Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
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-------- Original Message -------- Subject: USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA Date: Mon, 3 Nov 2003 11:05:09 -0600 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de
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Alisa Harrison (202) 720-4623 Jerry Redding (202) 720-6959
USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
Releases Risk Assessment by Harvard Center for Risk Analysis
WASHINGTON, Oct. 31, 2003--The United States Department of Agriculture today issued a proposed rule to amend its bovine spongiform encephalopathy (BSE) regulations to establish a new category of regions that recognizes those that present a minimal risk of introducing BSE into the United States via the importation of certain low-risk live ruminants and ruminant products.
USDA's Animal and Plant Health Inspection Service is seeking public comment on the proposal to allow the importation of certain live ruminants and ruminant products and byproducts from minimal risk regions under specified conditions. This proposed rule would place Canada on a list of countries considered a minimal risk for BSE, thus making Canada eligible to export certain live ruminant and ruminant products.
"The United States has a long history of having safeguards in place to prevent the introduction of BSE," said Agriculture Secretary Ann M. Veneman. "The continued protection of the U.S. food supply is our top priority. This proposal reflects a thorough review of the scientific evidence, which shows the risk to public health to be extremely low."
The proposed minimal risk region would include regions in which an animal has been diagnosed with BSE but in which specific preventive measures have been in place for an appropriate period of time that reduce the risk of BSE being introduced to the United States. Based on a comprehensive risk analysis and review, USDA believes that the surveillance, prevention and control measures implemented by Canada are sufficient to be included in the minimal risk category.
The proposed rule has a 60-day comment period. Once this period closes, USDA will consider the comments as it makes any final decisions on the importation of certain live ruminants and ruminant products from Canada and other minimal risk regions for BSE.
Under this proposal, ruminant and ruminant products eligible for entry into the United States from a BSE minimal risk region would include: 1) bovine animals less than 30 months of age for immediate slaughter; 2) bovine animals for feeding to be moved to a designated feedlot and then to slaughter at less than 30 months of age; 3) sheep and goats less than 12 months of age for immediate slaughter; 4) sheep and goats for feeding to be moved to a designated feedlot and then to slaughter at less than 12 months of age; 5) cervids for immediate slaughter; 6) fresh (chilled or frozen) meat from bovines less than 30 months of age; 7) fresh (chilled or frozen) whole or half carcasses of bovines less than 30 months of age; 8) fresh (chilled or frozen) bovine liver; 9) fresh (chilled or frozen) bovine tongues; 10) fresh (chilled or frozen) meat of sheep or goats less than 12 months of age; 11) fresh (chilled or frozen) carcasses of sheep or goats less than 12 months of age; 12) hunter-harvested wild ruminant products; 13) fresh (chilled or frozen) meat of cervids either farm-raised or harvested on a game farm or similar facility; 14) fresh (chilled or frozen) meat from wild- harvested caribou, musk ox, or other cervids; and 15) certain types of gelatin, tallow and offal. A full listing of the risk mitigation measures required to be eligible for entry into the United States can be found at http://www.aphis.usda.gov/.
The proposed rule is consistent with the approach taken by the World Organization for Animal Health (OIE) ? the standard setting organization for animal health for 164 member nations. In recent correspondence, the Director General of the OIE acknowledged that there has been an "increase in unjustified restrictions in international trade, particularly as it relates to cattle and cattle products." The letter was in response to a request from Secretary Veneman, Agricultural Minister Lyle Vanclief, Canada, and Agriculture Secretary Javier Usabiaga, Mexico, to the OIE to provide more practical guidance regarding the resumption of trade with countries that have reported cases of BSE. The United States continues to work with the OIE to ensure that countries establish import policy decisions based on standards that are commensurate with the BSE risks identified for each situation.
HARVARD RISK REASSESSMENT
USDA also released the findings of a second assessment conducted by the Harvard Center for Risk Analysis (HCRA) that confirms the findings of the initial study released in 2001. The study found that even if infected animals or ruminant feed material entered the U.S. animal agriculture system from Canada, the risk of it spreading extensively within the U.S. herd was low, that any possible spread would now have been reversed by controls put in place in the late 1990's, and that eventually, the disease would be eliminated from the United States.
"This study shows that the measures taken in the United States over the years greatly reduce the chance of BSE spreading and help ensure that the disease will not become a major animal or public health problem in America," said Dr. George Gray, executive director of HCRA.
The risk reassessment was commissioned by USDA shortly after the discovery of a single case of BSE in Canada on May 20, 2003. The study evaluates the potential for BSE to spread if it were introduced from Canada prior to May 20, when USDA banned all ruminant and ruminant products from Canada because of the discovery of the single case of BSE. The reassessment specifically examined scenarios for the likely introduction of BSE from Canada into the United States.
The scenarios used for this assessment included hypothetical introductions at various times of both infected animals and contaminated animal feed. These scenarios were entered into the HCRA computer model that simulates conditions in the U.S. cattle herd given the actions that have already been taken to minimize the risk of spreading the disease. In the worst case scenario, where infection was introduced as early as 1990, the results demonstrated that the disease could have spread with a peak infection rate occurring in 1997 and peak numbers of clinical cases occurring in 2000. When infection was introduced later in 1996 or 1998, there was minimal or no spread of the disease.
As with the initial study, which hypothetically introduced as many as 500 infected animals into the U.S. herd, the Food and Drug Administration's 1997 ban on feeding most mammalian protein back to other ruminants essentially stops the possible spread of the disease.
Even allowing for incomplete compliance with that feed ban, the HCRA analysis finds that, had infected animals or feed come in from Canada or elsewhere, by now the spread of BSE in the U.S. herd would have been reversed and that human exposure to contaminated animal tissue would have been very low.
A complete copy of the second Harvard Report can be obtained from USDA's official website at http://www.usda.gov/.
USDA PREVENTIVE ACTION
BSE is a progressive neurological disease among cattle that is always fatal. It belongs to a family of diseases known as transmissible spongiform encephalopathies. Also included in that family of illnesses is variant Creutzfeldt-Jakob Disease (vCJD), which is believed to be caused by eating neural tissue, such as brain and spinal cord, from BSE affected cattle.
BSE has never been detected in U.S. cattle. The USDA and other agencies have had preventive measures in place since recognition of BSE as a serious disease. Since 1989, USDA has banned the import of live ruminants, such as cattle, sheep and goats, and most ruminant products from the United Kingdom and other countries having BSE. The ban was extended to Europe in 1997. And, as more evidence was accumulated about how the disease spread, the Food and Drug Administration prohibited the use in 1997 of most mammalian protein in the manufacture of animal feed intended for cows and other ruminants.
Since 1990, USDA has had an aggressive BSE surveillance program in place to ensure detection and swift response in the event that an introduction of BSE were to occur. Last year, USDA tripled testing levels and this year testing reached an all-time high of 20,526 head, or 47 times the level recommended by the OIE. Because of the May 20, 2003 occurrence of a single case of BSE in Canada, APHIS is reviewing its current level of surveillance to continue to ensure a high confidence level.
USDA's Food Safety and Inspection Service is evaluating a proposal to further address specified risk material such as brain and spinal cord to continue to reduce any potential risk. These tissues are considered to be the most infectious in animals with BSE. Therefore, this measure could further reduce the already very low risk of BSE in the United States, thus providing additional protection for consumers.
TO COMMENT ON THE PROPOSAL
The notice of proposed rulemaking to permit entry of low-risk live animals from certain minimal risk regions is scheduled for publication in the Nov. 4 Federal Register. APHIS documents published in the Federal Register and related information, including the names of organizations and individuals who have commented on APHIS dockets, are available on the Internet at http://www.aphis.usda.gov/.
Consideration will be given to comments received on or before Jan. 5, 2004. Comments may be submitted by postal mail, commercial delivery or by e-mail. Send an original and three copies of postal or commercial delivery comments to Docket No. 03-080-1, Regulatory Analysis and Development, PPD, APHIS, Station 3C71, 4700 River Road Unit 118, Riverdale, Md. 20737-1238. If you use e-mail, address your comments to firstname.lastname@example.org. Comments must be contained in the body of the message; do not send attached files. Please include your name and address in the message and use "Docket No. 03-080-1" on the subject line.
Comments received may be reviewed at USDA, Room 1141, South Building, 14th Street and Independence Avenue, S.W., Washington, D.C., between 8 a.m. and 4:30 p.m., Monday through Friday, except holidays. Persons wishing to review comments are requested to call ahead on (202) 690-2817 to facilitate entry into the comment reading room.
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In Reply to: USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA [Docket No. 03-080-1] posted by TSS on November 3, 2003 at 10:21 am:
-------- Original Message --------
Subject: Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
Date: Mon, 03 Nov 2003 12:20:52 -0600
From: "Terry S. Singeltary Sr." To: email@example.com
I would like to kindly comment on Docket No. 03-080-1
USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA ;
Under this proposal, ruminant and ruminant products eligible for entry into the United States from a BSE minimal risk region would include:
1) bovine animals less than 30 months of age for immediate slaughter;
2) bovine animals for feeding to be moved to a designated feedlot and then to slaughter at less than 30 months of age;
6) fresh (chilled or frozen) meat from bovines less than 30 months of age; 7) fresh (chilled or frozen) whole or half carcasses of bovines less than 30 months of age; 8) fresh (chilled or frozen) bovine liver; 9) fresh (chilled or frozen) bovine tongues;
the myth that cattle under 30 months of age are free from BSE/TSE is just that, a myth, and it's a false myth !
the youngest age of BSE case to date is 20 months old; As at: 31 May 2003 Year of onset Age youngest case (mnths) Age 2nd youngest case (mnths) Age 2nd oldest case (yrs.mnths) Age oldest case (yrs.mnths) 1986 30 33 5.03 5.07 1987 30 31 9.09 10.00 1988 24 27 10.02 11.01(2) 1989 21 24(4) 12.00(2) 15.04 1990 24(2) 26 13.03 14.00 1991 24 26(3) 14.02 17.05 1992 20 26 15.02 16.02 1993 29 30(3) 14.10 18.10 1994 30(2) 31(2) 14.05 16.07 1995 24 32 14.09 15.05 1996 29 30 15.07 17.02 1997 37(7) 38(3) 14.09 15.01 1998 34 36 14.07 15.05 1999 39(2) 41 13.07 13.10 2000 40 42 17.08 19.09 2001 48(2) 56 14.10 14.11 2002 51 52 15.08 15.09(2) 2003 50 62 11.11 14.11
The implications of the Swiss result for Britain, which has had the most BSE, are complex. Only cattle aged 30 months or younger are eaten in Britain, on the assumption, based on feeding trials, that cattle of that age, even if they were infected as calves, have not yet accumulated enough prions to be infectious. But the youngest cow to develop BSE on record in Britain was 20 months old, showing some are fast incubators. Models predict that 200-300 cattle under 30 months per year are infected with BSE and enter the food chain currently in Britain. Of these 3-5 could be fast incubators and carrying detectable quantities of prion.
3) sheep and goats less than 12 months of age for immediate slaughter; 4) sheep and goats for feeding to be moved to a designated feedlot and then to slaughter at less than 12 months of age;
even if one believes that scrapie does not transmit to humans (without scientific proof and realizing scrapie transmits to primates) what about the potential for BSE in sheep/goats and what about the many different tissues that are infectious ?
Research into sheep TSEs - audit reports & IAH's response
5) cervids for immediate slaughter;
are you going to test all cervids coming into the USA from Canada for CWD/TSEs ? (this should be mandatory).
Commentary by European Microbiologist Roland Heynkes
August 26, 2003 Posted to BSE-L@UNI-KARLSRUHE.DE
SECRETARY VENEMAN: "Well, thank you, Tony, for your question. As you know, we've spent a considerable amount of time on this issue of Canada and the single case of BSE. The announcement we made on the 8th had several aspects. One was we were going to use a permit process to open the border with respect to boxed beef from animals under 30 months. As you know, animals under 30 months are generally thought to be of virtually no risk of having BSE. Now, we will also begin a regulatory process to look at the lowest risk animals, those under 30 months. That regulation is in process at this point, but it will take some time to actually do the regulation. That will include a risk assessment and so forth.
in my opinion this is a statement with intent to deceive and it is not correct. There have been several cases of clinical BSE in British cattle under 30 months and it is therefore hardly possible to think that cattle under 30 months have virtually no risk of having BSE. In 1988 the youngest British BSE case was 24, the second youngest 27 months old. In 1989 the youngest British BSE case was 21 and there were 4 cases only 24 months old. In 1990 there were two cases only 24 and one 26 months old. In 1991 the youngest British BSE case was 24 and there were 3 cases only 26 months old. In 1992 the youngest British BSE case was 20!, the second youngest 26 months old. In 1993 there was was a 29 months old case, in 1995 the UK had a 24 months old case and in 1996 one British BSE case was 29 months old.
But mainly this wrong statement is misleading, because not the clinically sick cows are the problem for consumers. The real problem are those animals that became infected as calves and are still incubating the infectivity during the incubation time of 5-6 years. For consumers it is therefore totally irrelevant that cattle are at low risk to reach the clinical stage before being 30 months old. Important for consumers is the fact that most British BSE cases became infected as calves ( http://www.heynkes.de/peaks.htm ) and that infected calves are already amplifying the infectivity. The advantage of young calves for consumers is that the infectivity in infected animals is low and still concentrated around the gastro- intestinal tract. But this is not necessarily true for bulls, which are usually slaughtered when they are 19-22 months old. They are too young to give positive results in the actual BSE tests, but they might be infective for consumers.
For US consumers it is of no importance whether a BSE-infected Canadian cow will show the first symptoms before or after it becomes 30 months old. Interesting for the consumers is only
1) if cattle are infected or not,
2) where in the animal is how much of the infectivity and
3) what happens to the infectivity during slaughtering?
If the US government is really interested to reduce consumers risk, it has to
1) stop cannibalism among farm animals (no farm animal protein and fat in feeding stuff for farm animals, no possibility of cross contamination of concentrate feed in mills and no lambing on pastures where scrapie might be a problem)
2) test slaughter cattle above 24 months for BSE,
3) avoid contamination of the beef with prions from CNS by changing slaughter methods (electrical stunning instead of captive bolt, no immobilisation with a pithing rod, no spreading of infectivity by sawing through the spinal cord),
4) destroy the high risk materials (brain, eyes, spinal cord, dorsal root ganglia and other peripheral ganglia, nervous and lymphatic tissue associated with intestine)
5) commit the whole chain from abattoir to counter in shop and restaurant to label products from cattle and sheep, because it is only a myth that scrapie is less infective than BSE.
In addition the US government should test all cattle and sheep which died or had to be killed because of illness. This measure should be hold out for at least one year in order to see the real BSE- and scrapie-incidence in the USA....
Microbiologist Roland Heynkes
Furthermore, for the USA to continue to flagrantly ignore the findings from Collinge/Asante et al that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD. These findings could have major implications for the medical and surgical arena and human health. this type sporadic CJD is very prevalent in the USA ;
HARVARD RISK REASSESSMENT
USDA also released the findings of a second assessment conducted by the Harvard Center for Risk Analysis (HCRA) that confirms the findings of the initial study released in 2001...
THESE FINDINGS WERE FLAWED FROM THE BEGINNING and the GAO proved this;
Reanalysis of Mad Cow Disease Confirms Risk is Low in the U.S.
Policies put in place in 1997 would reverse any possible disease spread
For immediate release: Friday, October 31, 2003
Boston, MA A study by the Harvard Center for Risk Analysis (HCRA) at the Harvard School of Public Health, assessing the likelihood of mad cow disease spreading in the United States cattle population, confirms the findings of the initial HCRA analysis done in 2001; that even if infected animals or contaminated ruminant feed material entered the American animal agriculture system from Canada, the risk of mad cow spreading extensively within the American herd would be low, and that any possible spread would by now have been reversed by controls put in place in the late 1990s.
The new study was initiated at the request of the United States Department of Agriculture following discovery in the summer of 2003 of a Canadian cow infected with bovine spongiform encephalopathy (BSE). The reanalysis also finds that any disease that might have been introduced would eventually be eliminated from the United States.
The reanalysis, done by George Gray, executive director and Joshua Cohen, senior researcher, both at HCRA, specifically examined scenarios for the likely introductions of BSE from Canada into the U.S. These hypothetical introductions included both infected animals (the study assumed 5 infected animals imported even though Canada has only identified one case to date) and contaminated animal feed. These scenarios were evaluated using the HCRA computer model that simulates conditions in the American agricultural system. The analysis found that if BSE infected animals had been introduced as early as 1990, up to 500-600 cattle in the U.S. might have become infected, and approximately 20-25 percent would have demonstrated signs of BSE. Such an outbreak was never detected, though it would have been below the prevalence level that surveillance systems in place at that time would likely have found. If the introduction took place later, the total number of animals infected in the U.S. would have been smaller.
The HCRA study found that the 1997 U.S. imposition of a ban on feeding rendered ruminant protein back to other ruminants essentially chokes off and then reverses any possible spread of the disease. Even accounting for incomplete compliance with that feed ban, the HCRA analysis found that had infected animals or contaminated feed come in from Canada or elsewhere, the spread of BSE in the American cattle population would have been reversed by now and that human exposure to contaminated animal tissue would have been very low.
HCRA has also delivered to the USDA the revised version of the November, 2001 BSE report following extensive peer review by both American and European experts.
The revised document is available on the HCRA website at http://www.hcra.harvard.edu/publications.html#Evaluation and the HCRA BSE computer model is available by contacting Joshua Cohen at HCRA (firstname.lastname@example.org ). For further information, please contact:
George Gray Executive Director Harvard Center for Risk Analysis 617-432-4341 email@example.com
Kevin C. Myron Office of Communications Harvard School of Public Health 617-432-3952 firstname.lastname@example.org
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BOUGHT AND PAID FOR (in partial or whole) by your local cattle dealler ;
In addition, USDA cannot rely on the Food and Drug Administrations (FDAs) 1997 BSE feed rule being rigorously enforced. Because of serious lapses, increased surveillance is needed. The USDA-sponsored Harvard risk assessment of the risk of BSE in the U.S. noted that compliance with FDAs 1997 BSE feed rule is the most important factor in preventing a BSE outbreak. Yet a pair of reports by GAOone published in September 2000 and the other published in January 2002have shown how lax FDA has been in ensuring compliance with the feed rule. The first report, published some three years after the BSE feed rule went into effect found fairly widespread non-compliance: inspection results of the 2,481 firms that were identified as handling prohibited materials . . . 699, or 28 percent, did not label their products with the required cautionary statements that the feed should not be fed to cattle or other ruminants. . . . In addition, of the 1,771 firms that manufacture both prohibited and non-prohibited material, 361, or 20 percent, did not have a system in place to prevent commingling and cross contamination, as required by the regulation (pp. 11-12 in http://www.gao.gov/new.items/rc00255.pdf ).
The 2002 GAO report found that, (C)oncerning the feed ban, FDA has not acted promptly to compel firms to keep prohibited proteins out of cattle feed and to label animal feed that cannot be fed to cattle. . . . Moreover, FDAs data on inspections are severely flawed and, as a result, FDA does not know the full extent of industry compliance. FDA acknowledges that it has not yet identified and inspected all firms subject to the ban (pg. 3 in
The report concludes that federal actions do not sufficiently ensure that all BSE-infected animals or products are kept out or that if BSE were found it would be detected promptly and not spread to other cattle through animal feed or enter the human food chain italics added (pg. 3 in http://www.gao.gov/new.items/d02183.pdf ). The failure of FDA to fully implement the 1997 BSE feed ban should spur USDA to exercise greater vigilance to ensure that if BSE occurred in the US that it would be found quickly. USDA should therefore dramatically expand the testing of cattle to ensure, at a minimum, that all downer cows (e.g. all emergency slaughter and all fallen stock) are tested for BSE using one of the rapid tests, preferably the one found to be the most accurate (e.g. with the lowest rate of false positives and false negatives).
We also believe that USDA should act to ensure that no CNS tissue is found in meat destined for human consumption. We note that the results of the Food Safety Inspection Services 2002 AMR survey found that about 74 percent (25 of 34) of the establishments tested in the AMR Survey of 2002 had positive laboratory results for CNS tissue in their final beef AMR products; the other 26 percent had negative laboratory results (see pg. 2 of http://www.fsis.usda.gov/OA/topics/AMRSurvey.pdf). The USDA should take appropriate action to ensure that there is zero CNS contamination of meat destined for human consumption...
Gerald Wells: Report of the Visit to USA, April-May 1989
The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised...
It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_...
PLEASE NOTE, WITH THE NEW ATYPICAL BSE/TSE CASES NOW DOCUMENTED IN CATTLE IN JAPAN AND ITALY, THE FINDINGS FROM MARSH ET AL SEEM MORE AND MORE IMPORTANT;
To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
R.F. Marsh* and G.R. Hartsough
â¬¢Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092
ABSTRACT Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.
Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source.
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.
Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months.
DISCUSSION These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy. We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed.
ACKNOWLEDGEMENTS These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations.
REFERENCES Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420.
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -10 Accepted - Volume 2
SCRAPIE 'USA' ANNUAL REPORT (105 newly infected flocks 2002) & CWD IN USA
As of September 30, 2002, there were 45 scrapie infected and source flocks (figure 3). There were 105 newly infected flocks, reported in FY2002 (figure 4). In addition, 379 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2002 (figure 5) and (figure 6). Five cases of scrapie in goats were reported in FY 2002 (figure 7), the last of which was confirmed in August 2002. New infected and source flocks numbers and the number of these flocks released in FY 2002 are depicted in chart 4. One hundred (100) flocks which is 67 percent of the scrapie infected and source flocks present in FY 2002 were released or put on clean-up plans in FY2002.
Slaughter Surveillance is currently in Phase II which is intended to determine the prevalence of scrapie in the US culled sheep population. Through September 2002 samples from 3,269 sheep were submitted to NVSL for testing. Samples from a total of 6,795 sheep have been submitted since the beginning of Phase II on April 1, 2002. Surveillance regions are depicted in (figure 8).
During FY 2002 11,751 animals have been tested for scrapie which includes: 2,711 regular necropsy cases, 1,343 third eyelid biopsies for the test validation project, 546 third eyelid biopsies for the regulatory program, and approximately 7,151 animals for Phase I & II of SOSS (chart 5). Laboratory testing has been taking 10 - 11 days on average with a range of 3 - 34 days.
Ear Tag Orders
During FY 2002 9.9 million plastic and 6.0 million metal tags were distributed by APHIS (chart 6).
NEW SCRAPIE INFECTED AND SOURCE FLOCKS
DISTRIBUTION OF CHRONIC WASTING DISEASE THROUGHOUT THE STATES (as of Oct. 2002)
CWD USA surveillance
DO NOT TAKE LIKELY, the early studies proving transmission of CWD to 5 cows and 1 sheep by inoculation. The oral route will take longer, if/when transmission occurs;
-------- Original Message -------- Subject: Re: CWD TO CATTLE by inoculation (ok,is it three or four OR NOW FIVE???) Date: Mon, 23 Jun 2003 12:36:59 -0500 From: "Janice M. Miller" Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de
Summary: After 5.75 years of observation we have 5 CWD transmissions to cattle from a group of 13 inoculates. These animals, which were necropsied 23, 24, 28, 59, and 63 months after inoculation, did not show the clinical signs or histopathologic lesions typical of a TSE, but PrPres was detected in brain samples by both immunohistochemistry and western blot. Five other animals necropsied during the 4th, 5th and 6th years of observation have not shown evidence of PrPres and the remaining 3 cattle are apparently healthy. Note that this study involved direct intracerebral inoculation of cattle with the CWD agent, which is an unnatural route of exposure. Likely, it would be more difficult to infect cattle by the oral route. Cattle have been inoculated orally at the University of Wyoming with the same inoculum used in this experiment, and 5.75 years into the study the animals remain healthy (personal communication, Dr. Beth Williams).
Experimental Transmission of CWD to sheep
Eight Suffolk sheep from the NADC scrapie-free flock were inoculated intracerebrally with the CWD brain suspension used to inoculate cattle. PRNP genotyping showed that 4 of the sheep were QQ at codon 171 and the other four were QR. Two of the QQ sheep were euthanized during the 3rd year of observation. At necropsy one of these animals had a urethral obstruction and PrPres was not detected in brain or lymphoid tissues. The other sheep, necropsied 35 months after inoculation, showed clinical signs and histopathologic lesions that were indistinguishable from scrapie. IHC tests showed typical PrPres accumulations in brain, tonsil, and some lymph nodes. The 2 remaining QQ sheep and all 4 QR sheep are apparently healthy 47 months after inoculation.
Summary: After 4 years of observation we have 1 transmission of CWD to a 171 QQ sheep. This animal, which was necropsied 35 months after inoculation, showed clinical signs and histopathologic lesions that were indistinguishable from scrapie. Another QQ sheep that was necropsied during the 3rd year showed no evidence of prion disease and all remaining sheep (2 QQ and 4 QR) are apparently healthy.
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
In recent correspondence, the Director General of the OIE acknowledged that there has been an "increase in unjustified restrictions in international trade, particularly as it relates to cattle and cattle products." The letter was in response to a request from Secretary Veneman, Agricultural Minister Lyle Vanclief, Canada, and Agriculture Secretary Javier Usabiaga, Mexico, to the OIE to provide more practical guidance regarding the resumption of trade with countries that have reported cases of BSE.
IF THE OIE CHANGES BSE/TSE GUIDELINES NOW (as weak as they are), just because the USA, Canada and Mexico does not like them. then all the work all other countries have done to erradicate this horrible disease from the planet over the last 3 decades will go for naught, and the agent will continue to spread...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518