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From: TSS ()
Subject: Scrapie program on hold in Vermont
Date: September 25, 2006 at 9:57 am PST

Scrapie program on hold in Vermont

September 24, 2006

By Susan Smallheer
Staff Writer

WINDSOR — Bill Yates remembers all too well his experience with scrapie 15 years ago.


Scrapie, which only affects sheep and goats, and mostly black-face breeds, such as Suffolk and Hampshire, is not transferred to humans. A sheep from a flock that has scrapie is safe to eat. The disease destroys the animal's brain, but it often takes more than five years to surface after exposure. There is no cure.


Scrapie is in the "mad cow" class of diseases. But scrapie and bovine spongiform encephalopathy are different diseases, according to USDA literature, and scrapie poses no risk to human health.

The USDA and the sheep industry have been trying to eradicate sheep scrapie since 1951 with limited success. A renewed effort, launched in 2001, called for a Sept. 30, 2006, deadline for states to have scrapie flock certification programs in place. Vermont is not yet in compliance with the federal regulation.

Vermont Agriculture Secretary Stephen Kerr said last week that Vermont will not be in compliance because of the state's now-shelved "premises registration" program.

Contact Susan Smallheer at

Susan Smallheer wrote;

> Scrapie, which only affects sheep and goats, and mostly black-face breeds, such as Suffolk

> and Hampshire, is not transferred to humans.


I am always amazed at just how ignorant the media is on this topic and how inept there reporting is most of the time. this article from the rutland herald is another fine example of just how inept the reporting of human and animal TSE are. I have followed the Faillace's plight with the USDA for years and years, watching your farms animals die from a TSE would be most disturbing to me, but you should try watching your loved one die from a TSE, and then have the USDA, FDA, CDC et al tell you it just happens spontaneously without any cause, and that there is no mad cows in the USA, or in this case in this newspaper article state that scrapie does not transmit to man or any other species other than sheep and goats. with scrapie in sheep and goats running rampant (has for decades here in the USA), with CWD running rampant here in the USA (has for decades), BSE and a new atypical BSE/TSE i.e. BASE in the USA cattle population (has been for a decades via Marsh's studies), and with TME also here in the USA (all of which have been rendered and fed back to other animals for human and animal consumption), the USA has the most documented TSE i.e. mad cow disease (catch fraise or maybe not? either way) Transmissible Spongiform Encephalopathy, but with all this, and especially the way the USDA handled those Belgium Sheep, I would not want any animal ID either, I would just let these TSE continue to spread to hell and back, and let the incubation fool everyone, all the while spreading through the various PROVEN routes and sources. ... i don't expect anyone to read this, they never do, just go stick your head in a hole in ground like everyone else, but these are the facts, like em or not. i have wasted 8+ years of my life daily with TSEs. nobody cares...

LETS FOR A CHANGE LOOK AT SOME FACTS, did i say that 'facts', most in the media do not know what the word means, it's all about ratings. ...

FACT is, scrapie transmits to primates by there non forced oral consumption, and there has never been any transmission studies done on humans. thats a fact, and there are a few others, IF anyone is interested ;



To minimize the risk of farmers' claims for compensation from feed

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by
maintaining the availability of meat and bone meal as a raw
material in animal feeds, and ensuring time is available to make any
changes which may be required.




MAFF remains under pressure in Brussels and is not skilled at
handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which
contain illegal traces of ruminant protein. More likely, a few positive
test results will turn up but proof that a particular feed mill knowingly
supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed
compounders are free of it. The longer we can avoid any direct
linkage between feed milling _practices_ and actual BSE cases,
the more likely it is that serious damage can be avoided. ...

SEE full text ;

J Infect Dis 1980 Aug;142(2):205-8

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

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

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

PMID: 6997404

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)


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.


Characterization of the CJD and Scrapie Strains. Controls were set up by transmitting one French and one U.S. scrapie isolate from ruminants as well as French sCJD and iCJD cases from humans. None of these revealed a lesion profile or transmission characteristics similar or close to those of BSE or vCJD, respectively, thus extending to the present French scrapie isolate the previous observation that the BSE agent was different from all known natural scrapie strains (4, 24).

The lesion profiles of sCJD and iCJD differed only slightly in severity of the lesions, but not in shape of the profile, revealing the identity of the causative agents. One of us reported the absence of similarity between sCJD (six cases) and U.K. scrapie (eight cases) in transmission characteristics in mice (4). Herein, we made the striking observation that the French natural scrapie strain (but not the U.S. scrapie strain) has the same lesion profile and transmission times in C57BL/6 mice as do the two human TSE strains studied. This strain “affiliation” was confirmed biochemically. There is no epidemiological evidence for a link between sheep scrapie and the occurrence of CJD in humans (25). However, such a link, if it is not a general rule, would be extremely difficult to establish because of the very low incidence of CJD as well as the existence of different isolates in humans and multiple strains in scrapie. Moreover, scrapie is transmissible to nonhuman primates (26). Thus, there is still a possibility that in some instances TSE strains infecting humans do share a common origin with scrapie, as pointed out by our findings.


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.

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


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.

ISSUED 13/05/1999


CWD to CJD in humans (why not?), as easy as BSE/Scrapie;

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.
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: Received June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.


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.


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.


Scrapie to Humans USA?

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.



Nobel Lecture, December 13, 1976


National Institutes of Health, Bethesda, Maryland, U.S.A.


In a study in Israel, an
overall prevalence in Jews of Libyan origin is 30 times as high as in Jews of

European origin (40). The custom of eating the eyeballs and brains of sheep

in the Jewish households of North African and Middle Eastern origin, as opposed

to Jewish households of European origin, has understandably given rise to the

conjecture that scrapie-infected sheep tissue might be the source of such CJD

infection (37).


The passage of sheep scrapie into other sheep and into goats, at least by the

route of feeding of material contaminated with placenta and embryonic

membrane (53), and into mink from feeding carcasses of scrapied sheep, are

established paths of scrapie transmission. In view of the experimental transmission

of scrapie to monkeys, there is serious cause for wonder whether kitchen

and butchery accidents involving the contamination of skin and eyes may not

be a possible source of CJD in man (36a, 37).


Scrapie has been transmitted

in our laboratory to five species of monkeys (Tables 9 and 10) (23, 31,

32), and such transmission has occurred using infected brain from naturally

infected sheep and from experimentally infected goats and mice (Figures

22a, b, c). The disease produced is clinically and pathologically indistinguishable

from experimental CJD in these species. .........

Figure 22. Scrapie has been transmitted to three species of New World monkeys and two

species of Old World monkeys (Tables 9, 10).

22a. Transmission of scrapie from the brain of a scrapie-infected Suffolk ewe (C506) in

Illinois to a cynomolgus monkey, and from the 4th mouse passage of this strain of scrapie

virus to two squirrel monkeys. Incubation period in the cynomolgus was 73 months and in

the squirrel monkeys 31 and 33 months. A chimpanzee and a rhesus monkey inoculated

109 months ago with this sheep brain remain well, as does a spider monkey inoculated 70

months ago with brain from the 4th passage of the C506 strain of scrapie in mice.


22b. Primary transmission of goat-adapted scrapie (Compton, England strain) to the

squirrel monkey and to mice and the transmission of mouse-adapted scrapie to two species

of Old World and three species of New World monkeys. Numbers in parentheses are the

number of months elapsed since inoculation, during which the animal remained asymptomatic.


22c. Transmission of mouse-adapted sheep scrapie (U. S. strain 434-3-897) to a squirrel

monkey 38 months following intracerebral inoculation with a suspension of scrapie-infected

mouse brain containing 10a7.3 infectious units of virus per ml. This animal showed signs of

ataxia, tremors and incoordination, and the disease was confirmed histologically. See (b)

for an explanation of symbols.


Figure 23. Transmissible mink encephalopathy (TME), a rare disease of American ranch

mink, is possibly a form of scrapie. The clinical picture and histopathological lesions attendant

in the brain, resemble that of scrapie, and scrapie sheep carcasses were fed to mink on

ranches on which TME appeared. The disease is transmissible to sheep, goats, certain

rodents and New and Old World monkeys. Illustrative data on the primary transmissions

of transmissible mink encephalopathy to one species of New World monkey and two species

of Old World monkeys, and serial passage of the virus in squirrel, rhesus and stumptailed

monkeys are presented in this Figure. Incubation periods are shown in months that elapsed

between inoculation and onset of clinical disease. (Figure includes information from our

laboratory and from R. F. Marsh, R. J. Eckroade, and R. P. Hanson.)

SNIP... end




Nobel Lecture, December 13, 1976


National Institutes of Health, Bethesda, Maryland, U.S.A.

Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr,
Gajdusek DC.

Proposed link between transmissible spongiform encephalopathies of man and animals.

Diringer H.

Robert Koch-Institut, Berlin, Germany.

A link between scrapie and Creutzfeldt-Jakob disease (CJD) is likely to exist. Based on old observations on scrapie, new experiments on bovine spongiform encephalopathy, and modern reviews on CJD, my proposal fits general rules of virus transmission

Transmission of Creutzfeldt-Jakob disease by handling of dura mater.
The Lancet Volume 341(8837) January 9, 1993 pp
Weber, Thomas; Tumani, Hayrettin; Holdorff, Bernd; Collinge, John; Palmer,
Mark; Kretzschmar, Hans A.; Felgenhauer, Klaus

Sir,- Creutzfeldt-Jakob disease (CJD) can be transmitted iatrogenically by
human pituitary growth hormone, corneal transplants, and dura mater grafts
(1). Possible accidental transmission has been reported in only four
people-a neurosurgeon (2), a pathologist (3), and two laboratory technicians
(4,5) . We have encountered an unusually rapid case of CJD probably acquired
through handling of sheep and human dura mater.
In May, 1992, a 55-year-old orthopaedic surgeon developed paraesthesia of
the left arm. A few days later he had spatial disorientation, apraxia, and
gait ataxia. In June he was admitted and a neurologist suspected CJD on the
basis of the clinical signs, typical electroencephalogram (EEG) pattern, and
history. An EEG in June revealed a typical pattern of periodic biphasic and
triphasic sharp wave complexes. We saw the patient in July, 1992. He was
awake and oriented, with dyscalculia, dysgraphia, disturbed vision, apraxia
mainly of the left side, rigidity of wrists, spasticity of all muscles,
myoclonus of the left arm, increased tendon reflexes, ataxia of limbs and
trunk, and incoordination of left arm. Within 3 weeks he had impaired
consciousness and attention, mildly impaired memory, and threatening visual
hallucinations with restless turning. He had periodic states with movements
of his head and eye-bulbs resembling tonic adversive seizures. During sleep
these motor disturbances stopped. 2 1/2 months later the patient died.

This patient had worked with sheep and human dura mater from 1968 to 1972.
He handled about 150 specimens of ovine origin and at least a dozen human
preparations for research. Handling involved opening skulls with a band saw,
removing dura, and testing them either fresh (usually), preserved, or
lyophilised for mechanical qualities. These specimens were sent to a company
that has sold dura mater preparations by which CJD was transmitted in six
instances. No information was available from the company about a possible
connection with this patient's disease and the earlier cases of transmitted
CJD. Brain biopsy was consistent with diagnosis of CJD. Cerebrospinal fluid
obtained in July showed neuron-specific enolase (NSE) at 82.0 ng/mL,
compared with 16.7 ng/mL in serum of other cases (6). Proton magnetic
resonance spectroscopy of parieto-occipital and temporal grey matter,
parietal white matter, and thalamus revealed a 20-30% reduction of
N-acetylaspartate, as described (7). DNA was genotyped with allele-specific
oligonucleotides (8) and was homozygous for methionine at the polymorphic
codon 129. Subsequent direct DNA sequencing for the PrP gene open-reading
frame demonstrated normal sequence on both alleles, excluding known or novel
pathogenic PrP mutations.

It is tempting to speculate that prions were transmitted to this patient
from sheep or human dura mater through small lacerations of his skin, but
the patient and his wife did not remember any significant injury during his
four years of working with these samples. It cannot be excluded that this
was a case of sporadic CJD although this assumption is unlikely in view of
the clinical course which was similar to iatrogenic CJD transmitted by
peripheral inoculation, such as with human pituitary growth hormone or
gonadotropin or to kuru (1). Iatrogenic cases resulting from intracerebral
inoculation with the transmissible agent, for instance following dura mater
grafts (2-5), present with a dementing picture, as is usual in sporadic CJD,
rather than with ataxia as in this case.

1. Brown P, Preece MA, Will RG. "Friendly fire" in medicine: hormones,
homografts, and Creutzfeldt-Jakob disease. Lancet 1992; 340: 24-27. [Medline
Link] [Context Link]

2. Schoene WC, Masters CL, Gibbs CJ Jr, et al. Transmissible spongiform
encephalopathy (Creutzfeldt-Jakob Disease): atypical clinical and
pathological findings. Arch Neurol 1981; 38: 473-77. [Medline Link] [Context

3. Gorman DG, Benson DF, Vogel DG, Vinters HV. Creutzfeldt-Jakob disease in
a pathologist. Neurology 1992; 42: 463. [Medline Link] [Context Link]

4. Miller DC. Creutzfeldt-Jakob disease in histopathology technicians. N
Engl J Med 1988; 318: 853-54. [Medline Link] [Context Link]

5. Sitwell L, Lach B, Atack E, Atack D, Izukawa D. Creutzfeldt-Jakob disease
in histopathology technicians. N Engl J Med 1988; 318: 854. [Medline Link]
[Context Link]

6. Wakayama Y, Shibuya S, Kawase J, Sagawa F, Hashizume Y. High
neuron-specific enolase level of cerebrospinal fluid in the early stage of
Creutzfeldt-Jakob disease. Klin Wochenschr 1987; 65: 798-801. [Medline Link]
[Context Link]

7. Bruhn H, Weber T, Thorwirth V, Frahm J. In-vivo monitoring of neuronal
loss in Creutzfeldt-Jakob disease by proton magnetic resonance spectroscopy.
Lancet 1991; 337: 1610-11. [Medline Link] [Context Link]

8. Collinge J, Palmer MS, Dryden AJ. Genetic predisposition to iatrogenic
Creutzfeldt-Jakob disease. Lancet 1991; 337: 1444-42. [Medlin


J Am Vet Med Assoc. 1992 Jan 15;200(2):164-7.
Recommendations of the International Roundtable Workshop on Bovine Spongiform Encephalopathy.
Gibbs CJ Jr,
Bolis CL,
Asher DM,
Bradley R,
Fite RW,
Johnson RT,
Mahy BW,
McKhann GM.
National Institutes of Health, Bethesda, MD 20892.

Recommendations of the working party were summarized as follows: Determine the status in all countries of their national cattle herds with respect to BSE. Attempt to develop a test to recognize BSE-infected animals before they become clinically ill. Establish procedures to prevent spread of BSE agent into the cattle populations, especially by eliminating feeds containing rendered ruminant proteins. Review the rendering processes, identify the sources and destinations of rendered products, and suggest appropriate changes if needed. Especially needed are standardized rendering procedures in regard to use of organic solvents, temperature, and duration of heat treatment. Review import and export regulations to reduce the risk of spreading BSE and to maximize opportunities for safe trading in cattle and cattle products. The scrapie-free certification program of the USDA was supported, and similar programs might be considered by other countries. If BSE/scrapie is diagnosed in a given country, determine baseline incidence of CJD in those countries and consider contributing to an international registry. The WHO should address the problems of BSE, formulate policy, participate in and coordinate research, and provide training opportunities for veterinary and human health care workers from eastern European countries and developing nations. Government and private agencies should consider increasing support for research on transmissibility and pathogenesis of CJD, BSE, CWD, scrapie, and transmissible mink encephalopathy. Prepare and publish a critical neuropathologic review of all spongiform encephalopathies, naturally and experimentally transmitted, defining the characteristics of each disease in the various species known to be susceptible. Consider producing guidelines for the biological and pharmaceutical industries with regard to sourcing, collecting, and processing bovine and ovine materials.




scrapie like syndrome 'cover up'




18. Following the conference, we prepared the full paper we had presented, for publication in

a book of this European Commission-sponsored conference and sent it to our superiors

for approval. (The correspondence which ensued in April and May 1991 is found at

YB91/4.16/1.1;YB91/4.22/2.1;YB91/4.30/1.1;YB91/5.3/3.1). Specifically, despite detailed

arguments supporting our statements, the following ultimatum was faxed to us from the

then Assistant Chief Veterinary Officer, making it plain that he was taking into account the

views of the then CVO:

“We are not willing for the paper to be published unless these references are

removed. This may be unacceptable to the authors, in which case permission to

publish is refused.”

19. Despite protestations that the body of the text would no longer agree with the already

published abstract, and our detailed knowledge on the subject notwithstanding, the edict

stood. We were left with little alternative but to amend the paper, which by this time had

missed the original deadline for submission and was in danger of not being published at all

(see correspondence above).

20. Subsequent to its publication in the conference book (ref 5), the paper was also published

in a refereed journal (ref 7). The original abstract from ref 5 was then also altered to agree

with the altered text. Specifically the words “with BSE” were removed from the phrase

“epidemiological association with BSE”. I had left MAFF before this paper was ever


21. This episode was described in Dispatches (Channel 4, 9pm Thursday 11th December

1997), and on two separate occasions in. The Independent newspaper (YB97/12.11/1.1

and YB98/1.26/1.1).

Outright rejection of manuscripts submitted for publication, during

"Refereeing/Scrutineering" by Journals

22. The peer review system is in itself generally reasonable. However, an issue of real concern

is that the Veterinary Record , the main channel of information for the veterinary

profession, failed to provide an open forum for discussion of the TSEs throughout the

period of the terms of reference of the Inquiry.

23. The following is a chronology of papers submitted to the Veterinary Record, but which

went unpublished:


1988: Letter entitled ‘Scrapie, Time to take HB Parry Seriously’ (YB88/6.8/4.1)

Time to take HB Parry Seriously’ (YB88/6.8/4.1)

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 notificable disease. ...

H. B. Parry, Scrapie Disease in Sheep--Historical, Clinical, Epidemiological, Pathological and Practical Aspects of the Natural Disease (Academic Press, London, 1983).

Author(s): PARRY HB
Source: NATURE 185 (4711): 441-443 1960
Document Type: Article
Language: English
Cited References: 7
IDS Number: ZQ043

ISSN: 0028-0836

Journal of the Royal Society ofMedicine Volume 78 April 1985 347

Letters to the Editor

Oncogenes in scrapie and

Creutzfeldt-Jacob disease

From Dr S J Oppenheimer

Department of Tropical Paediatrics

Liverpool School of Tropical Medicine

From a historical viewpoint it

should be noted that this point was first made

strongly in relation to scrapie by Parry (1962,

1983), to whose work Oppenheimer rightly draws






Date: February 12, 2006 at 1:03 pm PST


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.

To reduce/eliminate these problems, the Program has placed additional quality requirements on the testing laboratories: additional review of final reports, additional coding systems for testing operations, strict follow-up and reports to NVSL on corrective actions, dual data entry systems, and more frequent inspections. ...


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

Infected and Source Flocks

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


Scrapie Testing

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


Location: Animal Diseases Research

2005 Annual Report

1.What major problem or issue is being resolved and how are you resolving it (summarize project aims and objectives)? How serious is the problem? What does it matter?
The economic losses to the sheep industry due to ovine scrapie can be reduced by a coordinated program of live animal testing, replacement with sheep of lower susceptibility, and reducing transmission within the flock. Scrapie is a transmissible spongiform encephalopathy associated with deposition of an abnormal isoform of a mammalian glycoprotein, the prion protein, in tissues throughout the sheep. The highest level of accumulation is in the brain, although detectable levels are found in lymphoid tissues and placenta/fetal tissues. Detection of prions in peripheral lymphoid tissue can be used to identify and cull infected animals early in infection. Further, the susceptibility of sheep to clinical scrapie and to accumulation of prions is under genetic control. Quantitative determination of the level of protection associated with commonly occurring genotypes could enable producers and regulatory programs to integrate protective genetics with elimination of infected stock to reduce the amount of disease in U.S. flocks. Control of all domestic prion diseases is important in reducing trade barriers for U.S. sheep and germplasm and for assuring the present and future global markets for cattle. Ovine progressive pneumonia virus causes persistent viral infection and development of multi-organ inflammatory disease in some animals. The infection rates in US sheep flocks range from 9 to 49%. A variable and unpredictable percentage of infected animals will progress to clinical disease with high viral titers and increased risk of transmission to flockmates. This project has produced a serologic test for the disease. The current project includes development of a vaccine to reduce infected animals and identification of genes associated with decreased transmission in infected sheep. Sheep scrapie is a member of a group of diseases that includes bovine spongiform encephalopathy (BSE). Sheep scrapie is associated with minor direct losses to the industry. However, loss of international markets for sheep and sheep germplasm and loss of the domestic access to rendering facilities are major economic losses to the industry. Control programs based on epidemiology alone have failed to control the spread of scrapie throughout the U.S. since the disease was introduced in 1947. A control program based on a live animal diagnostic test supplemented by introduction of replacement stock of lower genetic susceptibility is urgently needed. Transmission barriers of these diseases are not understood. Therefore, the presence of any of these diseases within the U.S. represents a continuous threat for emergence in animals not yet found to have been infected in the U.S. The occurrence of BSE in U.S. cattle has caused economic losses in the U.S. cattle domestic market and the world markets. Animals with clinical signs of ovine progressive pneumonia virus represent the main risk of virus transmission because disease progression is associated with much higher virus loads than is nonprogressive persistent infection. Therefore, the immunogenetic basis of disease pathogenesis is an important consideration in SRLV research. The most significant problem associated with SRLV infection is the inability to determine which animals will progress to severe clinical disease and death. Our objectives are to reduce the clinical disease rates and viremia levels through a vaccination program targeting the type 1 immune responses and to determine the immunogenetics associated with this response. SRLV research will lead to methods for the induction of immunologic control and genetic predictors of animals with a low potential for transmission if infected. Our research concerning the transmissible encephalopathies and small ruminant lentiviruses address the following elements of our National Program in Animal Production, Product Value and Safety. Our research encompasses the National Program Initiative 103 Animal Health at 100%, and our research components include pathogen detection and diagnostics, animal immunology, mechanism of disease, genetic resistance to disease, and strategies to control infectious and non-infectious diseases.

2.List the milestones (indicators of progress) from your Project Plan.
Year 1 (FY2002)

Validate diagnostic and genetic tests; IHC test validation studies and PrP genotype continue from previous CRIS.

Define transmission route. Continue study on effect of maternal disease status and fetal genotype of PrP-Sc in placenta. Initiate studies on effect of pregnancy and placenta on PrP-Sc.

Initiate blood transfusion study. Complete methods for detecting and quantitating PrP-C and PrP-Sc in dissociated lymph nodes.

Induce type 1 response to CAEV and MVV. Immunize goats with plasmid DNA expressing CAEV env and boost with SU-FIA. Isolate and characterize wild type CAEV for challenge and challenge-immunized goats.

Identify MVV resistant MHC class II haplotypes. Complete titration and isotypes of antibodies from Dubois sheep.

Year 2 (FY2003)

Continue validation of IHC tests.

Continue studies on effect of pregnancy and placenta on PrP-Sc.

Continue FACS and IHC analysis of lymph node cells for PrP-C and PrP-Sc.

Continue examination of postchallenge parameters. Construct and characterize a recombinant plasmid expressing MVV8534 env.

Complete T cell proliferation assays and divide sheep.

Year 3 (FY2004)

Complete validation of IHC tests.

Complete studies on effect of pregnancy and placenta on PrP-Sc.

Complete FACS and IHC analysis of lymph node cells for PrP-C and PrP-Sc.

Continue examination of postchallenge parameters. Construct and characterize a recombinant plasmid expressing MVV8534 env.

Year 4 (FY2005)

Initiate studies on rapid, high volume diagnostic testing; complete PrP genotype study.

Complete study on effect of maternal disease status and fetal genotype of PrP-Sc in placenta Initiate studies on regulation of PrP-C by estrous cycle and pregnancy.

Complete PrP-C distribution and quantitation in peripheral blood cells; initiate immunomagnetic bead enrichment studies if indicated.

Immunize sheep with plasmid DNA expressing MVV8534 env and boost with MVV SU-FIA. Challenge immunized goats with MVV8534.

Complete PCR-RFLP of OvLa DRB-1 alleles.

Year 5 (FY2006)

Complete PrP-Sc rapid test development and transfer technology.

Complete studies on regulation of PrP-C by estrous cycle and pregnancy.

Complete blood transfusion study.

Continue examination of postchallenge parameters.

Identify OvLa DRB-1 alleles that associate with type 1 responses. Identify MMV-free sheep with appropriate DRB-1 haplotypes and challenge with MVV8534.

3a.List the milestones that were scheduled to be addressed in FY 2005. For each milestone, indicate the status: fully met, substantially met, or not met. If not met, why.

Initiate studies on rapid, high volume diagnostic testing; complete PrP genotype study.
Milestone Substantially Met

Complete study on effect of maternal disease status and fetal genotype of PrP-Sc in placenta Initiate studies on regulation of PrP-C by estrous cycle and pregnancy.
Milestone Substantially Met

Complete PrP-C distribution and quantitation in peripheral blood cells; initiate immunomagnetic bead enrichment studies if indicated.
Milestone Fully Met

Immunize sheep with plasmid DNA expressing MVV8534 env and boost with MVV SU-FIA. Challenge immunized sheep with MVV8534.
Milestone Not Met

Complete PCR-RFLP of OvLa DRB-1 alleles.
Milestone Fully Met

3b.List the milestones that you expect to address over the next 3 years (FY 2006, 2007, and 2008). What do you expect to accomplish, year by year, over the next 3 years under each milestone?
Year 5, 6 and 7 milestones are listed below with a description of the anticipated outcomes. The entire project will be completed during FY 2006, and a new project will be developed to undergo OSQR review, and subsequent implementation beginning FY 2007.

Year 5 (FY2006)

Complete rapid scrapie test development and transfer technology.

Complete PrP genotype study in goats.

Complete sequencing of expressed OvLa MHC Class II DRB-1 alleles.

Continue oral scrapie transmission study in goats.

Potential impact: A rapid test for scrapie will facilitate diagnosis. A map of the PrP gene and the mutations for goats will aid in determining if certain genotypes are more susceptible or resistant to scrapie once challenge experiments are initiated. Characterization of the expressed OvLa MHC Class II DRB1 alleles will allow development of a rapid high-throughput system for typing sheep.

Year 6 (FY 2007)

Continue oral scrapie transmission study in goats.

Initiate experimental inoculation of OPPV into sheep with specific OvLa MHC Class II DRB-1 expressed alleles.

Develop rapid MHC Class II DRB1-1 typing tests.

Potential impact: Data on oral transmission of scrapie to goats will aid in determining the impact of goats on scrapie transmission to sheep flocks in the US. Development of a rapid MHC Class II DRB1 typing test will allow rapid screening of sheep for specific MHC Class II types followed by experimental inoculation of OPPV.

Year 7 (FY 2008)

Continue experimental inoculation of OPPV into sheep with specific OvLa MHC Class II DRB-1 expressed alleles.

Initiate TSE strain studies.

Complete oral scrapie transmission study in goats.

Potential impact: Examining strains of scrapie will aid in understanding transmission of sheep scrapie. Data on oral transmission of scrapie to goats will aid in determining the impact of goats on scrapie transmission to sheep flocks in the US. Monitoring of experimental inoculation of OPPV into sheep with specific MHC Class II DRB1 types will allow associations to be made between disease progression and specific MHC Class II DRB1 types.

4a.What was the single most significant accomplishment this past year?
We found that multiple fetuses in the uterus of a pregnant ewe have an effect on PrPSc accumulation in the placental tissue. We previously showed that if a sheep fetus has a scrapie-resistant genotype, PrPSc does not accumulate in the placenta tissue of scrapie-infected ewes. We have now found, however, the placenta tissue associated with a fetus of a scrapie-resistant genotype can accumulate PrPSc if it is positioned next to a fetus of a scrapie susceptible genotype in utero in scrapie infected ewes. This has potential impact to the sheep industry in relying on the genetics to breed for resistance to scrapie.

4b.List other significant accomplishments, if any.
When applying OPPV diagnostic tests to the field, it is necessary to identify the immunodominant antigen in OPPV-infected sheep. One publication has resulted from identifying the surface envelope glycoprotein (SU) as the B-lymphocyte immunodominant antigen in mature OPPV-infected sheep. Because the CAEV cELISA detects anti-SU antibodies, this result ensures that most mature OPPV-infected sheep will have measurable titers of anti-SU antibodies which can be detected in the CAEV cELISA This result has direct implications for the sheep industry in terms of accurate OPPV diagnostic testing using the CAEV cELISA.

Previous studies have shown that sheep with Prnp diploid genotypes of AA, QR and AA, RR at codons 136, 171, respectively, are more resistant to scrapie. However, it is unknown whether breeding toward these scrapie-resistant Prnp diploid genotypes would affect lamb production traits. ADRU is currently collaborating with University of Wyoming (5348-32000-019-03S) to show that breeding flocks toward the scrapie resistant PrP genotypes does not influence lamb production. Results of this research have yielded one publication and has impact on the sheep industry.

We previously showed that if a sheep fetus has a scrapie-resistant genotype, PrPSc does not accumulate in the placenta tissue of scrapie-infected ewes. Another question we wanted to address, which relates to sheep with scrapie-resistant Prnp diploid genotypes, is whether ewes with scrapie resistant PrP genotypes born from scrapie-infected ewes will accumulate PrPSc in their placental tissue after being bred back to a ram with a scrapie susceptible PrP genotype. In addition, ADRU and North Dakota State University (5348-32000-019-04S) are collaborating to evaluate the natural passage of scrapie through a flock with Prnp diploid genotypes at 136 of AV and VV. Since this flock is the first documented case of valine 136-based scrapie in the U.S., it is extremely important to understand the Prnp genetics of all flock mates and the transmission of valine 136-based scrapie.

4c.List any significant activities that support special target populations.

4d.Progress report.

5.Describe the major accomplishments over the life of the project, including their predicted or actual impact.
A practical live animal test for scrapie and preclinical postmortem tests for scrapie were developed and transferred to the regulatory agencies for use in the US. Monoclonal antibodies useful in assays on routinely formalin fixed tissue from infected sheep, deer, elk, cattle, humans, mink, domestic cats and a wide variety of captive wildlife potentially exposed to prion diseases were developed. Mechanisms for preventing transmission of scrapie through genetic selection of sires were demonstrated. Along with sire testing, genetic testing in bred ewes will ensure less transmission of scrapie from ewe to lamb.

The specific immune cells in lymph nodes involved in PrPSc accumulation remain unknown. Therefore, we analyzed lymph nodes for the presence of PrPSc and macrophage or follicular dendritic cell (FDC) markers using dual immunohistochemistry. Results indicated that lymph node follicular macrophages acquire PrPSc by phagocytosis of CD21+ FDC processes and process full-length PrPSc to N-terminally truncated PrPSc. These data provide the first knowledge in determining the pathogenesis of sheep scrapie in FDC and macrophages.

A new caprine arthritis-encephalitis virus (CAEV) competitive inhibition enzyme-linked immunosorbent assay (cELISA) had previously been developed. We tested 200 goat sera for the presence of CAEV antibodies using cELISA against the standard of comparison, immunoprecipitations (IP) of [S35] methionine-labeled CAEV lysate. The CAEV cELISA validation resulted in 100% sensitivity and 96.4% specificity against the standard of comparison. By annually testing goats for CAEV using cELISA, a CAEV-free herd could be established.

Because of the high sensitivity and specificity of the CAEV cELISA in goats, validation of the CAEV cELISA in sheep also ensued. By using IP of [S35] methionine-labeled OPPV lysate as the comparable standard, detection of serum antibodies to ovine progressive pneumonia virus (OPPV) in sheep using the CAEV cELISA yielded a sensitivity 98.6% and a specificity of 96.9%. This indicates that one diagnostic test, the CAEV cELISA, can be utilized for detection of small ruminant lentiviruses.

When applying the CAEV cELISA diagnostic test to the field, it is necessary to identify OPPV field strains. We isolated 7 new OPPV field strains from the colostrum cells of 10 OPPV-infected sheep. We characterized and compared the surface envelope glycoprotein (SU) deduced amino acid sequences from these sheep against previously characterized OPPV, CAEV and maedi-visna virus strains. The new OPPV field strains had high sequence identity to OPPV and CAEV strains more than MVV strains. This result is important for future CAEV cELISA testing of U.S. sheep and sheep outside the U.S. infected with OPPV or MVV, respectively.

Standardized, validated diagnostic tests are needed for eradication of scrapie. In FY2001-FY2003, a cooperative ARS-APHIS-state test validation program resulted in submission of samples from more than 2,000 sheep. These samples are being used to validate the third eyelid live animal test, the postmortem immunohistochemistry test, and to develop novel rapid, high throughput tests suitable for slaughter surveillance. A panel of internationally accepted tests suitable for diagnostic and surveillance purposes will result.

Control of scrapie and the small ruminant lentiviruses (SRLV) directly benefits small farms that raise sheep and goats for supplementary income. Direct and indirect losses to these producers because of these diseases are significant. Control programs that include identification of infected flocks and animals should reduce the economic consequences of SRLV and prion diseases.

6.What science and/or technologies have been transferred and to whom? When is the science and/or technology likely to become available to the end-user (industry, farmer, other scientists)? What are the constraints, if known, to the adoption and durability of the technology products?
Two monoclonal antibodies to the prion protein and their use in combination as detection reagents for prions have been patented. Both antibodies are commercially available. Only non-exclusive licenses have been offered, to insure the widest possible use of these reagents in diagnostics, industry, and research. The antibodies are in use internationally and collaborative programs to train personnel in Canada, Mexico, and China are in progress. The preclinical test for scrapie has been transferred to the National Veterinary Services Laboratory. APHIS has established a national testing network, through which veterinary and state diagnostic laboratories will apply the technology under contract with APHIS. CAEV cELISA will be licensed and commercially available in the U.S. in 6-12 months.

7.List your most important publications in the popular press and presentations to organizations and articles written about your work. (NOTE: List your peer reviewed publications below).
1. Scrapie: Prions in the Placenta of AAQQ and AAQR sheep. Invited presentation at American Sheep Industry Convention, Reno, NV, January 28, 2005.

2. Prion accumulation in the sheep placenta / Goat scrapie genotyping project. Invited presentation at USAHA Sheep and Goat Committee, United States Animal Health Association Annual Meeting, Greensboro, NC, October 24, 2005.

3. Sheep scrapie: maternal and fetal genetics. Invited presentation at Animal Prion Diseases and the Americas, Ames, IA, October 14-16, 2005.

4. Using host immunogenetics as a prediction tool for ovine progressive pneumonia virus clinical disease. Invited presentation at the American Sheep Industry Convention, Reno, NV, January 2005.

5. Natural Sheep Scrapie: What have we learned? Invited presentation to the Department of Chemistry and Biochemistry at the University of Denver, Denver, CO, November 2004.

6. Predicting ovine progressive pneumonia virus loads using MHC Class II DRB1 immunogenetics. Invited presentation at the United States Animal Health Association Sheep and Goat Committee, Greensboro, NC, October 2004.

7. Lack of Natural Ovine Progressive Pneumonia Virus Transmission from OPPV-Infected Ewes to Their Lambs. Presentation at the Keystone Symposia HIV Pathogenesis, Banff, Canada, April 2005.

Review Publications
Alverson, J. 2005. Data sheet for scrapie. Animal Health and Production Compendium. Available:

Alexander, B.M., Stobart, R.H., Russell, W.C., Orourke, K.I., Lewis, G.S., Logan, J.R., Duncan, J.R., Moss, G.E. 2005. The incidence of genotypes at codon 171 of the prion protein gene (prnp) in five breeds of sheep and production traits of ewes associated with those genotypes. Journal of Animal Science. 83(2):455-459.

Herrmann, L.M., Mcguire, T.C., Hotzel, I., Lewis, G.S., Knowles Jr, D.P. 2005. Surface envelope glycoprotein is b-lymphocyte immunodominant in sheep naturally infected with ovine progressive pneumonia virus. Clinical and Diagnostic Laboratory Immunology. 12(6):797-800.

Herrmann, L.M. 2005. Needles: To Re-use or Not to Re-use?. Sheep Industry News. 9(5):2.

Johnson, M.L., Evoniuk, J.M., Stoltenow, C.L., Orourke, K.I., Redmer, D.A. 2005. Development of an assay to determine single nucleotide polymorphisms (snp) in the prion gene for the diagnosis of genetic susceptibility to scrapie in sheep. American Society of Animal Science. 56:151.

Evoniuk, J.M., Stoltenow, C.L., O'Rourke, K.I., Moore, B.L., Redmer, D.A. 2005. Assessment of the genetic risk and impact of lateral transmission in a valine-associated scrapie outbreak in sheep. American Journal of Veterinary Research. 66(8):1-6.


NOTICE CWD creeping its way to TEXAS, literally to it's border. ...

THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare to the other sample locations ;

THREE NEW CASES OF CWD were announced in this same location this month ;



SANTA FE - Three deer in southern New Mexico have tested positive for chronic wasting disease, bringing the total number of confirmed CWD-infected deer in the state to 15 since the first infected deer was discovered in 2002.

The Department received test results Wednesday from the state Veterinary Diagnostic Services laboratory in Albuquerque that two wild deer captured near the White Sands Missile Range headquarters east of Las Cruces had tested positive for chronic wasting disease. A third wild deer captured in the small community of Timberon in the southern Sacramento Mountains also tested positive for the disease.

The discoveries of the infected deer were part of the Department's ongoing efforts to monitor the disease, which to date has been confined to the southern Sacramento Mountains southeast of Cloudcroft and areas surrounding the Organ Mountains near Las Cruces. Two wild elk from the southern Sacramento Mountains tested positive for the disease in December 2005.

Chronic wasting disease is a fatal neurological illness that afflicts deer, elk and moose. There is no evidence of CWD being transmitted to humans or livestock. The disease causes animals to become emaciated, display abnormal behavior and lose control of bodily functions. To date, it has been found in captive and wild deer, elk and moose in eight states and two Canadian provinces.

For more information about CWD in New Mexico and how hunters can assist in research and prevention, please visit the New Mexico Department of Game and Fish Web site, . More information about CWD also can be found on the Chronic Wasting Disease Alliance site at .




Suppressed peer review of Harvard study October 31, 2002 [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of BovineSpongiform Encephalopathy (BSE) USDA Testing Protocols and Quality Assurance Procedures In November 2004, USDA announced that its rapid screening test produced an inconclusive BSE test result. A contract laboratory ran its rapid screening test on a brain sample collected for testing and produced three high positive reactive results. As required, the contract laboratory forwarded the inconclusive sample to APHIS’ National Veterinary Services Laboratories (NVSL) for confirmation. NVSL repeated the rapid screening test, which again produced three high positive reactive results. Following established protocol, NVSL ran its confirmatory test, an immunohistochemistry (IHC) test, which was interpreted as negative for BSE. Faced with conflicting results between the rapid screening and IHC tests, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded that no further testing was necessary since testing protocols were followed and the confirmatory test was negative. In our discussions with APHIS officials, they justified their decision to not do additional testing because the IHC test is internationally recognized as the "gold standard" of testing. Also, they believed that USDA/OIG-A/50601-10-KC/ Page iv conducting additional tests would undermine confidence in USDA’s testing protocols. OIG obtained evidence that indicated additional testing was prudent. We came to this conclusion because the rapid screening tests produced six high positive reactive results, the IHC tests conflicted, and various standard operating procedures were not followed. Also, our review of the relevant scientific literature, other countries’ protocols, and discussions with experts led us to conclude that additional confirmatory testing should be considered in the event of conflicting test results. To maintain objectivity and independence, we requested that USDA’s Agricultural Research Service (ARS) perform the Office International des Epizooties (OIE) Scrapie-Associated Fibrils (SAF) immunoblot test. The additional testing produced positive results. To confirm, the Secretary of Agriculture requested that an internationally recognized BSE laboratory in Weybridge, England (Weybridge) perform additional testing. Weybridge conducted various tests, including their own IHC tests and three Western blot tests. The tests confirmed that the cow was infected with BSE. The Secretary immediately directed USDA scientists to work with international experts to develop new protocols that include performing dual confirmatory tests in the event of an inconclusive BSE screening test. We attribute the failure to identify the BSE positive sample to rigid protocols, as well as the lack of adequate quality assurance controls over its testing program. Details of our concerns are discussed in Findings 3 and 4. snip...Section 2. Testing Protocols and Quality Assurance Controls In November 2004, USDA announced that its rapid screening test, Bio-Rad Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test result as part of its enhanced BSE surveillance program. The ELISA rapid screening test performed at a BSE contract laboratory produced three high positive reactive results.40 As required,41 the contract laboratory forwarded the inconclusive sample to the APHIS National Veterinary Services Laboratories (NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again produced three high positive reactive results.42 In accordance with its established protocol, NVSL ran its confirmatory test, an immunohistochemistry (IHC) test, which was interpreted as negative for BSE. In addition, NVSL performed a histological43 examination of the tissue and did not detect lesions44 consistent with BSE. Faced with conflicting results, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded no further testing was necessary because testing protocols were followed. In our discussions with APHIS officials, they justified their decision not to do additional testing because the IHC is internationally recognized as the “gold standard.” Also, they believed that conducting additional tests would undermine confidence in USDA’s established testing protocols. However, OIG obtained evidence that indicated additional testing was prudent to ensure that USDA’s testing protocols were effective in detecting BSE and that confidence in USDA’s testing procedures was maintained. OIG came to this conclusion because the rapid tests produced six high positive reactive results, confirmatory testing conflicted with the rapid test results, and various standard operating procedures were not followed. Also, our review of scientific literature, other country protocols, as well as discussions with internationally recognized experts led us to conclude that confirmatory testing should not be limited when conflicting test results are obtained. To maintain objectivity and independence in our assessment, we requested the USDA Agricultural Research Service (ARS) perform the Office International des Epizooties (OIE) Scrapie-Associated Fibrils (SAF) 40 ELISA test procedures require two additional (duplicate) tests if the initial test is reactive, before final interpretation. If either of the duplicate tests is reactive, the test is deemed inconclusive. 41 Protocol for BSE Contract Laboratories to Receive and Test Bovine Brain Samples and Report Results for BSE Surveillance Standard Operating Procedure (SOP), dated October 26, 2004. 42 The NVSL conducted an ELISA test on the original material tested at the contract laboratory and on two new cuts from the sample tissue. 43 A visual examination of brain tissue by a microscope. 44 A localized pathological change in a bodily organ or tissue.immunoblot.45 ARS performed the test at the National Animal Disease Center because NVSL did not have the necessary equipment46 (ultracentrifuge) to do the test. APHIS scientists observed and participated, as appropriate, in this effort. The additional tests conducted by ARS produced positive results. To confirm this finding, the Secretary requested the internationally recognized BSE reference laboratory in Weybridge, England, (Weybridge) to perform additional confirmatory testing. Weybridge conducted various tests, including their own IHC methods, as well as three Western blot methods. The tests confirmed that the suspect cow was infected with BSE. Also, Weybridge confirmed this case as an unequivocal positive case of BSE on the basis of IHC. As a result of this finding, the Secretary immediately directed USDA scientists to work with international experts to develop a new protocol that includes performing dual confirmatory tests in the event of another inconclusive BSE screening test. Finding 3 Rigid Protocols Reduced the Likelihood BSE Could be Detected APHIS relied on a single test method, as well as a histological examination of tissue for lesions consistent with BSE, to confirm the presence of BSE even though discrepant test results indicated further testing may be prudent. When IHC test results were interpreted as negative, APHIS concluded the sample tested negative for BSE. Subsequent independent tests initiated by OIG using a different testing method, as well as confirmatory testing by Weybridge, determined that the suspect sample was a positive case of BSE. APHIS Declares BSE Sample Negative Despite Conflicting Results When the tissue sample originally arrived at NVSL in November 2004 from the contract lab, NVSL scientists repeated the ELISA screening test and again produced three high positive reactive results. NVSL scientists cut out two sections of the brain sample for IHC testing. One section was used for an experimental procedure that was not part of the confirmatory testing protocol, and the other cut was for normal IHC testing using scrapie for a positive control.47 According to NVSL scientists, the experimental test results were inconclusive but the IHC test was interpreted as negative. The NVSL scientists were concerned with the inconsistencies and conducted 45 The OIE SAF immunoblot is an internationally recognized confirmatory test, often referred to as a Western blot test. There are different types of Western blots; the OIE SAF immunoblot includes enrichment steps taken with the sample prior to the standard Western blot steps. 46 APHIS has now ordered the necessary equipment for NVSL. USDA/OIG-A/50601-10-KC Page 3247 A positive control is a sample that is known to contain a given disease or react in the test. The sample then can be used to make sure that the test for that disease works properly. In the case of BSE, tissue infected with either scrapie or BSE can serve as a positive control for an IHC test for BSE since both are different forms of the same disease (transmissible spongiform encephalopathy or TSE).another IHC test using BSE as a positive control.48 The test result was also interpreted as negative. Also, according to the NVSL scientists, the histological examination of the tissue did not detect lesions consistent with BSE. After the second negative IHC test, NVSL scientists supported doing additional testing. They prepared a plan for additional tests; if those tests had been conducted, BSE may have been detected in the sample. The additional tests recommended by NVSL scientists, but not approved by APHIS Headquarters officials, were the IHC using other antibodies (IHC testing using different antibodies ultimately produced positive results); IHC testing of additional regions of the brain (the cerebellum tested positive); regular and enriched (OIE-like) Western blots (the obex and cerebellum tested positive); and variable rapid tests (the obex and cerebellum tested positive with two different rapid tests). NVSL officials also recommended that the sample be sent to Weybridge for confirmatory testing (to conduct IHC and OIE Western blot tests). In June 2005, Weybridge conducted IHC testing with three different antibodies, including the antibody used in the United States (tested positive), the OIE Western blot (tested positive), a modified commercial kit Western blot (negative) and the NaPTA49 Western blot (tested positive). We obtained information as to the differing protocols used by other countries. We found that while APHIS determined that additional testing was unnecessary after the IHC test, other countries have used multiple tests to confirm positives. In Japan, for example, all reactive screening test samples are examined by both IHC and a Western blot (different from the OIE SAF immunoblot). In the United Kingdom (U.K.), IHC and Western blot (different from the OIE SAF immunoblot) tests are used for all animals that test positive with a screening test. When IHC and the Western blot fail to confirm a positive rapid test, the U.K. resorts to a third test, the OIE SAF immunoblot. With these procedures in place, both Japan and the U.K. have found BSE cases that were rapid test reactive, IHC negative, and finally confirmed positive with a Western blot. Evidence Indicated Additional Testing Would Be Prudent We also spoke with an internationally recognized BSE expert regarding the advisability of limiting confirmatory testing when conflicting results are obtained. This official expressed concern about limiting confirmatory tests to the IHC despite its status as one of the “gold standard” tests. He advised that the IHC is not one test; it is a test method that can vary significantly in sensitivity from laboratory to laboratory. New antibodies can improve orUSDA/OIG-A/50601-10-KC Page 3348 The NVSL uses scrapie as the positive control as part of its normal IHC testing procedures. Due to the conflicting results between the ELISA and IHC tests, the NVSL conducted another IHC test with BSE as the positive control. Subsequently, the NVSL modified the Confirming Inconclusive Results from BSE Testing Laboratories at the NVSL SOP to show that all IHC tested BSE inconclusive samples from contract laboratories will use BSE as the positive control. 49 Sodium phosphotungstic acid.USDA/OIG-A/50601-10-KC Page 34reduce sensitivity, as can variations in many of the reagents50 used. He explained that his laboratory had experienced cases where an initial confirmatory IHC test was challenged by either a more extensive IHC test or “…applying a more sensitive immunoblot.” He emphasized the importance of having additional confirmatory testing to resolve discrepant results since there are many variables, and most of the variability appears to be due to test performance of the laboratory. OIG became concerned that APHIS relied on its confirmatory test methods when rapid screening tests produced high positive reactive results six times.51 Also, we found that APHIS did not pursue and/or investigate why the ELISA produced high reactive positives. An official from the manufacturer of the ELISA test kit told us that they requested, but did not receive, information on the inconclusive reported by USDA in November 2004. These officials requested this information in order to understand the reasons for the discrepant results. The Bio-Rad ELISA rapid screening test is internationally recognized as a highly reliable test and is the rapid screening test used for USDA’s surveillance effort. According to APHIS officials, they felt it would be inappropriate to collaborate on the one sample because Bio-Rad is a USDA-APHIS regulated biologics company and only one of several competing manufacturers. To maintain confidence in USDA’s test protocols, it would have been a prudent course of action for USDA to determine why such significant differing results were obtained. The fact that they did not pursue this matter caused concerns relating to testing quality assurance procedures. In this regard, we found lack of compliance with SOPs relating to laboratory proficiency and quality assurance (see Finding 4), and, in this case, the storage of sampled material and reporting of test results. We found that the NVSL did not prepare a report to document its confirmatory testing of the November 2004 sample. The SOP52 states that the BSE network laboratory initiating the inconclusive will receive a report of the case. NVSL officials could not explain why a final report had not been prepared. We also found that the inconclusive sample was frozen prior to IHC confirmatory testing. APHIS protocols state that samples are not to be frozen prior to laboratory submission. The OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals states that the tissues for histological or IHC examination are not to be frozen as this will provide artefactual53 lesions that may compromise the identification of vacuolation,54 and/or target site location. Although the sample was frozen, APHIS did not conduct a Western 50 A substance used in a chemical reaction to detect, measure, examine, or produce other substances. 51 The six high positive reactive results were from three tests of the submitted sample (multiple runs of the same test). 52 Confirming Inconclusive Results from Bovine Spongiform Encephalopathy Testing Laboratories at the NVSL SOP, dated August 13, 2004. 53 A structure or feature not normally present but visible as a result of an external agent or action, such as one seen in a microscopic specimen after fixation. 54 A small space or cavity in a tissue.USDA/OIG-A/50601-10-KC Page 35blot test on the sample. An NVSL official said freezing the sample does not make it unsuitable for IHC. APHIS determined that the sample was suitable for IHC and therefore, in accordance with its SOP, did not conduct a Western blot test. APHIS also handled the December 2003 BSE positive differently than the November 2004 sample. For the December 2003 BSE positive sample, APHIS conducted several confirmatory tests in addition to the IHC testing and histological examination (unlike the November 2004 sample tests, both of these were interpreted as positive). ARS performed two Western blots (Prionics Check Western blot and an ARS developed Western blot). When we questioned why the samples were handled differently, APHIS officials stated that the Western blots were done because the IHC in December 2003 was positive. The additional testing was done to further characterize the case, because it was the first U.S. case; the additional testing was not done to decide whether the case was positive or negative. We discussed our concerns with limiting confirmatory testing, particularly given conflicting results, with the APHIS Administrator and staff in May 2005. He explained that international standards recognized more than one “gold standard” test. In setting up its testing protocols, USDA had chosen one as the confirming test, the IHC test, and stayed with it. APHIS protocols only allow a Western blot in cases where the sample has become unsuitable for IHC tests (e.g., in cases where the brainstem architecture is not evident). International standards, he continued, accept a tissue sample as negative for BSE if its IHC test is negative. Once the test is run in accordance with protocols, additional tests undermine the USDA testing protocol and the surveillance program. He concluded that since APHIS’ protocols accepted the IHC test as confirming the presence or absence of BSE, no further testing was necessary. According to protocol, the tissue sample was determined to have tested negative for BSE. On June 24, 2005, USDA announced that the additional testing by the BSE reference laboratory in England confirmed the presence of BSE in the tissue sample. To obviate the possibility that a future sample would be declared negative and then found positive, the Secretary of Agriculture announced a change to APHIS’ testing protocols that same day. He called for “dual confirmatory tests in the event of another ‘inconclusive’ [reactive] BSE screening test.” He also indicated that he would reinforce proper procedures so that samples will not be frozen, and to spot-check the laboratories to see that they complete reports as required. APHIS issued a SOP on the new confirmatory testing protocols on November 30, 2005. contamination of dairy feeds with ruminant derived meat and bone meal. FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS The feed was manufactured from materials that may have been contaminated with mammalian protein. RECALL MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants". RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006 THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ; CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006 The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade. The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old. These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen. "The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that." Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive. USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general. "Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ... December 20,2005 Division of Dockets Management (HFA-305) Food and Drug Administration 5630 Fishers Lane Room 1061 Rockville, MD 20852 Re: Docket No: 2002N-0273 (formerly Docket No. 02N-0273) Substances Prohibited From Use in Animal Food and Feed Dear Sir or Madame: As scientists and Irecognized experts who have worked in the field of TSEs for decades, we are deeply concerned by the recent discoveries of indigenous BSE infected cattle in North America and appreciate the opportunity to submit comments to this very important proposed rule We strongly supported the measures that USDA and FDA implemented to protect public health after the discovery of the case of bovine spongiform encephalopathy (BSE) found in Washington State in 2003. We know of no event or discovery since then that could justify relaxing the existing specified risk material (SRM) and non-ambulatory bans and surveillance that were implemented at that time. Further, we strongly supported the codification of those changes, as well as additional measures to strengthen the entire feed and food system. The discovery of additional cases of indigenous BSE in North America since that time has validated our position and strengthened OUT convictions. We caution against using the 18 month enhanced surveillance as a justification to relax or impede further actions. While this surveillance has not uncovered an epidemic, it does not clear the US cattle herd from infection. While it is highly likely that US and Canadian cattle were exposed to BSE prior to the 1997 feed ban, we do not know how many cattle were infected or how widely the infection was dispersed. BSE cases are most likely clustered in time and location, so while enhanced surveillance provides an 18 month snapshot, it does uot negate the fact that US and Canadian cattle were exposed to BSE. We also do not know in any quantitative or controlled way how effective the feed ban has been, especially at the farm level. At this point we cannot even make a thorough assessment of the USDA surveillance as details such as age, risk category and regional distribution have not been released. see full text 18 pages ; [GAO-05-101 ] Mad Cow Disease: FDA's Management of the Feed Ban Has Improved, but Oversight Weaknesses Continue to Limit Program Effectiveness Size: 104986 , Score: 1000 , TEXT , PDF , SUMMARY [2] [GAO-05-101 ] Mad Cow Disease: FDA's Management of the Feed Ban Has Improved, but Oversight Weaknesses Continue to Limit Program Effectiveness Size: 104986 , Score: 1000 , TEXT , PDF , SUMMARY [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle 03-025IFA 03-025IFA-2 Terry S. Singeltary Subject: Substances Prohibited from Use in Animal Food or Feed, Proposed Rule, Docket No. 2002N-0273 C-534 VOL 45 (PhRMA) and Entered On February 17, 2006 Date: March 10, 2006 at 5:23 pm PST Marie A. Vodicka, PhD Assistant Vice President Biologics & Blotechnology Scientlflc & Regulatory Affairs SCIENCE & REG AFFAIRS Division of Dockets Management (HFA-305) Food and Drug Administration 5630 Fishers Lane, rrn . 1061 Rackville, MD 20862 Re: Substances Prohibited from Use in Animal Food or Feed, Proposed Rule, Docket No. 2002N-0273 February 14, 2006 Dear Sir or Madam : The Pharmaceutical Research and Manufacturers of America (PhRMA) is providing comment to the proposed rules issued. ...... snip... Subject: Docket No: 2002N-0273 (formerly Docket No. 02N-0273) Substances Prohibited From Use in Animal Food and Feed PAUL BROWN Date: January 20, 2006 at 9:31 am PST December 20,2005 Division of Dockets Management (HFA-305) Food and Drug Administration 5630 Fishers Lane Room 1061 Rockville, MD 20852 Re: Docket No: 2002N-0273 (formerly Docket No. 02N-0273) Substances Prohibited From Use in Animal Food and Feed Dear Sir or Madame: As scientists and Irecognized experts who have worked in the field of TSEs for decades, we are deeply concerned by the recent discoveries of indigenous BSE infected cattle in North America and appreciate the opportunity to submit comments to this very......... snip... Given that BSE can be transmitted to cattle via an oral route with just .OO1 gram of infected tissue, it may not take much infectivity to contaminate feed and keep the disease recycling. ........ THE SEVEN SCIENTIST REPORT *** Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle 03-025IFA 03-025IFA-2 Terry S. Singeltary 9/13/2005 Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission) Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION] Docket Management Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -10 Accepted - Volume 2 PART 2
BOOK RELEASE PARTY - Linda Faillace's MAD SHEEP WERE THE FINAL RESULTS OF THOSE MOUSE BIO-ASSAYS OF THOSE SAMPLES FROM THE MAD SHEEP OF MAD RIVER VALLEY ???>> -------- Original Message -------->> Subject: re-85th Meeting of SEAC - 30.11.04>> Date: Tue, 21 Dec 2004 16:56:55 -0000>> From: "Barlow, Tom (SEAC)">> To: "''">>>>>>>> Dear Mr Singeltary>>>> Thank you for you enquiry to the SEAC secretariat about mouse bioassays>> commissioned by the USDA to investigate TSE cases in imported sheep.>>> After making a number of enquiries, it appears that Defra were not>> involved>> with this work. However, it is possible that a UK research>> laboratory was>> contacted by the USDA about such tests but I have been unable to find>> out>> any further information. You may wish to make further enquiries with>> the>> USDA.>>>> Yours sincerely>>>> Tom Barlow>>>> Dr Tom Barlow>> Spongiform Encephalopathy Advisory Committee (SEAC) Secretariat>> Area 108, 1A Page Street, London SW1P 4PQ>>>> Tel: 0207 904 6267>> -----Original Message----->> From: Terry S. Singeltary Sr. []>> Sent: 02 December 2004 20:19>> To: Dale, Tabitha J (SEAC)>> Subject: re-85th Meeting of SEAC - 30.11.04>>>>>> Hello Tabitha,>>>> A kind greetings from Texas.>>>> I had signed up for the meeting and wanted to ask a>> question, but it took>> me too long to finally get everything working properly on my>> end with>> the viewing. finally got things going today and got into the>> audio of the>> meeting (will have to download an upgrade for my windows>> media).>>>> ASIDE from the disturbing points made about sCJD not being>> tied>> to BSE from some unpublished mouse bioassays (if i heard>> that right)>> and the fact that they still today base the increase of>> sporadic CJD in>> known BSE countries as a happenstance of better>> surveillance, I wish>> to kindly ask a question not pertaining to the above, as>> disturbing as>> it is (lost my mother to the hvCJD 12/14/97) and i simply>> have never>> accepted the spontaneous/sporadic aspects of this agent in>> 85%+ of>> all humans. never will, it's a pipe dream thought up in some>> back room>> in the 80s to protect the industries involved (my opinion).>>>> MY question is one about the VERMONT USA SHEEP that were>> imported to the USA from Belgium and confiscated by the USDA>> several>> years ago due to an atypical TSE, with the announcement that>> mouse studies would be immediately started. I was informed by>> Dr.>> Linda Detwiler that it>> was DEFRA that was responsible for these mouse studies being>> put on hold>> for 2 years. WHY were such important studies put off for 2>> years by DEFRA?>>>> HERE is my correspondence with Dr. Detwiler;>>>> Release No. 0141.02>>>> Ed Curlett (301) 734-3256>> Jerry Redding (202) 720-6959>>>>>> TESTING TO CONTINUE ON IMPORTED SHEEP CONFISCATED LAST YEAR>>>>>> WASHINGTON, April 11, 2002 -- The U.S. Department of>> Agriculture today announced that tests conducted on a flock>> of sheep>> confiscated last year from a farm in Vermont confirm that two>> of the 125 sheep>> tested positive for an atypical undifferentiated>> transmissible spongiform>> encephalopathy (TSE) of foreign origin. The flock of 125>> sheep was>> confiscated in March 2001 after four animals from an>> associated flock tested>> positive for TSE in July 2000. USDA will continue to conduct>> additional tests>> to determine the type of TSE in these sheep.>>>> "These results confirm our previous conclusions were correct>> and that we took the appropriate preventative actions in>> confiscating>> these animals," said Bobby Acord, administrator of USDA s Animal>> and Plant Health Inspection Service. "USDA s actions to>> confiscate,>> sample and destroy these sheep were on target. As a result of>> our>> vigilance, none of these confiscated animals entered the>> animal or human>> food supply.">>>> The sheep, imported from Belgium and the Netherlands in>> 1996, were placed under certain federal restrictions when>> they entered>> the country as part of USDA's scrapie control efforts. In>> 1998, USDA>> learned that it was likely that sheep from Europe were>> exposed to feed>> contaminated with bovine spongiform encephalopathy. At that>> time, the state of>> Vermont, at the request of USDA, imposed a quarantine on>> these flocks,>> which prohibited slaughter or sale for breeding purposes.>>>> On July 10, 2000, several sheep from the flock tested>> positive for a TSE, a class of degenerative neurological>> diseases that is>> characterized by a very long incubation period and a 100>> percent mortality>> rate in infected sheep. Two of the better known varieties of>> TSE are>> scrapie in sheep and BSE in cattle. There is no evidence that>> scrapie>> poses a risk to human health.>>>> On July 14, 2000, USDA issued a declaration of extraordinary>> emergency to acquire the sheep. This action was contested by>> the flock>> owners. A federal district court judge ruled in favor of USDA>> based on>> the merits of the case. The flock owners appealed to the>> Second Circuit>> Court requesting a stay, which was denied. The sheep were>> confiscated by USDA in March 2001 and transported to USDA's>> National Veterinary>> Services Laboratories in Ames, Iowa, where they were humanely>> euthanized. Tissue samples were collected from the sheep for>> diagnostic testing>> and USDA will continue with additional tests which could take>> up to 2>> - 3 years to complete. In all, USDA has acquired 380 sheep>> from a>> total of three flocks. All of the animals were humanely>> euthanized, sampled>> and disposed and did not enter the animal or human food supply.>>>> Our goal continues to be to prevent, detect and eradicate>> foreign animal diseases to protect American agriculture,>> natural resources>> and consumers," said Acord. "We will continue to utilize the>> scientific results of these and other tests conducted during>> the last>> several years to strengthen our extensive surveillance,>> monitoring and>> prevention efforts.">>>> For more information about USDA s ongoing surveillance,>> monitoring and prevention efforts as it relates to this>> situation, please>> visit>>>>>> #>>>>>> NOW, June 2004 those same test that we were told would start>> in>> 2002, have yet to be started. THE TSE those VERMONT sheep>> was supposedly to have had, has yet to be confirmed.>>>> WHY?>>>> Correspondence from Dr. Detwiler to me;>>>> -------- Original Message -------->> Subject: Sheep>> Date: Sat, 12 Jun 2004 14:26:04 EDT>> From: xxxxxxxxx>> To:>>>>>>>> Mr. Singeltary.>>>> I hope this finds you well. As you are aware I left the>> USDA last>> year. I can only update you on the sheep before that time.>> Contact was>> established with the UK on doing the bioassay studies. They>> agreed.>> However, we were prioritized after their own needs, hence>> the delay. I>> am aware that there are now additional labs in Europe>> running the mouse>> bioassay strain typing. You will have to contact USDA for>> further word.>>>>>> Linda Detwiler>> =========>>
> > -------- Original Message --------> > Subject: Re: hello Dr. Sutton...question please...scrapie...TSS> > Date: Thu, 20 May 2004 14:36:09 -0400> > From:> > To:>>> snip...>>> FULL TEXT AND THREAD BETWEEN TSS, MAFF, USDA AND DR. DETWILER HERE ;

Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


Volume 3, Number 8 01 August 2003


Tracking spongiform encephalopathies in North America

Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost

my mom to hvCJD (Heidenhain variant CJD) and have been searching for

answers ever since. What I have found is that we have not been told the

truth. CWD in deer and elk is a small portion of a much bigger problem...

he complained in a letter to the Journal of the American Medical

Association (JAMA 2003; 285: 733). I hope that the CDC does not

continue to expect us to still believe that the 85% plus of all CJD

cases which are sporadic are all spontaneous, without route or source.<<<

actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...

Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.





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

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