Feds confirm mad cow in Alabama

5 thoughts on “Feds confirm mad cow in Alabama”

1. Helpful discussion – I was fascinated by the information . Does someone know if my company might be able to find a template a form version to type on ?

2. Thursday, January 3, 2008

   ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)

   http://animalhealthreport2006.blogspot.com/

   Thursday, January 31, 2008

   SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 99th
   meeting held on 14th December 2007

   snip…

   snip…

   ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION

   40. The Chair explained that the purpose of the question and answer
   session was to give members of the public an opportunity to ask
   questions related to the work of SEAC. Mr Terry Singeltary
   (Texas, USA) had submitted a question prior to the meeting,
   asking: “With the Nor-98 now documented in five different states so
   far in the USA in 2007, and with the two atypical BSE H-base

   13
   © SEAC 2007

   cases in Texas and Alabama, with both scrapie and chronic
   wasting disease (CWD) running rampant in the USA, is there any
   concern from SEAC with the rise of sporadic CJD in the USA from
   ”unknown phenotype”, and what concerns if any, in relations to
   blood donations, surgery, optical, and dental treatment, do you
   have with these unknown atypical phenotypes in both humans and
   animals in the USA? Does it concern SEAC, or is it of no concern
   to SEAC? Should it concern USA animal and human health
   officials?”

   41. A member considered that this question …………

   snip… please see full text, sources, and comments here ;

   http://seac992007.blogspot.com/2008/01/spongiform-encephalopathy-advisory.html

   2008

   USDA CERTIFIED NON-AMBULATORY DOWNER COW SCHOOL LUNCH PROGRAM

   http://downercattle.blogspot.com/2008/02/beef-recall-nationwide-school-lunch.html

   Specified Risk Material SRM

   http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html

   Thursday, February 21, 2008

   TRANSCRIPT: Technical Briefing – Hallmark/Westland Meat Packing Company –
   (02/21/08)

   Release No. 0054.08

   http://downercattle.blogspot.com/

   http://downercattle.blogspot.com/2008/02/transcript-technical-briefing.html

   Sunday, February 17, 2008

   Release No. 0046.08 Statement by Secretary of Agriculture Ed Schafer Regarding Hallmark/Westland
   Meat Packing Company Two Year Product Recall

   Release No. 0046.08

   Contact:
   USDA Press Office (202) 720-4623

   http://cjdmadcowbaseoct2007.blogspot.com/2008/02/release-no-004608-statement-by.html

   Geographical BSE Risk (GBR) assessments covering 2000-2006

   Date : 01.08.2006

   http://www.efsa.europa.eu/EFSA/Scientific_Document/GBR_assessments_table_Overview_assessed_countries_2002-2006.pdf

   In this context, a word is in order about the US testing program. After the
   discovery of the first (imported) cow in 2003, the magnitude of testing was
   much increased, reaching a level of >400,000 tests in 2005 (Figure 4).
   Neither of the 2 more recently indigenously infected older animals with
   nonspecific clinical features would have been detected without such testing,
   and neither would have been identified as atypical without confirmatory
   Western blots. Despite these facts, surveillance has now been decimated to
   40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and
   invites the accusation that the United States will never know the true
   status of its involvement with BSE.

   http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm

   PAUL BROWN COMMENT TO ME ON THIS ISSUE

   Tuesday, September 12, 2006 11:10 AM

   “Actually, Terry, I have been critical of the USDA handling of the mad cow
   issue for some years, and with Linda Detwiler and others sent lengthy detailed
   critiques and recommendations to both the USDA and the Canadian Food
   Agency.”

   http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125

   BEEF RECALL – USA (05)
   **********************
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   TSS

3. Subject: SEAC Draft minutes of the open session of the 93rd meeting held on 6th July 2006 (atypical BSE USA)
   Date: August 22, 2006 at 3:03 pm PST
   SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE

   Draft minutes of the open session of the 93rd meeting held on 6th July 2006

   snip…

   The Chair noted that recent reports described two cases of BSE in cattle in the United States of America (USA) as being similar to atypical cases of BSE found in a number of European countries. The Chair suggested that the term “atypical BSE”, used in the USA report, is potentially confusing and that this would be discussed under any other business. Dr Danny Matthews (Veterinary Laboratories Agency [VLA]) explained that data from western blots of the USA cases resembled that of a small number of atypical cases of BSE in France. A study of the French cases had shown the condition to be transmissible to mice by intracerebral (ic) inoculation with the neuropathological phenotype maintained on transmission3. Claims have been made about the existence of atypical cases of BSE in other countries but these have yet to be confirmed. No study has yet examined the tissue distribution of abnormal prion protein (PrPSc) or infectivity in such atypical cases of BSE.

   3 Baron et al. (2006) Transmission of new bovine prion to mice. Emerging. Infect. Diseases. 12, 1125-1128.

   snip…

   http://www.seac.gov.uk/minutes/draft93.pdf

   However, based on analysis of molecular features of prion

   diseases in cattle, this situation is similar to that in humans

   (5), in which different subtypes of sporadic Creutzfeldt-

   Jakob disease agents are found.

   DISPATCHES

   1126 Emerging Infectious Diseases • http://www.cdc.gov/eid • Vol. 12, No. 7, July 2006

   http://www.cdc.gov/ncidod/EID/vol12no07/pdfs/vol12no07.pdf

   Medical Sciences
   Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease

   Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli *
   *Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d’Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico “Carlo Besta,” Via Celoria 11, 20133 Milan, Italy

   Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)

   Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called “species barrier” between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.

   ——————————————————————————–

   C.C. and G.Z. contributed equally to this work.

   ||To whom correspondence should be addressed.

   E-mail: [email protected].
   http://www.pnas.org/cgi/doi/10.1073/pnas.0305777101

   http://www.pnas.org/cgi/content/abstract/0305777101v1

   PLEASE NOTE!

   SINCE spontaneous scrapie or CWD does not occur, then why is it that only BSE and sproadic CJD are capable of spontaneous mutation $$$

   confusious is confused again;-) …TSS

   Science 24 September 2004:
   Vol. 305. no. 5692, pp. 1918 – 1921
   DOI: 10.1126/science.1103581

   Perspectives
   BIOMEDICINE:

   A Fresh Look at BSE

   Bruce Chesebro*

   Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle form of a family of progressive brain diseases. These diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease (CWD) in deer and elk. They are also known as either “prion diseases” because of the association of a misfolded cellular prion protein in pathogenesis or “transmissible spongiform encephalopathies” (TSEs) because of the spongelike nature of the damaged brain tissue (1).

   The recent discovery of two BSE-infected cows, one in Canada and one in the United States, has dramatically increased concern in North America among meat producers and consumers alike over the extent to which BSE poses a threat to humans as well as to domestic and wild animals. The European BSE epidemic of the late-1980s seems to have been initiated a decade earlier in the United Kingdom by changes in the production of meat and bone meal (MBM) from rendered livestock, which led to contamination of MBM with the BSE infectious agent. Furthermore, the fact that UK farmers fed this rendered MBM to younger animals and that this MBM was distributed to many countries may have contributed to the ensuing BSE epidemic in the United Kingdom and internationally (2).

   Despite extensive knowledge about the spread of BSE through contaminated MBM, the source of BSE in Europe remains an unsolved mystery (2). It has been proposed that BSE could be derived from a cross-species infection, perhaps through contamination of MBM by scrapie-infected sheep tissues (see the figure). Alternatively, BSE may have been an endemic disease in cattle that went unnoticed because of its low level of horizontal transmission. Lastly, BSE might have originated by “spontaneous” misfolding of the normal cellular prion protein into the disease-associated abnormal isoform (3), which is postulated to be the infectious agent or “prion.”

   Five possible sources of BSE in North American cattle. Sheep, deer, and elk could spread prion diseases (TSEs) to cattle through direct animal contact or contamination of pastures. Endemic BSE has not been proven to exist anywhere in the world, but it is difficult to exclude this possibility because of the inefficient spread of BSE infectivity between individual animals (2). BSE caused by spontaneous misfolding of the prion protein has not been proven.
   CREDIT: KATHARINE SUTLIFF/SCIENCE

   Spontaneous protein misfolding is not a new phenomenon as proteins are known to sometimes misfold after synthesis. Cells in turn have devised ingenious ways to deal with this problem. These include molecular chaperone proteins that bind to misfolded proteins and help them to unfold, and organelles called proteosomes that degrade misfolded or unwanted proteins. However, although misfolded prion proteins have been generated in test tubes as well as in cultured cells, it has been difficult to demonstrate that such misfolded abnormal prion proteins are infectious (4, 5). Even the most recent data do not prove conclusively that infectivity has been generated in vitro because misfolded synthetic prion proteins were not able to transfer disease directly to wild-type mice (6). To obtain infectivity and subsequent prion disease, the misfolded proteins had to be inoculated and incubated for 1 to 2 years in transgenic mice that overexpressed a mutant version of the prion protein. Previous data from this group showed that transgenic mice expressing high amounts of prion protein developed neurological disease without inoculation of misfolded prion protein (7). Thus, at the biochemical level, the critical attributes of the misfolded prion protein required for infectivity are not known, and misfolding of prion protein alone may not be sufficient to generate an infectious agent (8).
   Nevertheless, the idea that BSE might originate due to the spontaneous misfolding of prion proteins has received renewed interest in the wake of reports suggesting the occurrence of atypical BSE (9-11). These results imply that new strains of cattle BSE might have originated separately from the main UK outbreak. Where and how might such strains have originated? Although such rare events cannot be studied directly, any number of sources of the original BSE strain could also explain the discovery of additional BSE strains in cattle (see the figure). However, it would be worrisome if spontaneous BSE were really a valid etiology because such a mechanism would be impossible to prevent–unlike other possible scenarios that could be controlled by large-scale eradication of TSE-positive animals.

   Another way to look at this problem is to examine evidence for possible spontaneous TSE disease in other animals besides cattle. Spontaneous BSE would be extremely difficult to detect in cattle, where horizontal spread is minimal. However, in the case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at birth as well as between adults, spontaneous disease should be detectable as new foci of clinical infection. In the early 1950s scrapie was eradicated in both Australia and New Zealand, and the mainland of both these countries has remained scrapie-free ever since. This scrapie-free status is not the result of selection of sheep resistant to scrapie because sheep from New Zealand are as susceptible as their UK counterparts to experimental scrapie infection (12). These experiments of man and nature appear to indicate that spontaneous clinical scrapie does not occur in sheep. Similarly, because CWD is known to spread horizontally, the lack of CWD in the deer or elk of eastern North America but its presence in western regions would also argue against a spontaneous disease mechanism. This is particularly noteworthy in New Zealand, where there are large numbers of deer and elk farms and yet no evidence of spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer, this would suggest that spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are unlikely to be found in cattle or humans. The main caveat to this notion is that spontaneous disease may arise in some animal species but not others. In humans, sCJD–which is considered by some researchers to begin by spontaneous misfolding of the prion protein–usually takes more than 50 years to appear. Thus, in animals with a shorter life-span, such as sheep, deer, and cattle, an analogous disease mechanism might not have time to develop.

   What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? “Sporadic” pertains to the rarity of disease occurrence. “Spontaneous” pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, “idiopathic” BSE–that is, BSE of unknown etiology–might be a better term to describe the origin of this malady.

   What does all this imply about testing cattle for BSE in North America? Current testing in the United States indicates that BSE is rare (one positive result in 40,000 cattle tested). However, additional testing of 200,000 head of slaughtered cattle over the next 1 to 2 years, as recently proposed by the U.S. Department of Agriculture (USDA), should tell us the incidence more precisely. Nevertheless, if any rare cases are detected, we may still not know their origin. If evidence arises of a focal occurrence of BSE, we might gain important insight into unexpected sources of contamination. However, because current tests do not seem to be able to detect BSE in infected animals less than 30 months of age, even more extensive testing will not completely guarantee the negative status of younger animals in the food chain. Therefore, the alternative option of testing all slaughtered cattle, as implemented in some countries such as Japan, would appear to provide little additional benefit. This fact has been acknowledged as the basis for a new agreement between the United States and Japan aimed at reestablishing the beef trade between the two countries.

   One problem with the current U.S. testing program was the announcement a few months ago of unconfirmed positive BSE tests in two additional North American animals that were subsequently found to be negative when tested with the more accurate method of Western blotting. The public release of information about unconfirmed positive tests detected by the rapid test used for mass screening may be a good idea in the interest of openness, but it has the potential to create unwarranted anxiety. If unconfirmed positives are a frequent occurrence, it would seem reasonable to follow a more cautious approach and wait until confirmatory testing is complete before publicly announcing the details.

   Based on the experience of many European countries, the mainstays of controlling BSE in cattle and avoiding spread to humans are threefold: first, eliminate feeding of ruminant tissues to ruminants; second, remove high-risk cattle tissues from human food; and third, continue to test for BSE in cattle in order to monitor progress with the elimination of the disease on a local and national basis. In the next 12 months, after extensive USDA test results are available, the extent of any possible BSE spread in the United States will be better documented. But, in fact, the United States and Canada have already instituted the most important steps to prevent the spread of cattle BSE in advance of the results–that is, a ban on feeding ruminant MBM to other ruminants and removal of high-risk tissues from meat for human consumption. It is hoped that the new data will not deviate enough from previous predictions to require further measures for management of this problem. The most important line of defense against any possible spread of BSE will be to maintain strict vigilance in the implementation of the current regulations.

   References

   S. B. Prusiner, Proc. Natl. Acad. Sci. U.S.A 95, 13363 (1998) [Medline].
   P. G. Smith, R. Bradley, Br. Med. Bull. 66, 185 (2003) [Medline].
   C. Weissmann, A. Aguzzi, Curr. Opin. Neurobiol. 7, 695 (1997) [Medline].
   A. F. Hill et al., J. Gen. Virol. 80, 11 (1999) [Medline].
   R. Chiesa et al., J. Virol. 77, 7611 (2003) [Medline].
   G. Legname et al., Science 305, 673 (2004).
   D. Westaway et al., Cell 76, 117 (1994) [Medline].
   B. Chesebro, Science 279, 42 (1998).
   A. G. Biacabe et al., EMBO Rep. 5, 110 (2004) [Medline].
   Y. Yamakawa et al., Jpn. J. Infect. Dis. 56, 221 (2003) [Medline].
   C. Casalone et al., Proc. Natl. Acad. Sci. U.S.A. 101, 3065 (2004) [Medline].
   E. F. Houston et al., J. Gen. Virol. 83, 1247 (2002) [Medline].

   http://www.sciencemag.org/cgi/content/full/305/5692/1918

   US atypical BSE – further details

   As reported in the last BSE Report (Which? BSE May 2006) French research findings

   concerning the two most recent cases of BSE in the USA suggest that these cases were

   not typical of BSE in cattle and may reflect a sporadic form of the disease.

   I

   n the two US cases, discovered in herds in Texas and Alabama, threre was an absence

   of telltale spongy lesions caused by prions. In addition, the prions in brain tissue

   samples from these cows seemed to be distributed differently from the classic form.

   Laboratory studies on mice in France showed that both the classic and atypical strains

   could be spread from one animal to another, but the atypical strain might happen

   spontaneously in cattle. The Texas and Alabama cows were older animals, as were

   some of the other animals in Europe with seemingly atypical forms of BSE.31

   Linda Detwiler, a former Agriculture Department veterinarian who consults for major

   food companies, cautioned against making that assumption. “I think it’s kind of early to

   say that would be the case,” Detwiler said. Other theories, she said, suggest the

   atypical strain might come from a mutation of BSE or even from a related disease in

   sheep.

   The US Agriculture Department has stated that whatever the cause there is no reason

   to change federal testing or control measures. “It’s most important right now, till the

   science tells us otherwise, that we treat this as BSE regardless,” the department’s chief

   veterinarian, John Clifford, said in an interview. …

   http://www.which.co.uk/files/application/pdf/bserep0606-445-89308.pdf

   BSE, BOVINE – USA: ATYPICAL STRAIN (02)
   ***************************************
   A ProMED-mail post

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   [1]
   Date: Tue 6 Jun 2006
   From: Terry Singeltary
   Source: News.Farmpage.com [edited]

   USDA Confirms BSE Tests On U.S. Cows Found Identical To Atypical Cases In
   France
   ———————————————–
   A USDA official confirmed that the positive BSE tests in 2 U.S.-born cattle
   were indeed an “atypical” type of the disease.

   A USDA spokesman acknowledged Friday [2 Jun 2006] that positive BSE tests
   from 2 domestic-born cattle were from a rare strain of the disease found in
   a small number of European cases.

   BSE, scientifically known as bovine spongiform encephalopathy and commonly
   known as mad cow disease, is a degenerative, fatal disease affecting the
   central nervous system of adult cattle.

   USDA officials have declined in the past to provide such details, but
   released information Friday [2 Jun 2006] after a French researcher revealed
   earlier this week that the cases in Texas last year 2005 and Alabama last
   spring 2006 were identical to “atypical” cases of BSE found in France.

   Scientists from around the world are trying to quantify the significance of
   these rare cases. They also want to know whether these cases may be sporadic.

   In an e-mail, a USDA spokesman said the cases raise “many unanswered
   questions about these unusual findings, and additional research is needed
   to help characterize the significance — or lack of significance — of any
   of these findings.”

   The USDA spokesperson said nothing in the test results of the 2 cattle
   justifies any changes in surveillance, disease control or public-health
   measures already being taken in the U.S.

   —
   Terry Singeltary

   ******
   [2]
   Date: Tue 6 Jun 2006
   From: Terry Singeltary
   Source: Farmers Weekly [edited]

   Cattle disease might be unknown strain of BSE
   ———————————————–
   Scientists across Europe and the United States are following the emergence
   of a new Transmissible Spongiform Encephalopathy (TSE) in cattle that could
   be a new strain of BSE.

   Speaking last weekend at an international conference on prion diseases in
   domestic livestock (such as BSE in cows and scrapie in sheep and goats),
   scientists from France and Italy described how the disease had been
   detected in a small number of cattle ranging from 5 to 15 years old.

   The strain differs from BSE in that it has a longer incubation time and is
   consequently being found in older cattle.

   The new strain also demonstrates different characteristics from BSE in
   laboratory tests and was originally detected through active surveillance of
   live animals rather than during inspection of a suspect fallen animal.

   Marion Simmons of the Veterinary Laboratory Agency at Weybridge urged
   caution, saying there are not yet sufficient supporting data to suggest
   that the disease is a new strain of BSE.

   —
   Terry Singeltary

   [It has long been debated whether this atypical form is sporadic or whether
   the sporadic appearance was an atypical form. There does not seem to be a
   good explanation, which simply highlights the need for more research and
   understanding of this disease. – Mod.TG]

   [see also:
   BSE, bovine – USA: atypical strain 20060601.1525]
   ……….tg/msp/dk

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   Order Code RS22345

   Updated July 18, 2006

   CRS REPORT FOR CONGRESS

   BSE (“Mad Cow Disease”): A Brief Overview

   Geoffrey S. Becker

   Specialist in Agricultural Policy

   Resources, Science, and Industry Division

   snip…

   1 This report, which replaces CRS Issue Brief IB10127, Mad Cow Disease: Agricultural Issues

   for Congress, summarizes and updates information in other CRS reports, listed on page 6.

   Sources for facts and citation to reports and studies can be found in these CRS reports.

   Congressional Research Service ˜ The Library of Congress

   CRS Report for Congress

   Received through the CRS Web

   Order Code RS22345

   Updated July 18, 2006

   BSE (“Mad Cow Disease”): A Brief Overview

   Geoffrey S. Becker

   Specialist in Agricultural Policy

   Resources, Science, and Industry Division

   Summary

   The appearance of BSE (bovine spongiform encephalopathy or “mad cow disease”)

   in North America in 2003 raised meat safety concerns and disrupted trade for cattle and

   beef producers. A major issue for Congress has been how to rebuild foreign confidence

   in the safety of U.S. beef and regain lost markets like Japan and Korea. Among other

   issues are whether additional measures are needed to further protect the public and cattle

   herd, and concerns over the relative costs and benefits of such measures for consumers,

   taxpayers and industry. This report will be updated if significant developments ensue.1

   What Is BSE?

   BSE (bovine spongiform encephalopathy or “mad cow disease”) is a fatal

   neurological disease of cattle, believed to be transmitted mainly by feeding infected cattle

   parts back to cattle. More than 187,000 cases have been reported worldwide, 183,000 of

   them in the United Kingdom (UK) where BSE was first identified in 1986. The annual

   number of new cases has declined steeply since 1992. Humans who eat contaminated

   beef are believed susceptible to a rare but fatal brain wasting disease, variant Creutzfeldt-

   Jakob disease (vCJD). About 160 people, most in the UK, have been diagnosed with

   vCJD since 1986, but none has been linked to any Canadian or U.S. meat consumption.

   BSE in North America

   BSE has been reported in 11 North American cattle, 10 born here and one imported

   from the UK. The first native case was an Alberta, Canada, beef cow reported in May

   2003. Canada has since reported six more cases, most recently in July 2006 in a 50-

   month-old dairy cow in Manitoba. The first U.S. case was in a Canadian-born dairy cow

   found in Washington state in December 2003. The other two U.S. cases were a 12-yearold

   Texas-born and -raised beef cow, found in November 2004 but not confirmed until

   June 2005, and a 10-year-old Alabama beef cow found in late February 2006.

   CRS-2

   In epidemiological investigations of the three U.S. cases, the U.S. Department of

   Agriculture (USDA) was unable to track down all related animals of interest, but those

   that were located tested negative for the disease. Despite a beef recall, some meat from

   the first U.S. BSE cow may have been consumed, USDA said, adding, however, that the

   highest-risk tissues never entered the food supply. No materials from the other two U.S.

   cows entered the food supply, USDA also said. In the recent Alabama case, authorities

   were unable to determine the cow’s herd of origin. Animal health officials initially

   indicated that all of the North American cases were caused by the consumption of BSEcontaminated

   feed. However, USDA reportedly now believes that the two native-born

   U.S. cattle had “atypical” BSE, which differs from other cases. If these cases are

   determined to be “spontaneous,” that may affect future control strategies.

   snip…

   http://ncseonline.org/NLE/CRSreports/06Jul/RS22345.pdf

   Research Project: Study of Atypical Bse

   Location: Virus and Prion Diseases of Livestock

   Project Number: 3625-32000-073-07
   Project Type: Specific C/A

   Start Date: Sep 15, 2004
   End Date: Sep 14, 2007

   Objective:
   The objective of this cooperative research project with Dr. Maria Caramelli
   from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct
   comparative studies with the U.S. bovine spongiform encephalopathy (BSE)
   isolate and the atypical BSE isolates identified in Italy. The studies will
   cover the following areas: 1. Evaluation of present diagnostics tools used
   in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison
   of the U.S. BSE isolate and other typical BSE isolates with atypical BSE
   cases. 3. Studies on transmissibility and tissue distribution of atypical
   BSE isolates in cattle and other species.

   Approach:
   This project will be done as a Specific Cooperative Agreement with the
   Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del
   Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance
   program to analyze the effectiveness of the U.S diagnostic tools for
   detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE
   isolate with atypical BSE isolates will provide further characterization of
   the U.S. BSE isolate. Transmission studies are already underway using brain
   homogenates from atypical BSE cases into mice, cattle and sheep. It will be
   critical to see whether the atypical BSE isolates behave similarly to
   typical BSE isolates in terms of transmissibility and disease pathogenesis.
   If transmission occurs, tissue distribution comparisons will be made between
   cattle infected with the atypical BSE isolate and the U.S. BSE isolate.
   Differences in tissue distribution could require new regulations regarding
   specific risk material (SRM) removal.

   http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490

   Research Project: Study of Atypical Bse

   Location: Virus and Prion Diseases of Livestock

   2005 Annual Report

   This report serves to document research conducted under a specific
   cooperative agreement between ARS and the Italian Reference Centre for
   Animal TSE (CEA) at the Istituto Zooprofilattico Sperimentale, Turin, Italy.
   Additional details of research can be found in then report for the parent
   project 3625-32000-073-00D, Transmission, Differentiation, and Pathobiology
   of Transmissible Spongiform Encephalopathies. The aim of the cooperative
   research project conducted by the CEA and ARS is to compare the U.S. bovine
   spongiform encephalopathy (BSE) isolate and the bovine amyloidotic
   spongiform encephalopathy isolates (BASE) identified in Italy. The first
   objective was to determine whether diagnostic methods routinely used by USDA
   are able to identify the Italian BASE cases. For this purpose, CEA received
   the immunohistochemistry (IHC) protocol developed by APHIS-USDA. The IHC
   protocol was reproduced and standardized in the CEA laboratory and will be
   applied to the Italian BSE and BASE cases. Furthermore, fixed brainstem
   sections and frozen brainstem material from Italian BSE and BASE cases will
   be sent to ARS for analysis using USDA IHC and Western blot (WB) methods.
   These studies will enable us to determine whether the present diagnostic
   tools (IHC and WB) employed at the USDA will be able to detect the Italian
   BASE cases and also enable us to compare Italian BSE and BASE with the U.S.
   BSE cases.

   http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2005

   Research Project: Transmission, Differentiation, and Pathobiology of
   Transmissible Spongiform Encephalopathies

   Location: Virus and Prion Diseases of Livestock

   Title: Where We’ve Been and Where We’re Going with Bse Testing in the United
   States

   Authors
   item Hall, Mark – NVSL-APHIS-USDA
   item Richt, Juergen
   item Davis, Arthur – NVSL-APHIS-USDA
   item Levings, Randall – NVSL-APHIS-USDA

   Submitted to: American Association of Veterinary Laboratory Diagnosticians
   Publication Type: Abstract
   Publication Acceptance Date: September 1, 2005
   Publication Date: November 3, 2005
   Citation: Hall, M.S., Richt, J.A., Davis, A.J., Levings, R.L. 2005. Where
   We’ve Been and Where We’re Going with Bse Testing in the United States
   [abstract]. 48th Annual Meeting of the American Association of Veterinary
   Laboratory Diagnosticians. P. 20.

   Technical Abstract: A review of the laboratory aspects of the United States
   Department of Agriculture’s (USDA) Bovine Spongiform Encephalopathy (BSE)
   Surveillance Program from its beginning to the present day will be provided.
   Validated diagnostic tests for BSE require brain tissue. There are no ante
   mortem (blood/serum) tests for BSE available at present. From a historical
   perspective, diagnostic tests for BSE continue to evolve. The original
   diagnostic test method was histopathology in which sections of brain were
   examined under a microscope, and the classical vacuoles and spongiform
   change in specific areas of the brain would allow a diagnosis to be made.
   This method was accurate but only allowed a diagnosis to be made relatively
   late in the course of the disease. In the mid-1990s, immunohistochemistry
   (IHC) and Western blotting were developed which allow the detection of the
   abnormal form of the prion protein (PrPSc) and a diagnosis could be made
   prior to the development of spongiform changes and clinical signs. In the
   past decade, so-called “rapid tests” have been introduced commercially for
   BSE. Five commercial tests are currently licensed/permitted in the United
   States for BSE. These licensed tests include the Prionics Western blot,
   Prionics ELISA, Enfer/Abbott ELISA, IDEXX ELISA, and the BioRad ELISA. This
   presentation will discuss various attributes of the validated test methods
   available today. Both IHC and Western blot are considered confirmatory tests
   for BSE by the World Organisation of Animal Health (OIE). IHC provides for a
   specific immunological detection of PrPSc and enables the specific
   anatomical location to be determined. Western blot provides both
   immunological detection of PrPSc as well as specific molecular weight
   characterizations; certain Western blot procedures can be extremely
   sensitive due to various concentration procedures before analysis of the
   sample. The OIE recommended Western blot and IHC methods for confirmatory
   diagnosis of BSE used by USDA and the Veterinary Laboratories Agency in
   Weybridge, England, will be discussed. The overall enhanced testing plan
   that has been used for the past 18 months will be described including
   changes that have occurred during this time. The USDA’s BSE enhanced
   surveillance plan has been a very successful national surveillance testing
   program that has been a shared effort between state veterinary diagnostic
   laboratories as part of the National Animal Health Laboratory Network and
   the National Veterinary Services Laboratories.

   http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=183829

   http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf

   3.57 The experiment which might have determined whether BSE and scrapie were
   caused by the same agent (ie, the feeding of natural scrapie to cattle) was
   never undertaken in the UK. It was, however, performed in the USA in 1979,
   when it was shown that cattle inoculated with the scrapie agent endemic in
   the flock of Suffolk sheep at the United States Department of Agriculture in
   Mission, Texas, developed a TSE quite unlike BSE. 32 The findings of the
   initial transmission, though not of the clinical or neurohistological
   examination, were communicated in October 1988 to Dr Watson, Director of the
   CVL, following a visit by Dr Wrathall, one of the project leaders in the
   Pathology Department of the CVL, to the United States Department of
   Agriculture. 33 The results were not published at this point, since the
   attempted transmission to mice from the experimental cow brain had been
   inconclusive. The results of the clinical and histological differences
   between scrapie-affected sheep and cattle were published in 1995. Similar
   studies in which cattle were inoculated intracerebrally with scrapie inocula
   derived from a number of scrapie-affected sheep of different breeds and from
   different States, were carried out at the US National Animal Disease Centre.
   34 The results, published in 1994, showed that this source of scrapie agent,
   though pathogenic for cattle, did not produce the same clinical signs of
   brain lesions characteristic of BSE.

   http://www.bseinquiry.gov.uk/

   The findings of the initial transmission, though not of the clinical or
   neurohistological examination, were communicated in October 1988 to Dr
   Watson, Director of the CVL, following a visit by Dr Wrathall, one of the
   project leaders in the Pathology Department of the CVL, to the United States
   Department of Agriculture. 33

   http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf

   http://www.bseinquiry.gov.uk/

   The results were not published at this point, since the attempted
   transmission to mice from the experimental cow brain had been inconclusive.
   The results of the clinical and histological differences between
   scrapie-affected sheep and cattle were published in 1995. Similar studies in
   which cattle were inoculated intracerebrally with scrapie inocula derived
   from a number of scrapie-affected sheep of different breeds and from
   different States, were carried out at the US National Animal Disease Centre.
   34 The
   results, published in 1994, showed that this source of scrapie agent, though
   pathogenic for cattle, did not produce the same clinical signs of brain
   lesions characteristic of BSE.

   3.58 There are several possible reasons why the experiment was not performed
   in the UK. It had been recommended by Sir Richard Southwood (Chairman of the
   Working Party on Bovine Spongiform Encephalopathy) in his letter to the
   Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988, 35
   though it was not specifically recommended in the Working Party Report or
   indeed in the Tyrrell Committee Report (details of the Southwood Working
   Party and the Tyrell Committee can be found in vol. 4: The Southwood Working
   Party, 1988-89 and vol. 11: Scientists after Southwood respectively). The
   direct inoculation of scrapie into calves was given low priority, because of
   its high cost and because it was known that it had already taken place in
   the USA. 36 It was also felt that the results of such an experiment would be
   hard to interpret. While a negative result would be informative, a positive
   result would need to demonstrate that when scrapie was transmitted to
   cattle, the disease which developed in cattle was the same as BSE. 37 Given
   the large number of strains of scrapie and the possibility that BSE was one
   of them, it would be necessary to transmit every scrapie strain to cattle
   separately, to test the hypothesis properly. Such an experiment would be
   expensive. Secondly, as measures to control the epidemic took hold, the need
   for the experiment from the policy viewpoint was not considered so urgent.
   It was felt that the results would be mainly of academic interest. 38

   http://www.bseinquiry.gov.uk/

   REPORT OF THE COMMITTEE ON SCRAPIE

   Chair: Dr. Jim Logan, Cheyenne, WY

   Vice Chair: Dr. Joe D. Ross, Sonora, TX

   Dr. Deborah L. Brennan, MS; Dr. Beth Carlson, ND; Dr. John R. Clifford, DC; Dr. Thomas F. Conner, OH; Dr. Walter E. Cook, WY; Dr. Wayne E. Cunningham, CO; Dr. Jerry W. Diemer, TX; Dr. Anita J. Edmondson, CA; Dr. Dee Ellis, TX; Dr. Lisa A. Ferguson, MD; Dr. Keith R. Forbes, NY; Dr. R. David Glauer, OH; Dr. James R. Grady, CO; Dr. William L. Hartmann, MN; Dr. Carolyn Inch, CAN; Dr. Susan J. Keller, ND; Dr. Allen M. Knowles, TN; Dr. Thomas F. Linfield, MT; Dr. Michael R. Marshall, UT; Dr. Cheryl A. Miller, In; Dr. Brian V. Noland, CO; Dr. Charles Palmer, CA; Dr. Kristine R. Petrini, MN; Mr. Stan Potratz, IA; Mr. Paul E. Rodgers, CO; Dr. Joan D. Rowe, CA; Dr. Pamela L. Smith, IA; Dr. Diane L. Sutton, MD; Dr. Lynn Anne Tesar, SD; Dr. Delwin D. Wilmot, NE; Dr. Nora E. Wineland, CO; Dr. Cindy B. Wolf, MN.

   The Committee met on November 9, 2005, from 8:00am until 11:55am, Hershey Lodge and Convention Center, Hershey, Pennsylvania. The meeting was called to order by Dr. Jim Logan, chair, with vice chairman Dr. Joe D. Ross attending. There were 74 people in attendance.

   The Scrapie Program Update was provided by Dr. Diane Sutton, National Scrapie Program Coordinator, United States Department of Agriculture (USDA), Animal and Plant Health Inspection Services (APHIS), Veterinary Services (VS). The complete text of the Status Report is included in these Proceedings.

   Dr. Patricia Meinhardt, USDA-APHIS-VS-National Veterinary Services Laboratory (NVSL) gave the Update on Genotyping Labs and Discrepancies in Results. NVSL conducts investigations into discrepancies on genotype testing results associated with the Scrapie Eradication Program. It is the policy of the Program to conduct a second genotype test at a second laboratory on certain individual animals. Occasionally, there are discrepancies in those results. The NVSL conducts follow-up on these situations through additional testing on additional samples from the field and archive samples from the testing laboratories.

   For the period of time from January 1, 2005, until October 15, 2005, there were 23 instances of discrepancies in results from 35 flocks. Of those 23 instances, 14 were caused by laboratory error (paperwork or sample mix-up), 3 results from field error, 5 were not completely resolved, and 1 originated from the use of a non-approved laboratory for the first test. As a result of inconsistencies, one laboratory’s certification was revoked by APHIS-VS.

   snip…

   Infected and Source Flocks

   As of September 30, 2005, there were 105 scrapie infected and source flocks. There were a total of 165** new infected and source flocks reported for FY 2005. The total infected and source flocks that have been released in FY 2005 was 128. The ratio of infected and source flocks cleaned up or placed on clean up plans vs. new infected and source flocks discovered in FY 2005 was 1.03 : 1*. In addition 622 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2005, of which 130 were RSSS cases. Fifteen cases of scrapie in goats have been reported since 1990. The last goat case was reported in May 2005. Approximately 5,626 animals were indemnified comprised of 49% non-registered sheep, 45% registered sheep, 1.4% non-registered goats and 4.6% registered goats.

   Regulatory Scrapie Slaughter Surveillance (RSSS)

   RSSS was designed to utilize the findings of the Center for Epidemiology and Animal Health (CEAH) Scrapie: Ovine Slaughter Surveillance (SOSS) study. The results of SOSS can be found at http://www.aphis.usda.gov/vs/ceah/cahm/Sheep/sheep.htm . RSSS started April 1,

   2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks for clean-up. During FY 2005 collections increased by 32% overall and by 90% for black and mottled faced sheep improving overall program effectiveness and efficiency as demonstrated by the 26% decrease in percent positive black faced sheep compared to FY 2004. Samples have been collected from 62,864 sheep since April 1, 2003, of which results have been reported for 59,105 of which 209 were confirmed positive. During FY 2005, 33,137 samples were collected from 81 plants. There have been 130 NVSL confirmed positive cases (30 collected in FY 2004 and confirmed in FY 2005 and 100 collected and confirmed in FY 2005) in FY 2005. Face colors of these positives were 114 black, 14 mottled, 1 white and 1 unknown. The percent positive by face color is shown in the chart below.

   Scrapie Testing

   In FY 2005, 35,845 animals have been tested for scrapie: 30,192 RSSS; 4,742 regulatory field cases; 772 regulatory third eyelid biopsies; 10 third eyelid validations; and 129 necropsy validations (chart 9).

   Animal ID

   As of October 04, 2005, 103,580 sheep and goat premises have been assigned identification numbers in the Scrapie National Generic Database. Official eartags have been issued to 73,807 of these premises.

   *This number based on an adjusted 12 month interval to accommodate the 60 day period for setting up flock plans.

   http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf

   Published online before print October 20, 2005

   Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102
   Medical Sciences

   A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

   ( sheep prion | transgenic mice )

   Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *, Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte ||, Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude *
   *Virologie Immunologie Moléculaires and ||Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

   Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)

   Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and “cases” that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

   ——————————————————————————–

   Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B. contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data; and H.L. wrote the paper.

   A.L.D. and V.B. contributed equally to this work.

   To whom correspondence should be addressed.

   Hubert Laude, E-mail: [email protected]

   http://www.pnas.org/cgi/doi/10.1073/pnas.0502296102

   http://www.pnas.org/cgi/content/abstract/0502296102v1

   12/10/76
   AGRICULTURAL RESEARCH COUNCIL
   REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
   Office Note
   CHAIRMAN: PROFESSOR PETER WILDY

   snip…

   A The Present Position with respect to Scrapie
   A] The Problem

   Scrapie is a natural disease of sheep and goats. It is a slow
   and inexorably progressive degenerative disorder of the nervous system
   and it ia fatal. It is enzootic in the United Kingdom but not in all
   countries.

   The field problem has been reviewed by a MAFF working group
   (ARC 35/77). It is difficult to assess the incidence in Britain for
   a variety of reasons but the disease causes serious financial loss;
   it is estimated that it cost Swaledale breeders alone $l.7 M during
   the five years 1971-1975. A further inestimable loss arises from the
   closure of certain export markets, in particular those of the United
   States, to British sheep.

   It is clear that scrapie in sheep is important commercially and
   for that reason alone effective measures to control it should be
   devised as quickly as possible.

   Recently the question has again been brought up as to whether
   scrapie is transmissible to man. This has followed reports that the
   disease has been transmitted to primates. One particularly lurid
   speculation (Gajdusek 1977) conjectures that the agents of scrapie,
   kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
   mink are varieties of a single “virus”. The U.S. Department of
   Agriculture concluded that it could “no longer justify or permit
   scrapie-blood line and scrapie-exposed sheep and goats to be processed
   for human or animal food at slaughter or rendering plants” (ARC 84/77)”
   The problem is emphasised by the finding that some strains of scrapie
   produce lesions identical to the once which characterise the human
   dementias”

   Whether true or not. the hypothesis that these agents might be
   transmissible to man raises two considerations. First, the safety
   of laboratory personnel requires prompt attention. Second, action
   such as the “scorched meat” policy of USDA makes the solution of the
   acrapie problem urgent if the sheep industry is not to suffer
   grievously.

   snip…

   76/10.12/4.6

   http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf

   Subject: SCRAPIE and CWD USA UPDATE July 19, 2006
   Date: July 19, 2006 at 12:06 pm PST
   SCRAPIE USA UPDATE MAY 31, 2006

   Infected and Source Flocks

   As of May 31, 2006, there were 93 scrapie infected and source flocks (Figure 3). There were 12 new infected and source flocks reported in May (Figure 4) with a total of 67 flocks reported for FY 2006 (Figure 5). The total infected and source flocks that have been released in FY 2006 are 53 (Figure 6), with 7 flocks released in May. The ratio of infected and source flocks released to newly infected and source flocks for FY 2006 = 0.79 : 1. In addition, as of May 31, 2006, 216 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 33 were RSSS cases (Figure 7). This includes 33 newly confirmed cases in May 2006 (Figure 8). Eighteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat case was reported in March 2006. New infected flocks, source flocks, and flocks released for FY 2006 are depicted in Chart 3. New infected and source statuses from 1997 to 2006 are depicted in Chart 4.

   snip…

   Scrapie Testing

   In FY 2006, 26,185 animals have been tested for scrapie : 22,634 RSSS*; 2063 regulatory field cases; 61 necropsy validations, 5 rectal biopsy and 1427 regulatory third eyelid biopsies (Chart 9). …

   snip…END

   http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html

   TSS

4. Hello
   It is a good thing that you are doing, keeping a vigilant eye on things. I want to share with you what some important people are saying about mad Cow Disease and its cause.
   As there is currently a news story concerning Mad Cow Disease in Alabama, we are taking this opportunity to share this question.
   Encephalopathy is brain damage. Hexane is known to cause brain damage(Hexane MSDS), and Hexane is fed to cattle in large quantities (the EPA found one-half to one pound per ton of Hexane in food meals, in averages of nine vegetable oil-processing plants.).
   To find what does, and what does not cause the malady of Scrapie(aka Mad Cow Disease) one can look to the only two countries in the world known to be free of Scrapie and Mad Cow Disease; Australia and New Zealand. Look at what they feed to their livestock. Australian and New Zealand livestock are normally fed only grass and grass hay. Their livestock are not fed grain supplements from the vegetable oil extraction industry(which is the source of Hexane in high protein meals).
   Should we give credit where credit is due? The unpleasant chemical Hexane is fed to cows at levels 15-20 times higher than the OSHA occupational permissable Hexane exposure limit for humans(Time weighed averages). Hexane is the root cause for Mad Cow Disease.
   My letter includes the documentation and official government studies where the EPA found Hexane levels many times over the occupational exposure limits in the food meals that you and I eat(and the cows eat it too).
   (this passage is from a letter about Hexane being fed to cattle and its effects. The entire letter is at http://www.datacruz.com/~baneyred/index.html and it is called “My Story of Hexane”
   Given these frank associations, can Mad Cow Disease be explained in a more reasonable way?
   Is it strange to say and see that Spongiform Encephalopathy is brain damage? What causes brain damage anyway?
   Earnestly, Dale Baney

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