Stability properties of PrPSc from cattle with experimental transmissible
spongiform encephalopathies: use of a rapid whole homogenate, protease-free
assay
Catherine E Vrentas1 Email: catherine.vrentas@ars.usda.gov Justin J
Greenlee1 Email: justin.greenlee@ars.usda.gov Thierry Baron2 Email:
Thierry.BARON@anses.fr Maria Caramelli3 Email: Maria.Caramelli@izsto.it Stefanie
Czub4 Email: stefanie.czub@inspection.gc.ca Eric M Nicholson1* * Corresponding
author Email: eric.nicholson@ars.usda.gov
1 Virus and Prion Disease Research Unit, National Animal Disease Center,
USDA, Agricultural Research Service, 1920 Dayton Road, Ames, IA 50010, USA
2 Agence Nationale de Sécurité Sanitaire (Anses)-Lyon, 31 Avenue Tony
Garnier, 69364, Lyon Cedes 07, France
3 Istituto Zooprofilattico Sperimentale Piemonte Liguria e Valle d'Aost,
Via Bologna 148, 10154 Torino, Italy
4 National & OIE Reference Laboratories for BSE NCAD/CFIA, Township
Road 9-1 (Box 640), Lethbridge/Alberta, Canada
Abstract
Background
Transmissible Spongiform Encephalopathies (TSEs), including scrapie in
sheep, chronic wasting disease (CWD) in cervids, transmissible mink
encephalopathy (TME), and bovine spongiform encephalopathy (BSE), are fatal
diseases of the nervous system associated with accumulation of misfolded prion
protein (PrPSc). Different strains of TSEs exist, associated with different
PrPSc conformations that can be probed by the stability assay, in which PrPSc is
treated with increasing concentrations of the denaturant guanidine hydrochloride
(GdnHCl).
Results
Here, we provide the first comprehensive application of a rapid,
protease-free version of the GdnHCl stability assay to brain tissue from cattle
experimentally infected with various TSE isolates. Consistent with previous
findings from a single Japanese isolate, the L-type isolates of BSE are not
distinguishable from classical BSE in this assay. In contrast, H-type isolates
of BSE, including our unique isolate of E211K BSE, exhibit higher stability than
classical BSE, suggesting that its increased protection against protease
digestion at the BSE Nterminus is associated with a higher stability in GdnHCl.
While the difference in stability in our version of the assay is likely not
large enough for effective use in a diagnostic laboratory setting, the use of
alternative experimental conditions may enhance this effect. TSEs from other
natural host species that have been passaged in cattle, including CWD and TME,
were not distinguishable from classical BSE, while isolates of cattle passaged
scrapie exhibited a slight increase in stability as compared to classical
BSE.
Conclusions
These results suggest that the core of PrPSc, as probed in this assay, has
similar stability properties among cattle-passaged TSE isolates and that the
conformational differences that lead to changes in the proteinase K cleavage
site do not cause large changes in the stability of PrPSc from TSE-affected
cattle. However, the stability differences observed here will provide a basis of
comparison for new isolates of atypical BSE observed in the future and in other
geographic locations, especially in the case of H-type BSE.
snip...
Stability comparison of BSE to other cattle-passaged TSEs
In addition to comparing the different BSE strains, we also used the
stability assay to characterize the biochemical properties of other TSEs
passaged into cattle. Scrapie and CWD are both transmissible into cattle by IC
inoculation, leading to PrPSc accumulation--but not significant spongiform
changes--in the brain [29,30]. Transmissible mink encephalopathy has been
hypothesized to have originated from the feeding of downer cattle, possibly
carrying atypical, L-type BSE, to farm-raised mink [37]. We wanted to determine
if the profiles of PrPSc from these TSEs passaged in cattle brain were
distinguishable from each other or from other BSE strains, with potential
implications for understanding strain origins and/or improving (non-BSE) TSE
diagnosis in cattle.
snip...
Keywords
Bovine spongiform encephalopathy, BSE, ELISA, Prion, PrP, Scrapie,
Stability, Transmissible spongiform encephalopathy, TSE
ISSN 1746-6148 Article type Research article Submission date 12 April 2013
Acceptance date 12 August 2013 Publication date 15 August 2013 Article URL http://www.biomedcentral.com/1746-6148/9/167
Like all articles in BMC journals, this peer-reviewed article can be downloaded,
printed and distributed freely for any purposes (see copyright notice below).
Articles in BMC journals are listed in PubMed and archived at PubMed Central.
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Sunday, July 21, 2013
Biochemical Characteristics and PrPSc Distribution Pattern in the Brains of
Cattle Experimentally Challenged with H-type and L-type Atypical BSE
please see below from PRION2013 ;
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
AD.56: The emergence of novel BSE prions by serial passages of H-type BSE
in bovinized mice
Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki
Okada, Shirou Mohri and Takashi Yokoyama
National Institute of Animal Health; Tsukuba, Japan
H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE,
and has been detected in several European countries, and North America.
Transmission studies of H-type BSE led to the emergence of the classical BSE
(C-BSE) phenotypes during passages in inbred wild type and bovinized
PrP-overexpressing transgenic mice. In this study, we conducted serial passages
of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice
(TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods
of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage
were constant (~= 220 d), no clear differences were observed in their biological
and biochemical properties. However, at the forth passage, 2 different BSE
phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the
other is longer survival times. TgBoPrP mice with longer incubation period
showed the H-type phenotype of PrPsc profile and pathology. However, those of
shorter incubation period were different phenotypes from previously existed BSE
prions (C-BSE, L-type BSE, and H-type BSE). *** This study imply the possibility
that the novel BSE prions with high virulence in cattle will be emerged during
intraspecies transmission.
please see ;
Thursday, August 15, 2013
The emergence of novel BSE prions by serial passages of H-type BSE in
bovinized mice
Saturday, July 6, 2013
Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy
Research Article
Tuesday, July 2, 2013
APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals
Eliminating ALL remaining BSE barriers to export market
Thursday, June 13, 2013
Experimental interspecies transmission studies of the transmissible
spongiform encephalopathies to cattle: comparison to bovine spongiform
encephalopathy in cattle
Tuesday, June 11, 2013
Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant
deviations from requirements in FDA regulations that are intended to reduce the
risk of bovine spongiform encephalopathy (BSE) within the United States
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI
ratings as at June 5, 2013
Unsuccessful oral transmission of scrapie from British sheep to
cattle
snip...
I have often pondered if the whole damn mad cow follies started over here
in the USA, and somehow, the USA shipped it over to the UK ?
It happened with S. Korea and CWD, via Canada. see ;
The disease was confirmed only in elk in the Republic of Korea in 2001,
2004 and 2005. Epidemiological investigations showed that CWD was introduced via
importation of infected elk from Canada between 1994 and 1997.
but I still am not so sure that the mad cow follies did not start long ago
right here in the USA i.e. Richard Marsh and deadstock downer cattle to those
mink, and then the USA shipped it to hell and back. just pondering out loud
here. ...tss
The exact same recipe for B.S.E. existed in the U.S. for years
and years. In reading over the Qualitative Analysis of BSE
Risk Factors-1, this is a 25 page report by the
USDA:APHIS:VS. It could have been done in one page. The
first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous
rendering technology and the lack of usage of solvents,
however, large differences still remain with other risk factors
which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of
B.S.E. in the U.S., with nothing more than the cattle to sheep
ratio count, and the geographical locations of herds and flocks.
That's all the evidence they can come up with, in the next 24
pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific
continuous rendering technology which uses lower
temperatures and accounts for 25 percent of total output. This
technology was _originally_ designed and imported from the
United States. However, the specific application in the
production process is _believed_ to be different in the two
countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two
countries. The calculations are based on slaughter numbers,
fallen stock estimates, and product yield coefficients. This
approach is used due to variation of up to 80 percent from
different reported sources. At 3.6 million tons, the United
States produces 8 times more animal rendered product than
the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and
bone meal is more acute in both relative and absolute terms in
the United Kingdom (Figures 27 and 28). Note that sheep
meat and bone meal accounts for 14 percent, or 61 thousand
tons, in the United Kingdom versus 0.6 percent or 22 thousand
tons in the United States. For sheep greater than 1 year, this is
less than one-tenth of one percent of the United States supply."
"The potential risk of amplification of the BSE agent through
cattle meat and bone meal is much greater in the United States
where it accounts for 59 percent of total product or almost 5
times more than the total amount of rendered product in the
United Kingdom."
Considering, it would only take _one_ scrapie infected sheep
to contaminate the feed. Considering Scrapie has run rampant
in the U.S. for years, as of Aug. 1999, 950 scrapie infected
flocks. Also, Considering only one quarter spoonful of scrapie
infected material is lethal to a cow. Considering all this, the
sheep to cow ration is meaningless. As I said, it's 24 pages of
B.S.e.
To be continued...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA
_____________________________________________________________________
Qualitative Assessment Considering the comparative factors presented, with
the exception of some similarities in rendering practices, epidemiologic factors
believed conducive to the introduction of BSE in the United Kingdom are
significantly different in the United States. This is supported by the following
points: Similar changes in the rendering practices have occurred in both
countries. Continuous rendering accounts for the vast majority of all product
produced. From 1977 to 1982, the portion of United Kingdom product rendered
using hydrocarbon solvents dropped from 70 per-cent to 10 percent. Within the
United States the decline was at least 5 years earlier with very little if any
solvent in current use.
see full text ;
TME in mink was documented in the early 1960s. it was first thought that
the TME out break was from scrapie infected sheep, until a investigation was
done on feed practices at these mink facilities, and it was later found that the
mink had been fed 95%+ dead stock downer cows. and later, the Late Richard Marsh
tried to warn the feds of the pending mad cow debacle. they refused to listen.
... some interesting reading on pages 26 to 33
1979
TME originates from feeding mink, scrapie infected materials...
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
Tuesday, July 21, 2009
Transmissible mink encephalopathy - review of the etiology
Folia Neuropathologica 2/2009
full text of the article:
Transmissible mink encephalopathy – review of the etiology
Folia Neuropathol 2009; 47 (2): 195-204
snip...
A possible clue was provided during the Stetsonville TME outbreak in which
the rancher fed his mink commercial feed (e.g., poultry, fish, cereal) and fresh
meat primarily from sick or downer dairy cattle within a 50-mile radius of his
ranch [37]. He did not recall including sheep products in his homemade feed
ration. Upon reviewing prior TME outbreaks in the U.S. and Canada, in all four
cases in which records were available and were not linked to a commercial feed
plant, downer cattle were also included in the mink diet. The Stetsonville TME
isolate, and subsequently additional TME isolates, were transmitted to cattle by
intracerebral inoculation and the Stetsonville TME isolate was the first
confirmed case of experimental transmission of a TSE/prion disease to cattle.
What was striking was that upon experimental transmission of cattle TME back
into mink by the oral and intracerebral routes, the incubation periods were
similar to that found for mink passaged TME. Hence, the pathogenicity of the
Stetsonville TME agent in mink was not altered upon passage into cattle,
suggesting that a previously unrecognized TSE/prion disease in cattle may be the
source of TME infection. Additional studies strongly suggest that TME has
similarities to L-type BSE in transgenic mice compared to H-type or classical
BSE [2]. Since the L-type BSE does not appear to be an infectious form of
TSE/prion disease, the proposal by Marsh [35,37] that a rare TSE in cattle may
be the source of TME infection seems plausible. This is particularly the case in
Wisconsin, which has had the majority of TME in the USA and is a prominent dairy
state with aged cattle being a primary source of fresh meat for mink ration.
Since mink are a sentinel host it is not surprising that they may have been a
key host in amplifying a rare cattle TSE disease. Another possible explanation
for the high incidence of TME in Wisconsin is based on the recent identification
of a mutation in the prion protein gene in cattle with atypical BSE. There may
be cattle breeding stock in Wisconsin that carry a mutation in the prion protein
gene that is linked to late onset disease and are also the source of TSE
infection for mink TME outbreaks described in the 1960s and 1985.
snip...
To this end, mink were shown to be sensitive to scrapie [23,24]. Of
interest, following i.c. inoculation with the UK source of scrapie from a
Suffolk sheep only a single animal developed the disease. In contrast, American
sources B-834 and B-957 from Suffolk sheep readily transmitted to mink. Also, in
another outbreak of TME in Stetsonville, Wisconsin, USA, the affected mink were
apparently fed with downer cattle but not scrapie-affected sheep [32], and thus
TME may result from BSE transmission from cattle to mink [37]. TME is readily
transmitted to cattle [26]. The suggestion that TME may result from transmission
from infected cattle but not sheep was supported by recent data on phenotypic
similarities of TME in cattle and L-type bovine spongiform encephalopathy (BSE)
transmitted to ovine transgenic mice (TgOvPrP4) [2]. To this end, L-type of BSE
and TME in TgOvPrP4 presented similar molecular mass of all 3 bands of PrPd.
Unglycosylated PrPd in L-type BSE, bovine TME and typical BSE has the same
molecular mass of approximately 18 kDa in contrast to that of diglycosylated
PrPd species which was lower by 0.5-0.8 kDa in L-type BSE and bovine TME as
compared to typical BSE. Furthermore, L-type BSE and bovine TME transmitted to
TgOvPrP4 mice presented spongiform change of low intensity but PrPd was strongly
expressed including amyloid plaques. Mink were also susceptible to BSE [44]. ...
snip...
please see full text and more here;
http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html
Saturday, December 01, 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and
L-type Bovine Spongiform Encephalopathy in a Mouse Model
Volume 13, Number 12–December 2007 Research
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and
L-type Bovine Spongiform Encephalopathy in a Mouse Model
Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,*
andRichard A. Bessen†*Agence Française de Sécurité Sanitaire des Aliments–Lyon,
Lyon, France; and†Montana State University, Bozeman, Montana, USA
Abstract
Transmissible mink encepholapathy (TME) is a foodborne transmissible
spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant
TSE has been proposed as the cause, but the precise origin of TME is unknown. To
compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct
natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE,
and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4).
Transgenic mice were susceptible to infection with bovine-passaged TME, typical
BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain
lesions profiles, disease-associated prion protein brain distribution, and
biochemical properties of protease-resistant prion protein, typical BSE had a
distint phenotype in ovine transgenic mice compared to L-type BSE and bovine
TME.The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4
mice suggest that L-type BSE is a much more likely candidate for the origin of
TME than is typical BSE.
snip...
Conclusion
These studies provide experimental evidence that the Stetsonville TME agent
is distinct from typical BSE but has phenotypic similarities to L-type BSE in
TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely candidate for
a bovine source of TME infection than typical BSE. In the scenario that a
ruminant TSE is the source for TME infection in mink, this would be a second
example of transmission of a TSE from ruminants to non-ruminants under natural
conditions or farming practices in addition to transmission of typical BSE to
humans, domestic cats, and exotic zoo animals(37). The potential importance of
this finding is relevant to L-type BSE, which based on experimental transmission
into humanized PrP transgenic mice and macaques, suggests that L-type BSE is
more pathogenic for humans than typical BSE (24,38).
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus
Macaque
"BSE-L in North America may have existed for decades"
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Sophie Freire,1
Jürgen Richt,2 Justin Greenlee,3 Juan-Maria Torres,4 Paul Brown,1 Bob Hills5 and
Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Kansas State
University; Manhattan, KS USA; 3USDA; Ames, IA USA; 4INIA; Madrid, Spain;
5Health Canada; Ottawa, ON Canada†Presenting author; Email: emmanuel.comoy@cea.fr
The epidemiology of Transmissible mink encephalopathy (TME) indicates an
alimentary origin. Several inter-species transmission experiments have not
succeeded in establishing with certainty any natural reservoir of this prion
strain, although both ovine and bovine sources have been suspected. Cattle
exposed to TME develop a spongiform encephalopathy that is distinct from
classical Bovine Spongiform Encephalopathy (c-BSE).
Inoculation of c-BSE to cynomolgus macaque provided early evidence of a
possible risk to humans, and remains an important model to define the risk of
both primary (oral transmission from cattle to primate) and secondary
(intravenous intra-species transmission) exposures. We have also evaluated the
transmissibility of other cattle prion strains to macaques, including L- and H-
atypical forms of BSE, namely BSE-L and BSE-H, and cattle-adapted TME.
BSE-L induced a neurological disease distinct from c-BSE. Peripheral
exposures demonstrate the transmissibility of BSE-L by oral, intravenous, and
intra-cerebral routes, with incubation periods similar to c-BSE. Cattle-adapted
TME also induced a rapid disease in cynomolgus macaque. The clinical features,
lesion profile, and biochemical signature of the induced disease was similar to
the features observed in animals exposed to BSE-L, suggesting a link between the
two prion strains. Secondary transmissions to a common host (transgenic mouse
overexpressing bovine PrP) of cattle-TME and BSE-L before or after passage in
primates induced diseases with similar incubation periods: like the c-BSE
strain, these cattle strains maintained their distinctive features regardless of
the donor species and passages.
If the link between TME and BSE-L is confirmed, our results would suggest
that BSE-L in North America may have existed for decades, and highlight a
possible preferential transmission of animal prion strains to primates after
passage in cattle.
=====================end...tss====================
link url not available, please see PRION 2011 ;
ALSO, SEE Scrapie Mission, Texas, did not produce _typical_ BSE...
see page 17 here ;
3.57 The experiment which might have determined whether BSE and scrapie
were caused by the same agent (ie, the feeding of natural scrapie to cattle) was
never undertaken in the UK. It was, however, performed in the USA in 1979, when
it was shown that cattle inoculated with the scrapie agent endemic in the flock
of Suffolk sheep at the United States Department of Agriculture in Mission,
Texas, developed a TSE quite unlike BSE.339 The findings of the initial
transmission, though not of the clinical or neurohistological examination, were
communicated in October 1988 to Dr Watson, Director of the CVL, following a
visit by Dr Wrathall, one of the project leaders in the Pathology Department of
the CVL, to the United States Department of Agriculture.340 The results were not
published at this point, since the attempted transmission to mice from the
experimental cow brain had been inconclusive. The results of the clinical and
histological differences between scrapie-affected sheep and cattle were
published in 1995. Similar studies in which cattle were inoculated
intracerebrally with scrapie inocula derived from a number of scrapie-affected
sheep of different breeds and from different States, were carried out at the US
National Animal Disease Centre.341 The results, published in 1994, showed that
this source of scrapie agent, though pathogenic for cattle,
*** did not produce the same clinical signs of brain lesions characteristic
of BSE. ***
3.58 There are several possible reasons why the experiment was not
performed in the UK. It had been recommended by Sir Richard Southwood (Chairman
of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the
Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342
though it was not specifically recommended in the Working Party Report or indeed
in the Tyrrell Committee Report (details of the Southwood Working Party and the
Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89
and vol. 11: Scientists after Southwood respectively). The direct inoculation of
scrapie into calves was given low priority, because of its high cost and because
it was known that it had already taken place in the USA.343 It was also felt
that the results of such an experiment would be hard to interpret. While a
negative result 337 Fraser, H., Bruce, M., Chree, A., McConnell, I. and Wells,
G. (1992) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice,
Journal of General Virology, 73, 1891–7; Bruce, M., Chree, A., McConnell, I.,
Foster, J., Pearson, G. and Fraser, H. (1994) Transmission of Bovine Spongiform
Encephalopathy and Scrapie to Mice: Strain Variation and the Species Barrier,
Philosophical Transactions of the Royal Society of London, Series B, Biological
Sciences, 343, 405–11 338 Bruce, M., Will, R., Ironside, J., McConell, I.,
Drummond, D., Suttie, A., McCordie, L., Chree, A., Hope, J., Birkett, C.,
Cousens, S., Fraser, H. and Bostock, C. (1997) Transmissions to Mice Indicate
that ‘New Variant’ CJD is Caused by the BSE Agent, Nature, 389, 498–501 339
Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle
Experimentally Infected with the Scrapie Agent, American Journal of Veterinary
Research, 56, 606–12 340 YB88/10.00/1.1 341 Cutlip, R., Miller, J., Race, R.,
Jenny, A., Katz, J., Lehmkuhl, H., Debey, B. and Robinson, M. (1994)
Intracerebral Transmission of Scrapie to Cattle, Journal of Infectious Diseases,
169, 814–20 342 YB88/6.21/1.2 343 YB88/11.17/2.4 SCIENCE 84 would be
informative, a positive result would need to demonstrate that when scrapie was
transmitted to cattle, the disease which developed in cattle was the same as
BSE.344 Given the large number of strains of scrapie and the possibility that
BSE was one of them, it would be necessary to transmit every scrapie strain to
cattle separately, to test the hypothesis properly. Such an experiment would be
expensive. Secondly, as measures to control the epidemic took hold, the need for
the experiment from the policy viewpoint was not considered so urgent. It was
felt that the results would be mainly of academic interest.345 3.59
Nevertheless, from the first demonstration of transmissibility of BSE in 1988,
the possibility of differences in the transmission properties of BSE and scrapie
was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to
transmit BSE to hamsters had failed. Subsequent findings increased that
possibility.
1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE ?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF
CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS
SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN HISTOPATHOLOGY AND
INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS _NOT_ BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT ?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN
ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE,
AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE
AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. ...
Tuesday, November 17, 2009
SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM
THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS
"All of the 15 cattle tested showed that the brains had abnormally
accumulated PrP"
2009
''THE LINE TO TAKE'' ON IBNC $$$ 1995 $$$
1995
page 9 of 14 ;
30. The Committee noted that the results were unusual. the questioned
whether there could be coincidental BSE infection or contamination with scrapie.
Dr. Tyrell noted that the feeling of the committee was that this did not
represent a new agent but it was important to be prepared to say something
publicly about these findings. A suggested line to take was that these were
scientifically unpublishable results but in line with the policy of openness
they would be made publicly available and further work done to test their
validity. Since the BSE precautions were applied to IBNC cases, human health was
protected. Further investigations should be carried out on isolations from
brains of IBNC cases with removal of the brain and subsequent handling under
strict conditions to avoid the risk of any contamination.
31. Mr. Bradley informed the Committee that the CVO had informed the CMO
about the IBNC results and the transmission from retina and he, like the
Committee was satisfied that the controls already in place or proposed were
adequate. ...
snip... see full text
http://web.archive.org/web/20030327015011/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA
Final report
IN CONFIDENCE
BSE ATYPICAL LESION DISTRIBUTION
http://web.archive.org/web/20041226015813/http://www.bseinquiry.gov.uk/files/yb/1993/03/14001001.pdf
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
Thursday, May 02, 2013
Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING
OBEX ONLY
USDA 2003
We have to be careful that we don't get so set in the way we do things that
we forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain stem
and we're looking in only one area. In Norway, they were doing a project and
looking at cases of Scrapie, and they found this where they did not find lesions
or PRP in the area of the obex. They found it in the cerebellum and the
cerebrum. It's a good lesson for us. Ames had to go back and change the
procedure for looking at Scrapie samples. In the USDA, we had routinely looked
at all the sections of the brain, and then we got away from it. They've recently
gone back. Dr. Keller: Tissues are routinely tested, based on which tissue
provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another
important thing to get across to the public is that the negatives do not
guarantee absence of infectivity. The animal could be early in the disease and
the incubation period. Even sample collection is so important. If you're not
collecting the right area of the brain in sheep, or if collecting
lymphoreticular tissue, and you don't get a good biopsy, you could miss the area
with the PRP in it and come up with a negative test. There's a new, unusual form
of Scrapie that's been detected in Norway. We have to be careful that we don't
get so set in the way we do things that we forget to look for different emerging
variations of disease. We've gotten away from collecting the whole brain in our
systems. We're using the brain stem and we're looking in only one area. In
Norway, they were doing a project and looking at cases of Scrapie, and they
found this where they did not find lesions or PRP in the area of the obex. They
found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had
to go back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got away
from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip...
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
END...TSS
snip...see ;
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except
on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
snip...
PAGE 31
Appendix I
VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE
1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The experimental
results have not been published but there are plans to do this. This work was
initiated in 1978. A summary of it is:-
Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a
2nd Suffolk scrapie passage:-
i/c 1ml i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BSE-like disease.
Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus
2/6 went down similarly after 36 months.
Expt C Mice inoculated from brains of calves/cattle in expts A & B were
resistant, only 1/20 going down with scrapie and this was the reason given for
not publishing.
Diagnosis in A, B, C was by histopath. No reports on SAF were given.
Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally- (and naturally) infected sheep by ET. He had
found difficulty in obtaining emhryos from naturally infected sheep (cf SPA).
3. Prof. A Robertson gave a brief account of BSE. The US approach was to
PAGE 32
accord it a very low profile indeed. Dr A Thiermann showed the picture in
the "Independent" with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. BSE was not reported in USA.
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control Scheme was started there were
10-14 incidents, in 1978 - 1 and in 1988 so far 60.
5. Scrapie agent was reported to have been isolated from a solitary fetus.
6. A western blotting diagnostic technique (? on PrP} shows some promise.
7. Results of a questionnaire sent to 33 states on the subject of the
national sheep scrapie programme survey indicated;
17/33 wished to drop it 6/33 wished to develop it 8/33 had few sheep and
were neutral
Information obtained from Dr Wrathall's notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.
please see ;
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
see ;
EVIDENCE OF SCRAPIE IN SHEEP AS A
RESULT OF FOOD BORNE EXPOSURE
This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies.
THE RISK OF TRANSMISSION OF BSE TO SHEEP VIA FEED
Prusiner vs Maff on BSE brains, and delaying science for profits $
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus
Macaque
"BSE-L in North America may have existed for decades"
snip...see full text ;
Monday, June 3, 2013
Unsuccessful oral transmission of scrapie from British sheep to
cattle
Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013
Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010
http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html
Sent: Tuesday, August 13, 2013 3:58 PM
Subject: Idiopathic Brainstem Neuronal Chromatolysis (IBNC): a
novel prion protein related disorder of cattle?
Greetings Honorable Science Advisory Council et al @ DEFRA,
I wish to ask a question about something I have seen no updates on, that
concerns me.
IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS IBNC or what I some times call,
IBNC BSE.
I have seen nothing in the scientific literature updated on this in years,
since around 2008, then it was like it fell off the face of the earth ?
can you please give me some sort of update on the IBNC BSE science to date
?
how many cases of IBNC BSE have been detected ?
is there an ongoing surveillance for this the IBNC BSE, and are the BSE
test even capable of detecting it ?
could the USA and or North America even detect, if they were even looking
for it ?
latest studies, if any more since "All of the 15 cattle tested showed that
the brains had abnormally accumulated PrP" ?
thank you,
kind regards,
terry
references as follows ;
snip...end...tss
