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From: TSS ()
Subject: Scrapie: a Research Update
Date: May 11, 2006 at 7:53 pm PST

Research Project: Ovine Prion & Viral Infections: Scrapie & Ovine Progressive Pneumonia, Diagnosis & Control
Location: Animal Diseases Research

Title: Scrapie: a Research Update


Author

Alverson, Janet


Submitted to: Trade Journal Publication
Publication Type: Trade Journal
Publication Acceptance Date: February 23, 2004
Publication Date: March 1, 2004
Citation: Alverson, J. 2004. Scrapie: a Research Update. the Paddock. 1(1):1-2.

Interpretive Summary: Scrapie is best known as a degenerative fatal disease affecting the central nervous system of sheep, but it also can occur in goats. It is classified as a transmissible spongiform encephalopathy (TSE), and the infectious agent is thought to be an abnormal form of a protein normally found in sheep cells called a prion. Scrapie was first recognized as a disease of sheep in Great Britain and other countries of Western Europe more than 250 years ago, and is now endemic in many parts of the world. The first case of scrapie in the United States was diagnosed in 1947 in a Michigan flock where sheep of British origin had been imported through Canada for several years. Scrapie has primarily been reported in the Suffolk breed in the United States, but it has also been diagnosed in Border Leicester, Cheviot, Corriedale, Cotswold, Dorset, Finnsheep, Hampshire, Merino, Montadale, Rambouillet, Shropshire, Southdown, and a number of crossbreeds. Although there is no evidence suggesting that sheep scrapie poses a human health risk, it has the potential to cost the sheep industry millions of dollars in lost production. Infected flocks that contain a high percentage of susceptible animals can experience significant production losses. The presence of scrapie in the United States prevents the export of breeding stock, semen, and embryos to many other countries. The USDA has established a National Scrapie Eradication Program in the United States and encourages sheep and goat owners to participate.
Technical Abstract: Scrapie is best known as a degenerative fatal disease affecting the central nervous system of sheep, but it also can occur in goats. It is classified as a transmissible spongiform encephalopathy (TSE), and the infectious agent is thought to be an abnormal form of a protein normally found in sheep cells called a prion. Scrapie was first recognized as a disease of sheep in Great Britain and other countries of Western Europe more than 250 years ago, and is now endemic in many parts of the world. The first case of scrapie in the United States was diagnosed in 1947 in a Michigan flock where sheep of British origin had been imported through Canada for several years. Scrapie has primarily been reported in the Suffolk breed in the United States, but it has also been diagnosed in Border Leicester, Cheviot, Corriedale, Cotswold, Dorset, Finnsheep, Hampshire, Merino, Montadale, Rambouillet, Shropshire, Southdown, and a number of crossbreeds. Although there is no evidence suggesting that sheep scrapie poses a human health risk, it has the potential to cost the sheep industry millions of dollars in lost production. Infected flocks that contain a high percentage of susceptible animals can experience significant production losses. The presence of scrapie in the United States prevents the export of breeding stock, semen, and embryos to many other countries. The USDA has established a National Scrapie Eradication Program in the United States and encourages sheep and goat owners to participate.


http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=175594


Published online before print October 20, 2005

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

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

( sheep prion | transgenic mice )

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


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

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


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

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

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

To whom correspondence should be addressed.

Hubert Laude, E-mail: laude@jouy.inra.fr

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


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

Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*,, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*,
Domíníque Marcé*, François Lamoury*, Nicolas Kopp, Jean-Jacques Hauw§, James
Ironside¶, Moira Bruce, Dominique Dormont*, and Jean-Philippe Deslys*
* Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction
des Sciences du Vivant/Département de Recherche Medicale, Centre de
Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc,
BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Hôpital Neurologique Pierre
Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; § Laboratoire de
Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital,
75013 Paris, France; ¶ Creutzfeldt-Jakob Disease Surveillance Unit, Western
General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and
Institute for Animal Health, Neuropathogenesis Unit, West Mains Road,
Edinburgh EH9 3JF, United Kingdom

Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)


Abstract

There is substantial scientific evidence to support the notion that bovine
spongiform encephalopathy (BSE) has contaminated human beings, causing
variant Creutzfeldt-Jakob disease (vCJD). This disease has raised concerns
about the possibility of an iatrogenic secondary transmission to humans,
because the biological properties of the primate-adapted BSE agent are
unknown. We show that (i) BSE can be transmitted from primate to primate by
intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD
to humans could be readily recognized pathologically, whether it occurs by
the central or peripheral route. Strain typing in mice demonstrates that the
BSE agent adapts to macaques in the same way as it does to humans and
confirms that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. The agent responsible for French iatrogenic
growth hormone-linked CJD taken as a control is very different from vCJD but
is similar to that found in one case of sporadic CJD and one sheep scrapie
isolate. These data will be key in identifying the origin of human cases of
prion disease, including accidental vCJD transmission, and could provide
bases for vCJD risk assessment.


http://www.pnas.org/cgi/content/full/041490898v1

Like lambs to the slaughter
31 March 2001
Debora MacKenzie
Magazine issue 2284
What if you can catch old-fashioned CJD by eating meat from a sheep infected
with scrapie?
FOUR years ago, Terry Singeltary watched his mother die horribly from a
degenerative brain disease. Doctors told him it was Alzheimer's, but
Singeltary was suspicious. The diagnosis didn't fit her violent symptoms,
and he demanded an autopsy. It showed she had died of sporadic
Creutzfeldt-Jakob disease.

Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number
of campaigners who say that some sCJD, like the variant CJD related to BSE,
is caused by eating meat from infected animals. Their suspicions have
focused on sheep carrying scrapie, a BSE-like disease that is widespread in
flocks across Europe and North America.

Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in ...

The complete article is 889 words long.

full text;

http://www.newscientist.com/article.ns?id=mg16922840.300


The EMBO Journal, Vol. 19, No. 17 pp. 4425-4430, 2000
© European Molecular Biology Organization

Evidence of a molecular barrier limiting
susceptibility of humans, cattle and sheep to
chronic wasting disease

G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O?Rourke3,
L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M.
Smits2
and B. Caughey1,7

1NIAID/NIH Rocky Mountain Laboratories, Hamilton, MT 59840,
3USDA/ARS/ADRU, Pullman, WA 99164-7030, 4USDA/ARS/ABADRL,
Laramie, WY 82071, 5Colorado Division of Wildlife, Wildlife Research
Center, Fort Collins, CO 80526-2097, 6Department of Veterinary Sciences,
University of Wyoming, Laramie, WY 82070, USA and 2ID-Lelystad,
Institute for Animal Science and Health, Lelystad, The Netherlands
7Corresponding author e-mail: bcaughey@nih.gov Received June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.

Abstract

Chronic wasting disease (CWD) is a transmissible
spongiform encephalopathy (TSE) of deer and elk,
and little is known about its transmissibility to other
species. An important factor controlling
interspecies TSE susceptibility is prion protein (PrP)
homology between the source and recipient
species/genotypes. Furthermore, the efficiency with which
the protease-resistant PrP (PrP-res) of one
species induces the in vitro conversion of the normal PrP
(PrP-sen) of another species to the
protease-resistant state correlates with the cross-species
transmissibility of TSE agents. Here we
show that the CWD-associated PrP-res (PrPCWD) of cervids
readily induces the conversion of recombinant cervid PrP-sen
molecules to the protease-resistant state in accordance
with the known transmissibility of CWD between cervids. In contrast,
PrPCWD-induced conversions of human and bovine PrP-sen were
much less efficient, and conversion of ovine PrP-sen was
intermediate. These results demonstrate a barrier at the
molecular level that should limit the susceptibility of these non-cervid
species to CWD.

snip...

Clearly, it is premature to draw firm conclusions about CWD
passing naturally into humans, cattle and sheep, but the present
results suggest that CWD transmissions to humans would be as
limited by PrP incompatibility as transmissions of BSE or sheep
scrapie to humans. Although there is no evidence that sheep
scrapie has affected humans, it is likely that BSE has caused variant
CJD in 74 people (definite and probable variant CJD cases to
date according to the UK CJD Surveillance Unit). Given the
presumably large number of people exposed to BSE infectivity,
the susceptibility of humans may still be very low compared with
cattle, which would be consistent with the relatively inefficient
conversion of human PrP-sen by PrPBSE. Nonetheless, since
humans have apparently been infected by BSE, it would seem prudent
to take reasonable measures to limit exposure of humans
(as well as sheep and cattle) to CWD infectivity as has been
recommended for other animal TSEs.

snip...

http://www.emboj.org/current.shtml

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

snip...

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

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

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

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

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

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

snip...

76/10.12/4.6

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

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that
were exposed to the infectious agents only by their nonforced consumption of
known infectious tissues. The asymptomatic incubation period in the one
monkey exposed to the virus of kuru was 36 months; that in the two monkeys
exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months,
respectively; and that in the two monkeys exposed to the virus of scrapie
was 25 and 32 months, respectively. Careful physical examination of the
buccal cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has remained
asymptomatic during the 39 months that it has been under observation.


PMID: 6997404


http://www.ncbi.nlm.nih.gov/entrez/query.fcgicmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


1: Cent Eur J Public Health 2003 Mar;11(1):19-22

Analysis of unusual accumulation of Creutzfeldt-Jakob disease cases
in Orava and Liptov regions (northern Slovak focus) 1983-2000.

Mad'ar R, Maslenova D, Ranostajova K, Straka S, Baska T.

Institute of Epidemiology, Jessenius Faculty of Medicine, Comenius
University, Sklabinska 26, Martin, 037 53 Slovakia. MADAR@jfmed.uniba.sk

While familial cases of Creutzfeldt-Jakob disease are extremely rare
all over the world, 3 familial clusters were observed between
1983-2000 in a relatively small area situated in the North of
Slovakia. Prevalence of CJD in this area exceeded the overall
prevalence in Slovakia more than 8 times. The majority of CJD
patients admitted consuming sheep brain. Most patients lived in
small secluded villages with rather common familial intermarriage.
CJD affected both sexes equally. All patients were prior to the
disease mentally normal individuals. Shortly after the onset of CJD
their mental status deteriorated remarkably with an average survival
rate of 3.6 months.

PMID: 12690798

http://www.ncbi.nlm.nih.gov/entrez/query.fcgicmd=Retrieve&db=PubMed&list_uids=12690798&dopt=Abstract

1: Eur J Epidemiol 1991 Sep;7(5):520-3

"Clusters" of CJD in Slovakia: the first laboratory evidence of scrapie.

Mitrova E, Huncaga S, Hocman G, Nyitrayova O, Tatara M.

Institute of Preventive and Clinical Medicine, Bratislava.

Epidemic-like occurrence of Creutzfeldt-Jakob disease was observed in
1987 in Slovakia (Orava). Search for the cause of CJD focus indicated a
coincidence of genetic and environmental risks in clustering patients.
Since Spongiform Encephalopathies might be transmitted orally, (Bovine
Spongiform Encephalopathy), the possibility of zoonotic source of CJD
cases in Orava was also considered. A deficient knowledge about the
occurrence of scrapie in Slovakia stimulated an examination of sheep
with signs of CNS disorders in two flocks of Valasky breed in Orava. In
one flock, neurohistopathological examination revealed in sheep brains
lesions characteristic for scrapie. Frozen brain tissue of these animals
were used for the detection of scrapie associated fibrils. They were
found in 2 animals from the same flock. This is the first laboratory
confirmation of scrapie in Czecho-Slovakia. The possible epidemiological
and economical implications are emphasized.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgicmd=Retrieve&db=PubMed&list_uids=1761109&dopt=Abstract


STATEMENT OF DR HELEN GRANT MD FRCP
ISSUED 13/05/1999

BSE INQUIRY

http://www.bseinquiry.gov.uk/files/ws/s410.pdf


http://www.bseinquiry.gov.uk/files/ws/s410x.pdf

http://www.bseinquiry.gov.uk/evidence/ws/ws8.htm

1: Neuroepidemiology. 1985;4(4):240-9.


Sheep consumption: a possible source of spongiform encephalopathy in humans.

Davanipour Z, Alter M, Sobel E, Callahan M.

A fatal spongiform encephalopathy of sheep and goats (scrapie) shares many characteristics with Creutzfeldt-Jakob disease (CJD), a similar dementing illness of humans. To investigate the possibility that CJD is acquired by ingestion of contaminated sheep products, we collected information on production, slaughtering practices, and marketing of sheep in Pennsylvania. The study revealed that sheep were usually marketed before central nervous system signs of scrapie are expected to appear; breeds known to be susceptible to the disease were the most common breeds raised in the area; sheep were imported from other states including those with a high frequency of scrapie; use of veterinary services on the sheep farms investigated and, hence, opportunities to detect the disease were limited; sheep producers in the area knew little about scrapie despite the fact that the disease has been reported in the area, and animal organs including sheep organs were sometimes included in processed food. Therefore, it was concluded that in Pennsylvania there are some 'weak links' through which scrapie-infected animals could contaminate human food, and that consumption of these foods could perhaps account for spongiform encephalopathy in humans. The weak links observed are probably not unique to Pennsylvania.


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract

REPORT OF THE COMMITTEE ON SCRAPIE

Chair: Dr. Jim Logan, Cheyenne, WY

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

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

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

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

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

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


snip...

Infected and Source Flocks

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

Regulatory Scrapie Slaughter Surveillance (RSSS)

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

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

Scrapie Testing

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

Animal ID

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

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

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

SCRAPIE USA UPDATE AS of March 31, 2006 2 NEW CASES IN GOAT, 82
INFECTED SOURCE FLOCKS, 19 INFECTED RSSS

Date: April 30, 2006 at 4:49 pm PST
SCRAPIE USA UPDATE AS of March 31, 2006


2 NEW CASES IN GOAT, 82 INFECTED SOURCE FLOCKS, WITH 4 NEW INFECTED SOURCE
FLOCKS IN MARCH, WITH 19 SCRAPIE INFECTED RSSS REPORTED BY NVSL


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

Subject: Louping-ill vaccine documents from November 23rd, 1946
Date: Sat, 9 Sep 2000 17:44:57 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

THE VETERINARY RECORD
516 No 47. Vol. 58
November 23rd, 1946

NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND

ANNUAL CONGRESS, 1946

The annual Congress, 1946, was held at the Royal Veterinary College,
Royal College Street, London, N.W.I. from September 22nd to September
27th.

Opening Meeting

[skip to scrapie vaccine issue...tss]

Papers Presented to Congress

The papers presented to this year's Congress had as their general theme
the progressive work of the profession during the war years. Their
appeal was clearly demonstrated by the large and remarkably uniform
attendance in the Grand Hall of the Royal Veterinary College throughout
the series; between 200 and 250 members were present and they showed a
keen interest in every paper, which was reflected in the expression of
some disappointment that the time available for discussion did not
permit of the participation of more than a small proportion of
would-be contributors.

In this issue we publish (below) the first to be read and discussed,
that by Dr. W. S. Gordon, M.R.C.V.S., F.R.S.E., "Advances in Veterinary
Research." Next week's issue will contain the paper on "Some Recent
Advances in Veterinary Medicine and Surgery in Large-Animal Practice"
by Mr. T. Norman Gold, M.R.C.V.S. In succeeding numbers of the Record
will be reproduced, also with reports of discussions, that by Mr. W. L.
Weipers, M.R.C.V.S., D.V.S.M., on the same subject as relating to
small-animal practice, and the papers by Mr. J. N. Ritchie, B.SC.,
M.R.C.V.S., D.V.S.M., and Mr. H.W. Steele-Bodger, M.R.C.V.S., on
"War-time Achievements of the British Home Veterinary Services."

The first scientific paper of Congress was read by Dr. W. S.
Gordon, M.R.C.V.S., F.R.S.E. on Monday, September 23rd, 1946,
when Professor J. Basil Buxton, M.A., F.R.C.V.S, D.V.H., Prinicipal
of the Royal Veterinary College, presided.

Advances in Veterinary Research

by

W.S. GORDON, PH.D., M.R.C.V.S., F.R.S.E.

Agriculteral Research Council, Field Station, Compton, Berks.

Louping-ill, Tick-borne Fever and Scrapie

In 1930 Pool, Browniee & Wilson recorded that louping-ill was
a transmissible disease. Greig et al, (1931) showed that the infective
agent was a filter-passing virus with neurotropic characters and
Browniee & Wilson (1932) that the essential pathology was that of an
encephalomyelitis. Gordon, Browniee, Wilson & MacLeod (1932) and
MacLeod & Gordon (1932) confirmed and extended this work. It was
shown that on louping-ill farms the virus was present in the blood
of many sheep which did not show clinical symptoms indicating
involvement of the central nervous system and that for the perpetuation
and spread of the disease these subclinical cases were probably of
greater importance that the frank clinical cases because, in Nature,
the disease was spread by the tick, lxodes ricinus L. More recently
Wilson (1945, 1946) has described the cultivation of the virus in a
chick embryo medium, the pathogenic properties of this culture
virus and the preparation of louping-ill antiserum.

Between 1931 and 1934 I carried out experiments which resulted
in the development of an effective vaccine for the prevention
of louping-ill.* This vaccine has been in general use since 1935
and in his annual report to the Animal Diseases Research Association
this year, Dr. Greig stated that about 227,000 doses of vaccine
had been issued from Moredun alone.

Dr. Gordon illustrated this portion of his paper by means of graphs
and diagrams projected by the epidiascope.

This investigation, however, did not begin and end with the
study of louping-ill; it had, by good fortune, a more romantic
turn and less fortunately a final dramtic twist which led almost
to catastrope. After it had been established that a solid immunity
to louping-ill could be induced in sheep, a group of
immunized and a group of susceptible animals were placed together
on the tick-infected pasture of a louping-ill farm. Each day all
the animals were gathered and their temperatures were recorded.
It was anticipated that febrile reactions with some fatalities would
develop in the controls while the louping-ill immunes would remain
normal. Contrary to expectation, however, every sheep, both immune
and control, developed a febrile reaction. This unexpected
result made neccessary further investigation which showed that the
febrile reaction in the louping-ill immunes was due to a hitherto
undescribed infective agent, a Rickettsia-like organism which could
be observed in the cytoplasm of the grannular leucocytes, especially
the neutrophil polymorphs (MacLeod (1932), Gordon, Browniee,
Wilson & MacLeod. MacLeod & Gordon (1933). MacLeod (1936).
MacLeod collected ticks over many widely separated parts of
Scotland and all were found to harbour the infective agent of
tick-borne fever, and it is probable that all sheep on tick-infested
farms develop this disease, at least on the first occasion that they
become infested with ticks. When the infection is passed in series
through susceptible adult sheep it causes a sever, febrile reaction,
dullness and loss of bodily condition but it rarely, if ever, proves
fatal. It is clear, however, that it aggravates the harmful effects
of a louping-ill infection and it is a serious additional complication
to such infections as pyaemia and the anacrobic infections which
beset lambs on the hill farms of Northern Britain.

Studying the epidemiology of louping-ill on hill farms it became
obvious that the pyaemic condition of lambs described by
M'Fadyean (1894) was very prevalent on tick infested farms
Pyaemia is a crippling condition of lambs associated with tick-bite
and is often confused with louping-ill. It is caused by infection
with Staphylococcus aureus and affected animals may show abscess
formation on the skin, in the joints, viscera, meninges and elsewhere
in the body. It was thought that tick-borne fever might
have ben a predisposing factor in this disease and unsuccessful
attempts were made by Taylor, Holman & Gordon (1941) to reproduce
the condition by infecting lambs subcutaneously with the
staphylococcus and concurrently produceing infections with tickborne
fever and louping-ill in the same lambs. Work on pyaemia
was then continued by McDiarmid (1946a, 1946b, 1946c), who
succeeded in reproducing a pyaemic disease in mice, guinea-pigs
and lambs similar to the naturally occuring condition by intravenous
inoculation of Staphylococcus aureus. He also found a
bacteraemic form of the disease in which no gross pyaemic lesions
were observed. The prevention or treatment of this condition
presents a formidable problem. It is unlikely that staphylococcal
???oid will provide an effective immunity and even if penicillin
proved to be a successful treatment, the difficulty of applying it
in adequate and sustained dosage to young lambs on hill farms
would be almost insurmountable.

>From 1931 to 1934 field trials to test the immunizing value
and harmlessness of the loup-ill vaccine were carried out on a
gradually increasing scale. Many thousands of sheep were vaccinated
and similar numbers, living under identical conditions
were left as controls. The end result showed that an average
mortability of about 9 percent in the controls was reduced to less
than 1 percent in the vaccinated animals. While the efficiency
of the vaccine was obvious after the second year of work, previous
bitter experience had shown the wisdom of withholding a biological
product from widespread use until it had been successfully produced
in bulk, as opposed to small-scale experimental production
and until it had been thoroughly tested for immunizing efficiency
and freedom from harmful effects. It was thought that after
four years testing this stage had been reached in 1935, and in
the spring of that year the vaccine was issued for general use. It
comprised a 10 percent saline suspension of brain, spinal cord
and spleen tissues taken from sheep five days after infection with
louping-ill virus by intracerebral inoculation. To this suspension
0-35 percent of formalin was added to inactivate the virus and
its safety for use as a vaccine was checked by intracerbral inoculation
of mice and sheep and by the inoculation of culture medium.
Its protective power was proved by vaccination sheep and later
subjecting them, along with controls, to a test dose of living virus.

Vaccine for issue had to be free from detectable, living virus
and capable of protecting sheep against a test dose of virus applied
subcutaneously. The 1935 vaccine conformed to these standards
and was issued for inoculation in March as three separate batches
labelled 1, 2, and 3. The tissues of 140 sheep were employed
to make batch 1 of which 22,270 doses were used; 114 to make
batch 2 of which 18,000 doses were used and 44 to make batch 3
of which 4,360 doses were used. All the sheep tissues incorporated
in the vaccine were obtained from yearling sheep. During 1935
and 1936 the vaccine proved highly efficient in the prevention
of loup-ill and no user observed an ill-effect in the inoculated
animals. In September, 1937, two and a half years after vaccinating
the sheep, two owners complained that scrapie, a disease which
had not before been observed in the Blackface breed, was appearing
in their stock of Blackface sheep and further that it was confined
to animals vaccinated with louping-ill vaccine in 1935. At that
stage it was difficult to conceive that the occurrence could be
associated with the injection of the vaccine but in view of the
implications, I visited most of the farms on which sheep had been
vaccinated in 1935. It was at this point that the investigation
reached its dramatic phase; I shall not forget the profound effect
on my emotions when I visited these farms and was warmly welcomed
because of the great benefits resulting from the application
of louping-ill vaccine, wheras the chief purpose of my visit was
to determine if scrapie was appearing in the inoculated sheep.
The enquiry made the position clear. Scrapie was developing in
the sheep vaccinated in 1935 and it was only in a few instances
that the owner was associating the occurrence with louping-ill
vaccination. The disease was affecting all breeds and it was
confined to the animals vaccinated with batch 2. This was clearly
demonstrated on a number of farms on which batch 1 had been
used to inoculate the hoggs in 1935 and batch 2 to inoculate
the ewes. None of the hoggs, which at this time were three-
year-old ewes. At this time it was difficult to forecast whether all
of the 18,000 sheep which had received batch 2 vaccine would
develop scrapie. It was fortunate, however, that the majority of
the sheep vaccinated with batch 2 were ewes and therfore all
that were four years old and upwards at the time of vaccination
had already been disposed of and there only remained the ewes
which had been two to three years old at the time of vaccination,
consequently no accurate assessment of the incidence of scrapie
could be made. On a few farms, however, where vaccination was
confined to hoggs, the incidence ranged from 1 percent, to 35 percent,
with an average of about 5 percent. Since batch 2 vaccine
had been incriminated as a probable source of scrapie infection,
an attempt was made to trace the origin of the 112 sheep whose
tissues had been included in the vaccine. It was found that they
had been supplied by three owners and that all were of the
Blackface or Greyface breed with the exception of eight which
were Cheviot lambs born in 1935 from ewes which had been in
contact with scrapie infection. Some of these contact ewes
developed scrapie in 1936-37 and three surviving fellow lambs to
the eight included in the batch 2 vaccine of 1935 developed
scrapie, one in September, 1936, one in February, 1937, and one
in November, 1937. There was, therefore, strong presumptive
evidence that the eight Cheviot lambs included in the vaccine
althought apparently healthy were, in fact, in the incubative stage
of a scrapie infection and that in their tissues there was an
infective agent which had contaminated the batch 2 vaccine,
rendering it liable to set up scrapie. If that assumption was
correct then the evidence indicated that:-

(1) the infective agent of scrapie was present in the brain, spinal
cord and or spleen of infected sheep:
(2) it could withstand a concentration of formalin of 0-35 percent,
which inactivated the virus of louping-ill:
(3) it could be transmitted by subcutaneous inoculation;
(4) it had an incubative period of two years and longer.

Two Frenchmen, Cuille & Chelle (1939) as the result of experiments
commenced in 1932, reported the successful infection of
sheep by inoculation of emulsions of spinal cord or brain material
by the intracerebral, epidural, intraocular and subcutaneous routes
The incubation period varied according to the route employed,
being one year intracerebrally, 15 months intraocularly and 20
months subcutaneously. They failed to infect rabbits but succeeded
in infecting goats. Another important part of their work
showed that the infective agent could pass throught a chamberland
1.3 filter, thus demonstrating that the infective agent was a
filtrable virus. It was a curious coincidence that while they
were doing their transmission experiments their work was being
confirmed by the unforeseeable infectivity of a formalinized tissue
vaccine.

As a result of this experience a large-scale transmision experiment
involving the ue of 788 sheep was commenced in 1938 on a
farm specially taken for the purpose by the Animal Diseases
Research Association with funds provided by the Agricultural
Research Council. The experiment was designed to determine the
nature of the infective agent and the pathogenesis of the disease.
It is only possible here to give a summary of the result which
showed that (1) saline suspensions of brain and spinal cord tissue
of sheep affected with scrapie were infective to normal sheep
when inoculatted intracerebrally or subcutaneously; (2) the incubation
period after intracerebral inoculation was seven months and
upwards and only 60 percent of the inoculated sheep developed
scrapie during a period of four and a half years; (3) the incubation
period after subcutaneous inoculation was 15 months and upwards
and only about 30 percent of the inoculated sheep developed
the disease during the four and a half years: (4) the infective
agent was of small size and probably a filtrable virus.

The prolonged incubative period of the disease and the remarkable
resistance of the causal agent to formalin are features of
distinct interest. It still remains to determine if a biological test
can be devised to detect infected animals so that they can be
killed for food before they develop clinical symptoms and to
explore the possibilities of producing an immunity to the disease.
==================================================================

Greetings List Members,

pretty disturbing document. now, what would stop this from happening
with the vaccineCJD in children???

kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA

TSS




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