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From: Terry S. Singeltary Sr. (
Subject: Re: Case of BSE in a goat confirmed: Commission extends testing programme
Date: January 29, 2005 at 8:14 am PST

In Reply to: Re: Case of BSE in a goat confirmed: Commission extends testing programme posted by TSS on January 28, 2005 at 8:11 am:

-------- Original Message --------
Subject: Re: Case of BSE in a goat confirmed: Commission extends testing programme
Date: Fri, 28 Jan 2005 21:32:35 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
References: <> <>

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

Greetings list members,

> The level of TSE infection in goats seems however to be extremely low
> and any possible risk to consumers is minimal.

IS this assessment based on true science or Gov. PR science?

FROM what i have been told, the goat prion protein sequence is fairly
different from cow, so no one has any idea of what the species barrier
would be, tissue distribution infectivity, infectivity in milk or
cheese, (if any) or whether it would primarily
transmit to met met or equally to val val. fact is no one really knows
yet. why do they continue to claim things with which
they have no scientific data to back it up with, while continuing to
ignore other data.

goat/cow are identical at 247/256 amino acid positions, ie different at 8

>Capra hircus (goat)




>Bos taurus (cow)








COMPARISION of goat and cow a

Identities = 247/256 (96%), Positives = 252/256 (98%)







goat to human

Identities = 227/253 (89%), Positives = 246/253 (97%)






cow to human

Identities = 233/261 (89%), Positives = 249/261 (95%)








> Markos Kyprianou, EU Commissioner responsible for Health and Consumer
> Protection, said “I want to reassure consumers that existing safety
> measures in the EU offer a very high level of protection.

I firmly dispute this, for whatever that is worth.

JUST echos of the past.

WITH BABs still showing up, feed ban was ignored there as well.

WHO knows if it was not lateral or vertical transmission of BSE to GOAT?

Environmental Sources of Prion Transmission in Mule Deer

Michael W. Miller,*Comments
Elizabeth S.
Williams,† N. Thompson Hobbs,‡ and Lisa L. Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; †University
of Wyoming, Laramie, Wyoming, USA; and ‡Colorado State University, Fort
Collins, Colorado, USA


Our findings show that environmental sources of infectivity may
contribute to CWD epidemics and illustrate the potential complexity of
such epidemics in natural populations. The relative importance of
different routes of infection from the environment cannot be discerned
from our experiment, but each could play a role in sustaining natural
epidemics. Although confinement likely exaggerated transmission
probabilities, conditions simulated by this experiment do arise in the
wild. Mule deer live in established home ranges and show strong fidelity
to historic home ranges (24-26
). As a result of
such behavior, encounters with contaminated environments will occur more
frequently than if deer movements were random. Feces and carcass remains
are routinely encountered on native ranges, thus representing natural
opportunities for exposure. Social behavior of deer, particularly their
tendency to concentrate and become sedentary on their winter range, also
may increase the probability of coming into contact with sources of
infection in their environment.

The ability of the CWD agent to persist in contaminated environments for
>2 years may further increase the probability of transmission and
protract epidemic dynamics (8
). Because
infectivity in contaminated paddocks could not be measured, neither the
initial levels nor degradation rate of the CWD agent in the environment
was estimable. However, the observed persistence of the CWD agent was
comparable to that of the scrapie agent, which persisted in paddocks for
?1 to 3 years after removal of naturally infected sheep (7
). Similarities
between the CWD and scrapie agents suggest that environmental
persistence may be a common trait of prions. Whether persistence of the
BSE prion in contaminated feed production facilities or in environments
where cattle reside contributed to BSE cases in the United Kingdom after
feed bans were enacted (27
) remains
uncertain but merits further consideration.

Indirect transmission and environmental persistence of prions will
complicate efforts to control CWD and perhaps other animal prion
diseases. Historically, control strategies for animal prion diseases
have focused on infected live animals as the primary source of
infection. Although live deer and elk represent the most plausible
mechanism for geographic spread of CWD, our data show that environmental
sources could contribute to maintaining and prolonging local epidemics,
even when all infected animals are eliminated. Moreover, the efficacy of
various culling strategies as control measures depends in part on the
rates at which the CWD agent is added to and lost from the environment.
Consequently, these dynamics and their implications for disease
management need to be more completely understood.


HOWEVER, we do know this ;

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

Corinne Ida Lasmézas*,dagger
, Jean-Guy
Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François
Lamoury*, Nicolas KoppDagger , 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; Dagger
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)


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.

Transmission of vCJD and BSE to Nonhuman Primates. vCJD transmitted
readily to the cynomolgus macaque after 2 years of incubation, which was
comparable to the transmission obtained from first-passaged macaque BSE
and much shorter than the interspecies transmission of BSE. Starting
with 100 mg of BSE-macaque brain material, dilutions up to 4 µg still
provoked disease. These data suggest that the BSE agent rapidly adapts
to primates accompanied by enhanced virulence.

Examination of macaque brain inoculated with vCJD revealed a similar
pathology to that with second-passage BSE. The distribution of
vacuolation and gliosis, as well as the pattern of PrP deposition,
including the dense, sometimes florid plaques, were similar to the human
vCJD and the BSE hallmarks of the first passage (1
, 2
). These data show
that the phenotype of BSE in primates is conserved over two passages.
Moreover, they confirm that the BSE agent behaves similarly in humans
and macaques, a precious finding that will prove useful in the near
future for the design of pathogenesis or therapeutic studies. Because of
the number of macaques examined in this study, we can now reliably state
that the pathology, in particular the PrP deposition pattern provoked by
BSE, is similar in older and very young animals. However, plaque
deposition is greater, and mature florid plaques were more numerous, in
the young, which may be correlated with a longer duration of the
clinical phase observed in this animal (2
). This is
important with regard to the fact that vCJD has been diagnosed mainly in
teenagers and young adults, which raises the concern that older patients
may have been misdiagnosed because of an alternative phenotype of the
disease. One should bear in mind, however, that cynomolgus macaques are
all homozygotes for methionine at codon 129 of the PrP gene. Thus, our
observations may not be relevant to humans carrying one or both valine
alleles; however, all patients with vCJD reported to date have been M/M
at this position (27

Intravenous Transmissions to Nonhuman Primates. Brain pathology was
identical in macaques inoculated i.c. and i.v. The i.v. route proved to
be very efficient for the transmission of BSE, as shown by the 2-year
survival of the animals, which is only 5 months longer than that
obtained after inoculating the same amount of agent i.c. As the i.v.
injection of the infectious agent implies per se a delayed neuroinvasion
compared with a direct inoculation in the brain, this slight lengthening
of the incubation period cannot, at this stage, be interpreted as a
lower efficiency of infection as regards the i.c. route.

These data should be taken into account in the risk assessment of
iatrogenic vCJD transmission by i.v. administration of biological
products of human origin. They also constitute an incentive for a
complete i.v. titration.

From BSE and vCJD transmissions in nonhuman primates, a number of
conclusions can be drawn that are of major importance for human health:
(i) human-adapted BSE appears to be a variant of the BSE agent that is
more virulent for humans than cattle BSE and is efficiently transmitted
by the peripheral route; (ii) the detection of vCJD in unusually young
patients is probably not because of a lack of diagnosis of cases in
older patients, thus raising the question of the source of human
contamination with BSE early in life; and (iii) iatrogenic transmissions
from patients with vCJD would be readily recognized by using the same
diagnostic criteria as those applied to vCJD [clinical and pathological
criteria (27 )
comprising neuronal loss and gliosis in the thalamus correlated with
high MRI signal (28
, 29
)], whether such
contaminations had occurred by the central or i.v. route. Primary and
iatrogenic cases of vCJD could be distinguished on the basis of the
patient's clinical history.

The risk assessment of biological products of human origin, notably
those derived from blood, has been deeply modified by the appearance of
vCJD. We confirm that the BSE agent has contaminated humans not only in
the U.K. and the Republic of Ireland but also in France, and we show
that its pathogenic properties for primates are being enhanced by a
primary passage in humans. Considering the flow of potentially
contaminated bovine-derived products between 1980 and 1996, it is
obvious that further vCJD cases may occur outside the U.K. Thus, and in
the light of the present study, it is necessary to sustain worldwide CJD
surveillance regardless of national BSE incidence and to take all
precautionary measures to avoid iatrogenic transmissions from vCJD.


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

PMID: 6997404

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?


Terry S. Singeltary Sr. wrote:

> ##################### Bovine Spongiform Encephalopathy
> #####################
> Progress report on actions from the meeting on 25th
> November, 2004, Rue Froissart.
> Report drafted by Marion Simmons and John Spiropoulos using data and
> analysis supplied by VLA Weybridge, IAH (NPU) Edinburgh, AFSSA and
> Executive summary
> These investigations have been pursued by the transfer of materials from
> experimentally inoculated mice to the Veterinary Laboratories Agency
> and the
> Institute for Animal Health, for blind peer review. In addition,
> experimental
> caprine BSE was provided to AFSSA by the IAH for further Western
> immunoblotting of the suspect sample alongside appropriate controls.
> Codes for mouse brain groups were held by a third party (Professor
> Bostock)
> so that all examinations at the VLA and IAH were blinded. Results were
> reported to Professor Bostock, who broke the codes and reported the
> outcome to the VLA for compilation of this report. The report is
> therefore
> compiled by the VLA on behalf of the Expert Group, and has been agreed
> with Professor Bruce (IAH).
> A more comprehensive report of our findings has been provided to the
> French
> scientists who submitted the samples.
> Conclusion
> Our findings, and interpretation of the western immunoblotting work
> done at
> AFSSA, support the conclusion that the French caprine isolate (CH636) is
> likely to contain the BSE strain.
> Dr Marion M Simmons
> On behalf of the EU CRL for TSE
> 28th January 2005
> Terry S. Singeltary Sr. wrote:
>> ##################### Bovine Spongiform Encephalopathy
>> #####################
>> Référence: IP/05/105 Date: 28/01/2005
>> EN
>> DE
>> EL
>> PDF: FR
>> EN
>> DE
>> EL
>> DOC: FR
>> EN
>> DE
>> EL
>> IP/05/105
>> Brussels, 28 January 2005
>> Case of BSE in a goat confirmed: Commission extends testing programme
>> A suspected case of BSE in a goat slaughtered in France in 2002 has
>> been confirmed today by a panel of European scientists
>> (
>> The European Commission proposes to step up testing to determine if
>> this is an isolated incident. Although this is the first time that
>> BSE has been found in a goat under natural conditions, precautionary
>> measures to protect consumers from this eventuality have been applied
>> in the EU for several years. The level of TSE infection in goats
>> seems however to be extremely low and any possible risk to consumers
>> is minimal. The European Commission asked the French authorities to
>> submit their preliminary findings to the Community Reference
>> Laboratory (CRL) for TSEs based in Weybridge, UK (see IP/04/1324
>> ).
>> TSEs are transmissible spongiform encephalopathies, namely BSE
>> affecting cattle and scrapie affecting goats and sheep.
>> Markos Kyprianou, EU Commissioner responsible for Health and Consumer
>> Protection, said “I want to reassure consumers that existing safety
>> measures in the EU offer a very high level of protection. This case
>> was discovered thanks to the EU testing system in place in France.
>> The testing programme has shown us that there is a very low incidence
>> rate of TSEs in goats and allowed us to detect suspect animals so
>> that they can be taken out of the food chain, as was done with this
>> goat and its entire herd. I am proposing to extend testing further to
>> determine whether this is an isolated incident.”
>> Existing safety measures
>> For many years, safety measures have been applied to all farmed
>> ruminants (cattle, goats, sheep) to offer maximum public health
>> protection in case BSE in goats was ever confirmed. These safety
>> measures include the ban on feeding animal proteins in the form of
>> meat-and-bone meal (MBM), the removal of specified risk materials
>> (i.e. the removal of tissues such as brain, spinal cord, part of the
>> intestines) from the food and feed chain, the slaughtering of herds
>> affected by scrapie (a disease of goats and sheep similar to BSE but
>> not infectious for humans), and a TSE monitoring and testing
>> programme in all Member States. Over 140,000 goats have been tested
>> since April 2002, including random testing of healthy animals, sick
>> animals and those that die on the farm.
>> Extension of testing regime
>> Following this confirmation, the Commission is proposing increased
>> testing for BSE among goats for at least 6 months (200 000 tests of
>> healthy goats in the EU) to determine if this is an isolated
>> incident. The extent of the monitoring programme will be based on the
>> goat population in each Member State and will focus primarily on
>> Member States where BSE is present in the cattle population. All
>> confirmed TSE cases will be subjected to a three-step testing scheme,
>> already in use, which will make it possible to differentiate between
>> scrapie and BSE. These additional measures will be submitted for
>> Member States approval at the next meeting of the Standing Committee
>> on the Food Chain and Animal Health scheduled on 2-3 February 2005..
>> Does this BSE case indicate a widespread problem?
>> The conditions that existed when the affected goat was born in 2000
>> no longer exist and available evidence would suggest that even if the
>> infection still exists in goats, the level would be extremely low.
>> The feeding of meat-and-bone meal (MBM) to ruminants is generally
>> considered to be the transmission route of BSE. In January 2001 the
>> existing ban on feeding MBM to all ruminants was extended to a total
>> ban on feeding MBM to all farmed animals. Goats in the EU generally
>> only live for a few years, which means that the majority of goats in
>> the EU today were born after the total feed ban was put in place.
>> Are goat milk, cheese and meat safe?
>> The European Food Safety Authority has advised that based on current
>> scientific knowledge, goat milk and derived products are unlikely to
>> present any risk of TSE contamination if the milk comes from healthy
>> animals:
>> Currently, as a precautionary measure and following scientific
>> advice, milk and meat from goats which are affected by TSE cannot be
>> used. These rules were in place before the case of BSE in a goat was
>> discovered. As for cattle and sheep, specified risk materials (the
>> tissues most likely to carry infectivity if the disease is present)
>> are also removed from all goats even if there is no infection
>> detected. While it is not possible to say that there is absolutely no
>> risk, any potential risk will be mitigated by the safety measures put
>> in place.
>> In light of the above, the European Commission advises no change in
>> current consumption of goat milk, cheese and meat. The European
>> Commission has asked EFSA to carry out a quantitative risk assessment
>> for goat meat and goat meat products, which is expected to be ready
>> by July 2005.
>> Background
>> Following the findings by a research group in France of a suspected
>> BSE infection in a goat, the European Commission immediately made the
>> findings public on 28 October 2004 (see IP/04/1324
>> ).
>> The supporting data were submitted on 5 November, as foreseen by the
>> EU procedure, by the French authorities to the Community Reference
>> Laboratory (CRL) for TSEs based in Weybridge (UK), for an evaluation
>> by an expert panel. The CRL expert panel reported their findings
>> today
>> (
>> The infected goat was born in March 2000 and slaughtered in France in
>> October 2002. The results are only now becoming available as the
>> series of confirmatory tests included testing on mice (a so-called
>> “mouse bioassay”), which takes two years to complete.
>> The goat and its herd were disposed in accordance with EU rules and
>> did not enter either the food or feed chain, and therefore do not
>> represent a risk to public health. This goat was detected as part of
>> the EU wide surveillance programme designed to detect suspicious TSE
>> strains in small ruminants, and was the only one in its herd of 300
>> goats to develop BSE. Over 140,000 goats have been tested across
>> Europe since April 2002.
>> See also MEMO/05/29
>> .
>> TSS
>> #########
>> ##########
> #########
> ##########

######### ##########

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