or tissue attached.
  • Upper canine teeth, also known as "buglers," "whistlers," or "ivories."
  • Finished taxidermy.

A summary of state-by-state carcass transportation regulations is provided in Column J of the regulations on each state page (accessible from the home page) or on the map. Since these regulations are continually evolving, it is recommended that before hunting you check the CWD regulations in your home state, the state in which you will be hunting and states in which you will travel through en route home from your hunting area. Most state wildlife agencies provide regulations information on their websites, and may be accessed via the clickable map on the home page.

The Carcass Transport and Disposal Working Group of the Association of Fish and Wildlife Agencies (AFWA) Fish and Wildlife Health Committee developed the following guidelines for regulatory and non-regulatory approaches to carcass transport and disposal. The intent of the working group is to encourage states to adopt policies that minimize risk; do not hinder hunting, wild cervid population management, or disease control; are easily understood; and promote compliance because they are consistent and well-justified. The recommendations are based on current knowledge of CWD and may be updated when new information becomes available. The Working Group recognizes state wildlife management agencies will tailor their approach to fit individual concerns and situations, and asks that agency directors, through AFWA, give serious and urgent consideration to this matter so that this potential risk of CWD spread can be minimized.

Transport and Disposal of Hunter-killed Cervid Carcasses: Recommendations to Wildlife Agencies to Reduce Chronic Wasting Disease Risks [PDF]

US Legislation

---April 6, 2004---
Senate Hearing on S1366 - Chronic Wasting Disease Financial Assistance Act of 2003

Senate Environment and Public Works Subcommittee on Fisheries, Wildlife and Water
April 6, 2004

CWD Alliances’ Testimony PDF document
Other Testimony

---January 9, 2004---
S 2007 - BSE and Other Prion Disease Prevention and Public Health Protection Act

To provide better protection against bovine spongiform encephalopathy and other prion diseases.
S 2007 PDF document
S 2007 Word document

---June 19, 2003---
Congressional Hearing on HR 2057

U.S. House of Representatives
House Resources Committee
Subcommittees on Forests and Forest Health, and
Fisheries Conservation, Wildlife and Oceans
Thursday, June 19, 2003


---June 9, 2003---
HR 2431 - Chronic Wasting Disease Task Force Establishment Act of 2003 (Introduced in House)

To establish a National Chronic Wasting Disease Task Force, and for other purposes.
HR2431 Word document

---June 9, 2003---
HR 2430 - Chronic Wasting Disease Research, Monitoring, and Education Enhancement Act of 2003 (Introduced in House)

To amend the Fish and Wildlife Coordination Act to coordinate and strengthen scientific research and monitoring, and to promote public outreach, education, and awareness, of Chronic Wasting Disease affecting free-ranging populations of deer and elk, and for other purposes.
HR2430 Word document

---June 9, 2003---
S 1366 - Chronic Wasting Disease Financial Assistance Act of 2003 (Introduced in Senate)

To authorize the Secretary of the Interior to make grants to State and tribal governments to assist State and tribal efforts to manage and control the spread of chronic wasting disease in deer and elk herds, and for other purposes.
S1366 PDF document | Word document

---June 9, 2003---
HR 2636 - Chronic Wasting Disease Financial Assistance Act of 2003 (Introduced in House)

To authorize the Secretary of the Interior to make grants to State and tribal governments to assist State and tribal efforts to manage and control the spread of chronic wasting disease in deer and elk herds, and for other purposes.
HR2636 PDF document | Word document

---May 9, 2003---
S 1036 - Chronic Wasting Disease Support Act of 2003

Introduce in the Senate May 9, 2003 by Senator Allard (CO)
S1036 Word document
S1036 PDF document

---May 9, 2003---
HR 2057 - Chronic Wasting Disease Support for States Act of 2003

Introduced in the House of Representatives May 9, 2003 by Rep. McInnis (CO)
HR2057 Word document
HR2057 PDF document

---April 18, 2003---
FY 2004 Budget - Conservation Organizations Request Congressional Support for CWD

24 organizations sign letter requesting funding for National CWD Plan- April 18, 2003
Letter Word document

---May 16, 2002---
Congressional Hearing on Chronic Wasting Disease

U.S. House of Representatives
House Resources Committee
Subcommittees on Forests and Forest Health, and
Fisheries Conservation, Wildlife and Oceans
May 16, 2002
CWD Alliances’ Testimony PDF document | Word document

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Category Archives: National News

Colorado State Awarded $2.5 Million NSF Grant to Study Prevalence and Spread of Chronic Wasting Disease

FORT COLLINS – A Colorado State University research team has been awarded a $2.5 million National Science Foundation grant to study transmission of chronic wasting disease.

Chronic wasting disease, or CWD, affects members of the deer family and is similar to diseases like scrapie in sheep and mad cow disease – or bovine spongiform encephalopathy – in cattle. CWD is caused by misfolded proteins that resist breakdown by enzymes within cells. These proteins cause fatal, neurological damage.

The disease was first discovered in deer in northeastern Colorado and southeastern Wyoming by Colorado State scientists in the 1960s.

Understanding and managing CWD depends on developing predictive models that track how the disease spreads. CWD remains an important challenge for managing wildlife resources in Colorado.

“An important goal for disease ecologists is to predict how diseases change in populations. This study will enhance our ability to predict the dynamics of CWD but also will improve models of all types of diseases,” said Tom Hobbs, CSU professor and project leader. “Predicting the spread of disease is similar to forecasting the weather. It is crucial to understand all of the sources of uncertainty in model predictions. If you don’t do that, you will probably make forecasts that are falsely optimistic. Our contribution will be to increase the reliability of disease models using sophisticated methods for bring together mathematics, statistics and data.”

In this NSF-funded project, CSU scientists will model the impact of CWD on deer populations in an effort to better understand dynamics of transmission.

Investigators will conduct field studies on wild mule deer populations in northern Colorado and will focus on studying the mechanism of transmission. Additionally, they will take a look at how many susceptible individuals are infected by a single infected deer. Lastly, research will study how an individual’s genetic make-up makes it more or less susceptible to being infected with CWD.

The research team will investigate free-ranging populations where CWD is prevalent. The study will not cause any animal to become infected and will not change their risk of infection. Instead, the project scientists will learn about the disease by observing ongoing processes of disease transmission.

“We will be taking a close look at why some deer get sick with CWD and why some don’t. Is their susceptibility to the disease controlled by the environment where they live? By their genetics? By the other deer they contact? We want to understand the things that determine individual variation in disease transmission,” Hobbs said.

Beyond the primary field research aims of this project, some broad impacts include innovative training of graduate students; curriculum development and research experience for local K-12 teachers; outreach to Rocky Mountain National Park visitors; collaboration on disease management with wildlife agencies in western North America; and training for researchers in the modeling methods used in this project.

The interdisciplinary CSU team of researchers awarded the grant will be led by Hobbs and Mike Miller from the Colorado Division of Wildlife. Team members include, Randy Boone, research scientist from the Natural Resource Ecology Laboratory; Mike Antolin, biology professor; Jennifer Hoeting, associate professor of statistics ; and Simon Tavener, professor of math.

Prions Found in Feces of Deer Asymptomatic for Chronic Wasting Disease

Scientists have discovered that deer asymptomatic for a fatal brain condition known as chronic wasting disease excrete the infectious prions that cause the disease in their feces. The finding, they say, suggests a plausible explanation for transmission of the disease among deer and, possibly, elk and moose in the environment.

The study is reported as an advance online paper on September 9, 2009 in the journal “Nature.”

While the study reveals that prions are shed in feces of symptomatic deer as well, the discovery that the infected deer shed prions (PREE-ons) in their feces many months before they show clinical symptoms has particularly provocative implications, according to the research team, at University of California, San Francisco and the Colorado Division of Wildlife’s Wildlife Research Center.

Deer, elk and moose inadvertently consume feces and soil in the course of their daily grazing. Given this, the team set out to determine whether the animals could develop chronic wasting disease through long-term consumption of contaminated feces. They did so by measuring the amount of prions contained in the feces of orally infected deer up until the time they became symptomatic and then calculated whether prolonged exposure to the concentrations of prions in these feces would be enough to cause the disease.

“Prion levels in feces samples of asymptomatic deer were very low compared to those in the brains of the same deer at the time of death,” says the lead author of the study, Erdem Tamguney, PhD, an assistant professor at the Institute for Neurodegenerative Diseases, based at UCSF. “However, the total number of prions excreted over time was sufficiently high enough to cause disease in other deer.”

The susceptibility of animals to infection, he says, might be increased by the simultaneous ingestion of clay soil, which is thought to enhance the infectivity of prions, possibly by slowing their clearance from the gastrointestinal tract.

“Our findings suggest that prolonged fecal prion excretion by infected deer provides a plausible explanation for the high level of transmission of chronic wasting disease within deer herds, as well as prion transmission among deer and other cervid species. Our work may also explain transmission of scrapie prions among sheep and goats,” says senior author and Nobel laureate Stanley B. Prusiner, MD, UCSF professor of neurology and director of the UCSF Institute for Neurodegenerative Diseases.

The study did not examine whether chronic wasting disease could be transmitted to humans via exposure to deer feces. To date, transgenic mouse studies have indicated that chronic wasting disease does not transmit to humans, but scientists remain open to the possibility that it could.

“We can only say that prions of chronic wasting disease have not transmitted to mice genetically engineered to carry the normal, healthy form of human prion protein in earlier studies,” says Prusiner. “That said, we do not know for sure that deer or elk prions cannot be transmitted to humans.”

The prion is an infectious form of the normal prion protein, which has been found in all mammals examined, including humans. The lethal, infectious form induces the normal protein to twist into a malconformation, initiating a disease process that ravages the brain. Prion diseases, seen in cervids, sheep, cows and humans, are also referred to as spongiform encephalopathies. Prusiner won the Nobel Prize in Physiology or Medicine in 1997 for the discovery of prions as a new biological principle of infection.

The new study sheds light on a question that has puzzled scientists for a number of years: how chronic wasting disease spreads so widely through herds and species in contrast to bovine spongiform encephalopathy in cattle, in which horizontal transmission between animals is rare.

First detected in a research facility in Colorado in 1967, chronic wasting disease has since been detected in fourteen states in the U.S. and in two Canadian provinces, predominantly in the West, both in the wild and on commercial farms. In wild herds, it can sometimes be found in up to 30 percent of animals; in captivity nearly entire herds can be affected.

Studies have shown that the disease can be transmitted orally – deer experimentally fed infected brain tissue become sick – but the animals are not carnivores, nor cannibalistic. And while prions have been reported in the saliva, blood, muscle, urine and antler velvet of symptomatic animals with late-stage disease, there is little evidence that these sources are responsible for high incidence of the disease within herds.

Epidemiological findings argue that chronic wasting disease spreads efficiently across populations. When healthy deer grazed on pastureland previously used by deer with chronic wasting disease, the healthy deer eventually develop the disease. But there has been no clear mechanism of transmission of prions in this way.

The UCSF scientists teamed up with co-investigators led by Michael Miller, DVM, PhD, of the Colorado Division of Wildlife’s Wildlife Research Center, to investigate the issue. Five deer were orally infected with one gram of brain tissue from a deer that had died of chronic wasting disease. Then fecal samples from the animals were collected at five time points – once before they were infected (as a control group), and then post infection at 3-4 months, 9-10 months, 13-14 months and 16-20 months (when animals show symptoms of the disease). Symptoms include inability to hold the head erect, excessive salivation, unsteady gait and poor grooming skills.

The UCSF scientists irradiated the deer feces to kill all bacteria and viruses, and inoculated the fecal material into the brains of mice genetically engineered to over-express the normal, healthy version of the elk prion protein.

An analysis showed that feces collected before infection and at 3-4 months post infection did not transmit the disease to the mice. At all subsequent time points, however, many fecal samples did transmit the disease. Prion infectivity was found in 14 of the 15 samples collected from the five deer as early as 7-11 months before neurological symptoms developed.

To measure the prions in feces, the team conducted a separate experiment in which they correlated the time required for mice to become ill from various prion concentrations in infected elk brain tissue (brain samples were diluted with varying amounts of water). Then they compared this data to the incubation times of the mice inoculated with contaminated feces, determining the amount of infectivity of the samples at different time points. While the number of prions in individual samples was low, the amount that accumulated over a 10-month period was similar to that in brain at the end-stage of the disease.

The findings offer strong evidence, says Prusiner, that prion contamination of forest, shrub-steppe and grassland habitats may be largely responsible for the high incidence of the disease both within and between cervid species and account for geographic spread as deer move between seasonal ranges.

Other co-authors of the study are Lisa L. Wolfe, MS, DVM, and Tracey M. Sirochman, BA, of the Colorado Division of Wildlife, Wildlife Research Center; David V. Glidden, PhD, professor of epidemiology and biostatistics, Christina Palmer, MS, Azucena Lemus, BS, of pathology, and Stephen J. DeArmond, MD, PhD, professor of pathology, all of UCSF.

The study was funded by the Larry L. Hillblom Foundation, the Colorado Division of Wildlife, grants from the U.S. Department of Defense National Prion Research Program and the National Institutes of Health.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

Species Barrier May Protect Macaques from Chronic Wasting Disease

Data from an ongoing multi-year study suggest that people who consume deer and elk with chronic wasting disease (CWD) may be protected from infection by an inability of the CWD infectious agent to spread to people. The results to date show that 14 cynomolgus macaques exposed orally or intracerebrally to CWD remain healthy and symptom free after more than six years of observation, though the direct relevance to people is not definitive and remains under study. Cynomolgus macaques often are used as research models of human disease because they are very close genetically to humans and are susceptible to several forms of human brain-damaging disease. Thus, it was decided to see whether exposure to CWD could induce disease in the macaques. The study appears online in the journal Emerging Infectious Diseases.

CWD is a type of brain-damaging disease known as a transmissible spongiform encephalopathy (TSE) or prion disease. CWD primarily affects deer, elk, and moose. Other TSE diseases include mad cow disease, or bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep, and sporadic Creutzfeldt-Jakob disease (CJD) in humans. Humans are not susceptible to sheep scrapie, but BSE appears to have infected about 200 people, primarily in Europe in the 1990s. Those findings provided the rationale for the present CWD-macaque study, which began in 2003.

“We plan to continue this study for at least several more years because, although the risk to macaques so far appears to be low, we know that these diseases can take more than 10 years to develop,” says Bruce Chesebro, M.D., chief of the Laboratory of Persistent Viral Diseases at Rocky Mountain Laboratories (RML) in Hamilton, Mont. RML is part of the National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health (NIH). The RML group is leading the study with collaborators from the Colorado Division of Wildlife; State University of New York Downstate Medical Center; New York State Institute for Basic Research in Developmental Disabilities; American Red Cross; and the University of Wyoming.

The findings by the RML group support published field studies done by others in regions of Colorado and Wyoming where CWD is endemic. Between 1979 and 2001, there were no significant increases in human TSE diseases despite the likelihood that hunters in those areas were exposed to CWD through contact with infected animal tissue and contaminated hunting tools such as knives and saws. Extensive laboratory data also supports a human species barrier against CWD.

Notably, the RML study also included identical testing in squirrel monkeys, which are genetically less similar to humans than macaques. Of 15 squirrel monkeys exposed orally to CWD, two displayed disease symptoms 69 months after infection. Of 13 squirrel monkeys exposed intracerebrally to CWD, 11 displayed symptoms between 33 and 53 months after infection. In symptomatic animals, the presence of the CWD agent was confirmed in brain, spleen and lymph nodes.

The results in squirrel monkeys were not surprising because a study elsewhere in two squirrel monkeys yielded similar results. The study by the RML group was different, however, in that it tested oral exposure to CWD and also studied eight CWD samples from different areas of the country. The results in squirrel monkeys confirmed that disease progression in that species appears consistent with disease progression in deer and elk, where severe weight loss is nearly always present.

“The fact that the squirrel monkeys, like the deer and elk, suffered severe weight loss suggests that chronic wasting disease might affect a common region of the brain in different species,” notes Dr. Chesebro.

NIAID conducts and supports research — at NIH, throughout the United States, and worldwide—to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web.

The National Institutes of Health (NIH) — The Nation’s Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit the NIH website.

USDA Proposes to Amend Final Rule on Chronic Wasting Disease Herd Certification Program for Captive Deer, Elk and Moose

WASHINGTON, March 30, 2009–The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service (APHIS) is proposing changes to a final rule that establishes a herd certification program to eliminate chronic wasting disease (CWD) from farmed or captive cervids in the United States. In the final rule, participating deer, elk and moose herds would have to follow CWD herd certification program requirements for animal identification, testing, herd management and movement of animals into and from herds. APHIS’ proposed changes involve the recognition of state bans on the entry of farmed or captive cervids for reasons unrelated to CWD, the number of years an animal must be monitored for CWD before it may move interstate, interstate movement of cervids that originated from herds in proximity to a CWD outbreak, herd inventory procedures and several other matters. These actions are intended to help eliminate CWD from the farmed or captive cervid herds in the United States. The proposed rule is in response to petitions and public comments requesting reconsideration of several requirements to the previous final rule. APHIS believes that the comments identified several areas where the CWD final rule could be more effective or less burdensome, and that the CWD final rule could be improved by making several changes to its requirements. CWD is a transmissible spongiform encephalopathy (TSE) of cervids (members of Cervidae, the deer family) that, as of October 2008, has been found only in wild and captive animals in North America and in captive animals in the Republic of Korea. First recognized as a clinical “wasting” syndrome in 1967, the disease is typified by chronic weight loss leading to death. There is no known relationship between CWD and any other TSE of animals or people. Species known to be susceptible to CWD via natural routes of transmission include Rocky Mountain elk, mule deer, white-tailed deer, black-tailed deer and moose. In the United States, CWD has been confirmed in free-ranging deer and elk in Colorado, Illinois, Kansas, Nebraska, New Mexico, New York, South Dakota, Utah, West Virginia, Wisconsin and Wyoming, and, as of October 2008, in 32 farmed elk herds and 11 farmed or captive white-tailed deer herds in Colorado, Kansas, Michigan Minnesota, Montana, Nebraska, New York, Oklahoma, South Dakota and Wisconsin. The disease was first detected in U.S. farmed elk in 1997. It was also diagnosed in a wild moose in Colorado in 2005. This proposed supplemental rule is scheduled to be published for public comment in the Federal Register on March 31.

Consideration will be given to comments received on before June 1. Send two copies of postal mail or commercial delivery comments to Docket No. 00-108-7, Regulatory Analysis and Development, PPD, APHIS, Station 3A-03.8, 4700 River Road, Unit 118, Riverdale, MD 20737-1238. Please state that your comment refers to Docket No. 00-108-7. If you wish to submit a comment using the Internet go to the Federal eRulemaking portal.

Comments are posted on the Web site and may also be reviewed at USDA, Room 1141, South Building, 14th St. and Independence Ave., S.W., Washington, D.C., between 8 a.m. and 4:30 p.m., Monday through Friday, excluding holidays. To facilitate entry into the comment reading room, please call (202) 690-2817

The proposed rule may be downloaded from the Federal Register in pdf format.

Please note that the comment period for this proposed rule is open until June 1, 2009.

Common Soil Mineral Degrades the Nearly Indestructible Prion

In the rogues’ gallery of microscopic infectious agents, the prion is the toughest hombre in town.

Warped pathogens that lack both DNA and RNA, prions are believed to cause such fatal brain ailments as chronic wasting disease (CWD) in deer and moose, mad cow disease in cattle, scrapie in sheep and Creutzfeldt-Jakob disease in humans. In addition to being perhaps the weirdest infectious agent know to science, the prion is also the most durable. It resists almost every method of destruction from fire and ionizing radiation to chemical disinfectants and autoclaving, which reduce prion infectivity but fail to completely eliminate it.

Now, however, a team of Wisconsin researchers has found that a common soil mineral, an oxidized from of manganese known as birnessite, can penetrate the prion’s armor and degrade the protein.

The new finding, which was reported earlier this month (Jan. 2) in the Journal of General Virology, is important because it may yield ways to decontaminate soil and other environments where prions reside.

“Prions are resistant to many of the conventional means of inactivating pathogens,” says Joel Pedersen, a UW-Madison environmental chemist and the senior author of the new study. For example, autoclaving, a standard method for sterilization in the laboratory, will reduce the concentration of prions in solution, but fails to eliminate them altogether, as it does for virtually all other types of pathogens.

Because prions infect both wild and domesticated animals, the agent can contaminate barnyards and other areas where infected livestock are kept, as well as persist in natural environments where deer, elk and other animals can become infected by contact with contaminated soil.

Other studies have shown that prions can survive in the soil for at least three years, and that soil is a plausible route of transmission for some animals, Pedersen says. “We know that environmental contamination occurs in deer and sheep at least,” he notes.

Prion reservoirs in the soil, Pedersen explains, are likely critical links in the chain of infection because the agent does not appear to depend on vectors — intermediate organisms like mosquitoes or ticks — to spread from animal to animal.

That the birnessite family of minerals possessed the capacity to degrade prions was a surprise, Pedersen says. Manganese oxides like birnessite are commonly used in such things as batteries and are among the most potent oxidants occurring naturally in soils, capable of chemically transforming a substance by adding oxygen atoms and stripping away electrons. The mineral is most abundant in soils that are seasonally waterlogged or poorly drained.

“A variety of manganese oxide minerals exist and one of the most common is birnessite. They are common in the sense that you find them in many soils, but in low concentrations,” says Pedersen. “They are among the strongest oxidants in soil.”

The new study, which was led by Fabio Russo of the University of Naples and Christopher J. Johnson of UW-Madison, was conducted on prions in solution in the laboratory. The group’s working hypothesis, according to Pedersen, is that the mineral oxidizes the prion, a chemical process that can be seen in things like iron oxidizing to form rust or how cut pears and apples turn brown when exposed to oxygen.

The next step, Pedersen says, is to mix the mineral with contaminated soil to see if it has the same effect. If it does, birnessite may become a useful tool for cleaning up contaminated farmyards and other places where the prion may be concentrated in the soil.

“I expect that its efficacy would be somewhat diminished in soil,” says Pedersen. “It’s something we’ll explore.”

In addition to Pedersen, Russo and Christopher Johnson, co-authors of the new study include Chad J. Johnson of the UW-Madison School of Veterinary Medicine, and Judd Aiken and Debbie McKenzie of the University of Alberta. The work was supported by grants from the National Science Foundation, the U.S. Environmental Protection Agency and the U.S. Department of Defense.