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MAD COWS, TYPICAL OR ATYPICAL, WHO EXPORTED WHAT TO WHOM

flounder

Well-known member
Greetings,

Thought some of you might be interested in the USDA exports of potential
USDA CERTIFIED ATYPICAL AND TYPICAL MAD COW BRAINS, SWEETBREADS, BOVINE
FROZEN OFFAL, AND LIVE CATTLE. Interestingly, the USA may be the one to
blame from there consistent lies and deceit and what they have exported
globally for decades, to blame for spreading sporadic CJD around the globe.


Looking from stats at ;


http://www.fas.usda.gov/ustrade/ustlists/ExCmdty.asp?QI=370619655344&type=1&code=02


then searching here ;


http://www.fas.usda.gov/ustrade/USTEXHS10.asp?QI=370619655344



SEEMS that Mexico received from the USA a boat load of potential mad cow
brains 0206290030 between 2001 to 2005, Mexico received the most compared to
COTE D'IVOIRE which was next in line, followed by ROMANIA, GREECE,
SINGAPORE, GERMANY AND SWEDEN. ...

NEXT, looking at SWEETBREADS 0206290040 the USA exported, and whatever
phenotype of TSE that went along, we have as follows;
MEXICO AGAIN receiving a boat load of sweetbreads, followed by ARGENTINA,
JAPAN, URUGUAY, COLOMBIA, ISRAEL, BULGARIA, HONG KONG, VENEZUELA, United
Arab Emirates, Switzerland, Singapore, Netherlands, The Bahamas, and the
Dominican Republic. ...

THE LIST for BOVINE OFFAL FROZEN 020629 EXPORTED FROM THE USA ACROSS THE
GLOBE IS PHENOMENAL WITH JAPAN RECEIVING THE MOST FROM 1998 TO 2003,
FOLLOWED BY MEXICO, and from here the list is staggering along with the
amount of potential TSE tainted materials. ...

FINALLY, LIVE CATTLE WITH CANADA RECEIVING THE MOST, FOLLOWED BY MEXICO,
KOREA REPUBLIC OF, followed by many more countries with smaller amounts. ...

WHEN the OIE did away with the BSE GBR risk assessments to ride saddle with
GW and his legal tool to trade TSE globally i.e. the BSE MRR policy, 20
years of fighting this disease went down the drain, just so he could trade
his precious commodities and futures. THIS BSe about how now the USA having
an epidemic of a spontaneous TSE in cattle and humans, as sporadic CJD
triples in 3 years in the USA, is simply absurd. nothing is spontaneous
about it, there is absolutely no science to back these 'spontaneous'
statements up. ...



US "Atypical" Mad Cow Threat Was Predicted

http://www.prwatch.org/node/4883



TSS
 

Murgen

Well-known member
Flounder, do you believe the UK/Canadian strain may have been a result of the strain now found in the US?

From what I have read, this "atypical" strain was very difficult to find/determine with previous testing methods.

So it may have been present pre UK BSE, and may have been the cause also.

thanks for your input
 

Murgen

Well-known member
Or is it just a coincidence that the Country that export the most MBM/SRM's in the world is also the location of the highest rate of TSE's?
 

flounder

Well-known member
Murgen wrote;


Flounder, do you believe the UK/Canadian strain may have been a result of the strain now found in the US?

From what I have read, this "atypical" strain was very difficult to find/determine with previous testing methods.

So it may have been present pre UK BSE, and may have been the cause also.

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

o.k., i will try and answer this best i can, but may take some space, so sorry for long answer.


THIS goes back further than 85 in my opinion. the exact date between the U.K. and the USA as far as who started using the low temp continuous rendering is up for guess i suppose, but i once read where the USA sent the technology to the UK about 5 years before the USA started using it. BUT, whatever sparked off the species jump, and when that was from scrapie/tme/cwd/bse/tse to whatever species, is another guess. could go way back. consider the rabies in cattle and how much of that was really TSE, pre 1985 ??? IF one believes in the spontantous crap, then it would have been happening all along, and why did not anyone document a case earlier? why have countries going with feed ban etc, why did these countries BSE cases decline dramatically if spontaneous BSe is correct? also, an unthinkable, a mutated strain from consumption and or casual contact from CWD that transmits to cattle the same way, a frightening thought, one that i hope never comes true.
i simply don't buy the ukbsenvcjd only theory, especially if we look at what collinge/asante et al found,
that BSE can propagate as nvCJD and or sCJD in mice ;



BSE prions propagate as either variant CJD-like or

sporadic CJD-like prion strains in transgenic mice

expressing human prion protein




Emmanuel A.Asante, Jacqueline M.Linehan,

Melanie Desbruslais, Susan Joiner,

Ian Gowland, Andrew L.Wood, Julie Welch,

Andrew F.Hill, Sarah E.Lloyd,

Jonathan D.F.Wadsworth and

John Collinge1

MRC Prion Unit and Department of Neurodegenerative Disease,

Institute of Neurology, University College, Queen Square,

London WC1N 3BG, UK

1Corresponding author

e-mail: [email protected]

Variant Creutzfeldt±Jakob disease (vCJD) has been

recognized to date only in individuals homozygous for

methionine at PRNP codon 129. Here we show that

transgenic mice expressing human PrP methionine

129, inoculated with either bovine spongiform

encephalopathy (BSE) or variant CJD prions, may

develop the neuropathological and molecular phenotype

of vCJD, consistent with these diseases being

caused by the same prion strain. Surprisingly, however,

BSE transmission to these transgenic mice, in

addition to producing a vCJD-like phenotype, can also

result in a distinct molecular phenotype that is indistinguishable

from that of sporadic CJD with PrPSc

type 2. These data suggest that more than one BSEderived

prion strain might infect humans; it is therefore

possible that some patients with a phenotype consistent

with sporadic CJD may have a disease arising

from BSE exposure.

Keywords: BSE/Creutzfeldt±Jakob disease/prion/

transgenic

Introduction ...



snip...



These studies further strengthen the evidence that vCJD

is caused by a BSE-like prion strain. Also, remarkably, the

key neuropathological hallmark of vCJD, the presence of

abundant ¯orid PrP plaques, can be recapitulated on BSE

or vCJD transmission to these mice. However, the most

surprising aspect of the studies was the ®nding that an

alternate pattern of disease can be induced in 129MM

Tg35 mice from primary transmission of BSE, with a

molecular phenotype indistinguishable from that of a subtype

of sporadic CJD. This ®nding has important potential

implications as it raises the possibility that some humans

infected with BSE prions may develop a clinical disease

indistinguishable from classical CJD associated with type 2

PrPSc. This is, in our experience, the commonest molecular

sub-type of sporadic CJD. In this regard, it is of interest

that the reported incidence of sporadic CJD has risen in the

UK since the 1970s (Cousens et al., 1997). This has been

attributed to improved case ascertainment, particularly as

much of the rise is reported from elderly patients and

similar rises in incidence were noted in other European

countries without reported BSE (Will et al., 1998).

However, it is now clear that BSE is present in many

European countries, albeit at a much lower incidence than

was seen in the UK. While improved ascertainment is

likely to be a major factor in this rise, that some of these

additional cases may be related to BSE exposure cannot be

ruled out. It is of interest in this regard that a 2-fold

increase in the reported incidence of sporadic CJD in 2001

has recently been reported for Switzerland, a country that

had the highest incidence of cattle BSE in continental

Europe between 1990 and 2002 (Glatzel et al., 2002). No

epidemiological case±control studies with strati®cation of

CJD cases by molecular sub-type have yet been reported.

It will be important to review the incidence of sporadic

CJD associated with PrPSc type 2 and other molecular subtypes

in both BSE-affected and unaffected countries in the



light of these ®ndings. If human BSE prion infection can

result in propagation of type 2 PrPSc, it would be expected

that such cases would be indistinguishable on clinical,

pathological and molecular criteria from classical CJD. It

may also be expected that such prions would behave

biologically like those isolated from humans with sporadic

CJD with type 2 PrPSc. The transmission properties of

prions associated with type 2 PrPSc from BSE-inoculated

129MM Tg35 mice are being investigated by serial

passage.

We consider these data inconsistent with contamination

of some of the 129MM Tg35 mice with sporadic CJD

prions. These transmission studies were performed according

to rigorous biosafety protocols for preparation of

inocula and both the inoculation and care of mice, which

are all uniquely identi®ed by sub-cutaneous transponders.

However, crucially, the same BSE inocula have been used

on 129VV Tg152 and 129MM Tg45 mice, which are

highly sensitive to sporadic CJD but in which such

transmissions producing type 2 PrPSc were not observed.

Furthermore, in an independent experiment, separate

inbred lines of wild-type mice, which are highly resistant

to sporadic CJD prions, also propagated two distinctive

PrPSc types on challenge with either BSE or vCJD. No

evidence of spontaneous prion disease or PrPSc has been

seen in groups of uninoculated or mock-inoculated aged

129MM Tg35 mice.

While distinctive prion isolates have been derived from

BSE passage in mice previously (designated 301C and

301V), these, in contrast to the data presented here, are

propagated in mice expressing different prion proteins

(Bruce et al., 1994). It is unclear whether our ®ndings

indicate the existence of more than one prion strain in

individual cattle with BSE, with selection and preferential

replication of distinct strains by different hosts, or that

`mutation' of a unitary BSE strain occurs in some types of

host. Western blot analysis of single BSE isolates has not

shown evidence of the presence of a proportion of

monoglycosylated dominant PrPSc type in addition to the

diglycosylated dominant pattern (data not shown).

Extensive strain typing of large numbers of individual

BSE-infected cattle either by biological or molecular

methods has not been reported.

Presumably, the different genetic background of the

different inbred mouse lines is crucial in determining

which prion strain propagates on BSE inoculation. The

transgenic mice described here have a mixed genetic

background with contributions from FVB/N, C57BL/6 and

129Sv inbred lines; each mouse will therefore have a

different genetic background. This may explain the

differing response of individual 129MM Tg35 mice, and

the difference between 129MM Tg35 and 129MM Tg45

mice, which are, like all transgenic lines, populations

derived from single founders. Indeed, the consistent

distinctive strain propagation in FVB and C57BL/6 versus

SJL and RIIIS lines may allow mapping of genes relevant

to strain selection and propagation, and these studies are in

progress.

That different prion strains can be consistently isolated

in different inbred mouse lines challenged with BSE

prions argues that other species exposed to BSE may

develop prion diseases that are not recognizable as being

caused by the BSE strain by either biological or molecular

strain typing methods. As with 129MM Tg35 mice, the

prions replicating in such transmissions may be indistinguishable

from naturally occurring prion strains. It

remains of considerable concern whether BSE has transmitted

to, and is being maintained in, European sheep

¯ocks. Given the diversity of sheep breeds affected by

scrapie, it has to be considered that some sheep might have

become infected with BSE, but propagated a distinctive

strain type indistinguishable from those of natural sheep

scrapie.

Materials and methods

The EMBO Journal Vol. 21 No. 23 pp. 6358±6366, 2002

snip...end...TSS



ALSO, if we go back to the first documented mad cow in the UK, Carol Richardsons the vet that diagnosed that cow at the Stent farm, that cow was really mad in 1984 (please note some urls may be duplicated). ...TSS



http://www.bseinquiry.gov.uk/files/yb/1985/09/19001001.pdf



Carol Richardson’s Pathology Report as amended by Gerald Wells



http://www.bseinquiry.gov.uk/files/yb/1985/09/19002001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/09/19003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/09/23001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/09/26001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/10/04001001.pdf





seems files are missing here;

28.6.84 - BS Cos No 226



http://www.bseinquiry.gov.uk/files/yb/1984/06/26001001.pdf




http://www.bseinquiry.gov.uk/files/yb/1984/06/28001001.pdf



Minutes of the 23nd Meeting held at the Central Veterinary Laboratory on Tuesday 14 May 1985.

http://www.bseinquiry.gov.uk/files/yb/1985/05/14001001.pdf



pitsham farm mr stent 25.5.85

http://www.bseinquiry.gov.uk/files/yb/1985/05/28001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/05/29001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/05/30001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/06/04001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/06/13002001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/07/18001001.pdf



2-9-85

''PITSHAM FARM SYNDROME''

The Friesian cow brand 142 was received in a recumban condition showing considerable twitching movements

http://www.bseinquiry.gov.uk/files/yb/1985/09/03001001.pdf



10-9-85 MAFF AND 'NERVOUS COWS'



http://www.bseinquiry.gov.uk/files/yb/1985/09/10001001.pdf



REPORTED BY C. RIGHARDSON 19/9/85

http://www.bseinquiry.gov.uk/files/yb/1985/09/10002001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/09/10003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/09/17001001.pdf



CAROL RICHARDSON PATHOLOGY REPORT

http://www.bseinquiry.gov.uk/files/yb/1985/09/19001001.pdf



Carol Richardson’s Pathology Report as amended by Gerald Wells



http://www.bseinquiry.gov.uk/files/yb/1985/09/19002001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/09/19003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/09/23001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/09/26001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1985/10/04001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1986/09/22001001.pdf



21/10/85 CJD



http://www.bseinquiry.gov.uk/files/yb/1985/10/21001001.pdf




IF the disease turned out to be bovine scrapie it would have severe repercussions to the export trade and possibly also for humans if for example it was discovered that humans with spongiform encephalopathies had close association with the cattle. IT is for these reasons I have classified this document CONFIDENTIAL...

(THUS THE BSE/nvCJD 'CHOSEN ONES theory was born sometimes after this...TSS)

snip...

NEVERTHELESS an open mind should be kept. At present I would recommend playing at low key because a simple explanation may be forthcoming as a result of current investigations which will allay fears.

YOU may also find the information valuable for defence of the CVL in a POLITICAL SENSE.....

http://www.bseinquiry.gov.uk/files/yb/1986/12/19001001.pdf



Dr. Boothby has understandably fallen victim to that well recognised RUSE of PATHOLOGISTS, confounding all but here own, in sometimes ascribing similar names to histological apperances of quite differing natures......



http://www.bseinquiry.gov.uk/files/yb/1988/01/28001001.pdf



or who knows, maybe 1981 ???



http://www.bseinquiry.gov.uk/files/yb/1984/01/30001001.pdf



ANOTHER THING, was it from a scrapie strain and or a strain of TME that started this? IF you look at the outbreaks of TME, look at the Stetsonville outbreak and what those mink were fed way back then ??? ;



OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



IN CONFIDENCE Perceptions of unconventional slow virus disease of animals in the USA



G A H Wells


REPORT OF A VISIT TO THE USA APRIL-MAY 1989



http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf




Subject: First Confirmed Case of BSE April 1985 (ANNEX 6) $ BOVINE [[ However all routes of transmission were considered possible]]
Date: November 1, 2000 at 11:38 am PST


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

Greetings List Members,

found this in a pile, i have failed to post........sorry

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

MEETING HELD ON 8 JUNE 1988 TO DISCUSS THE IMPLICATIONS OF BSE TO
BIOLOGICAL PRODUCTS CONTAINING BOVINE - EXTRACTED MATERIAL

Chairman - Dr Little
Mr Bradley
Mr Dawson
Mrs Evans
Mr Gray
Mr Kidd
Mr Luff
Dr Thornton
Mr Wilesmith

BACKGROUND

The first cases of BSE were identified in November/December 1986, but
with reviewing previous data the first confirmed clinical case was found
to be in April 1985.

The incidence of BSE was highest in the South of England but incidents
had occurred from the Shetlands down to Guernsey.

The youngest recorded age at which BSE was confirmed in a cow was 2
years 9 months, while the peak incidence appeared to be in 4 year old
cattle.

It was considered that exposure to the disease had occurred from 1982
onwards and that the incubation period ranged from 3-6+ years.

Calves appeared to be at 30x greater risk than adult cattle and
incidents were significantly more prevalent in dairy rather than beef
suckler herds.

The major source of infection was considered to be infected meat and
bonemeal feedstuffs. It was noted that meat and bonemeal feedstuffs were
exported to Europe and the third world.

BSE AGENT

Characterisation of the protein fibrils of the agent showed it to be a
spongiform encephalopathy agent and as yet no differences between BSE
and scrapie, other than host, have been found.

So far there has been no evidence on BSE transmissibility to other
species, but experiments are underway.

Discussion continued with scrapie being used as the model for BSE
distribution in lymphoid tissues and subsequent treatment.

The tissues most at risk of containing, and consequently transmitting,
scrapie were the brain, spinal cord and lymphoid tissues. Scrapie had
been found in many other tissues including the placenta, pancreas and
lung. However all routes of transmission were considered possible so use
of any bovine derived tissues were considered to be of some degree of
risk.

88/06.08/11-1

BOVINE BIOLOGICAL PRODUCTS

The bovine tissues used in biological products were outlined as:

SERUM

This was the main concern as it was included in the majority of
biological products.

Serum was considered likely to be of low risk for transmission of the
agent. However, utilization of a closed farm with no known clinical
cases would be preferable for serum production. If non-UK serum were to
be included in products it would need to be irradiated to remove any
other viruses or bacteria.

PEPTONE/MEAT DIGEST

For growth media and also used as a freeze-drying stabiliser.
Autoclave treated.


PITUITARY EXTRACT

This was used to help cows super ovulate. This tissue was considered to
be of greatest risk of containing BSE and consequently transmitting the
disease.

BEEF BRAIN AND BRAIN INFUSION BROTHS

Considered to be of great risk.

TISSUE CULTURES DERIVED FROM PRIMARY BOVINE TISSUES

Milk proteins - serapie had not been found in milk as yet.

OX BILE

FAECES

Scrapie was suspected of being excreted in the faeces, but had not been
isolated
yet.
RECOMMENDATION

The greatest concern was the use of pituitary gland products. It was
agreed that the Medicines Unit should prepare a paper to advise Animal
Medicines Division, Tolworth on the course of action to be taken.

It was agreed that B P & S should draw up a full list of all the tissues
involved in biological products. Medicines Unit would produce a list for
pharmaceutical products. A chart of risk assessment should be made for
each of the tissues in relation to the products, together with
appropriate treatments for each tissue.

It was agreed that some form of guidance should be given to companies at
the next NOAH meeting on 11 July.

MEDICINES UNIT
June 1988

88/06.08/11.2
=============
TSS

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

Greetings List,

dont know if this will help calm nerves a bit, but
you might find what you want here, in one of those reference
YB numbers. her hand-written notes on the case would be;
YB85/9.10/3.1-3.2

>It was not, therefore, immediately apparent from the
>post-mortem histopathological examination of the brain
>of one animal in this herd that it was the first and
>unprecedented case of a new disease. Even though it
>can now be seen, with hindsight, that such was the case.

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

The Stent farm cases

12. On 10th September, 1985 specimens (brain, kidney and
spinal cord) from a cow owned by a Mr Stent of
Pitsham Farm was referred to the CVL by the Winchester VI
Centre (Mr J. Watkin-Jones, Veterinary Officer
(VO)) for histopathological examination. Referrals from the VI
Centres were dealt with on a rota system by the
Consultative Pathology Unit (see paragraph 9 above). The
veterinary pathologist on duty when the case came in
to the Pathology Department was Ms Carol Richardson. At the
time both Carol Richardson and I held the
position of Senior Research Officer Grade II (SROII), both of
us reporting directly to Ray Bradley. Carol
Richardson worked in a section of the Department called
Ruminant Reproductive Pathology and I believe that she
had been working mainly on reproductive disorders in cattle
and sheep, with a particular interest in research into
infections producing foetal damage. She would, however, have
dealt with scrapie cases through some of her
previous work with Dr Stanley Terlecki, a former pathologist
in the Department.

13. When such diagnostic cases came into CVL from a VI Centre
the technician on duty at the time completed a
VL99 card summarising the clinical history of the cow and the
herd it originated from (based on information
provided in the referral letter from the relevant VI Centre).
The duty veterinary pathologist prepared the necessary
pathological material for histological processing. Sections
were then produced from the animal tissues for
subsequent examination. The VL99 card for this particular case
from Mr Stent's farm is found at
YB85/9.10/3.1-3.2. This card and the prepared sections would
then have been passed back to the duty veterinary
pathologist for examination, which in this instance was Carol
Richardson.

14. Carol Richardson conducted the histopathological
examination and reported her findings on 19th September,
1985 (YB85/9.10/3.1-3.2). Her hand-written notes on the
examination are on the VL99 card (see
YB85/9.10/3.1-3.2). The final pathology report prepared by
Carol Richardson, which was sent to Mr
Watkin-Jones at Winchester VI Centre, is found at
YB85/9.19/3.2. It should be noted that the purpose of the
pathology reports prepared by the veterinary pathologists for
such referrals from VI Centres is to make
morphological diagnoses based on an examination of specimens
provided. As far as is possible the pathologist
then tries to place the diagnosis in the context of the
clinical history of the particular animal and its herd or flock to
reach conclusions or speculations on an aetiological diagnosis
(the cause of the observed changes). This is the
purpose of the "Remarks" section of the pathology report.
Carol Richardson's examination reported "moderate
spongiform encephalopathy" and "mild renal nephrosis" (the
morphological diagnoses) and she attributed these
observed changes to "a toxicity of some description" (the
possible aetiological diagnosis). This was what was
reported to the VI Centre. It is notable that nowhere in her
report does she mention scrapie or indicate that her
observations lead her to suspect any "scrapie-like" disease.
The fact that the report mentions "moderate
spongiform encephalopathy" is not conclusive in that respect.
As highlighted by my short paper on vacuolation
previously referred to in paragraph 8, spongiform conditions
of the brain can arise from several different causes,
including as a reaction to the ingestion of toxic substances,
so this observation was consistent with her suggested
aetiological diagnosis.

15. At the time this case came in from Mr Stent's farm, I was
attending a meeting of the Charles Davis DVM
Foundation for Veterinary Pathology in Cheshire. As is often
the practice between pathologists in the event of
encountering unusual or unexplained findings, Carol Richardson
left the specimens and her pathology report for
me to examine immediately on my return. A copy of Carol
Richardson's report of 19th September, 1985 as
annotated in manuscript by myself, is found at YB85/9.19/3.1.
When sections are left for colleagues to examine it
is not expected that any particular action would be taken by
the colleague on his or her own initiative in respect of
those sections. The purpose would be simply to offer a view on
the material and then return the sections and
report to the original examining pathologist, as was the case
in this instance. Carol Richardson was absent from
the Department on sick leave from 29th December, 1986, and
this subsequently became maternity leave on 31st
May, 1987. She returned to the Department on 29th December,
1987. Had Carol Richardson felt strongly
thatabout the observations she had originally made were those
of scrapie in cattle, and my subsequent opinion on
her report, I would have expected that she would have come
back to me to discuss the matter subsequently or
take the matter further herself. in the period between seeing
my annotations on her original report on the Stent
case in September 1985 and her absence at the end of December
1985.

16. My re-examination of the sections "reinforcedwas
consistent with" her original diagnosis in so far as I agreed
with her overall observations and that such observations were
not artefactual i.e. caused as a result of
post-mortem changes or in the preparation of sections. My
conclusion was that the brain lesions observed in this
case could not in my experience be attributed to a specific
disease, but a speculative comment was made that they
could possibly be the result of chronic bacteraemia or an
endotoxaemia (the production of poisons in the blood
due to infection). Whilst the clinical history as described by
the referring VI Centre (see YB85/9.10/3.1) describes
that seven out of 130 cows were "nervous", this does not
equate necessarily to the occurrence of a specific
neurological disorder. The history indicated the occurrence of
complex metabolic problems within the Stent herd
(see paragraph 17 below).

17. Samples from three other cows in the Stent herd which had
died or were killed on the farm had been referred
to CVL for examination earlier in March, April and May of 1985
(CVL references VLO11453/85/0286,
VLO11453/85/0640 and VLO12473/85/0831 respectively).
Following, as far as I can recall, a telephone call
from Mr J. Watkin-Jones, on 26th September, 1985 I reviewed
the history of the submissions from the Stent herd
and discussed them with him. This again, was standard practice
where the VIS were investigating a persistent herd
problem. A copy of my note of this event, together with the VI
Centre referral letters and pathology reports for
each case from the Stent farm (with manuscript comments made
by myself at the time of this review) are found at
YB85/9.26/1.1; YB85/9.10/3.1; YB85/9.19/3.1; YB85/4.31/1.1;
YB85/5.9/1.1; YB85/4.6/1.1; YB85/4.16/1.1;
YB85/2.13/1.1 and YB85/3.1/1.1 respectively. None of the
samples for the three earlier cases included brain
tissue and the main post-mortem finding in these cases was
internal bleeding. Taken in isolation and in the light of
these factors, the case in September 1985 did not at that time
suggest that a new disease had been identified.
Vacuolar changes in the brain of that particular animal were
not severe and there was previous, and current,
evidence of other disease problems. The herd from which these
animals came had clearly experienced a lot of
other health problems including haemorrhagic disorder
(internal bleeding), hypocalcaemia (lack of calcium), septic
arthritis (pus in joints), renal damage, bovine viral
diarrhoea and peritonitis (inflammation of the abdominal cavity)
associated with foetal death. This was a complex pattern in a
dairy herd indicating that a variety of different
diseases might be occurring. It was not, therefore,
immediately apparent from the post-mortem histopathological
examination of the brain of one animal in this herd that it
was the first and unprecedented case of a new disease.
Even though it can now be seen, with hindsight, that such was
the case.

18. Further samples of nervous system tissues and other organs
were received at CVL from a cow in the Stent
herd on 10th September, 1986 (YB86/9.22/1.1-1.2). These were
examined by Dr S. Done, a veterinary
pathologist who joined the Pathology Department in 1983. A
copy of the VL99 card for this case is found at
YB86/9.22/1.1-1.2. Histopathogical examination of the central
nervous system (CNS) tissues submitted from this
case showed mild spongiform change in the medulla (hind
brain). Other brain regions are described as having
either no visible lesions or mild focal haemorrhage. See
paragraph 31 for further discussion of this case.

http://www.bse.org.uk/witness/htm/stat065.htm



4.The single case of BSE that I examined in September 1985 was the one
and only case that I have seen.

5.The first officially reported case of BSE

Memory recalls a sequence of events the importance of which can
only be made by informed judgement. The following
account of an interesting and exciting event is taken largely from
my memory. I have used copies of the original
letter,case card, diagnostic report, accession books and my 1985
organiser diary to make this account as accurate as
possible.

6.I had returned from annual leave and was on rota as duty
pathologist. The senior technician of the diagnostic unit asked
me to examine an adult bovine brain; the vet wanted a diagnosis
a.s.a.p.

7.The history was of 7/130 cows showing nervous symptoms over the
previous 5 months; most had gone for casualty
slaughter and no gross abnormality had been seen in the viscera.
(YB85/9.10/1.1).The Pathology Department had
examined pieces of liver, kidney, heart and lung from three
previous cases from this farm (YB85/2.15/1.1; YB85/4.9/1.1;
YB85/5.3/1.1) (2 adults and 1 calf)and had found chronic mild
hepatitis(1),acute hepatic necrosis (1) moderate
pulmonary oedema (1) and chronic mild interstitial nephritis (2).

8.The history of these earlier cases was one of internal haemorrhage
and samples had been sent for organic mercurial
poisoning assay. There had been metabolic problems in this herd and
active BVD infection in the calves. The case card
numbers of these three cases can be seen in the cross-reference
column on the case card of the September specimen-
MS1509/85 (YB85/9.10/2.1). In addition to the nervous signs seen in
this cow, abscessation of the stifle was also
present. On gross examination, the brain was well fixed and
relatively undamaged; pieces of spinal cord and a piece of
kidney were included and were grossly unremarkable. The meninges
appeared thickened but this was probably normal
for an adult cow.

9.In the absence of gross abnormality, I made multiple incisions and
took standard blocks (13) for histological processing
and the production of H&E (see procedures) sections. Blocks of
spinal cord and kidney were also sent for processing
(11/9/85).

10.I have a set sequence for examining brain sections; when these
sections were returned to me (13/9/85) I examined the
frontal cerebrum first and progressed caudally scanning each
section from dorsal to ventral surface. In this case there
seemed to be a mild vacuolation of the cerebral neuropil. At this
time Gerald Wells had been investigating the possibility
that prolonged exposure of nervous tissue to 70% alcohol could
produce neuropil vacuolation. Such prolonged exposure
would occur over the week-end but I checked with the technician to
ensure that such exposure had not occurred in this
case before resuming my examination. I noted finding a mild
multifocal non-suppurative peri-vascular infiltration with
some eosinophils and in the caudal cerebrum mild focal gliosis. No
abnormality was found in the thalamus (cranial
midbrain) but mild neuropil vacuolation of the reticular formation
in the colliculi. The medulla (a pathogonomic site for
Scrapie in sheep) showed moderate neuronal and neuropil
vacuolation. I found no abnormality in the cerebellum but the
section of lumbar spinal cord showed mild neuropil vacuolation of
the dorsal horns. There were two types of lesion in the
section of kidney;a chronic mild /moderate non-suppurative
interstitial reaction with tubular regeneration and fibrosis; a
peracute reaction of a mild multifocal tubular necrosis with
hydropic change (protein reabsorption).

11.These sections were reviewed by Gerald Wells in 1987 with
essentially similar findings but more refined. (See case card
at YB85/9.10/2.1).

12.Although I had never seen this type of lesion before in a cow I had
frequently seen the combination of neuronal and
neuropil vacuolation with this distribution in Scrapie. To me,this
was Scrapie in a cow.

13.Before writing the report I sought a second opinion; I needed the
opinion of a ruminant neuropathologist and therefore
placed the sections, my findings and a request for re-examination
on Martin Jeffrey’s bench. I was eager to hear his
opinion and immediately after lunch went to collect the slides.
Martin had left a note on which was written "Bovine
scrapie". As I left his room I met him in the doorway. Apparently
this was the first case he had seen but he informed me
that Gerald had examined two cases and was expecting another two
cases.

14.Interestingly, we apparently had more than one case here from
different farms but obviously Gerald was dealing with it.
In all my experience, there has not been a case of a novel disease
in cattle affecting more than one farm initially: this
should have caused alarm bells to ring. If there are several cases
at different farms, it is important to cross-reference for
the purposes of disease surveillance. A site visit to the Pitsham
farm would have resulted in further well-preserved
specimens, and more background information.

15.On the 17th-18th Sept. I drafted a batch of diagnostic reports
including my report to Winchester VIC (YB85/9.19/1.1).

16.The report is a reiteration of my findings except that the
histo-anatomical term `reticular formation’ should have been
typed in the sentence above and not under the findings in the
medulla. When it came to stating a diagnosis I decided that
since the pathological term used for the clinical disease Scrapie
of sheep is ovine spongiform encephalopathy then this
"new" entity must also be classified as a "spongiform
encephalopathy". I called it mild because again projecting onto the
sheep situation with only a few sites affected the inclusion of
mild as a descriptive term seemed correct. Although there
was a chronic interstitial nephritis , I decided to highlight the
peracute nephrosis which was probably related to a
bacterial toxaemia associated with the stifle abcess.

17.From the history of the case on the Stent farm, it seemed as if the
clinical course of the disease was fairly rapid in that
metabolic disorders of short duration and heavy metal toxicities
were being considered on the farm. Therefore, it seemed
likely that the cause(s) of the spongiform changes were a result of
an acute clinical disease (rather than a chronic illness)
and in the absence of a more likely aetiology, toxicity seemed to
be the most appropriate catagory that fitted both
symptoms and findings.

18.I dismissed the possibility that a bacterial toxaemia had caused
the spongiform change; in my limited experience of
ruminant neuropathology, toxaemia was likely to produce frank
neuronal necrosis rather than degenerative vacuolation
(cf. Clostridial toxaemia).

19.The report was sent for typing; returned and despatched on the 19th
September. The second copy and the original letter
was filed on VlO 12467, the diagnostic file for cattle diseases. I
asked the technician, Dorothy Wells (no relation to
Gerald) to cross-reference with similar cases. I always asked the
technician to do this, to enter the case numbers of
similar cases on the pathology card. In this case I asked Dorothy
to cross-reference for the two cases that Gerald had
appaerntly already seen.

20.I heard nothing further about my 1985 case.

21.I left the CVL at Christmas 1986, on maternity leave.

http://www.bse.org.uk/witness/htm/stat069.htm



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

Greetings List Members,

in looking over some other files and documents, i found this,
and thought i would pass it on;

STRICTLY PRIVILEGED
AND CONFIDENTIAL - PREPARED
FOR THE PURPOSES OF EXTERNAL

THE BSE INQUIRY

SCIENTIFIC EVIDENCE PHASE 1

STATEMENT FOR THE PERIOD 1985 TO 3RD FEBRUARY, 1989

OF RAYMOND BRADLEY


33. Around this time, I believe (but I cannot specifically
recall) a review of pathology reports of brain
examinations from cases of neurological disease in adult
cattle examined at CVL was initiated to see if there was
evidence, with the new knowledge we had acquired, that cases
of BSE had occurred earlier than the first reported
cases in November/December 1986. It uncovered a case from
September 1985. Carol Richardson, a pathologist
in the Pathology Department at CVL, had examined this cow
brain and had reported spongiform change and also
kidney disease. The herd of origin appeared to be affected by
an unidentified toxicological problem and kidney
disease. In view of the history of the herd, at the time it
was suggested that the illness might be due to an unknown
toxic condition and this was indicated in Carol Richardson's
initial report, with which Gerald Wells agreed in
substance, although he made some amendments to the detail.
When this case was later reviewed and with the
benefit of experience of the new disease it was recognised
that it had been a case of this disease.

http://www.bse.org.uk/witness/htm/stat071.htm



BUT, even more interesting, i find in Dr. Gibbs document,
i have not scanned and posted yet;

Reprinted from Clarence J. Gibbs, Jr.
Editor

Bovine Spongiform Encephalopathy

The BSE Dilemma

1996 Springer-Verlag New York, Inc.
Printed in the United States of America

Preliminary Observations on the Pathogenesis of Experimental Bovine
Spongiform Encephalopathy

Gerald A. H. Wells, Michael Dawson, Stephen A. C. Hawkins, Anthony R.
Austin, Rober B. Green, Ian Dexter, Mark W. Horigan, and Marion M.
Simmons

3. Preliminary Observations on the Pathogenesis of Experimental BSE

First, uniformity of the pathology defined by the pattern of
distribution and severity of the vacuolar changes in the brains of
affected cattle, in both natural disease and in cases experimentally
induced by parenteral inoculation, provided an indication of the
phenotypic stability of the infection and gave rise to the view that the
epidemic in Britain involved a single strain of scrapie-like
pathogen (16, 21, 22). A later finding showed further that on primary
transmission, to a standard panel of isogenic mice, seven different
cases of BSE presented uniformity of the pathologic phewnotype in each
mouse strain (16). "It can be concluded that this bovine-adapted agent
was established in cattle prior to clinical recognition of the disease,
and since four of the seven cases strain typed were present in the
national herd in 1982, this was perhaps as early as the time of putative
initial exposure of cattle to a scrapie-like agent (2, 23).

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

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



Murgen,



SCRAPIE is and has been rampant and uncontrolable in the USA for decades, and fed back to humans and animals for human consumption, along with TME, CWD, TSE in cattle of multiple strains. Scrapie transmits naturally to primates by there non-forced oral consumption of tainted feed. sporadic CJD of humans also transmits to primates by the same mode of transmission. FROM here, one must make up there own mind. mine is and has been made up, i.e. amplfication and transmission, it's not rocket science, just science ignored. origin, ill leave that for the scientist. we must act on what we know, amplification and transmission.



SO, Murgen, to answer your question finally ;



> Flounder, do you believe the UK/Canadian strain may have been a result

> of the strain now found in the US?


who knows? i dont. possible, anything is possible. with the enormous amount of product shipped across our borders between mexico, canada, and the usa, who know's, but again, why overlook the obvious and most important i.e. amplification and transmission, we must adhere to the feed ban, strengthen it, and by all means we must be very vigilant, especially in the medical and surgical i.e. friendly fire of human and animal TSEs. MOST IMPORTANTLY, the BSE MRR policy of GWs and the OIE, this thing must be REPELLED AT ONCE. the bse mrr policy was nothing more than a legal tool to trade all strains of TSE globally, and it worked. the BSE GBR risk assessments must be adhered too, and strengthened to include all TSE, until those TSE are proven safe via transmission studies.


Murgen wrote;


> From what I have read, this "atypical" strain was very difficult to find/determine with previous testing methods


These so-called atypical cases match results in seven cases discovered in France, says Dr. Jean-Philippe Deslys, project coordinator for NeuroPrion, the European Network of Excellence, but are dissimilar to three other French cases as well as a handful in Italy and Germany, among others. The U.S. cases are so-called "high-weight" on a molecular basis, while the other atypical cases are "low-weight." (Results of ongoing experiments on this topic are due to be presented at Prion2006 in Turin, Italy in October.)

What it means is anyone's guess. Deslys says it could mean one of three things: that the "classic" BSE infection has mutated, much like a virus; that these cases are linked to scrapie in sheep or are truly spontaneous like most CJD (Creutzfeldt-Jakob disease) cases in humans and present little or no infective risk; or most ominously, that a new pattern of infectivity has emerged and may not be identified for years. ...end


ALSO ;


Q&A Dr. Jean-Philippe Deslys

1. What is the standard regime for testing of suspect animals in the EU?

The regime is an initial screening by a high-output test, the Bio-Rad
test. If a result raises suspicion, a confirmatory test is conducted
with the Western blot test.

2. How long has this been the case?

Its a fairly recent development. Only recently has the Western blot
test become sensitive enough, with the addition of phospohtungstic acid
precipitation step. The Bio-Rad test (which Deslys helped develop) is
extremely sensitive, and the standard Western blot is extremely reliable
with high-signal test results. However, it had to be made more sensitive
for low-signal (samples with low density of malformed prions) samples.
It has been made more sensitive.

Reproducibility is the problem with the IHC test. It is not
standardized; depending on the lab and its protocols, or even on the
technician involved in the test, one can get conflicting results.

3. Is there a way to measure the three tests in sensitivity, accuracy
and objectivity?

Historically, yes. The IHC was the gold standard at one point, but we
have shifted to the Western blot. It requires less work, it is more
sensitive and its results are reproducible. IHC relies on localization.
If you have a weak signal case, you may get lucky and test a spot with a
high concentration of prions. But the opposite it true too; you can miss
an infection by testing a sample with low concentrations. Western blot
is much better for low signal situations.

4. The USDA in 2003 used the Western blot to confirm the BSE case in
Washington state, and it sent samples to the U.K. for independent
testing. In the case this November, which it announced was negative, it
instead used the IHC test and did not send samples to the U.K. Is this
good science?

Its not logical. If you have two consecutive questionable screenings,
you do another test. I can only advise, its managements duty at USDA
to make the decisions. But when you have a discrepancy between the rapid
test and the IHC, it is only logical to confirm it with another test.

5. We are hearing now about a new strain of BSE, atypical BSE or aBSE.
Or BaSE. We have heard that IHC, the so-called gold standard, cannot
detect the variant. Is this true?

Yes. There have been a few cases, one in Italy, one in Belgium, one here
in France. It seems to only affect very old animals. The distribution in
the brain is very different than we see with BSE, it looks very
different. The IHC test will come back negative.

This his a very recent phenomenon. I have no opinion on its virulence.
We do not know where it comes from. It could be a version of sporadic
infection. Western blot caught them, but we would not even know it
existed if we werent running systematic testing in the EU.

BSE was around for a long time before we caught it and by then, it was
everywhere. It had become highly infectious. It probably amplified due
to low-temperature rendering. The disease was recycled through the food
chain, and was given time to amplify. By the time it was identified,
even good cooking couldnt eliminate it.

I cant stress enough that systematic testing is necessary. Withdrawing
all positives from the food chain is the best way to break the cycle.

What can happen with testing of only cattle that are clearly at risk is
that several can remain undetected. Canada has tested about 30,000 head
of cattle and has three positives. That would indicate that there are
probably undiscovered cases. And what happens then is that the disease
is allowed to amplify. You have to maintain testing.

When people choose to protect their economic interests over public
health, it can have a boomerang effect. It happened all through Europe.
They always deny; its not OUR problem, it is our neighbors problem.
And then a single case is discovered and the public reacts. The economic
results are devastating. It would be better to just assume BSE is
present and use systematic testing as protection. That way, the public
is reassured that it is not entering the food supply.

By systematic testing, I mean doing as we do in the EU, which is to test
every animal over 30 months of age when it is slaughtered. In Europe,
three times as many cases of BSE have been caught by systematic testing
as by clinical testing (of clearly sick animals). In 2004, eight
clinical cases were discovered, 29 were discovered at rendering plants,
and 17 at slaughter. We should be using these tests as a weapon to
protect the public and to give them assurance that the food supply is
being protected.

6. USDAs list of specified risk materials excludes some products, like
blood and bone meal, that are banned in the EU and UK. Is our feed
supply safe?

With SRMs, where do you stop? Tests have found prions in meat, nerves
travel through meat, and so on. The main infectivity is in the brain and
the spinal cord. A blood and bone meal ban in animal feed is not really
necessary, because except in cases of highly infective animals, it is
unlikely that they are dangerous in themselves. If you combine
systematic testing and targeted SRM removal, the brain and the spinal
column in cattle over 30 months, you can have a compromise that is both
safer and less costly than expanded feed bans.

Certainly, you can stop the spread of BSE with a total ban on offal. But
it has to be a total ban. It cant be given to sheep or swine or
poultry. It would be very expensive and virtually impossible to
accomplish. You can have farmers using the wrong feed or transportation
errors.

Systematic testing makes far more sense. I think of it as a thermometer.
It not only allows us to catch the disease, it also allows us to monitor
its progress. We can watch the levels of infectivity and if they start
going up instead of down, we can take measures.

To an extent, our environment is contaminated. About 10 percent of wild
animals test positive for TSEs. If you recycle these agents, they can
evolve and get more dangerous. This is probably what happened with BSE.
It wasnt very dangerous until it evolved to the disease we know today.

People complain that testing is very expensive. It is much more
expensive to kill and test whole herds.

7. In your opinion, is infected feed the sole method of transmission of
BSE, apart from the very rare maternal transmission?

Feed is the main problem. However, we are seeing some other
possibilities, including through fat and greases. Calves are fed milk
extracts, with the cream removed. To make it nutritious, they are using
fat and grease from cattle.

(FOLLOW QUESTION: Would that allow BSE to develop into an infective
level in cattle younger than 30 months, assuming they might be getting
infected at a younger age?)

8. You were involved in a study that tested two primates who were fed
infected brain tissue. One eventually died of TSE; the other survived.
The press reported that the main finding was that it would take
something on the order of 1.5 kilograms of infected matter to create an
infection, but that seems to be an oversimplification. Could you explain
it further?

The findings suggest that as little as five grams is enough to infect.
The 1.5 kilo figure is the amount of infected tissue that would have to
be ingested from an animal that would be below the threshold of
infection, and would test negative. In other words, even though a
younger animal may be developing the disease, it would take a
considerable amount of tissue to transmit the disease.

An animal could be just below the testing level, and not be particularly
dangerous. But that is why you have to keep testing. Once it reaches the
threshold, it can become highly infective.

9. BSE is a pretty horrifying disease, but overall, it has killed less
than 200 humans, and only a handful in recent years. Listeria, by
comparison, kills thousands every year. Overall, how do you rate the
threat from BSE?


The overall risk is not particularly high. Over two million infected
animals went into the food chain in Europe, 400,000 of them before the
SRMs, the brains and spinal column, were removed from the carcass. Less
than 200 died, and less than 4,000 are at risk of developing the
disease. What we know now is that one particle is not going to kill you.
There has to be condensation of the prions to be truly dangerous.

This is not a sterile world. But the danger is that now that the crisis
appears to be over, attention will turn elsewhere and that will allow
the disease to amplify again. Just as we stopped paying attention to
AIDS when medication seemed to control it, then were surprised when a
new and more infectious and aggressive strain appeared, we could be
surprised by a more serious strain of BSE. That is why I support
systematic testing for the long term. The object is to keep levels of
BSE low, and to recognize the danger if it suddenly pops back up. ...END

TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########



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.





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




Murgen wrote;


> Or is it just a coincidence that the Country that export the most MBM/SRM's in the world is also the location of the highest rate of TSE's?



indeed, this is what you call being bush whacked, dixie chicked, and or screwed by more BSe, at least that is what USDA et al wants us to believe. that's political science, here are facts, i.e. 'sound science'


http://www.efsa.eu.int/science/tse_assessments/gbr_assessments/573/sr03_biohaz02_usa_report_v2_en1.pdf


http://www.efsa.eu.int/science/tse_assessments/gbr_assessments/564/sr02_biohaz02_canada_report_v2_en1.pdf


http://www.efsa.eu.int/science/tse_assessments/gbr_assessments/565/sr04_biohaz02_mexico_report_v2_en1.pdf




Murgen, I propose once again the following for the ones still with me here ;


HUMAN and ANIMAL TSE Classifications i.e. mad cow
disease and the UKBSEnvCJD only theory



TSEs have been rampant in the USA for decades in many
species, and they all have been rendered and fed back
to animals for human/animal consumption. I propose that
the current diagnostic criteria for human TSEs only
enhances and helps the spreading of human TSE from the
continued belief of the UKBSEnvCJD only theory in 2005.
With all the science to date refuting it, to continue
to validate this myth, will only spread this TSE agent
through a multitude of potential routes and sources
i.e. consumption, surgical, blood, medical, cosmetics
etc. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis,
Marsh, et al and many more, that the world of TSE
Tranmissible Spongiform Encephalopathy is far from an
exact science, but there is enough proven science to
date that this myth should be put to rest once and for
all, and that we move forward with a new classification
for human and animal TSE that would properly identify
the infected species, the source species, and then the
route. This would further have to be broken down to
strain of species and then the route of transmission
would further have to be broken down. Accumulation and
Transmission are key to the threshold from subclinical
to clinical disease. Key to all this, is to stop the amplification

and transmission of this agent, the spreading of, no matter what

strain. BUT, to continue with this myth that the U.K. strain of
BSE one strain in cows, and the nv/v CJD, one strain in
humans, and that all the rest of human TSE is one
single strain i.e. sporadic CJD (when to date there are
6 different phenotypes of sCJD), and that no other
animal TSE transmits to humans, to continue with this
masquerade will only continue to spread, expose, and
kill, who knows how many more in the years and decades
to come. ONE was enough for me, My Mom, Heidenhain

Variant of Creutzfeldt Jakob disease, hvCJD, DOD
12/14/97 confirmed, which is nothing more than another
mans name added to CJD, like CJD itself, Jakob and
Creutzfeldt, or Gerstmann-Straussler-Scheinker
syndrome, just another CJD or human TSE, named after
another human. WE are only kidding ourselves with the
current diagnostic criteria for human and animal TSE,
especially differentiating between the nvCJD vs the
sporadic CJD strains and then the GSS strains and also
the FFI fatal familial insomnia strains or the ones
that mimics one or the other of those TSE? Tissue
infectivity and strain typing of the many variants of
the human and animal TSEs are paramount in all variants
of all TSE. There must be a proper classification that
will differentiate between all these human TSE in order
to do this. With the CDI and other more sensitive
testing coming about, I only hope that my proposal will
some day be taken seriously. ...




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