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Chronic Wasting Disease:  Implications for Human Health

NOTE:  This report represents the medical/scientific literature on this subject as of June 2005.

Resolution 422 (A-04), introduced by the New York Delegation at the 2004 AMA Annual Meeting and referred to the Board of Trustees, asks:

That the American Medical Association study the health issues associated with chronic wasting disease, including but not limited to, facilities processing both game and non-game animals.

This report reviews the recent literature on the human health risks associated with chronic wasting disease (CWD) in the deer and elk population, and briefly describes the responsibilities of, and actions taken by, the Food and Drug Administration (FDA) and the U.S. Department of Agriculture (USDA) in regard to this issue. Based on these findings, the Council also offers recommendations for consideration by the House of Delegates.

Data Sources

• Literature searches conducted in the PUBMED database for English-language articles published between 1980 and 2005 using the search term chronic wasting disease yielded a total of 126 references; 38 articles directly relevant to the human health impact of CWD and/or the regulations established to prevent potential transmission of CWD to the human population, published from 1980 to 2005, were selected for further review.  Fifteen additional references were culled from the bibliographies of these references.
• Lexis/Nexis news databases and the World Wide Web (using the Google search engine) were searched for current developments using the search term chronic wasting disease AND human health. Relevant Web references were examined for accuracy and appropriateness.

Introduction

CWD is a transmissible spongiform encephalopathy (TSE) of cervids (members of the deer family) and specifically of only mule and white-tailed deer, farmed black-tailed deer, and Rocky Mountain elk.  TSEs are fatal, neurodegenerative disorders in humans and animals that include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeldt-Jakob disease (CJD) in humans.1-6  TSEs are caused when infection with an abnormal form of a proteinaceous agent called a prion protein (PrP) occurs in the animal or human.  While originally controversial, the prion hypothesis of disease now has significant data to support it.2,4,6-8  This hypothesis proposes that TSEs are caused by abnormal, protease-resistant forms (PrPres) of the normal cellular prion protein (PrPc).4  PrPc are coded for and normally produced within the body’s lymphoid and central nervous system tissues.3,4,9  The abnormal forms of PrP are believed to arise when post-translational modifications occur to PrPc, resulting in decreased α-helical content and increased β-sheet tertiary structure.10  Thus, TSEs can spontaneously arise when these modifications of the PrPc occur over time, but the sporadic forms of TSE have only been defined in humans.11 TSEs are generally transmitted between animals when PrPres enter the body.  PrPres promotes a slow conversion/production process wherein the body’s normal PrPc are converted into PrPres.  Because of their lack of nucleic material, prions have a remarkable resistance to environmental conditions, and a wide variety of agents known to deactivate conventional infectious agents are not effective against prions.2,12  As with BSE and other TSEs, immunohistochemical analysis identifies CWD prions in the spinal cord, brain, eyes, peripheral nerves, and lymphoreticular tissues of infected cervids.13,14  The Council has previously published a detailed review on the mechanisms proposed for the transmission of TSEs (CSA Report 6, A-98).2

Chronic Wasting Disease. In the 4 susceptible cervid species, CWD manifests as chronic weight loss leading to death.15,16 CWD most closely resembles scrapie in sheep but recent concern surrounding BSE has brought the disease to wider public attention.15 CWD was first recognized in 1967 in captive mule deer in wildlife research facilities in northern Colorado and was identified as a TSE in 1978.17  Deer in these facilities originated from several sources, including free-ranging populations, and were also routinely interchanged with deer from wildlife facilities in Wyoming.16  Shortly after the initial identification of CWD as a TSE in 1978, CWD began to be diagnosed in captive mule deer in Wyoming.  Identification of CWD in captive elk in the wildlife research facilities soon followed.16

In 1981, CWD was diagnosed in the free-ranging elk population in Colorado and Wyoming16,18 and later was diagnosed in free-ranging mule deer (1985) and white-tailed deer (1990).16  Surveillance and modeling data suggest that CWD may have circulated in the free-ranging cervid population for as long as 20 years or more before its initial identification in the captive population in the 1960s.19  Comparison of the histological lesions and immunohistochemical staining of prion proteins from captive and free-ranging deer have shown them to be indistinguishable, suggesting a common etiological source.20  Data also suggest that horizontal transmission of CWD in deer is remarkably effective, producing an incidence of disease in a herd as high as 89%.21  Thus, horizontal transmission has a major role in sustaining the CWD epidemic.  Additionally, environmental sources of CWD prions, such as excreta or decomposing carcasses, have been implicated in the transmission of disease.22  Accordingly, these factors make it difficult to identify the precise time and location where CWD first emerged.  Regardless, it is clear that in a contiguous area in northeastern Colorado and southeastern Wyoming, CWD is endemic.19  In 2001, CWD was identified in free-ranging white-tailed deer in Wisconsin and in a single mule deer in southern New Mexico, and in 2003 the disease was identified in a mature buck deer in northeastern Utah.23  Other states that have now also identified CWD in wild cervids include Illinois, South Dakota, and Nebraska. (U.S. Department of Agriculture, Animal and Plant Health Inspection Service  [USDA-APHIS], personal communication, April 2005)

The potential for dissemination of CWD via the commercial exchange of farmed elk exists24 and indeed, in 1996, CWD diagnosed in farmed elk in Canada was traced back to elk imported from a South Dakota farm before 1989 as the source of infection.16  Thus, by 2002, various elk herds from South Dakota, Nebraska, Oklahoma, Colorado, Montana, Kansas, Minnesota, Wisconsin, and Canada had been identified with CWD and it is likely that a fair amount of cross-dissemination occurred between these locations.16  An elk with CWD was imported to South Korea from Canada in 1997.16  Based on epidemiological studies, it is believed that CWD has existed in the farmed elk population since at least the 1980s.16  Recent data indicate that CWD-infected farmed elk may have also served as a source of infection for free-ranging local deer populations and that CWD can “cross the fence” in both directions.16,19 In 3 states, free-ranging deer with CWD have also been culled from within the confines of elk farms.16

There are two identified CWD epidemics that appear to explain the disease’s current distribution.  One is in free-ranging cervids in a core endemic area in Colorado, Wyoming and Nebraska, and in foci of CWD in Saskatchewan, South Dakota, Utah, Illinois, New Mexico, and Wisconsin.  Natural geographic spread of the free-ranging epidemic seems to be following predictable and natural movements of the infected deer and elk in the endemic regions.25  With respect to the foci of infection, many of these likely represent spillover from infected farmed elk facilities near each of these foci.  Finally, no one original event links all CWD foci at this time.23 

The other epidemic is occurring within farmed elk, but most infected herds are quickly depopulated within months of detection of CWD.  Unlike the natural geographic movement of CWD in free-ranging cervids, the spread of disease among farmed elk is much more unpredictable; the movements of the animals are random, commercial, and frequently unregulated.16  CWD spread in farmed elk will likely continue undetected until more rigorous and uniform surveillance programs are implemented.16 It is important to note that the USDA’s Animal and Plant Health Inspection Service (APHIS) will soon implement its CWD Herd Certification Program (see below), and that this program when finalized and operational will likely improve surveillance, help control CWD, and eventually lead to its eradication in farmed and captive cervids.  The development of new screening techniques to identify infected animals will be invaluable in accomplishing this.26,27  Given the long latency period of TSEs in general, and the relative ease of horizontal transmission, it is not surprising that many gaps in knowledge exist about the epidemiology of CWD.

March 2005 identification of CWD in New York:  On March 30, 2005, New York became the ninth state to detect CWD in captive cervids with a positive test at a white-tailed deer farm (USDA-APHIS, personal communication, April 2005).  USDA-APHIS is working cooperatively with the New York Department of Agriculture and Markets (NY DAM) and the New York Department of Environmental Conservation ( NY DEC) on the CWD occurrences in Oneida County, NY.  Two animals in captive herds on 2 properties have been diagnosed with CWD.  The index case was identified as part of routine surveillance efforts and was not reported to have shown signs of disease.  All deer from both properties have been depopulated with the assistance of APHIS Wildlife Services personnel and tested for CWD.  To date, diagnostic laboratory testing has confirmed one animal on each property as CWD-positive.  Three more presumptive positives from the index herd have not yet been confirmed by laboratory testing.  Several other properties/captive herds that have been epidemiologically tied to the index herd are under state quarantine.  APHIS is currently working with the NY DAM on the epidemiological tracing of other potentially infected animals and will provide appraisal, indemnity, depopulation, and disposal services as appropriate.  With respect to the wild cervid population, the NY DEC is undertaking the harvesting and sampling of some 420 wild deer in the area surrounding the 2 positive properties to determine if the disease has spread to wild deer.  No test results are yet available.  Finally, because meat from the index case was served at a local fundraising dinner, public health concerns have been raised, but as discussed below, there is no known association between CWD exposure and human CJD disease.

Transmission of CWD from Cervids to Other Species

The ability of CWD to transmit between captive and free-ranging cervids is well documented.  However, significant concern exists, particularly after the emergence of BSE,2,28 about whether CWD can transmit to other domestic animals, such as cattle.  As with surveillance of inter-cervid transmission, rapid screening methods that can identify the source of CWD following cross-species transmission would be invaluable to ascertain whether and to what extent the host range of CWD is expanding.  Indeed, if there were significant transmission to domestic species, the risk of increased human exposure to the CWD prion would also increase.23  Additionally, passage of the CWD agent through a secondary host could yield a prion protein that could become potentially infective of humans.  This is likely what happened with the scrapie agent, which never infected humans until its passage through cattle as BSE.2,29

While CWD does not appear to exist outside the cervid population, it can be experimentally transmitted via intracerebral injection into other species, such as mice, monkeys, and goats.16  In vitro conversion of the normal, protease-sensitive cattle prion (PrPc) into an abnormal, protease-resistant state (PrPres) by the CWD prion does not occur effectively.30  However, transmission did occur in 3 of 13 cattle intracerebrally injected with the CWD prion.31  This is substantially lower than the transmission seen when cattle were intracerebrally injected with the scrapie prion.32  With the more plausible oral route of infection, after 6 years of observation, no cattle fed with CWD prion have developed a TSE.23  Cattle living with CWD-infected cervids for more than 6 years also have not become infected with the CWD prion.23  A survey of potentially high-risk adult cattle in CWD-endemic regions in Colorado failed to detect TSE-like illness in more than 262 brains taken from 4-years’-old cattle.33  This suggests that the large-scale spread of CWD from deer and elk to cattle under natural range conditions in CWD-endemic regions is unlikely.33  Finally, domestic cattle, sheep, and goats residing in research facilities in close proximity with CWD-infected cervids did not develop TSE-like diseases, suggesting that transmission of the CWD prion in natural conditions to other domestic species is limited, if not extremely rare.23

The Potential for Transmission of CWD to Humans

Analysis of abnormal prion protein glycoform patterns from CWD-infected cervids, scrapie-infected sheep , and BSE-infected cattle demonstrate minimal differences between the 3, suggesting a commonality with respect to the causative agent for these 3 diseases.34,35  It is thus speculated that CWD did emerge from a cross-species transmission of the scrapie prion into cervids.34  Whether this might result in increased ability for CWD to transmit to humans remains unknown.34

In the late 1990s, with the increasing incidence of CWD in cervids and the potential foodborne transmission of BSE to humans as variant CJD (vCJD),2,29 concern about the potential transmission of CWD to humans was raised when CJD was identified in 3 patients who were <30 years of age and were deer hunters or had eaten deer or elk meat. However, epidemiologic and laboratory investigations into these cases revealed no causal link between CWD and the patients’ CJD.36  For example, the deer and elk eaten by the hunters did not originate from a region in the United States that was endemic for CWD.  Additionally, when brains from more than 1000 deer from the area were examined for CWD, none was found to have a TSE.36  There also was a lack of homogeneity in the clinical expression of disease between the 3 hunters, which would be expected if they had been infected with CWD.  There was also a lack of homogeneity in the protein structure of abnormal prions causing disease in the hunters, suggesting a spontaneous origin of disease rather than a common source of infection. 

Significantly, extensive laboratory and epidemiologic investigations have been conducted into cases of human TSE that may be associated with cervid exposure.  In 2001, a 25-year-old man developed a TSE and died after an illness of 22 months’ duration.23  This man’s grandfather was an avid deer and elk hunter throughout the 1980s and 1990s in the known CWD-endemic area of southeastern Wyoming and regularly shared the meat with his family.  However, analysis of the prion protein structure revealed that the man had died from Gerstmann-Straussler Scheinker (GSS) syndrome.  What is unknown is whether the potential exposure to CWD-infected meat may have contributed to the unusually early onset of GSS syndrome in the patient.

Also in 2001, 2 patients aged 26 and 28 years died from CJD in Michigan.37 The 26-year-old patient did not hunt and while family members did not provide any history of venison consumption, it is believed that the patient might have consumed deer meat from the Upper Peninsula of Michigan while in college.  However, Michigan deer have not been shown to be CWD-infected, and the patient was eventually determined to have had sporadic CJD.23  The 28-year-old patient also did not hunt but may have had exposure to venison from Michigan when he was 1 to 2 years of age.  While the lack of samples prevented a prion protein analysis on the patient, an analysis of his parents indicated GSS syndrome mutation, suggesting that he died from GSS syndrome.23

In 2002, Wisconsin officials reported that 3 men who had participated in “wild game feasts” had died from rare neurologic disorders.38  These were the only neurologic cases among more than 50 people who had attended the feast.  Analysis of brain tissue from the 3 men indicated that 2 had no evidence of a TSE while the third had prion characteristics consistent with sporadic CJD.23  Furthermore, the deer and elk meat served at these feasts did not appear to have come from CWD-endemic regions of the United States.23

Finally, in 2003, 3 hunters were identified from across the United States who died from strikingly similar neuropathologic symptoms.39  Further investigation revealed that none of them had hunted in or eaten venison from CWD-endemic regions.23  Prion protein analysis verified that all 3 died from sporadic CJD.

Thus far, none of the cases described can be linked to consumption of deer or elk meat from CWD-endemic regions.  Indeed, only 2 known cases of sporadic CJD have been positively associated with a history of exposure to deer or elk meat from a CWD-endemic area.  In one of these cases, a 64-year-old woman who died in 2000, analysis of the brain following autopsy confirmed that she died from sporadic CJD.23  In the other, a 66-year-old man who died in 2002, analysis following autopsy also verified sporadic CJD as the cause of death.  Additionally, tests on the brains of the 2 deer the man apparently ate, revealed no signs of CWD in the animals.23

If CWD were transmitting to humans, the incidence of TSE deaths in CWD-endemic states would be expected to be higher than in other states.  However, this is not the case.  In fact, even with the long-term endemic nature of CWD in Colorado and Wyoming, the incidence and age distribution (early onset of disease symptoms is a classic feature of vCJD in humans) of CJD in these states are no different from the rest of the United States.23  Indeed, between 1979 and 2000, the only person under the age of 30 years in Colorado who developed CJD did so because of receipt of human growth hormone injections, and in Wyoming no CJD case was detected in any person under age 55,23

With the onset of BSE and vCJD in humans, laboratory methods have been crucial to study and establish the transmission of BSE from cattle to humans.2,23,40  As discussed in CSA Report 6 (A-98), the likelihood of successful disease transmission between species is dependent on the homology between the infecting abnormal PrPres and the host endogenous PrPc,2 with a higher degree of homology generally indicating a species barrier that would be easily overcome.  Thus, laboratory studies have examined how well the CWD PrPres converts human prion protein into an abnormal form via an in vitro, cell-free conversion reaction assay.30  This technique measures the degree of molecular homology between 2 prion protein isoforms. A study by Raymond and co-workers demonstrated that while the CWD PrPres effectively induces the conversion of normal, protease-sensitive cervid PrPc into abnormal, protease-resistant prion protein, it was much less effective at converting normal human PrPc into abnormal protease-resistant forms.  Additionally, the same study indicated that cattle PrPc-susceptibility to conversion was slightly greater than that of humans.30  These data, coupled with the epidemiologic data showing cattle to be relatively resistant to infection with CWD, suggest that the species barrier between cervids and humans for CWD prions is fairly high.  Recent  (as yet unpublished) studies of transgenic mice that express human prion genes indicate that these mice have very low susceptibility to CWD transmission from infectious cervid prions, further supporting the hypothesis that the risk of CWD transmission is very low (USDA-APHIS, personal communication, April 2005).

Finally, glycoform ratio analysis of the CWD PrPres when compared to that of human CJD-associated PrPres indicates that the diglycosylated form was predominant in the CWD-associated prion, while the monoglycosylated form was dominant in human CJD-associated prions.23  This fundamental molecular difference further reinforces the epidemiologic data indicating that the risk of transmission of CWD to humans is very low.41

FDA Actions to Control the Risk of CWD Transmission to the Human Population

In response to the BSE scare in the 1990s, the FDA established several regulatory steps to prevent the transmission of BSE to the human population.2  Many of these regulations will serve to indirectly protect the human population from potential CWD transmission as well.  For example, the ban on the use of specific risk material, such as brain and spinal cord, from cattle in human food will remove the risk of cattle serving as a intermediate source of transmission of CWD to humans.42  The USDA has also implemented a similar ban on the use of specific risk material from cattle in the food products that fall under its jurisdiction.

In 2003, the FDA published a draft guidance on the use of rendered materials from deer and elk in animal feed.43  This guidance (http://www.fda.gov/cvm/guidance/guide158.pdf, 200 KB, requires Adobe® Reader®)  is intended to prevent the possibility of CWD transmission to other animals via animal feed.  While the FDA concedes that potential risks of transmission of CWD to humans and other animals appear low, these risks are poorly understood.  Thus, the FDA recommends that any material from CWD-positive deer or elk not be used in any animal feed or feed ingredients.  According to Sec. 402(a)(5) of the Federal Food, Drug, and Cosmetic Act, animal feed and feed ingredients containing material from a CWD-positive animal would be considered adulterated and should be recalled.43

Additionally, the FDA recommends that materials from deer and elk considered at high risk for CWD no longer enter the animal feed system.  At this time, the FDA does not require that feed made from deer and elk from a non-endemic area be recalled should a state later declare that area endemic for CWD or a CWD-eradication zone.  Similarly, at this time, the FDA does not require feed made from deer and elk believed to be from a captive herd that contained no CWD-positive animals be recalled if that herd is subsequently found to contain a CWD-positive animal.  It is important to keep in mind that under the current FDA BSE feed regulation (21 CFR 589.2000) most material from any deer or elk is prohibited from use in animal feed for ruminant animals (eg, cattle, goats, sheep).43  Finally, the FDA states that materials from deer and elk not considered at high risk for CWD may be used in feed for non-ruminant animals.

USDA Actions to Control the Risk of CWD Transmission

The goal of USDA-APHIS is to eradicate CWD from farmed and captive cervids while assisting the states and Native American tribes in addressing the disease in free-ranging deer and elk.44  The USDA began surveillance for CWD in 1997 and has continued to work with state agricultural and wildlife agencies on a variety of CWD activities.44  Since 2002, USDA-APHIS has offered indemnity and covered costs of testing, depopulation, and disposal for the voluntary depopulation of  CWD-positive farmed herds, CWD-exposed farmed herds, and trace animals from epidemiologic investigations.44  The alternative to depopulation for farmers is state-imposed quarantine.  USDA-APHIS has also instituted a voluntary program of buying and depopulating high-risk farmed or captive herds in areas where CWD has become established in wildlife.  Herds in Colorado and Nebraska have been purchased and depopulated under this program.  Currently, indemnity is provided at 95% of appraised value and is capped at $3,000 per animal.44  Owners of depopulated herds must complete herd and premises plans, which include guidelines for cleaning, disinfection, and restocking. 

On December 24, 2003, USDA-APHIS published a proposed rule for a voluntary CWD Herd Certification Program with restrictions on interstate movement.45  The plan includes requirements for inventory, animal identification, surveillance testing, and fencing.  Once the rule is finalized, only owners of herds participating in the program will be allowed to ship animals interstate.  State programs that meet federal criteria will be grandfathered into the federal program.

USDA-APHIS also provides cooperative agreement funding to state wildlife agencies and tribes to support CWD surveillance and management activities in wildlife.44  Since 2003, all 50 state wildlife agencies have shared in this funding based on a formula developed in consultation with the International Association of Fish and Wildlife Agencies.  The funding provided to the Native American Fish and Wildlife Society and an increasing number of individual tribes totaled $500,000 in FY03 and $750,000 in FY04 and FY05.

In 2002, at the urging of Congress, USDA-APHIS worked with other federal agencies, the states, and the local tribes to develop the Plan for Assisting States, Federal Agencies, and Tribes in Managing Chronic Wasting Disease in Wild and Captive Cervids.  USDA-APHIS continues to work with these partners to implement this plan.

The USDA has urged hunters to immediately report any deer or elk they see displaying signs of CWD, such as abnormal head posture, drooping ears, lack of coordination, and weight loss.  Also, USDA cooperative agreement funding provided to state wildlife agencies supports an active surveillance program on hunter-killed deer and elk.  In the 2002-2003 hunting season, more than 91,000 samples were submitted for APHIS-funded testing. Of these, 302 were positive.46

Many states where CWD is endemic and where CWD has been identified have provided guidance to hunters on the consumption of deer and elk meat.  Typical of these guidelines are the following (issued by the Colorado Division of Wildlife)47:

• Do not shoot, handle, or consume any animal that appears sick; contact the Division of Wildlife if you see or harvest an animal that appears sick.
• Wear rubber gloves when field dressing and processing animals.
• Bone out the meat from your animal.
• Minimize the handling of brain and spinal tissues, and wash hands and instruments thoroughly after field-dressing.
• Wash hands and instruments thoroughly after field dressing is completed.
• Avoid consuming brain, spinal cord, eyes, spleen, tonsils, pancreas, and lymph nodes of harvested animals. Normal field dressing, coupled with boning out a carcass, will remove most, if not all, of these body parts. Cutting away all fatty tissue will remove remaining lymph nodes.
• Do not consume meat from animals known to be infected with CWD.
• Knives, saws, and cutting table surfaces can be disinfected by soaking in a solution of 50% unscented household bleach and 50% water for an hour. Afterward, allow them to air dry.

Conclusions

Evidence is lacking that CWD can transmit to the human population.41  Epidemiologic investigations of several potential cases have shown that these were either familial human TSEs (eg, GSS syndrome) or sporadic cases of CJD.  Coupled with the fact that CWD has been endemic in Colorado and Wyoming for several decades without a corresponding increase in CJD incidence in those states, it is likely that the risk of transmission of the CWD prion to humans is low.  Additionally, laboratory studies of the CWD prion indicate a significant lack of homology between the CWD prion and human CJD prions.  These same studies also suggest an inefficient conversion of normal, protease-sensitive human prions into abnormal, protease-resistant human prions by CWD prion, implying a substantial species barrier.  These laboratory studies also support the conclusion that transmission of CWD to humans is unlikely.

However, these same laboratory studies also imply that while the risk may be very low, the potential still exists that CWD may either transmit to humans inefficiently, or may play a role in enhancing the onset of CJD in already genetically vulnerable humans.  The experience with BSE also suggests that with sufficient exposure over time, the species barrier alone is insufficient to protect humans from animal prion diseases.  As such, while unlikely, it is possible that human exposure to CWD has simply been insufficient to cause transmission of disease to humans.23  Accordingly, it is important that surveillance efforts on the incidence of CJD in humans continue, not just for possible transmission of CWD, but also for BSE.  Additionally, continued efforts to control and/or eradicate CWD are justified.  Continued research, both epidemiologic and laboratory-based, into the potential that CWD may transmit to humans should be encouraged.  Some research along this line is already occurring.  Epidemiologic studies to survey for TSEs in humans with an increased risk of exposure to CWD-infected deer or elk meat are ongoing,48 and laboratory studies are underway to better elucidate the potential for the CWD prion to cause human disease.23,49

In summary, significant measures are in place to prevent the potential exposure of humans to CWD, both direct and indirect.  The FDA has a feed ban in place prohibiting the use of materials from any deer or elk in ruminant animals, and in 2003 issued a guidance prohibiting the use of CWD-positive material in animal feed.  Additionally, the ban prohibiting high-risk material from ruminants from entering the human food chain will serve to indirectly protect humans from CWD that may have passaged through a domestic ruminant, such as cattle.  The USDA-APHIS and USDA-Agricultural Research Service have dedicated significant resources to CWD research, control, and eradication, and are working with state governments, Native American tribes, and hunters to provide surveillance of the incidence of CWD in free-ranging deer and elk.  Many states have also provided guidance to hunters on how to reduce their exposure to potentially CWD-infected animals.

Thus, the risk of CWD transmission to the human population appears very low.  Appropriate measures are in place to protect the human population from CWD.  However, as indicated in CSA Report 6 (A-98), adherence to current guidances and enforcement of existing regulations is critical for the protection of the human population.2

RECOMMENDATIONS

The following statements, recommended by the Council on Scientific Affairs, were adopted by the AMA House of Delegates as AMA policy and directives at the 2005 AMA Annual Meeting:

  1. The AMA reaffirms Policy H-150.959 (3), (5), and (6): Risk of Transmission of Bovine Spongiform Encephalopathy to Humans in the United States, and Policy H-150.950, Regulation of Meat Plants That Process Wild Game (AMA Policy Database). (Reaffirm Policy)
  2. The AMA urges the Food and Drug Administration (FDA) to: (1) continue aggressive enforcement of existing regulations to prevent the transmission of animal-transmissible spongiform encephalopathies to humans; and (2) consider making Draft Guidance Document 158, Use of Material From Deer and Elk in Animal Feed, into a regulation. (Directive)
  3. The AMA encourages continued research into the potential transmission of chronic wasting disease (CWD) to other animals and humans. (Directive)
  4. The AMA supports continued surveillance of the CWD epidemic in cervids and continued investigation into human cases of CJD that appear to have an epidemiological link to exposure to CWD. (Directive)

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 14.  Sigurdson CJ, Spraker TR, Miller MW, Oesch B, Hoover EA. PrP(CWD) in the myenteric plexus, vagosympathetic trunk and endocrine glands of deer with chronic wasting disease.  J Gen Virol. 2001;82:2327-2334.
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