Environmental Sources of Scrapie Prions

Journal of Virology, November 2010, p. 11560-11562, Vol. 84, No. 21 0022-538X/10/$012.00+0 doi:10.1128/JVI.01133-10 Copyright © 2010, American Society for Microbiology. All Rights Reserved.

Environmental Sources of Scrapie Prions

Ben C. Maddison,1 Claire A. Baker,1 Linda A. Terry,2 Susan J. Bellworthy,2 Leigh Thorne,2 Helen C. Rees,1 and Kevin C. Gough3* ADAS UK, Department of Biology, University of Leicester, University Road, Leicester LE1 7RH, United Kingdom,1 Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, United Kingdom,2 School of Veterinary Medicine and Science, the University of Nottingham, Sutton Bonington Campus, College Road, Sutton Bonington, Leicestershire LE12 5RD, United Kingdom3

Received 27 May 2010/ Accepted 11 August 2010

Ovine scrapie and cervine chronic wasting disease show considerable horizontal transmission. Here we report that a scrapie-affected sheep farm has a widespread environmental contamination with prions. Prions were amplified by protein-misfolding cyclic amplification (sPMCA) from seven of nine environmental swab samples taken, including those from metal, plastic, and wooden surfaces. Sheep had been removed from the areas from which the swabs were taken up to 20 days prior to sampling, indicating that prions persist for at least that long. These data implicate inanimate objects as environmental reservoirs for prion infectivity that are likely to contribute to facile disease transmission.

--------------------------------------------------------------------------------

* Corresponding author. Mailing address: School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington Campus, College Road, Sutton Bonington, Leicestershire LE12 5RD, United Kingdom. Phone: 44-115-9516272. Fax: 44-115-9516440. E-mail: kevin.gough@nottingham.ac.uk

Published ahead of print on 25 August 2010.

--------------------------------------------------------------------------------

Journal of Virology, November 2010, p. 11560-11562, Vol. 84, No. 21 0022-538X/10/$012.00+0 doi:10.1128/JVI.01133-10 Copyright © 2010, American Society for Microbiology. All Rights Reserved.


http://jvi.asm.org/cgi/content/short/84/21/11560



16 February 2011 • Andrew Walker

ADAS research finds scrapie prion material detectable in the environment

ADAS scientists and their university colleagues have found that survival of scrapie prion pathogens in the environment may be a long term source of infection to sheep and cattle. These findings could indicate that previous understanding of TSE infectivity may be incomplete.

Thanks to rigorous health controls, robust biosecurity procedures and the implementation of a selective breeding program in sheep the prevalence of transmissible spongiform encephalopathies (TSEs) in UK farmed livestock has fallen to very low levels, and these diseases no longer impose a serious economic or epidemiological burden on British farmers. The two most well-known forms of TSE, that is scrapie in sheep and BSE in cattle, are, like all TSEs, fatal neurological disorders caused by a protein known as a prion. The infectious or pathological form of the scrapie prion is known to be excreted or secreted by sheep in body fluids, and this knowledge led ADAS scientists and their university colleagues to hypothesise that the survival of these pathogens in the environment - in fields or in buildings for example, may be a long-term source of infection. If correct, this may have implications for healthy flocks moving onto farms thought to have been thoroughly decontaminated following previous cases of the disease.

To test the hypothesis, ADAS carried out environmental sampling at a sheep farm with a detailed history of endemic scrapie. These samples were analysed using an innovative amplification technique which is capable of detecting the presence of very low numbers of prions.

These tests revealed that a number of environmental prion reservoirs did indeed exist at the test site. The results showed that metal gates, water troughs, feed troughs, penning structures, and both plastic and wooden fence posts, were harbouring prions at least three weeks after their last contact with infected animals. By contrast, similar structures from a different farm, housing sheep known to be scrapie-free, had no detectable contamination.

The key implication from these investigations is that our previous understanding of the risks of TSE infectivity may be incomplete. We do not know if the levels of environmental contamination that ADAS were able to detect are sufficient to cause disease in exposed animals, but further and more detailed research may yield the answer to that question.

For further information about this project, and about ADAS’s disease diagnostics capability, please contact Dr Ben Maddison via email ben.maddison@adas.co.uk , or on 0115 9516272.

The research described above was published in the Journal of Virology, November 2010, pp 11560-11562, where details of all the authors can be found.

http://aplus.adas.co.uk/Services/AHW/ADAS-research-finds-scrapie-prion-material-detectable-in-the-environment.aspx




Wednesday, February 16, 2011

IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE

http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html




Friday, February 11, 2011

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html




Published online 11 February 2011 | Nature | doi:10.1038/news.2011.87

News

Livestock plagues are spreading As farming intensifies, researchers warn that the developing world is "dangerously behind" on controlling animal diseases.

Natasha Gilbert


http://www.nature.com/news/2011/110211/full/news.2011.87.html



http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf




Chronic Wasting Disease—Prion Disease in the Wild

Citation: Bunk S (2004) Chronic Wasting Disease—Prion Disease in the Wild. PLoS Biol 2(4): e121. doi:10.1371/journal.pbio.0020121

Published: April 13, 2004

In 1967, mule deer in a research facility near Fort Collins, Colorado, in the United States apparently began to react badly to their captivity. At least, that was the guess of researchers working on the natural history and nutrition of the deer, which became listless and showed signs of depressed mood, hanging their heads and lowering their ears. They lost appetite and weight. Then they died—of emaciation, pneumonia, and other complications—or were euthanized. The scientists dubbed it chronic wasting disease (CWD), and for years they thought it might be caused by stress, nutritional deficiencies, or poisoning. A decade later, CWD was identified as one of the neurodegenerative diseases called spongiform encephalopathies, the most notorious example of which is bovine spongiform encephalopathy (BSE), more commonly known as mad cow disease. Nowadays, CWD is epidemic in the United States. Although no proof has yet emerged that it's transmissible to humans, scientific authorities haven't ruled out the possibility of a public health threat. The media have concentrated on this concern, and politicians have responded with escalated funding over the past two years for fundamental research into the many questions surrounding this mysterious disease.

Quite apart from how little is yet known about CWD, media interest is reason enough to step up investigation of it, says Mo Salman, a veterinary epidemiologist at Colorado State University in Fort Collins. He's been scientifically involved with BSE, since it was first discovered among cattle in the United Kingdom in 1986. He recalls predicting that lay interest in BSE would wane after five years. Instead, the disease was found in the mid-1990s to be capable of killing humans who ate tainted beef. “I was wrong, and it really changed my way of thinking, to differentiate between scientific evidence and the public perception,” Salman admits. “Because CWD is similar to BSE, the public perception is that we need to address this disease, to see if it has any link to human health.”

http://www.plosbiology.org/article/info:doi%2F10.1371%2Fjournal.pbio.0020121




* Williams reported in the same scientific paper that ``a few surplus deer and elk'' from CWD-infected state-run pens near Fort Collins had been released back into the wild. How many and in what years remains unclear. State officials say they can find few records.

http://www.highbeam.com/doc/1G1-87932644.html




Within the facilities, deer have had irregular and discontinuous contact with other wild ruminants and with domestic cattle, goats and sheep. In addition, other feral mammalian species either reside within or traverse the facilities’ pens.

Journal of Wildlife Diseases Vol. 16. No. 1, January, 1980 B Mice (Peromyscus sp., Mus musculus), rabbit (Lepus sp., Syluilagus sp.), raccoon (Procyon lotor), skunk (Mephitis

http://www.jwildlifedis.org/cgi/reprint/16/1/89



The Fort Collins facility became a CWD death trap. Between 1970 and 1981, 90 percent of the deer that stayed more than two years died from the disease or had to be euthanized. In 1980 the scourge emerged outside Colorado, at the Sybille Research Unit in southeastern Wyoming, 120 miles northwest of Fort Collins. The two facilities had exchanged deer for breeding purposes, thus indicating that the disease was infectious--even to a different species: soon the elk at the facilities contracted the disease. (Deer and elk both belong to the cervid family.)

For years, researchers thought CWD resulted from nutritional deficiencies, poisoning, or stress from confinement. But in 1977 Elizabeth S. Williams, studying for her doctorate at Colorado State University, discovered that this view was mistaken. When Williams looked at brain slices from infected animals, she saw that the tissue was full of microscopic holes. "I happened to be taking a course in neuropathology and had studied a lot of brain lesions," she recalls. The holes were unmistakably like scrapie, the sheep sickness that was the first documented spongiform encephalopathy.

In fact, CWD appears to have originated from scrapie. Richard E. Race of the National Institutes of Health Rocky Mountain Laboratories in Hamilton, Mont., conducted test tube studies that revealed no distinction between the malformed PrP of scrapie sheep and CWD cervids. Consistent with this discovery, Amir Hamir of the U.S. Department of Agriculture's National Animal Disease Center in Ames, Iowa, found no difference in the appearance of brain samples from elk with CWD and elk experimentally infected with scrapie. (BSE also probably arose from scrapie, after cows ate feed derived from infected sheep.)

Philip Yam is Scientific American's news editor. This article is adapted from his book, The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases, published in June. Overview/Chronic Wasting Disease

snip...end...tss

How did CWD get started? 17 Mar 98 webmaster opinion My best guess as to what really happened:

in the early days of the Ft. Collins facility, before they went to wild animal diseases, they studied scrapie and other diseases in sheep. The facility became contaminated, just like the pasture in Iceland. They hoped it wouldn't cross the species barrier.

Then they brought in mule deer. These became infected. No post-mortems were done, no tissues were saved, no records were kept; one worker there in 1967 wrote me to say they suspected scrapie at the time. They hoped it would go away.

The facility became grossly contaminated, 90% of the animals dying. No autopsies were supposedly done until 13 years into the disease, even though this was a disease research facility. They hoped it would go away.

Deer infected elk and other cervids. They hoped it would go away.

Pre-clinical animals were shipped to Wyoming, zoos, game farms, and released back into the wild. Wild animals infected each other at winter feeding stations at much higher rates than anyone expected. They hoped it would go away.

Infected wild animals were brought into various facilities. No monitoring had been done on wild animals. They hoped it would go away.

Tens of thousands of hunters ate contaminated meat from venison pooled into sausage. They hoped hunters wouldn't get CJD.

Some hunters subsequently donated blood which were pooled into batches of 50,000 doses or more. They hoped medical recipients wouldn't get CJD.

CWD is not scrapie, though it was probably originally triggered by scrapie. It is a different prion, a different amino acid sequence, after initial passage. CWD is probably not caused or spread through rendered downer protein feed like BSE. Its properties in humans are entirely unknown, the symptoms might be quite different from known forms of CJD.

http://www.mad-cow.org/elk_cwd.html#ddd




But the blanket slaughter programmes achieve little more than masking the superficial evidence of TSE, since they are merely taking out those susceptible populations that are at high risk of developing TSE. Meanwhile, the causal prerequisites remain well and truly cemented as Lendemic' into the bedrock of the TSE cluster environment. A good example of this is illustrated by the Colorado Division of Wildlife's failed attempts to annihilate so-called Chronic Wasting Disease (CWD) when they bulldozed the top six inches of soil from their CWD endemic deer facility at Fort Collins. CWD still returned. ...

http://www.mad-cow.org/99feb_cwd_special.html




DOW/CSU has never disclosed what happened to the original captive mule deer in 1967 -- were they released into the wild after the experiment, did any escape, did they exchange animals with the Wyoming facility, what were they fed, had there been prior scrapie sheep in the enclosure? It is ludicrous that they have never released the details -- as if the people who worked didn't keep lab notebooks.

My guess is that relevent documents were shredded long ago when they realized that the disease had gotten out of their facility -- with potentially devastating consequences to game tag sales and hence the very revenues that pay their salaries, never mind the legal liability. Now they are in too deep to confess. Just like MAFF.

The only other scenario that makes sense to me is a western Stetsonville: winter-ranged protein-caked deer, some of these got accidentally brought into the captive study.

http://www.mad-cow.org/colorado_exp.html




Monday, January 05, 2009

CWD, GAME FARMS, BAITING, AND POLITICS

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html




Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer

http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html




Wednesday, March 18, 2009

Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay

http://chronic-wasting-disease.blogspot.com/2009/03/detection-of-cwd-prions-in-urine-and.html




Tuesday, June 16, 2009

Infectious Prions in Pre-Clinical Deer and Transmission of Chronic Wasting Disease Solely by Environmental Exposure

http://chronic-wasting-disease.blogspot.com/2009/06/infectious-prions-in-pre-clinical-deer.html




Wednesday, October 14, 2009

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html




AS THE CROW FLIES, SO DOES CWD

Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html




ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html




http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf



Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010 PRION 2010

International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria

snip...

PPo4-4:

Survival and Limited Spread of TSE Infectivity after Burial

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.

The authors gratefully acknowledge funding from DEFRA.

PPo8-13:

Degradation of Pathogenic Prion Protein and Prion Infectivity by Lichens

Christopher J. Johnson,1 James P. Bennett,1 Steven M. Biro,1,2 Cynthia M. Rodriguez,1,2 Richard A. Bessen3 and Tonie E. Rocke1

1USGS National Wildlife Health Center; 2Department of Bacteriology; University of Wisconsin, Madison; 3Department of Veterinary Molecular Biology; Montana State University; Bozeman, MT USA

Key words: prion, lichen, bioassay, protease, degradation

Few biological systems have been identified that degrade the transmissible spongiform encephalopathy (TSE)-associated form of the prion protein (PrPTSE) and TSE infectivity. Stability of the TSE agent allows scrapie and chronic wasting disease agents to persist in the environment and cause disease for years. Naturally-occurring or engineered processes that reduce infectivity in the environment could aid in limiting environmental TSE transmission. We have previously identified that species of at least three lichens, unusual, symbiotic organisms formed from a fungus and photosynthetic partner, contain a serine protease capable of degrading PrPTSE under gentle conditions. We tested the hypothesis that lichen extracts from these three species reduce TSE infectivity by treating infected brain homogenate with extracts and examining infectivity in mice. We found lichen extracts diminished TSE infectious titer by factors of 100 to 1,000 and that reductions in infectivity were not well-correlated with the extent of PrPTSE degradation observed by immunoblotting. For example, treatment of brain homogenate with Cladonia rangiferina extract caused <100-fold reduction in PrP immunoreactivity but ~1,000-fold decrease in infectivity, suggesting that some PrPTSE remaining after extract treatment was rendered uninfectious or that the lichen protease favors more infectious forms of PrPTSE. Our data also indicate that lichen species closely related to those with prion-degrading protease activity do not necessarily degrade PrPTSE. Characterization of the lichen species-specificity of PrPTSE degradation within the genera Cladonia and Usnea and comparison with known lichen phylogeny has yielded clusters of species on which to focus searches for anti-prion agents.


PPo8-14:


Enzymatic Digestion of Chronic Wasting Disease Prions Bound to Soil


Samuel E. Saunders,1 Jason C. Bartz,2 Kurt C. Vercauteren3 and Shannon L. Bartelt-Hunt1 1Department of Civil Engineering; University of Nebraska-Lincoln; Peter Kiewit Institute; Omaha, Nebraska USA; 2Department of Medical Microbiology and Immunology; Creighton University; Omaha, Nebraska USA; 3USDA; Animal and Plant Health Inspection Service; Wildlife Services; National Wildlife Research Center; Fort Collins, CO USA


Chronic wasting disease (CWD) and sheep scrapie can be transmitted via indirect environmental routes, and it is known that soil can serve as a reservoir of prion infectivity. Given the strong interaction between the prion protein (PrP) and soil, we hypothesized that binding to soil enhances prion resistance to enzymatic digestion, thereby facilitating prion longevity in the environment and providing protection from host degradation. We characterized the performance of a commercially available subtilisin enzyme, the Prionzyme, to degrade soil-bound and unbound CWD and HY TME PrP as a function of pH, temperature, and treatment time. The subtilisin enzyme effectively degraded PrP adsorbed to a wide range of soils and soil minerals below the limits of detection. Signal loss occurred rapidly at high pH (12.5) and within 7 d under conditions representative of the natural environment (pH 7.4, 22°C). Serial PMCA of treated soil samples suggests a greater than 6-log decrease in infectious titer compared with controls. We observed no apparent difference in enzyme effectiveness between bound and unbound CWD PrP. Our results show that although adsorbed prions do retain relative resistance to enzymatic digestion compared with other brain homogenate proteins, they can be effectively degraded when bound to soil. Our results also suggest a topical application of a subtilisin enzyme solution may be an effective decontamination method to limit disease transmission via environmental ‘hot spots’ of prion infectivity.


snip...

see much more here ;


http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html



Saturday, January 24, 2009 Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report


http://bse-atypical.blogspot.com/2009/01/research-project-detection-of-tse.html


Wednesday, January 07, 2009


CWD to tighten taxidermy rules Hunters need to understand regulations


http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.html


Thursday, December 25, 2008


Lions and Prions and Deer Demise


http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.html



Monday, February 14, 2011


THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER


Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011


http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html

http://chronic-wasting-disease.blogspot.com/


Saturday, January 29, 2011


Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate


Jpn. J. Infect. Dis., 64 (1), 81-84, 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html


Thursday, December 23, 2010


Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002–2009


Volume 17, Number 1–January 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html


Wednesday, January 19, 2011


EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html


http://transmissiblespongiformencephalopathy.blogspot.com/



COMERCIAL IN CONFIDENCE SPREADING OF UNPROCESSED BLOOD ON LAND


http://web.archive.org/web/20040315202749/www.bseinquiry.gov.uk/files/yb/1991/02/15003001.pdf



Friday, February 04, 2011


NMLB and USDA allow scrapie prion infected mutton to enter food chain on the Navajo Reservation in New Mexico


----- Original Message -----


From: Terry S. Singeltary Sr.

To: President.BenShelly

Cc: sroanhorse ; opvp.nelson ; alaughing; georgehardeen; pressoffice

Sent: Thursday, February 03, 2011 12:15 PM

Subject: NMLB and USDA allow scrapie prion infected mutton to enter food chain on the Navajo Reservation in New Mexico

Greetings Honorable People of the Great Navajo Nation, and the Honorable President Ben Shelly,

I send this to you with great concern. ...


http://scrapie-usa.blogspot.com/2011/02/nmlb-and-usda-allow-scrapie-prion.html




Tuesday, February 01, 2011


Sparse PrP-Sc accumulation in the placentas of goats with naturally acquired scrapie

Research article

http://scrapie-usa.blogspot.com/2011/02/sparse-prp-sc-accumulation-in-placentas.html


----- Original Message -----


From: "BioMed Central Comments"

To:

Sent: Wednesday, February 16, 2011 4:13 AM

Subject: Your comment on BMC Veterinary Research 2011, 7:7

Your discussion posting "Scrapie cases Goats from same herd USA Michigan" has been rejected by the moderator as not being appropriate for inclusion on the site.

Dear Mr Singeltary,

Thank you for submitting your comment on BMC Veterinary Research article (2011, 7:7). We have read your comment with interest but we feel that only the authors of the article can answer your question about further investigation of the route of infection of the five goats in Michigan. We advise that you contact the authors directly rather than post a comment on the article.

With best wishes,

Maria

Maria Kowalczuk, PhD Deputy Biology Editor BMC-series Journals

BioMed Central 236 Gray's Inn Road London, WC1X 8HB

+44 20 3192 2000 (tel) +44 20 3192 2010 (fax)

W: www.biomedcentral.com E: Maria.Kowalczuk@xxxxxxxxx

Any queries about this decision should be sent to comments@biomedcentral.com

Regards

BMC Veterinary Research


=======================


Terry wrote ;


> Could this route of infection be the cause of the many cases of Goat

> scrapie from the same herd in Michigan USA ?

> Has this been investigated ?


=======================



OLDER DATA JANUARY 2003 AND EARLIER ;


CWD/TSEs & ENVIRONMENT CONTAMINATION

I believe it to be very irresponsible to dispose of clinical/sub-clinial cases of CWD or any animal with TSEs in landfills...

TSS

Aguzzi warns of CWD danger

The TSE family of diseases also includes chronic wasting disease (CWD) in deer, a condition that has spread in the US in recent years (Nature 416, 569; 2002). Speaking at the Days of Molecular Medicine conference in La Jolla in March, prion expert Adriano Aguzzi issued a strong warning against underestimating this form of TSE.

"For more than a decade, the US has by-and-large considered mad cows to be an exquisitely European problem. The perceived need to protect US citizens from this alien threat has even prompted the deferral of blood donors from Europe," he said. "Yet the threat-from-within posed by CWD needs careful consideration, since the evidence that CWD is less dangerous to humans than BSE is less-than-complete. Aguzzi went on to point out that CWD is arguably the most mysterious of all prion diseases.

"Its horizontal spread among the wild population is exceedingly efficient, and appears to have reached a prevalence unprecedented even by BSE in the UK at its peak. The pathogenesis of CWD, therefore, deserves a vigorous research effort. Europeans also need to think about this problem, and it would be timely and appropriate to increase CWD surveillance in Europe too." Aguzzi has secured funding from the National Institutes of Health to investigate CWD, and the effort will be lead by Christina Sigurdson in his department at the University of Zurich. KAREN BIRMINGHAM, LONDON

This quote from Dr. Gambetti is especially significant since he is the rather cautious TSE researcher under contract with the Centers for Disease Control to examine the brains of individuals who have died of CJD. -----------------

Pierluigi Gambetti, director of the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, said all deer should be tested for chronic wasting disease before any processing is done.

"There is no way around it," he said. "Nobody should touch that meat unless it has been tested."

http://www.ledger-enquirer.com/


TSEs And The Environment

The LANCET Volume 351, Number 9110 18 April 1998

BSE: the final resting place

How to dispose of dangerous waste is a question that has vexed the human race for hundreds of years. The answer has usually been to get it out of sight--burn it or bury it. In Periclean Athens, victims of the plague were incinerated in funeral pyres; in 14th century Venice, a law stipulated that Black Death corpses should be buried to a minimum depth of 5 feet; and now, as the 20th century draws to a close, we are challenged by everything from industrial mercury to the smouldering reactors of decommissioned atomic submarines.

The Irish Department of Agriculture will convene an expert panel on April 27-29 to discuss the disposal of tissues from animals with bovine spongiform encephalopathy (BSE). Proper disposal of tissues from infected cattle has implications for both human and animal safety. Safety for human beings is an issue because there is now unassailable if still indirect evidence that BSE causes infections in man in the form of "new variant" Creutzfeld-Jakob disease (nvCJD).1-3 Safety for animals is also an issue because BSE-affected cattle could possibly transmit disease to species other than cattle, including sheep, the species that was almost surely the unwitting source of the BSE epidemic.

The first matter to consider is the distribution of infectivity in the bodies of infected animals. The brain (and more generally, the central nervous system) is the primary target in all transmissible spongiform encephalopathies (TSE), and it contains by far the highest concentration of the infectious agent. In naturally occuring disease, infectivity may reach levels of up to about one million lethal doses per gram of brain tissue, whether the disease be kuru, CJD, scrapie, or BSE. The infectious agent in BSE-infected cattle has so far been found only in brain, spinal cord, cervical and thoracic dorsal root ganglia, trigeminal ganglia, distal ileum, and bone marrow.4 However, the much more widespread distribution of low levels of infectivity in human beings with kuru or CJD, and in sheep and goats with scrapie, suggests that caution is advisable in prematurely dismissing as harmless other tissues of BSE-infected cattle.

A second consideration relates to the routes by which TSE infection can occur. Decades of accumulated data, both natural and experimental, have shown clearly that the most efficient method of infection is by direct penetration of the central nervous system; penetration of peripheral sites is less likely to transmit disease. Infection can also occur by the oral route, and the ingestion of as little as 1 g of BSE brain tissue can transmit disease to other cattle.5 Infection by the respiratory route does not occur (an important consideration with respect to incineration), and venereal infection either does not occur or is too rare to be detected.

How can tissue infectivity be destroyed before disposal? The agents that cause TSE have been known almost since their discovery to have awesome resistance to methods that quickly and easily inactivate most other pathogens. Irradiation, chemicals, and heat are the three commonest inactivating techniques. Irradiation has proved entirely ineffective, and only a handful of a long catalogue of chemicals have produced more than modest reduction in infectivity. The most active of these are concentrated solutions of sodium hypochlorite (bleach) or sodium hydroxide (lye). As for heat, even though the agent shares with most other pathogens the feature of being more effectively damaged by wet heat than by dry heat, boiling has little effect, and steam heat under pressure (autoclaving) at temperatures of 121ºC is not always sterilising. To date, the most effective heat kill requires exposure of infectious material to steam heat at 134ºC for 1 h in a porous-load autoclave.6 Exposure to dry heat even at temperatures of up to 360ºC for 1 h may leave a small amount of residual infectivity.7 The standard method of incineration, heating to about 1000ºC for at least several seconds, has been assumed to achieve total sterilisation, but needs experimental verification in the light of suggestions that rendered tissue waste might find some useful purpose as a source of heating fuel.

Thus, TSE agents are very resistant to virtually every imaginable method of inactivation, and those methods found to be most effective may, in one test or another, fail to sterilise. It seems that even when most infectious particles succumb to an inactivating process, there may remain a small subpopulation of particles that exhibit an extraordinary capacity to withstand inactivation, and that, with appropriate testing, will be found to retain the ability to transmit disease. Also, almost all available inactivation data have come from research studies done under carefully controlled laboratory conditions, and it is always difficult to translate these conditions to the world of commerce. Even when the data are applied in the commercial process, the repetitive nature of the process requires vigilance in quality control and inspection to ensure adherence to its regulations.

The final issue that must be addressed is the "lifespan" of the infectious agent after disposal if it has been only incompletely inactivated beforehand. Given the extraordinary resistance of the agent to decontamination measures, the epidemiological and experimental evidence indicating that TSE agents may endure in nature for a long time should come as no surprise. The first real clue to this possibility came from the Icelandic observation that healthy sheep contracted scrapie when they grazed on pastures that had lain unused for 3 years after having been grazed by scrapie-infected sheep.8

Support for this observation was obtained from an experiment in which scrapie-infected brain material was mixed with soil, placed in a container, and then allowed to "weather" in a semi-interred state for 3 years.9 A small amount of residual infectivity was detected in the contaminated soil, and most of the infectivity remained in the topmost layers of soil, where the tissue had originally been placed--in other words, there had been no significant leaching of infectivity to deeper soil layers.

It is therefore plausible for surface or subsurface disposal of TSE-contaminated tissue or carcasses to result in long-lasting soil infectivity. Uncovered landfills are a favourite feeding site for seagulls, which could disperse the infectivity.10 Other animals might do likewise, and if the landfill site were later used for herbivore grazing, or tilled as arable land, the potential for disease transmission might remain. A further question concerns the risk of contamination of the surrounding water table, or even surface waste-water channels, by effluents and discarded solid waste from treatment plants.

A reasonable conclusion from existing data is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge number of uncertainties and assumptions that attend each stage of the disposal process.

On the positive side, spongiform encephalopathy can be said to be not easily transmissible. Although the level of infectivity to which creatures are exposed is not known, it is probably very low, since sheep that die from scrapie, cattle that die from BSE, and human beings who die from nvCJD represent only a small proportion of their respective exposed populations.

Whatever risk exists is therefore extremely small, but not zero, hence all practical steps that might reduce the risk to the smallest acceptable level must be considered. What is practical and what is acceptable are concepts that will be hammered out on the anvil of politics: scientific input, such as it is, already waits in the forge. A fairly obvious recommendation, based on the science, would be that all material that is actually or potentially contaminated by BSE, whether whole carcasses, rendered solids, or waste effluents, should be exposed to lye and thoroughly incinerated under strictly inspected conditions. Another is that the residue is buried in landfills to a depth that would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source. Certainly, it has been, and will continue to be, necessary in many instances to accept less than the ideal.

Paul Brown

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA

1 Will RG, Ironside JW, Zeidler M, et al. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 1996; 347: 921-25 [PubMed].

2 Bruce M, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 1997: 389: 498-501.

3 Collinge J, Sidle KCL, Heads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996; 383: 685-90 [PubMed].

4 Wells GAH, Hawkins SAC, Green RB, et al. Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet Rec 1998; 142: 103-06 [PubMed].

5 Collee JG, Bradley R. BSE: a decade on--part 2. Lancet 1997; 349: 715-21 [PubMed].

6 Taylor DM. Exposure to, and inactivation of, the unconventional agents that cause transmissible degenerative encephalopathies. In: Baker HF, Ridley RM, eds. Methods in molecular medicine: prion diseases. Totawa NJ: Humana Press, 1996: 105-18.

7 Brown P, Liberski PP, Wolff A, Gajdusek DC. Resistance of scrapie infectivity to steam autoclaving after formaldehyde fixation and limited survival after ashing at 360°C: practical and theoretical implications, J Infect Dis 1990; 161: 467-72 [PubMed].

8 Palsson PA. Rida (scrapie) in Iceland and its epidemiology. In: Prusiner SB, Hadlow WJ, eds. Slow transmissible diseases of the nervous system, vol I. New York: Academic Press, 1979: 357-66.

9 Brown P, Gajdusek DC. Survival of scrapie virus after 3 years' interment. Lancet 1991; 337; 269-70.

10 Scrimgoeur EM, Brown P, Monaghan P. Disposal of rendered specified offal. Vet Rec 1996; 139: 219-20 [PubMed].

http://www.thelancet.com/newlancet/sub/issues/vol351no9110/body.commentary1146.html


snip...

88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed. 89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence. 90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.

91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.

92. This review and recommendations from Brown have particular importance. Brown is one of the world's foremost authorities on TSEs and is a senior researcher in the US National Institutes of Health (NIH). It is notable that such a respected authority is forthright in acknowledging the existence of potential risks, and in identifying the appropriate measures necessary to safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical distribution of variant CJD in the UK (excluding Northern Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41 (02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD (variant CJD) might live closer to rendering factories than would be expected by chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were studied. The incubation period of vCJD is not known but by analogy with other human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure to rendering products, such exposure might plausibly have occurred 8-10 years before the onset of symptoms. The authors were able to obtain the addresses of all rendering plants in the UK which were in production in 1988. For each case of vCJD, the distance from the place of residence on 1st January 1998 to the nearest rendering plant was calculated

snip...


http://web.archive.org/web/20030326042814/http://www.bseinquiry.gov.uk/files/ws/s019b.pdf



Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).

http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf



PAUL BROWN SCRAPIE SOIL TEST


http://collections.europarchive.org/tna/20080102120203/http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf



Some unofficial information from a source on the inside looking out -

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

----------

You can take that with however many grains of salt you wish, and we can debate these issues all day long, but the bottom line, this is not rocket-science, all one has to do is some experiments and case studies. But for the life of me, I don't know what they are waiting on?

Kind regards,

Terry S. Singeltary Sr. Bacliff, Texas USA


More here:


http://collections.europarchive.org/tna/20080102173630/http://www.bseinquiry.gov.uk/files/ws/s018.pdf




INCINERATION TEMPS

Requirements include:

a. after burning to the range of 800 to 1000*C to eliminate smell;

well heck, this is just typical public relations fear factor control. do you actually think they would spend the extra costs for fuel, for such extreme heat, just to eliminate smell, when they spread manure all over your veg's. i think not. what they really meant were any _TSE agents_.

b. Gas scrubbing to eliminate smoke -- though steam may be omitted;

c. Stacks to be fitted with grit arreaters;

snip...

1.2 Visual Imact

It is considered that the requirement for any carcase incinerator disign would be to ensure that the operations relating to the reception, storage and decepitation of diseased carcasses must not be publicly visible and that any part of a carcase could not be removed or interfered with by animals or birds.

full text;


http://web.archive.org/web/20040521230540/www.bseinquiry.gov.uk/files/yb/1989/04/03006001.pdf



New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

Paul Brown*, [dagger ] , Edward H. Rau [Dagger ] , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§

* Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and [Dagger ] Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999

Abstract Top Abstract Introduction Materials and Methods Results Discussion References

One-gram samples from a pool of crude brain tissue from hamsters infected with the 263K strain of hamster-adapted scrapie agent were placed in covered quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual infectivity in the treated samples was assayed by the intracerebral inoculation of dilution series into healthy weanling hamsters, which were observed for 10 months; disease transmissions were verified by Western blot testing for proteinase-resistant protein in brains from clinically positive hamsters. Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded 6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600°C completely ashed the brain samples, which, when reconstituted with saline to their original weights, transmitted disease to 5 of 35 inoculated hamsters. No transmissions occurred after exposure to 1,000°C. These results suggest that an inorganic molecular template with a decomposition point near 600°C is capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy | scrapie | prion | medical waste | incineration

Introduction Top Abstract Introduction Materials and Methods Results Discussion References

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin. It also has been assumed that the replication of these agents is a strictly biological process (1), although the notion of a "virus" nucleant of an inorganic molecular cast of the infectious [beta ] -pleated peptide also has been advanced (2). In this paper, we address these issues by means of dry heat inactivation studies.

snip...

GUTTING DEER/ELK AND THOSE THIN GLOVES;

Distribution of prion protein in the ileal Peyer's patch of scrapie-free lambs and lambs naturally and experimentally exposed to the scrapie agent

Ragna Heggeb'z1, Charles McL. Press1, Gjermund Gunnes1, Kai Inge Lie1, Michael A. Tranulis2, Martha Ulvund3, Martin H. Groschup4 and Thor Landsverk1

Department of Morphology, Genetics and Aquatic Biology1 and Department of Biochemistry, Physiology and Nutrition2, Norwegian School of Veterinary Science, PO Box 8146 Dep., N-0033, Oslo, Norway Department of Sheep and Goat Research, Norwegian School of Veterinary Science, Kyrkjevegen 332/334, 4300 Sandnes, Norway3 Federal Research Centre for Virus Diseases of Animals, Paul-Ehrlich-Str. 28, 72076 TÃbingen, Germany4

Author for correspondence: Charles Press. Fax +47 22964764. e-mail Charles.Press@veths.no

A sensitive immunohistochemical procedure was used to investigate the presence of prion protein (PrP) in the ileal Peyer?s patch of PrP-genotyped lambs, including scrapie-free lambs and lambs naturally and experimentally exposed to the scrapie agent. The tyramide signal amplification system was used to enhance the sensitivity of conventional immunohistochemical procedures to show that PrP was widely distributed in the enteric nervous plexus supplying the gut wall. In scrapie-free lambs, PrP was also detected in scattered cells in the lamina propria and in the dome and interfollicular areas of the Peyer?s patch. In the follicles, staining for PrP was mainly confined to the capsule and cells associated with vascular structures in the light central zone. In lambs naturally exposed to the scrapie agent, staining was prominent in the dome and neck region of the follicles and was also found to be associated with the follicle-associated epithelium. Similar observations were made in lambs that had received a single oral dose of scrapie-infected brain material from sheep with a homologous and heterologous PrP genotype 1 and 5 weeks previously. These studies show that the ileal Peyer?s patch in young sheep may be an important site of uptake of the scrapie agent and that the biology of this major gut-associated lymphoid tissue may influence the susceptibility to oral infection in sheep. Furthermore, these studies suggest that homology or heterology between PrP genotypes or the presence of PrP genotypes seldom associated with disease does not impede uptake of PrP.

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BSE, KURU, DENTAL AND ___CUT ABRASIONS___ from gutting a deer perhaps;

snip...

Since there was a suggestion that kuru had been transmitted through the gums and/or gum abrasions...

snip...


http://collections.europarchive.org/tna/search/?query=http%3A%2F%2Fwww.bseinquiry.gov.uk%2Ffiles%2Fyb%2F1989%2F04%2F17005001.pdf&where=url&x=28&y=12





[PDF]
BSE INQUIRY
Statement of behalf of the Environment Agency ... File Format: PDF/Adobe Acrobat - View as HTML ... his Statement of March 1998 to the BSE Inquiry ... systems subject to regular or intermittent contamination by rapid movement of recharge water ...


www.bse.org.uk/files/ws/s490.pdf.......DEAD


http://www.bseinquiry.gov.uk/files/ws/s490.pdf...........DEAD



http://web.archive.org/web/20030331222937/http://www.bseinquiry.gov.uk/files/ws/s490.pdf





BSE INQUIRY

Statement of behalf of the Environment Agency Concerning Thruxted Mill By Mr C. P. Young Principal Hydrogeologist, Soil Waste and Groundwater Group WRc plc; Medmenham, Bucks

http://www.bseinquiry.gov.uk/files/ws/s490.pdf

http://web.archive.org/web/20030331222937/http://www.bseinquiry.gov.uk/files/ws/s490.pdf






Very important to those hunters looking for healthy deer/elk to eat...TSS


MRC-43-00 [ ] [Text only version of this site] [Print this page] Issued: Monday, 28 August 2000 NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a 'sub-clinical' form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the 'species barrier' - the main protective factor which limits the ability of prions2 to jump from one species to infect another. They found the mice had a 'sub-clinical' form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain.

In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters.

The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust.

Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection. This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures."

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET BY THE JOURNAL.

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011 (OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009 (OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly formed MRC Prion Unit based at The Imperial College School of Medicine at St Mary's Hospital. He is also a member of the UK Government's Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit is was set up in 1999, and its work includes molecular genetic studies of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad cow disease) in animals. In some circumstances prions from one species of animals can infect another and it is clear that BSE has done this to cause the disease variant CJD in the UK and France. It remains unclear how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain (also known as 263K) which infects hamsters, and until now was assumed not to infect mice.

This research was funded by the Medical Research Council and Wellcome Trust.

The Medical Research Council (MRC) is a national organisation funded by the UK tax-payer. Its business is medical research aimed at improving human health; everyone stands to benefit from the outputs. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and the academic world. MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. About half of the MRC's expenditure of £345 million is invested in over 50 of its Institutes and Units, where it employs its own research staff. The remaining half goes in the form of grant support and training awards to individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with a spend of some £600 million in the current financial year 1999/2000. The Wellcome Trust supports more than 5,000 researchers, at 400 locations, in 42 different countries to promote and foster research with the aim of improving human and animal health. As well as funding major initiatives in the public understanding of science, the Wellcome Trust is the country's leading supporter of research into the history of medicine.

©2002 Medical Research Council Data Protection policy | Contact the MRC


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Subject: OPINION ON THE USE OF BURIAL FOR DEALING WITH ANIMAL CARCASSES AND OTHER ANIMAL MATERIALS THAT MIGHT CONTAIN BSE/TSE

Date: Wed, 22 Jan 2003 14:58:53 -0600

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

######## Bovine Spongiform Encephalopathy #########


C:\WINNT\Profiles\bredagi.000\Desktop\Burial_OPINION_0301_OPINION_FINAL.doc

EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL Directorate C - Scientific Opinions C1 - Follow-up and dissemination of scientific opinions OPINION ON THE USE OF BURIAL FOR DEALING WITH ANIMAL CARCASSES AND OTHER ANIMAL MATERIALS THAT MIGHT CONTAIN BSE/TSE ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE MEETING OF 16-17 JANUARY 2003 1 OPINION On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to advice on the examples of conditions under which safe burial of potentially TSE-infected (animal) materials can be achieved. The details of the SSC's evaluation are provided in the attached report. The SSC concludes as follows: (1) The term "burial" includes a diversity of disposal conditions. Although burial is widely used for disposal of waste the degradation process essential for BSE/TSE infectivity reduction is very difficult to control. The extent to which such an infectivity reduction can occur as a consequence of burial is poorly characterised. It would appear to be a slow process in various circumstances. (2) A number of concerns have been identified including potential for groundwater contamination, dispersal/transmission by birds/animals/insects, accidental uncovering by man. (3) In the absence of any new data the SSC confirms its previous opinion that animal material which could possibly be contaminated with BSE/TSEs, burial poses a risk except under highly controlled conditions (e.g., controlled landfill). The SSC reiterates the consideration made in its opinion of 24-25 June 1999 on "Fallen Stock"1. The limited capacity for destruction of animal wastes in certain countries or regions in the first place justifies the installation of the required facilities; it should not be used as a justification for unsafe disposal practices such as burial. However, the SSC recognises that for certain situations or places or for certain diseases (including animals killed and recycled or disposed of as a measure to control notifiable diseases), the available rendering or incinerator or disposal capacity within a region or country could be a limiting factor in the control of a disease. Thus if hundreds or even millions of animals need to be rendered after killing or if the transport of a material to a rendering or disposal plant proved to be impractical, an appropriate case by case risk assessment2 should be carried out before deciding upon the most appropriate way of disposal. In principle, the risk is expected to be the lower for small incinerators3 as compared to burial. As such decisions in practice may have to be taken at very short notice, risk management scenarios according to various possible risks should be prepared in advance to allow for a rapid decision when the need arises.

1 Scientific Opinion on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials. Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999. (and re-edited at its meeting of 22-23 July 1999). 2 See also the relevant sections and footnotes on risk assessment in the report accompanying the SSC opinion of 24-25 June 1999. 3 See SSC opinion of 16-17 January 2003 on the use of small incinerators for BSE risk reduction. 2

THE USE OF BURIAL FOR DEALING WITH CARCASSES AND OTHER MATERIALS THAT MIGHT CONTAIN BSE/TSE REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to advice on the examples of conditions under which safe burial of potentially TSE-infected animal materials can be achieved. The SSC appointed Prof.J.Bridges as rapporteur. His report was discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by the SSC at its meeting of 16-17 January 2003.

2. GENERAL CONSIDERATIONS

"Burial" covers a range of disposal situations ranging from the practice of burying animals on farms and other premises in a relatively shallow trench (with or without treatment such as lining) to deep disposal to a lined and professionally managed landfill site (SSC 2001). Buried organic material is normally decomposed by microbial and chemical processes. However this is not a process amenable to control measures. As noted by the SSC "Opinion on Fallen Stock" (SSC 25th June 1999) there is little reliable information on the extent and rate of infectivity reduction of BSE/TSEs following burial. An old paper by Brown and Gajdusek 1991 assumed a reduction of 98% over 3 years. However it is noted that the rate of degradation of materials following burial can vary very considerably between sites. This is not surprising because the degradation process is strongly influenced by factors such as water content of the site, temperature inside the site, nature of adsorptive "material" present etc. The previous SSC opinion noted that BSE/TSEs appear to be resistant to degradation when stored at room temperature over several years. It also raised concerns that mites could serve as a vector and/or reservoir for the infected scrapie material. Burial sites may have a thriving animal population. Uncovering of risk material that is not deeply buried is therefore possible. The SSC in its opinion of 28th-29th June 2001 set out a framework for assessing the risk from different waste disposal processes. These criteria may be applied to burial as follows:

(1) Characterisation of the risk materials involved.

Unlike many other waste disposal options there are no technical or economic factors that would limit the nature of the material that can be disposed of by burial. Moreover in many cases the location of burial sites is uncertain. The potential for transmission of BSE/TSEs for SRM that is buried near the surface is also poorly characterised.3

(2) Risk reduction.

The extent to which the infectivity is reduced is likely to vary substantially according to the nature of the site depth of burial whether pre-treatment by burning or through the addition of lime is used etc. There appears to be no scientific basis at present for the prediction of the rate of loss of infectivity. In the absence of such data, as a worst case, it has to be assumed that over a three-five year period the loss of infectivity may be slight. In principle on a well-managed fully contained landfill the risks from infective material can approach zero. However this requires rigorous management over many years. This is difficult to guarantee.

(3) Degree to Which the Risks can be Contained

The principal concerns are:

* Prevention of access to the SRM by animals that could result in the transmission (directly or indirectly) of the BSE/TSE.

* Penetration of prions into the leachate/groundwater. It is noted that on some landfill sites leachate is sprayed into the air to facilitate oxidation of some organic components. Such a practice could in principle lead to dispersal of BSE/TSEs. It is also noted that it is not uncommon for landfill sites to be re-engineered to increase their stability, gas and leachate flow and/or total capacity. If this re-engineering involved an area where previous burial of BSE/TSE contaminated material had taken place and additional risk could accrue. The possibility of contaminated material being dug up in shallow and unmarked burial sites on farms etc constitutes a considerably greater risk.

3. FURTHER INVESTIGATIONS

Research is needed on specific aspects of the behaviour of prion like molecules in controlled landfills i.e.:

* Potential for adsorption to other material present in the waste that might limit their mobility.

* Principal factors influencing rates of degradation.

* Effectiveness of encasement in cement in controlling/reducing the risk.

4. CONCLUSION

In the absence of new evidence the opinion of the SSC "Opinion on Fallen Stock" (SSC 25th June 1999) must be endorsed strongly that land burial of all animals and material derived from them for which there is a possibility that they could incorporate BSE/TSEs poses a significant risk. Only in exceptional circumstances where there could be a considerable delay in implementing a safe means of disposal should burial of such materials be considered. Guidelines should be made available to aid on burial site selection.


http://europa.eu.int/comm/food/fs/sc/ssc/out309_en.pdf





C:\WINNT\Profiles\bredagi.000\Desktop\Burning_OPINION_0301_OPINION_FINAL.doc


EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL Directorate C - Scientific Opinions C1 - Follow-up and dissemination of scientific opinions

OPINION ON

OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL MATERIALS

ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 16-17 JANUARY 2003

2 OPINION

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to advice on the examples of conditions under which safe burning of potentially TSE-infected (animal) materials can be achieved. The details of the SSC's evaluation are provided in the attached report. The SSC concludes as follows:

(1) "Burning" covers a wide variety of combustion conditions. This opinion is concerned with the process of open burning e.g. bonfires.

(2) There are serious concerns regarding the use of open burning for the destruction of pathogen contaminated animal waste, particularly for waste which may be contaminated with relatively heat stable pathogens. Issues include: the potentially very high variability of the pathogen inactivation, the nature of the gaseous and particulate emissions, and the risks from the residual ash.

(3) The SSC recommends that open burning is only considered for pathogen destruction under exceptional circumstances following a specific risk assessment. In the case of animal waste possibly contaminated with BSE/TSE in view of the uncertainty of the risk open burning should be considered a risk. Suitable monitoring methods for TSE contamination of both air and ash are needed. Protocols for safe burning in emergency situations need to be established. The SSC reiterates the consideration made in its opinion of 24-25 June 1999 on "Fallen Stock"1. The limited capacity for destruction of animal wastes in certain countries or regions in the first place justifies the installation of the required facilities; it should not be used as a justification for unsafe disposal practices such as burial. However, the SSC recognises that for certain situations or places or for certain diseases (including animals killed and recycled or disposed of as a measure to control notifiable diseases), the available rendering or incinerator or disposal capacity within a region or country could be a limiting factor in the control of a disease. Thus if hundreds or even millions of animals need to be rendered after killing or if the transport of a material to a rendering or disposal plant proved to be impractical, an appropriate case by case risk assessment2 should be carried out before deciding upon the most appropriate way of disposal. In principle, the risk is expected to be the lower for small incinerators3 as compared to open burning. As such decisions in practice may have to be taken at very short notice, risk management scenarios according to various possible risks should be prepared in advance to allow for a rapid decision when the need arises. 1 Scientific Opinion on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials. Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999. (and re-edited at its meeting of 22-23 July 1999). 2 See also the relevant sections and footnotes on risk assessment in the report accompanying the SSC opinion of 24-25 June 1999. 3 See SSC opinion of 16-17 January 2003 on the use of small incinerators for BSE risk reduction. 3

OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL MATERIALS REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to advice on the examples of conditions under which safe burning of potentially TSE-infected animal materials can be achieved. The SSC appointed Prof.J.Bridges as rapporteur. His report was discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by the SSC at its meeting of 16-17 January 2003.

2. GENERAL CONSIDERATIONS

Burning is a combustion process to which a range of control measures may be applied to contain emissions and to ensure the completeness of the degradation process for organic matter. Depending on the source (waste) material the burning process may or may not require addition of other energy sources. Incineration/pyrolysis are contained combustion processes are contained combustion processes and therefore have the potential for a high level of control. (However see opinion on small incinerators). At the other end of the control spectrum is open burning; such as bonfires. Typically combustion of animal waste requires the addition of a high calorific fuel in order to initiate (and for some materials to sustain) the process. It is recognised that open burning of animal waste is a very cheap and convenient method of disposal. However uncontained burning has a number of problems in terms of the potential risks involved:

(1) In the open burning situation a range of temperatures will be encountered. It is difficult therefore to ensure complete combustion of the animal waste. If the waste is contaminated with pathogens there will remain considerable uncertainty as to the degree of their inactivation.

(2) Gaseous and particulate emissions to the atmosphere will occur and consequently worker and public exposure is likely. There is very little data to indicate whether or not some pathogens could be dispersed to air as a consequence of open burning.

(3) The supporting/secondary fuel may be a source of contamination itself. For example in the recent foot and mouth disease outbreak in the UK timbers were used at some sites that were heavily contaminated with pentachlorophenol.

(4) The residual ash must be considered to be a risk source. Its safe disposal needs to be assured (see opinion on small incinerators) to prevent human and animal contact and protect from groundwater contamination. While careful selection of burning sites can reduce the risks open burning should only be considered in emergency situations. For each such emergency situation a specific risk assessment should be conducted which must include the risk 4 from the pathogen of immediate concern but also other pathogens that might be present.

3. RISK ASSESSMENT OF OPEN BURNING FOR BSE

The SSC, at its meeting of 28th-29th June 2001, recommended "a framework for the assessment of the risk from different options for the safe disposal or use of meat and bone meal (MBM) and other products which might be contaminated with TSEs and other materials. Applying the framework to the practice of open burning, the following conclusions can be drawn:

3.1. Nature of the materials handled Potentially a wide variety of materials can be used provided suitable secondary fuel is available. The burning process is very simple in principle and difficult in practice to regulate effectively.

3.2. Risk reduction due to open burning There is no reliable data to indicate the extent of risk reduction that could be achieved by open burning. It is reasonable however to assume that overall it will be rather less effective in reducing the infectivity of BSE/TSE than wellconducted incineration. Moreover the reproducibility of the risk reduction is likely to be very variable even at a single location.

3.3. Airborne emissions and residue ash The composition of airborne emissions and residue ash is rarely monitored. From a risk assessment viewpoint particular attention needs to be given to the potential for the airborne dispersal of relatively heat stable pathogens as a consequence of open burning. In the absence of reliable data both airborne emissions and residual ash must be considered to constitute a significant risk if animal waste that might be contaminated with TSEs is being burnt.

4. FURTHER INVESTIGATION

Research is needed particularly on: * The potential for airborne dispersal of relatively heat stable pathogens. * Methodologies to improve the efficacy of the combustion process to ensure the inactivation of pathogen contaminated animal waste.

5. CONCLUSION

Open burning potentially represents a significant risk where the animal waste has the possibility of being contaminated with BSEs/TSEs. Suitable monitoring methods for TSE contamination of both air and ash are needed. Protocols for safe burning in emergency situations need to be established.


http://europa.eu.int/comm/food/fs/sc/ssc/out310_en.pdf



C:\WINNT\Profiles\bredagi.000\Desktop\Incinerator_OPINION_0301_FINAL.doc


EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL

Directorate C - Scientific Opinions C1 - Follow-up and dissemination of scientific opinions OPINION ON

THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION

SCIENTIFIC STEERING COMMITTEE MEETING OF 16-17 JANUARY 2003

2 OPINION On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to (i) evaluate a risk assessment1 prepared for the UK's Spongiform Encephalopathy Advisory Committee (SEAC), on the potential risk arising from the use of small incinerators to dispose of specified risk materials and (ii) to advise on the safety with regard to TSE risks of the use of such small incinerators.

The details of the SSC's evaluation are provided in the attached report. The SSC concludes as follows:

(i) The SSC, at its meeting of 28th -29th June 2001, recommended "a framework for the assessment of the risk from different options for the safe disposal or use of meat and bone meal (MBM) and other products which might be contaminated with TSEs and other materials." This framework comprised five components:

(1) Identification and characterisation of the risk materials involved, the possible means for their transmission and potential at risk groups.

(2) The risk reduction achieved by the particular process.

(3) The degree to which the risks can be contained under both normal and emergency operating conditions. This inevitably includes consideration of the effectiveness of control measures.

(4) Identification of interdependent processes for example transport, storage, loading of any TSE related risk materials.

(5) The intended end-use of the products for example disposal, recycling etc. The risk assessment prepared for SEAC focuses on the risks involved steps 1 and 2 in respect of BSE/TSEs only and is based on a visit to 10 incinerators out of a total of 263 in the UK of which 60% had after burners. The risk assessment is also using a number of assumptions and data that may be valid for certain incinerator types under certain conditions, but are not necessarily applicable either for all types of materials to be disposed of, or to the whole range of types of small incinerators in use the EU and the UK.

(ii) Small incinerators are widely used to meet the needs of local communities. These incinerators vary greatly in their design, nature of use and performance characteristics and the quality of their management. As a consequence of this variability there are many uncertainties in identifying risks posed by small incinerators that are used to treat SRM materials and each type should eventually receive its own assessment. Also, general operating and control criteria should be established for

1 DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and Food. Revision 2 of the Draft report, February 2001. 24 pages. 3

Potential risk sources arising from the incineration process include: gaseous emissions and residual ash. Research is currently ongoing mimicking incineration of TSE-infected brain tissue to assess the infectivity clearance level under various scenarios2. However, there are no final reported measurements that enable the risk to be assessed from either the emissions or the ash from small incinerators. It has been argued that the protein content of the ash is a reasonable surrogate measure of the degree of risk deduction caused by the incineration process. This assumption is questionable in view of the resistance to heat of prions as compared to other proteins. Protein measurements in ash are however probably a useful general measure of the overall efficiency and reproducibility of the incineration process. Results in the aforementioned report1 indicate a large degree of variability in performance among the small incinerators in the UK that have been evaluated. It is anticipated that small incinerators, used by other Member States will also show a considerable variation in performance. In evaluating the risk of small incinerators, consideration should be given to the risk of potential contamination of the ash and of the gaseous emissions. In the absence of generally accepted and enforced performance standards for small incinerators handling SRMs each such facility therefore needs to be the subject of a specific risk assessment. The SSC considers that the standards set up by the new Waste Incinerator Directive (2000/76/EC) and in its opinion of June 1999 on waste disposal should serve as guidance. In the absence of reliable data on the possible residual infectivity of the ash, it should be disposed of, i.e., in controlled landfills as described in the SSC opinion of June 1999 on safe disposal of waste. The SSC finally wishes to emphasise the need for suitable monitoring methods in order that risks can be assessed readily for individual types of small incinerators. 2 P.Brown, pers.comm., December 2002. Publication in progress.4

THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to (i) evaluate a risk assessment3 prepared for the UK's Spongiform Encephalopathy Advisory Committee (SEAC), on the potential risk arising from the use of small incinerators to dispose of specified risk materials and (ii) to advise on the safety with regard to TSE risks of the use of such small incinerators.

The SSC appointed Prof. J. Bridges as rapporteur. His report was discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by the SSC at its meeting of 16-17 January 2003.

2. CURRENT LEGISLATIVE FRAMEWORK

Until 2000, small incinerators were exempt from the emission limits set by the EC for MSW and hazardous waste incinerators with throughputs greater than 50 kg/hour. An "incineration plant" is defined by the new Incineration of Waste Directive (2000/76/EC) as "any stationary or mobile technical equipment dedicated to the thermal treatment of waste with or without recovery of the combustion heat generated". This definition would appear to exclude open burning of waste. The new Directive, which must be transposed into the legislation of each Member State by December 2002, replaces a range of previous directives on incineration. It applies to all new incinerator installations from December 28th 2002 and all existing installations from December 28th 2005. The principal aim of the Directive is to prevent and/or limit negative environmental effects due to emissions into air, soil, surface and ground water and the resulting risks to human health from the incineration and co-incineration of waste. It covers many aspects from a requirement for afterburners to airborne emission limits and criteria for the composition of residual ash. Previous EC legislation has exempted small incinerators (i.e. those operating at less than 50 kg per hour). The Waste Incinerator Directive (WID) (2000) allows such small incinerators to be exempt from licensing at the national level however they will still be subjected to the same onerous requirements of the WID as larger incinerators.

In the UK it is proposed that in future incinerators dealing with non-hazardous waste but with a throughput of less than 1 tonne per hour will be regulated by local authorities whereas those with a larger throughput will be regulated by the national authority. It is possible that different regulatory mechanisms may result in differences in the rigour with which the new standards are enforced. The position on the disposal of animal waste is complicated. Animal carcass incineration use not covered by the WID and therefore the existing regulatory framework (90/66/EEC which covers animal and public health requirements to ensure destruction of pathogens) will continue to be applied. A new Animal By-Products Regulation

3 DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and Food. Revision 2 of the Draft report, February 2001. 24 pages. 5

(ABPR) will apply in Member States during the first part of 2003. The relationship to WID has been included in the ABPR. It is important that it does not result in less strict standards being applied for animal carcass incineration. In contrast to whole carcasses WID will apply to the burning of meat and bone meal, tallow or other material (even if they burn animal carcasses too). Additional specific directives will continue to apply to waste that could be contaminated with BSE/TSEs. (96/449/EC)

3. CURRENT USE OF SMALL INCINERATORS TO DISPOSE OF ANIMAL WASTE Small incinerators are used for a variety of purposes and in a range of locations among Member States. Many are located alongside small abattoirs, knackers, hunt kennels, or laboratories. Thus they meet the needs of relatively small communities. Across Member States these small incinerators include a variety of designs and operating conditions (as indicated above in principle they will probably be required to meet specific standards for emissions and for the composition of the residual ash by December 28th 2005). In the UK there are indications (see DNV Report 2001) that a considerable quantity of SRM which would have previously been sent for rendering is now being incinerated directly in small incinerators. Thus evaluation of the risks from such incinerators is of increasing importance.

4. RISK ASSESSMENT FOR SMALL INCINERATORS

The SSC, at its meeting of 28th -29th June 2001, recommended "a framework for the assessment of the risk from different options for the safe disposal or use of meat and bone meal (MBM) and other products which might be contaminated with TSEs and other materials. This framework comprised five components:

(1) Identification and characterisation of the risk materials involved, the possible means for their transmission and potential at risk groups.

(2) The risk reduction achieved by the particular process.

(3) The degree to which the risks can be contained under both normal and emergency operating conditions. This inevitably includes consideration of the effectiveness of control measures.

(4) Identification of interdependent processes for example transport, storage, loading of any TSE related risk materials.

(5) The intended end-use of the products for example disposal, recycling etc. Recently a report has been prepared by DNV consulting (2001) for the UK Ministry of Agriculture, Fisheries and Food (now known as DEFRA) that assesses the risks from small incinerators in the UK that receive SRMs. This report focuses on the risks involved steps 1 and 2 in respect of BSE/TSEs only. 10 incinerators out of a total of 263 in the UK were visited of which 60% had after burners.

(1) Nature of the materials handled.

The DNV report 2001 starts with the assumption that "the materials incinerated at small abattoirs will be mainly SRM and bones from animals that are fit for human consumption. It may also include material from animals failed by meat inspectors. The likelihood of there being an animal 6 with significant BSE infectivity is very small and certainly much less than for the fallen stock handled by hunt kennels and knackers4. For this reason the study has concentrated on the latter type of operation". The Report notes that "the material handled by both knacker and hunt kennels is highly variable and difficult to characterise". In terms of input the key factors to consider are:

* The number of adult bovines processed and the proportion of these carcasses that are likely to be infected.

* The extent of infectivity (in terms of human oral Infectious Units) that may occur (average and worst case).

In the DNV (2001) risk assessment only the BSE risk from processing bovine SRMs was considered. For quantitative risk assessment purposes the mean value of the oral ID50 for cattle was taken as 0.1 gram. A range of values was taken to cover uncertainty in the inter-species barrier from 104 to 1 (as recommended by the SSC 2000). In order to assess the likelihood that a particular carcass could be infected, UK and Swiss monitoring data was used. An incidence rate based on Prionics test findings of between 0.013 and 0.0025 was calculated. The DNV Report notes that prevalence rates are progressively reducing from these 1998/99 figures. Finally the report concludes that the SRM from an infected bovine could contribute 700 Infectious Units.

(2) Risk reduction due to incineration

Once a carcass/SRM has been introduced into a small incinerator there are two main sources for the potential release of BSE infectivity

(a) Airborne emissions (b) Residual ash

There is no direct data on the TSE levels that may occur in those two media. The SSC however is aware of currently ongoing heat studies mimicking various incineration conditions and scenarios and aiming at assessing the TSE clearance efficacy of these processes (P.Brown, pers.comm., 16.01.03) on both the residual ash and the trapped emission gases. In the absence of final data from such experiments for individual (small) incinerator types, the DNV Report (2001) assumes that measurement of the total protein content of ash is a relevant surrogate for BSE/TSE material. Protein content is a useful indicator of the general performance of an incinerator. However it is much more problematic whether it is also a valid marker for possible BSE/TSE contamination as it known that BSE/TSE are relatively heat resistant as compared to other proteins. Failure to detect certain amino acids present in prions is encouraging but the sensitivity limits for amino acids are relatively poor for reassurance purposes. Equally important, the data provided in the DNV report shows moderate split sample 4 It may be mentioned that this assumption may be valid for the UK as a whole, but note necessarily for all other Member States. 7 variation but often substantial inter sampling variation (up to 600 fold). This indicates a wide span of performance standards among the small SRM incinerators in the UK and most likely across the whole of the EU. Typically performance was substantially poorer than is the case for larger incinerators. Unburned material is not uncommonly noted in the ash from small incinerators. If the reduction in protein content due to incineration is accepted as a valid indicator, typical infectivity reduction can be calculated to be of the order of 1600 (DNV Report 2001). Incinerators are known to emit particulate matter from their stacks. Larger incinerators have much higher stacks to facilitate disposal of emissions, they also have gas cleaning equipment to minimise the emission of particulate matter, metals and acidic gases. Small incinerators generally do not have any gas cleaning equipment. It can be speculated (as in the DNV Report 2001) that unburned materials (and therefore potentially infections is much less likely to be emitted in the form of particulate matter than burnt material. Nonetheless there is no data to support this assumption.

(3) Other considerations.

(a) Disposal of ash.

In the case of small incinerators ash is often dispersed of locally to a trench, which is typically neither lined, nor is the residue buried deeply. In contrast for larger incinerators in the UK ash is normally disposed of to a contained landfill. The risk from disposal to a trench is difficult to gauge in the absence of reliable data on the possible infectivity of the ash.

(b) Management factors.

Almost inevitably the level of expertise available for the management of small incinerators is highly variable because few such facilities can afford to employ specialists in incineration. This is also likely to be often the case for the inspectors as well. While such considerations cannot formally be taken into account in a risk assessment, they are not the less relevant factors that need to be considered in assessing the risk from a particular plant.

(c) Benchmarking.

The DNV 2001 risk assessment relies greatly on the assumption that BSE/TSE contaminated material is very unlikely to be processed. The Report seeks to compare the risks from a small incinerator with that from large SRM incinerators which the author had assessed previously (DNV, 1997). It identifies that the risk is four-five -fold less from a typical small incinerator because the scale of activities is much lower. However it is noted that the amount of experimental data to back this conclusion is extremely limited and does not take into account either risks from the residual ash or any consequences of a substantially lower stack height limiting the dilution of the emitted particulate and gaseous matter. 8

5. FURTHER INVESTIGATIONS

In view of the uncertainty regarding the risks due to BSE/TSE contamination of the fly and bottom ash and airborne emissions it is recommended that further research is conducted to identify the residual risks (along with attendant uncertainties) from the burial of ash (without further treatment,) in uncontained sites. It is essential that suitable monitoring methods are developed.

6. LITERATURE

EC (European Commission), 1999. Opinion on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials. Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999 and re-edited at its meeting of 22-23 July 1999. DNV Consulting (Det Norske Veritas), 1997. Risks from disposing of BSE infected cattle in animal carcass incinerators. Report prepared for the UK Environment Agency. DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and Food. Revision 2 of the Draft report, February 2001. 24 pages. SEAC (Spongiform Encephalopathy Advisory Committee, UK), 2001. Public summary of the SEAC meeting of 25 April 2001.


http://europa.eu.int/comm/food/fs/sc/ssc/out311_en.pdf




TSS

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Friday, February 11, 2011

AN EPIDEMIOLOGIC CRITIQUE OF CREUTZFELDT-JAKOB DISEASE Vol. 2, 1980 Paul Brown vs Zohreh Davanipour and Scrapie

EPIDEMIOLOGIC REVIEWS

http://scrapie-usa.blogspot.com/2011/02/epidemiologic-critique-of-creutzfeldt.html



Friday, February 11, 2011

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html



Sunday, April 18, 2010

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html




Wednesday, February 16, 2011

IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE

http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html




BSE: TIME TO TAKE H.B. PARRY SERIOUSLY

If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf




Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518