From: TSS (216-119-139-107.ipset19.wt.net)
Subject: Re: BSE aka MAD COW UPDATE (USA still not looking to find$$$)
Date: February 14, 2003 at 2:03 pm PST
In Reply to: BSE aka MAD COW UPDATE (USA still not looking to find$$$) posted by TSS on February 14, 2003 at 1:57 pm:
please note, there has never been transmission
studies done on man.
so, lets look at primates;
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus)
that were exposed to the infectious agents only by their nonforced
consumption of known infectious tissues. The asymptomatic incubation
period in the one monkey exposed to the virus of kuru was 36 months;
that in the two monkeys exposed to the virus of Creutzfeldt-Jakob
disease was 23 and 27 months, respectively; and that in the two monkeys
exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the
monkeys failed to reveal signs or oral lesions. One additional monkey
similarly exposed to kuru has remained asymptomatic during the 39 months
that it has been under observation.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
20 year old died from sCJD in USA in 1980 and a 16 year
old in 1981. A 19 year old died from sCJD in
France in 1985. There is no evidence of an iatrogenic
cause for those cases....
http://www.bseinquiry.gov.uk/files/yb/1995/10/04004001.pdf
cover-up of 4th farm worker ???
http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/20006001.pdf
CONFIRMATION OF CJD IN FOURTH FARMER
http://www.bseinquiry.gov.uk/files/yb/1995/11/03008001.pdf
now story changes from;
SEAC concluded that, if the fourth case were confirmed, it would be
worrying, especially as all four farmers with CJD would have had BSE
cases on their farms.
to;
This is not unexpected...
was another farmer expected?
http://www.bseinquiry.gov.uk/files/yb/1995/11/13010001.pdf
4th farmer, and 1st teenager
http://www.bseinquiry.gov.uk/files/yb/1996/02/27003001.pdf
DAIRY FARM WORKERS ARE _5_ TIMES MORE LIKELY TO DEVELOP
CJD THAN THE AVERAGE POPULATION (but it's only sporadic ???)
Deer Hunters?
http://www.bseinquiry.gov.uk/files/yb/1995/01/31004001.pdf
The EMBO Journal, Vol. 19, No. 17 pp. 4425-4430, 2000
© European Molecular Biology Organization
Evidence of a molecular barrier limiting
susceptibility of humans, cattle and sheep to
chronic wasting disease
G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O?Rourke3,
L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M.
Smits2
and B. Caughey1,7
1NIAID/NIH Rocky Mountain Laboratories, Hamilton, MT 59840,
3USDA/ARS/ADRU, Pullman, WA 99164-7030, 4USDA/ARS/ABADRL,
Laramie, WY 82071, 5Colorado Division of Wildlife, Wildlife Research
Center, Fort Collins, CO 80526-2097, 6Department of Veterinary Sciences,
University of Wyoming, Laramie, WY 82070, USA and 2ID-Lelystad,
Institute for Animal Science and Health, Lelystad, The Netherlands
7Corresponding author e-mail: bcaughey@nih.gov Received June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.
Abstract
Chronic wasting disease (CWD) is a transmissible
spongiform encephalopathy (TSE) of deer and elk,
and little is known about its transmissibility to other
species. An important factor controlling
interspecies TSE susceptibility is prion protein (PrP)
homology between the source and recipient
species/genotypes. Furthermore, the efficiency with which
the protease-resistant PrP (PrP-res) of one
species induces the in vitro conversion of the normal PrP
(PrP-sen) of another species to the
protease-resistant state correlates with the cross-species
transmissibility of TSE agents. Here we
show that the CWD-associated PrP-res (PrPCWD) of cervids
readily induces the conversion of recombinant cervid PrP-sen
molecules to the protease-resistant state in accordance
with the known transmissibility of CWD between cervids. In contrast,
PrPCWD-induced conversions of human and bovine PrP-sen were
much less efficient, and conversion of ovine PrP-sen was
intermediate. These results demonstrate a barrier at the
molecular level that should limit the susceptibility of these non-cervid
species to CWD.
snip...
Clearly, it is premature to draw firm conclusions about CWD
passing naturally into humans, cattle and sheep, but the present
results suggest that CWD transmissions to humans would be as
limited by PrP incompatibility as transmissions of BSE or sheep
scrapie to humans. Although there is no evidence that sheep
scrapie has affected humans, it is likely that BSE has caused variant
CJD in 74 people (definite and probable variant CJD cases to
date according to the UK CJD Surveillance Unit). Given the
presumably large number of people exposed to BSE infectivity,
the susceptibility of humans may still be very low compared with
cattle, which would be consistent with the relatively inefficient
conversion of human PrP-sen by PrPBSE. Nonetheless, since
humans have apparently been infected by BSE, it would seem prudent
to take reasonable measures to limit exposure of humans
(as well as sheep and cattle) to CWD infectivity as has been
recommended for other animal TSEs.
snip...
http://www.emboj.org/current.shtml
Volume 357, Number 9261
31
March 2001 Articles
Geographical distribution of variant Creutzfeldt-Jakob disease in
Great Britain, 1994-2000
snip...
Table 3 shows data from the Dietary and Nutritional Survey of British
Adults12 on consumption of food items most relevant to putative
transmission of BSE. Those items most likely to have contained
mechanically recovered meat or high-titre BSE agent material from the
central nervous system (burgers and kebabs, sausages, meat pies and
pastries, and other meat products) showed no consistent pattern of
higher consumption in northern regions. People in the
north ate more meat pies and pastries than those in the south, but those
in southeast England consumed the most burgers and kebabs and other meat
products.
Table 4 shows data on meat consumption from the Household Food
Consumption and Expenditure report for 1988,13 for 1984-86. Four
categories of meat or meat products were distinguished. Carcass meat
included: joints; steaks; chops; and mince of beef, pork, and lamb. The
products most likely to have contained bovine mechanically recovered
meat or high-titre BSE agent material from the central nervous
system were classed as other meat and meat products. Consumption of
other meat and meat productsshowed some correlation with vCJD
incidence (r=0·72, p=0·03) (figure 3), whereas for both carcass
meat and poultry the correlation was negative (r=-0·70,
p=0·04; and r=-0·68, p=0·04, respectively), and bacon consumption was
not correlated (r=0·12,p=0·77).
snip...
We identified a group of five people with vCJD in Leicestershire as the
most likely cluster (p=0·004). There were no other significant
(p<0·05) clusters. In particular, the cases in Kent which have been
much debated17 were not identified as a cluster. The
population of Leicestershire at the 1991 census was about 870 000, which
gave a local cumulative vCJD incidence of about 5·7 per million,
whereas overall cumulative incidence in Great
Britain was about 1·5 per million. Four of the five Leicestershire
people lived in the district of Charnwood. Charnwood had a population of
about 142 000 in 1991, which gave a cumulative
incidence for this district of about 28·2 per million. The fifth person
lived a few km outside Charnwood District; the greatest distance between
any two of the Leicestershire cases was less than
10 km. Apart from the closeness of place of residence, these cases did
not seem different from others from elsewhere in the country. Two were
women and ages at onset ranged from about 17 to
33 years. All five people were reported to have eaten beef products and
one had worked as a farm labourer.
snip...
Discussion
When we first reported11 an excess of people with vCJD in the north
compared with the south of Great Britain, we were cautious about
interpretation in the absence of an a priori hypothesis that incidence
of vCJD might be higher in the north. Our results show that a similar
excess has been maintained in subsequent cases, which suggests that the
original observation was not a chance finding. We also showed that five
people with vCJD in Leicestershire (which is in the south in our
classification) formed a cluster. Both these findings are based on
analyses of place of residence on Jan 1, 1991. Our findings are not,
however, sensitive to this choice of date; distribution of cases in 1985
(46 in the north of Great Britain, 37 in the south, and one overseas)
and at onset (45 in the north vs 39 in the south) also suggest higher
incidence among individuals living in the north.
Such regional differences could have arisen if ascertainment of people
with vCJD is more complete in the north, perhaps because the CJD
Surveillance Unit is located there (in Edinburgh, Scotland). However,
the similarity of the regional rates for sporadic CJD and for vCJD
referrals who do not have the disease does not lend support to the
hypothesis that there are major differences in ascertainment of CJD
between the two regions.
The socioeconomic profile of the places of residence of individuals with
vCJD was close to that of the whole population, suggesting that the
difference in cumulative incidence between north and south cannot solely
be explained by regional variations in socioeconomic circumstances. The
leading hypothesis for the mode of transmission of the BSE agent to the
human population is that infection occurred through dietary exposure to
contaminated bovine products. Data from the Dietary and Nutritional
Survey of British adults,12 showed no clear pattern of higher
consumption in the north of Great Britain of food items thought most
likely to contain high BSE agent titre material. Data from the Household
Food Consumption and Expenditure report,13 on the other hand, showed a
correlation between consumption of other meat and meat products and vCJD
incidence. Consumption of poultry and carcass meat showed an inverse
relation with vCJD incidence, perhaps because of an inverse correlation
between the consumption of poultry and carcass meat and that of other
meat and meat products.
The positive regional correlation of vCJD incidence with other meat and
meat products is difficult to interpret. Because the analysis was
ecological, the correlation could be attributable to some confounding
factor which is, or was, more prevalent in the north. Furthermore, no
clear correlation was identified between vCJD incidence and the data
from the Dietary and Nutritional Survey of British Adults.12 Regional
rates of vCJD have not correlated with BSE incidence, which has tended
to be higher in the south than in the north.18 These findings might
indicate merely that beef and beef products were generally consumed far
from the place where the cattle were raised.
Exposure routes that might distinguish cases at a national level have
not yet been established--eg, all people with vCJD had eaten beef and
beef products at some time during their lives, but then so have most of
the population. Recent results19 from an investigation of a cluster of
people with vCJD in Leicestershire, led by the local public health
department, indicate that most of these individuals were probably
infected through their diet. Beef carcass meat was unwittingly cross
contaminated with the BSE agent in local butchers' shops where cattle
heads were split. The proportion of other people with vCJD who might
have been infected in a similar way is as yet unknown.
We think the regional differences in cumulative vCJD incidence are not
likely to be attributable to ascertainment bias. Although the general
view is that there are regional differences in diet, do these
differences cause the variations in incidence of vCJD? First, we are
unsure about which food items carried the highest risk, if indeed the
BSE agent was transmitted to human beings through their diet. Second,
the limitations of ecological analyses, including the difficulty of
controlling confounding, are well known even when they provide
consistent results. Our analyses with two independent data sources do
not provide consistent results. A national case-control study of vCJD is
presently underway, which includes an investigation of potential dietary
risk factors in individuals. However, unbiased dietary data from years
past will be difficult to obtain. Relatives rather than the person with
vCJD will have to provide the information and there has been substantial
media coverage of a possible link between diet and risk of vCJD. Results
from the Leicestershire investigation suggest that it might not be only
the type of food consumed that determines risk of vCJD, but also where
and how items were prepared.
http://www.thelancet.com/
http://www.thelancet.com/journal/vol357/iss9261/full/llan.357.9261.original_research.15646.1
Scrapie to Humans?
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract
NEW SCIENTIST MAGAZINE 4/02/01
NEW SCIENTIST EDITORIAL PAGE 3
MAD SHEEP DISEASE?
IF THERE is one categorical pronouncement you
can safely make about prion diseases like BSE
or CJD, it is that one should not make
categorical pronouncements. "British beef is
safe" and "there is no BSE in Germany" come
to mind. Now there are two more: "scrapie is
safe", and "people don't catch sporadic CJD".
Scrapie is the most widespread prion
disease, infecting untold numbers of
sheep worldwide. Sporadic CJD is the
old-fashioned pre-BSE kind that is supposed
to happen spontaneously in unlucky people.
But a surprise observation in France suggests
some sCJD cases--though by no means all--may
be linked to scrapie after all (see p 4).
For years, British authorities asserted that
BSE was harmless because it was a form of
scrapie. In fact, the only evidence scrapie
is safe is some broad-brush epidemiology, good
as far as it goes but unable to reveal
occasional risks for some people from some
sheep. Alarm bells should have rung in 1980
when researchers gave monkeys scrapie by
feeding them infected brains. But that
research, like so much other work on
prion diseases, was never followed up.
We still have little idea what BSE does
in pigs and chickens. The Queniborough
vCJD outbreak (see p 5) would be easier
to understand if we knew how much brain
we must eat to be infected. As for scrapie,
it shouldn't take a chance finding to
tell us that there may be dangerous sheep
out there.
Suspect symptoms
What if you can catch old-fashioned CJD by
eating meat from a sheep infected with
scrapie?
Exclusive from New Scientist magazine
Four years ago, Terry Singeltary watched his
mother die horribly from a degenerative brain disease.................
full text url follows
By Debora MacKenzie
Suspect Symptoms
http://www.newscientist.com/hottopics/bse/suspectsymptoms.jsp
if url dead, go here for 'SUSPECT SYMPTOMS'
you can access article here also;
http://www.organicconsumers.org/meat/scrapiecjd.cfm
Then follow up with PNAS studies from which
new scientist article written from;
Published online before print March 20, 2001
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.041490898
Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*, Virginie Nouvel*,
Hermann Boe*, DomÃnÃque Marcé*, François Lamoury*, Nicolas Kopp [Dagger
] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique
Dormont*, and Jean-Philippe Deslys*
* Commissariat à l'Energie Atomique, Service de Neurovirologie,
Direction des Sciences du Vivant/Département de Recherche Medicale,
Centre de Recherches du Service de Santé des Armées 60-68, Avenue du
Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; [Dagger
] Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003
Lyon, France; § Laboratoire de Neuropathologie, Hôpital de la
Salpêtrière, 83, Boulevard de l'Hôpital, 75013 Paris, France; ¶
Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital,
Crewe Road, Edinburgh EH4 2XU, United Kingdom; and [||] Institute for
Animal Health, Neuropathogenesis Unit, West Mains Road, Edinburgh EH9
3JF, United Kingdom
Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)
Abstract
There is substantial scientific evidence to support the notion that
bovine spongiform encephalopathy (BSE) has contaminated human beings,
causing variant Creutzfeldt-Jakob disease (vCJD). This disease has
raised concerns about the possibility of an iatrogenic secondary
transmission to humans, because the biological properties of the
primate-adapted BSE agent are unknown. We show that (i) BSE can be
transmitted from primate to primate by intravenous route in 25 months,
and (ii) an iatrogenic transmission of vCJD to humans could be readily
recognized pathologically, whether it occurs by the central or
peripheral route. Strain typing in mice demonstrates that the BSE agent
adapts to macaques in the same way as it does to humans and confirms
that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. The agent responsible for French iatrogenic
growth hormone-linked CJD taken as a control is very different from vCJD
but is similar to that found in one case of sporadic CJD and one sheep
scrapie isolate. These data will be key in identifying the origin of
human cases of prion disease, including accidental vCJD transmission,
and could provide bases for vCJD risk assessment.
Introduction
The recognition of a variant of the human transmissible spongiform
encephalopathy (TSE) Creutzfeldt-Jakob Disease (vCJD) in the U.K. in
1996 raised the major concern that it would correspond to human
infection with the agent responsible for bovine spongiform
encephalopathy (BSE; ref. 1). Transmission of BSE to macaques provided
the first experimental evidence as it produced a disease close to vCJD
in humans (2). Strain typing in inbred mice (consisting of measuring the
incubation period and establishing lesion profiles corresponding to the
strain-specific distribution of brain vacuolation) allows reliable
identification of TSE strains (3). This method, together with
biochemical methods, has revealed a single phenotype for the agents of
BSE and the British cases of vCJD (4-6). Mice expressing only the bovine
prion protein (PrP) were highly susceptible to vCJD and BSE, which
induced the same disease (7). Thus, it is now well established that BSE
has caused vCJD, probably by alimentary contamination. In this respect,
the finding of abnormal PrP labeling in the gastrointestinal tract and
lymphatic tissues of orally BSE-contaminated lemurs shows that the BSE
agent can infect primates by the oral route (8). About 1 million
contaminated cattle may have entered the human food chain, and the
future number of vCJD cases could range from 63 to 136,000 depending on
the incubation period of BSE in humans (9). Unlike sporadic CJD (sCJD)
and iatrogenic CJD (iCJD) linked to the administration of contaminated
growth hormone extracted from human hypophyses, in vCJD, the infectious
agent seems to be widely distributed in lymphoid organs, as pathological
PrP (PrPres) can be detected in tonsils, lymph nodes, spleen, and
appendix even in the preclinical phase of the disease (10, 11). This
raises a public health issue with regard to the risk of iatrogenic
transmission of vCJD through surgical instruments, grafts, blood
transfusion, or parenteral administration of biological products of
human origin. However, this risk is difficult to assess, because it
largely depends on factors such as the virulence of the BSE agent
adapted to primates and the efficiency of secondary transmission to
humans by a peripheral route such as the i.v. one. A further issue is
whether vCJD accidentally acquired from humans would be recognized. The
latter poses the question of a phenotypic variation of the BSE agent
after successive transmissions in humans: does it retain its strain
characteristics, and does it induce a pathology similar to that observed
in the previous host? A 9-year history of transmission of BSE to
primates and mice enables us today to clarify a number of these
important points.
Although BSE has mainly affected the U.K., two definite cases and one
probable case of vCJD have now been reported in France in people who
have never resided in the U.K. (12, 13). We strain-typed the first of
these cases to establish its origin. Strain typing in C57BL/6 mice of
BSE, French, and British vCJD was compared with that of BSE passaged in
nonhuman primates, thus allowing us to study the effect of serial
passages in primates. Comparisons were also made with French cases of
sCJD and iCJD and two strains of scrapie (one of French and one of U.S.
origin). Our findings provide experimental demonstration that the same
agent, namely that responsible for the cattle disease BSE, has caused
vCJD both in France and in the U.K., in line with biochemical data and
with the fact that, until 1996, about 10% of the beef consumed in France
was imported from the U.K. We found that the BSE agent in nonhuman
primates is similar to that causing vCJD in humans and tends to evolve
rapidly toward a primate-adapted variant. Furthermore, we showed that
the strain responsible for iCJD is closely related to that of one
patient with sCJD, and, more unexpectedly, that these agents were
similar to the French scrapie strain studied (but different from the
U.S. scrapie strain). This finding requires a cautious interpretation
for several reasons, not least because of the inevitably limited number
of TSE strains that can be studied by such a cumbersome method as strain
typing. Nonetheless, it also prompts reconsideration of the possibility
that, in some instances, sheep and human TSEs can share a common origin.
snip...
http://www.pnas.org/cgi/content/full/041490898v1
STATEMENT OF DR HELEN GRANT MD FRCP
ISSUED 13/05/1999
BSE INQUIRY
http://www.bseinquiry.gov.uk/files/ws/s410.pdf
http://www.bseinquiry.gov.uk/files/ws/s410x.pdf
http://www.bseinquiry.gov.uk/evidence/ws/ws8.htm
kind regards,
terry
Terry S. Singeltary Sr.
Bacliff, TEXAS USA 77518
CJD WATCH
http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm
CJD Watch message board
http://disc.server.com/Indices/167318.html
MADCOW NEWS TSEs/TSS
http://www.vegsource.com/talk/madcow/index.html
just looken for the truth...tss
