• If you are having problems logging in please use the Contact Us in the lower right hand corner of the forum page for assistance.

'Mad cow' proteins successfully detected in blood

Help Support Ranchers.net:

Kathy, I have NOT ignored you and MY feelings are hurt if you think so.
I just haven't had much time lately.

Having said that, you must be careful of posting stuff as you did below because some will doubt you because of "Hamster" experiments. :wink:

Make me a list of questions to ask Dr. "V". I will get them to him.

The conversion of cellular prion protein (PrP(C)) to the disease-associated misfolded isoform (PrP(Sc)) is an essential process for prion replication. This structural conversion can be modelled in protein misfolding cyclic amplification (PMCA) reactions in which PrP(Sc) is inoculated into healthy hamster brain homogenate, followed by cycles of incubation and sonication.
 
TimH, you are actually quite correct. The section of the Paper I quoted did not mention the injection of muscle tissue into muscle tissue. Read the rest of the paper and you will see that the muscle tissue from some of the dead mink was in fact used as an inocula for subsequent testing that proved the same result. Narang et al also used muscle tissue to inoculate other animals [sheep & goats] and these experiments also proved the theory to be true.
 
"Sensitive Detection of Prion Protein in Human Urine", Harash K. Narang, Ayuna Dagdanova, Zhiliang Xie, Qiwei Yang, and Shu G. Chen. I have the abstract only.

Dr. Narang stated in a followup to his BSE inquiry, that scrapie and BSE are caused by viruses, with single strand DNA. He also stated that scrapie (virus-strain) would prevent BSE, and BSE (virus strain) would prevent scrapie. Whichever is domaninat, holds back the other.

This would allow scrapie to be used as an vaccine against BSE. So how does all this fit with the lab transmission experiments. They are using PrPSc (scrapie)!! ??

BSE-tester, send me all you got. Please bore me with the details. I do not subscribe to the journals and get most of my research off the internet or from "the horse's mouth". The Devil is in the details!!!

As I have stated before, I am a cow-calf producer. Just not your ordinary kind, I guess.

PS - a wise doctor from our town said, the least effective way to poison someone is to have them ingest the poison. And the most effective method is to inject the poison (toxic agent), as it will travel all around the body is 5 seconds.
 
hamsters are one thing, PRIMATES are another. it is totally unethical and illegal for human transmission study. please observe the dose rate too;

For personal use. Only reproduce with permission from Elsevier Ltd
Research Letters
Up to 400 000 cows with undiagnosed bovine spongiform
encephalopathy (BSE) infection are estimated to
have been slaughtered for food before brain and spinal
cord were banned from human consumption in 1989.
More restricted exposure to BSE could have continued
through 1995 from consumption of processed meat
products containing mechanically recovered meat
contaminated with central nervous system (CNS) tissue
and spinal ganglia.1 The discovery of BSE in Canada and
the USA, where consumption of brain and other viscera
was allowed until 2003, and of secondary cases of variant
Creutzfeldt-Jakob disease (vCJD) in the UK, possibly
attributable to contaminated blood donated by people
with pre-clinical primary infection, reinforces the need
for an experimental assessment of the risk of oral
exposure to BSE. We therefore investigated oral
transmission of BSE to non-human primates.
We chose cynomolgus macaques for the study because
these old-world monkeys have a digestive physiology
similar to that of human beings, are methionine
homozygous at codon 129 of the PRNP gene, and have a
BSE neuropathology similar to that of vCJD.2,3 We gave
two 4-year-old adult macaques a 5 g oral dose of brain
homogenate from a BSE-affected cow. We tested for
proteinase-resistant prion protein (PrPres) in this
homogenate with a commercial BSE-testing ELISA kit
(Bio-Rad, Marnes-la-Coquette, France). A sample of the
100% homogenate brain paste inoculum that was fed to
the primates was rehomogenised at 20% weight-pervolume
in the kit buffer. Serial dilutions were made with
a pool of 20% weight-per-volume BSE-negative brain
homogenate in the same buffer. Testing was done
according to the manufacturer's instructions and results
were confirmed by a western blot test (Bio-Rad) with a
similar process of PrPres dilution. With both methods,
dilutions of up to 1 in 300 provided a positive signal
(figure A).
One macaque developed neurological disease
60 months after exposure and was killed at 63 months
because of recumbency. Histopathological examination
of the brain of this animal showed the typical pathology
of vCJD (figure B) and an accumulation of PrPres
associated with the follicular dendritic cells in tonsils
(figure C), spleen, and intestine. A western blot showed
similar patterns of PrPres in a brain sample from the
macaque and the BSE-infected bovine inoculum
(figure D). The other macaque remained free of clinical
signs 76 months after exposure, and a tonsil biopsy done
at 72 months was negative (figure E).
In a previous study, two macaques orally dosed with
5 g of brain from a macaque with terminal clinical BSE
became ill after 44 and 47 months.4 The results of the
present study suggest that the incubation period for
interspecies transmission of BSE can be considerably
Published online
January 27, 2005
http://image.thelancet.com/
extras/05let1056web.pdf
Commissariat à l'Energie
Atomique/Direction des
Sciences du Vivant/Départment
de Recherche Médicale,
18 Route du Panorama, 92265
Fontenay-aux-Roses, France
(C I Lasmézas DrMedVet,
E Comoy DrMedVet,
C Herzog DipBiol,
F Mouthon DipBiol, F Auvré,
E Correia,
N Lescoutra-Etchegaray DipBiol,
Prof N Salès PhD, J-P Deslys MD);
Veterinary Laboratories
Agency, New Haw, Addlestone,
UK (S Hawkins MIBiol,
T Konold DrMedVet,
G Wells BVetMed); and 7815
Exeter Road, Bethesda, MD
20814, USA (P Brown PhD)
Correspondence to:
Dr Jean-Philippe Deslys
e-mail: [email protected]
www.thelancet.com Published online January 27, 2005 http://image.thelancet.com/extras/05let1056web.pdf 1
Risk of oral infection with bovine spongiform
encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,
Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant
Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the efficiency of oral infection
and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral
transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the
other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a
preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public
health measures can prevent transmission of BSE to man.
B
C
E
A
Dilution
D
3·215
1·989
0·984
0·302
0·131
0·065
0·052
1/10
1/30
1/100
1/300
1/1000
1/3000
Neg
36 kDa
36 kDa
22 kDa
22 kDa
16 kDa
1 2 3 4
ELISA detection of PrPres (absorbance units)
Figure: PrPres content of brain homogenate and histopathological assessment of macaque tissues
(A) Results of in-vitro testing for PrPres in BSE-infected inoculum by ELISA and western blot. Neg=normal bovine
brain material. (B) Typical florid plaque in the occipital cortex of the macaque that developed disease.
PrPres detected by proteinase K treatment with SAF32 anti PrP monoclonal antibody (kindly provided by Jacques
Grassi, CEA Saclay). The dense core of PrPres is surrounded by several vacuoles in a fibrillar proteinaceous corona;
bar=10 m. (C) Positive PrPres staining in tonsil (80% of follicules stained positive) of the macaque that developed
disease; bar=50 m. (E) Negative PrPres staining in tonsil of the macaque that did not develop disease; bar=50 m.
(D) Western blot showing similar PrPres patterns in samples from a patient with vCJD (lane 1), the macaque that
developed disease (lane 3), and the bovine BSE inoculum (lane 4). By contrast, a macaque inoculated intracerebrally
with material from a patient with sporadic CJD showed a different PrPres pattern (lane 2).
For personal use. Only reproduce with permission from Elsevier Ltd
Research Letters
longer than that of intraspecies transmission (60 months
vs 44 and 47 months, representing 36% and 28%
increases, respectively). The interval between the period of
peak exposure to infectious BSE tissue and the hitherto
peak incidence of vCJD is about 10–15 years, but
incubation periods of up to 40 years have followed oral
infection with kuru between human beings.5 Therefore,
maximum incubation periods might exceed 50 years in
cases of oral transmission of BSE from cattle to man.
The present data do not provide a definitive minimum
infective dose for transmission of cattle BSE to primates,
but they do give enough information for a preliminary
assessment of the adequacy of existing measures to
protect the human food chain. Results of ongoing
experiments provide a rough estimation of the intraspecies
transmission rates in cattle. The BSE brain
inoculum to which the cattle were exposed had an
infectivity titre of 103·5 mouse infectious (intracerebral
and intraperitoneal) units ID50 per g (ID50 is the dose at
which 50% of animals become infected). Interim results
at 6 years after exposure suggest that the oral ID50 in
cattle may be between 100 mg and 1 g (table 1; S A C
Hawkins, T Konold, G A H Wells, unpublished data).
Since the brain of a cow weighs 500 g and a spinal cord
200 g, CNS tissues from a cow with clinical signs of BSE
could contain enough infective agent to transmit disease
orally to 490–1400 cows (70% of 700 g if 1g is needed, or
20% of 700 g if 100 mg is sufficient), or to 70 primates
(50% of 700 g if 5 g represents the oral ID50).
The accuracy of estimates of the oral ID50 for man will
not be improved until completion, several years from
now, of a large dose-response European study (QLK1-
2002-01096) in macaques, in which the minimum dose
is 50 mg. However, because similar inocula were used in
both the cattle and macaque studies,6 a tentative comparison
can be made between the efficiency of oral infection
in cattle and that in primates. On this basis, a factor of
7–20 could be considered as the range of magnitude of a
bovine-to-primate species barrier for oral BSE infection
(70 primates infected compared with 490 or 1400 cows,
with a similar dose).
Elimination from the human food chain of CNS
tissues from cows with clinical BSE is estimated to have
reduced the risk of human exposure to the disease by
about 90%.7 Risk was further reduced in continental
Europe by systematic screening for the diagnostic
presence of PrPres in the brainstem of all cattle older than
30 months, and in the UK by the total interdiction of
cows older than 30 months. In an oral exposure study to
assess the pathogenesis of BSE in cattle, in which the
same European Union-evaluated test as we used in the
present study was applied to CNS tissues, some
preclinical cases of the disease were diagnosed.8
Using the same test, pooled brainstem from cows with
clinical BSE has yielded a endpoint titre of PrPres
corresponding to a 1-in-300 to 1-in-1000 dilution of
positive brainstem.6,9 If people were to eat CNS tissues
from a cow with preclinical BSE with a concentration of
PrPres just below the test detection limit of 1 in 300, they
would need to ingest at least 1·5 kg to reach the degree
of exposure equivalent to that in the 5 g of brain used for
oral transmission to the macaque in the present study. If
the oral ID50 for man was one log below this dose (ie,
similar to that in cattle, and not accounting for any
species barrier between cattle and man; see table), 150 g
of CNS tissue that tested falsely negative could represent
an infective dose. Because use of cattle brain and spinal
cord for human consumption is prohibited, and in view
of the existing mechanically recovered meat regulations,
a person would be very unlikely to ingest this amount of
cattle CNS tissue.
The minimum sensitivity of screening tests to detect
100% of BSE-infected animals has yet to be ascertained.
However, our results provide reassurance that BSE
screening procedures combined with CNS removal are
effective measures to protect the human food chain.
Contributors
J-P Deslys, C Lasmézas, and E Comoy were responsible for design and
management of this study. G Wells, S Hawkins, and T Konold were
responsible for the pathogenesis study in ruminants. C Lasmézas,
C Herzog, and N Lescoutra-Etchegaray were in charge of the primate
experiments. F Auvré undertook the biochemical analyses. N Salès was
responsible for the immunohistochemical analyses, which were done
by E Correia. C Lasmézas, E Comoy, F Mouthon, G Wells, P Brown, and
J-P Deslys drafted the manuscript.
Conflict of interest statement
Commissariat à l'Energie Atomique owns a patent covering the BSE
diagnostic test commercialised by Bio-Rad. All authors had full access to
all data and had responsibility to submit for publication. The funding
sources had no role in the collection, analysis, and interpretation of
data, writing of the report, or decision to submit the paper for
publication.
2 www.thelancet.com Published online January 27, 2005 http://image.thelancet.com/extras/05let1056web.pdf
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
For personal use. Only reproduce with permission from Elsevier Ltd
Research Letters
Acknowledgments
We gratefully acknowledge the expert care of the primate animals
provided by René Rioux, Sébastien Jacquin, and Anthony Fort, and the
technical expertise of Dominique Marcé, Capucine Dehen,
Sophie Freire, and Aurore Jolit Charbonnier. This work has received
financial support from the French Ministry of Research (GIS Prion). It is
now continued within the framework of the EU consortium QLK1-2002-
01096 and the European network of Excellence NeuroPrion. Ongoing
studies by the Veterinary Laboratories Agency in cattle are funded by the
UK Department for Environment, Food, and Rural Affairs.
References
1Anderson RM, Donnelly CA, Ferguson NM, et al. Transmission
dynamics and epidemiology of BSE in British cattle. Nature 1996;
382: 779–88.
2 Lasmézas CI, Deslys JP, Demaimay R, et al. BSE transmission to
macaques. Nature 1996; 381: 743–44.
3 Lasmézas CI, Fournier JG, Nouvel V, et al. Adaptation of the bovine
spongiform encephalopathy agent to primates and comparison with
Creutzfeldt-Jakob disease: implications for human health. Proc Natl
Acad Sci USA 2001; 98: 4142–47.
4 Herzog C, Salès N, Etchegaray N, et al. Tissue distribution of bovine
spongiform encephalopathy agent in primates after intravenous or
oral infection. Lancet 2004; 363: 422–28.
5 Klitzman RL, Alpers MP, Gajdusek DC. The natural incubation
period of kuru and the episodes of transmission in three clusters of
patients. Neuroepidemiol 1984; 3: 3–20.
6 Deslys JP, Comoy E, Hawkins S, et al. Screening slaughtered cattle
for BSE. Nature 2001; 409: 476–78.
7 European Commission. Opinion of the Scientific Steering
Committee on the Human Exposure Risk via food with respect to
BSE. Adopted on 10 December 1999. http://europa.eu.int./comm/
food/fs/sc/ssc/out67_en.pdf (accessed Jan 17, 2004).
8 Grassi J, Comoy E, Simon S, et al. Rapid test for the preclinical
postmortem diagnosis of BSE in central nervous system tissue.
Vet Rec 2001; 149: 577–82.
9 Moynagh J, Schimmel H. Tests for BSE evaluated. Bovine
spongiform encephalopathy. Nature 1999; 400: 105.
www.thelancet.com Published online January 27, 2005 http://image.thelancet.com/extras/05let1056web.pdf 3tss
 
##################### Bovine Spongiform Encephalopathy #####################

From: TSS ()
Subject: Re: Detection of prions in blood Joaquín Castilla1, Paula Saá1, 2 &
Claudio Soto1
Date: August 30, 2005 at 12:12 pm PST

30 August 2005


An Easy Assay for Prions?

An innovative new technique could finally lead to an early diagnostic test
for diseases such as Bovine Spongiform Encephalitis (BSE), or "mad cow", and
its human counterpart, variant Creutzfeldt-Jacob Disease (vCJD). Researchers
say the results in lab animals, while encouraging, need to be replicated and
note that competing tests are also under development.


Batty bovines. Cows with bovine spongiform encephalitis have holes in their
grey matter, which give their brains a spongy look.
CREDIT: Al Jenny/APHIS/USDA
BSE, vCJD, and several other neurodegenerative diseases are believed to be
caused by so-called prion proteins, which can occur in two forms: the normal
variety, called PrPc, and a misfolded variant that forms clumps in the brain
(PrPSc). The diseases are infectious, most researchers think, because PrPSc
has the peculiar ability to impose its abnormal folding on PrPc. So far,
scientists can only detect prion diseases in the brain, after death. The
problem is that levels of prions circulating in blood plasma are extremely
low, so any test would need to be exquisitely sensitive.

In previous studies, Claudio Soto and colleagues at the University of Texas
Medical Branch in Galveston had shown that they could amplify these minute
amounts of prions in a cyclical process reminiscent of the way the
polymerase chain reaction amplifies DNA (ScienceNOW, 21 April). The
researchers added normal prion proteins to a sample in the test tube, let
the misfolded proteins "convert" the normal ones, broke up the resulting
clumps with a sound pulse, and then repeated the process over and over until
the PrPSc became detectable with ordinary methods. In a new study published
online this week in Nature Medicine, Soto and his colleagues show that a
vastly optimized and automated version of their test correctly identified 16
out of 18 prion-infected hamsters, without false positives in a control
group of 12 uninfected hamsters.

Perluigi Gambetti, who directs the National Prion Disease Pathology
Surveillance Center at Case Western Reserve University in Cleveland, Ohio,
has a few criticisms: The hamsters were infected by injecting the protein
directly into the brain, for instance, which is "like creating a stab wound"
through which protein may have entered the blood stream. Still, "this is a
breakthrough," he says.

Replication is needed, says Paul Brown, a retired prion researcher at the
National Institute of Neurological Disorders and Stroke in Bethesda,
Maryland. Other labs have had trouble achieving the prion amplification
levels reported by Soto's group in previous papers, he says: "There's some
nervousness about that." Soto acknowledges there were difficulties with
replication at first but says these have largely been overcome.

Several competing tests are in the works as well, adds Jean-Philippe Deslys,
who heads the Prions Research Group at the Atomic Energy Commission in
France. Deslys says he has seen data on two promising ones that will be
presented at an upcoming meeting. "It's really too early to say which test
will be the best one," he says.

--MARTIN ENSERINK

Related sites
The report
More on prion diseases

http://sciencenow.sciencemag.org/cgi/content/full/2005/830/1

21 April 2005

Proof Positive for Prions

A new study has taken another step toward proving the "prion hypothesis"—the
idea that rogue proteins are responsible for a host of fatal neurological
diseases, including Mad Cow Disease and scrapie.


Prion factory. A schematic representation of the cyclic process by which a
molecule of PrPc (left side of circle) interacts with and is converted into
PrPSc (right side of circle). PrPSc damages normal brain tissue (left panel)
by forming long fibers (right panel).
CREDIT: Eric Smith, Harvard University
According to the prion hypothesis, the disease-causing protein, PrPSc, makes
copies of itself inside the brain, multiplying until it forms fibers that
destroy neurons and eventually kill the animal. PrPSc has the same amino
acid sequence as a normal brain protein called PrPc, but folds into a
different three-dimensional shape. It replicates by corrupting any PrPc it
encounters, twisting it into a new PrPSc, which in turn transforms more
PrPc. Although recent research has overwhelmingly supported the prion
hypothesis [ScienceNOW 15 October, 2003], one vital experiment was missing:
No one had induced a prion disease in a healthy animal using pure PrPSc made
in a test tube.

In work reported in the 22 April Cell, neurobiologist Claudio Soto of the
University of Texas Medical Branch in Galveston and colleagues come close to
achieving that goal. To generate high levels of PrPSc, Soto's group
performed 20 rounds of "infection" in a test tube. In the first round, the
group mixed ground up healthy brain with brain material from a
scrapie-infected animal. Just as in an intact animal, the PrPc in the
healthy brain material was converted to PrPSc. In subsequent rounds, they
used material from the previous round to infect fresh healthy brain
material. The procedure yielded billions of molecules of PrPSc from just a
few starting molecules. Although some of the original scrapie brain material
was carried through the early rounds of the experiment, it eventually became
diluted to the point where it disappeared from the sample. Nonetheless, the
material was very infectious, efficiently causing scrapie when injected into
the brains of hamsters.
The caveat, UCSF neurobiologist Giuseppe Legname notes, is that because the
researchers started with scrapie brain, not pure PrPSc, something else that
contributes to scrapie may have been amplified along with PrPSc. However,
Legname says, this system could be used to detect the low levels of prions
present in the blood of infected animals. Such a test is "desperately
needed," he says, to reduce the chances that prions will be spread through
food or medical blood products.

--KAREN ROSS

Related sites

http://sciencenow.sciencemag.org/cgi/content/full/2005/421/3


January 2004

NIAID Research on Prion Diseases
Overview

Prion diseases are a related group of rare, fatal brain diseases that affect
animals, including humans. Also known as transmissible spongiform
encephalopathies (TSE), they include bovine spongiform encephalopathy (BSE,
or "mad cow" disease) in cattle; Creutzfeldt-Jakob disease (CJD) in humans;
scrapie in sheep; and chronic wasting disease in deer and elk.

Much about TSE diseases remains to be discovered. The diseases are
characterized by certain misshapen protein molecules that appear in brain
tissue. Normal forms of these prion protein molecules reside on the surface
of many types of cells, including brain cells, but scientists do not
understand what normal prion protein does. On the other hand, scientists
believe that abnormal prion protein, which clumps together and accumulates
in brain tissue, is the likely cause of the brain damage that occurs in TSE
diseases. Scientists do not have a good understanding of what causes the
normal prion protein to take on the misshapen abnormal form.

The National Institute of Allergy and Infectious Diseases (NIAID) conducts
TSE disease research in its Rocky Mountain Laboratories (RML) in Hamilton,
MT, and also funds prion disease research in university labs. Two other
National Institutes of Health Institutes also fund prion disease research —
the National Institute of Neurological Disorders and Stroke and the National
Institute on Aging.

Variant Creutzfeldt-Jakob Disease

In some cases, TSE diseases appear to be infectious. For example, there is
good evidence that a newly discovered TSE disease — variant CJD (vCJD) — was
first spread to humans from cattle infected with BSE, although that type of
transmission is believed to be very inefficient. Identifying the
transmissible agent is still an ongoing area of research. A leading
hypothesis about the origin of vCJD is that abnormal forms of prion protein
ingested through diseased meat sicken people by causing normal human prion
protein to form incorrectly. This change from normal to abnormal prion
protein spreads to the brain, where the misshapen protein aggregates in the
spaces between brain cells and produces disease. An alternative hypothesis
is that the disease is transmitted by a virus, which subsequently triggers
the process of forming abnormal prion protein.

Health officials in the United Kingdom have responded to the possibility
that beef infected with BSE may have spread vCJD to humans. Since the 1980s,
when the mad cow epidemic began in the United Kingdom, millions of cattle in
Europe have been destroyed. Worldwide, there have been 153 reported cases of
vCJD, according to the Centers for Disease Control and Prevention (CDC). All
of these cases were among people who ate beef in a country with a BSE
outbreak, and nearly all — 143 of the cases — were in the United Kingdom.

The first North American case of mad cow disease was found in Canada in May
2003. Discovery of the first U.S. case of mad cow disease followed in
December 2003 in a Washington state cow. Although no cases of endemic vCJD
have been reported in the United States, more research is needed to confirm
whether vCJD is spread to humans from cattle with mad cow disease.

An older human TSE, Creutzfeldt-Jakob disease, is similar to vCJD but
progresses much more quickly and affects older people. Medical experts
believe it can be both inherited and transmitted through infection, although
some cases occur sporadically without a known cause.

Chronic Wasting Disease

A different TSE disease called chronic wasting disease has been detected in
U.S. deer and elk populations. So far, scientists have uncovered no evidence
that deer or elk with chronic wasting disease might transmit some form of
TSE disease to people who eat deer or elk or have close contact with them.
More research must be done to determine with certainty whether chronic
wasting disease poses any risk to humans, particularly because it is
spreading over a wider geographical area in the United States.

Basic Research

NIAID scientists at RML are examining how abnormal prion protein molecules
cause TSE diseases. RML is one of the world's premiere laboratories for
studying TSE diseases: scientists there co-discovered and were among the
first to clone the prion protein gene. NIAID scientists also discovered that
abnormal prion protein can convert normal prion protein to the abnormal
form. This also may account for the disease process in the brain.

RML scientists are working to insert genes into mice that would allow the
mice to carry the prion protein of deer and elk. These mice would react to a
prion protein infection as a deer or an elk would. Thus, scientists can
study the disease in these mice rather than in the larger animals, which are
much more expensive and labor-intensive to maintain.

At Colorado State University, NIAID has established an emerging diseases
research center focused on studying chronic wasting disease. This center is
investigating the mechanics of chronic wasting disease infection in deer and
elk, especially in the lymph nodes of their immune systems. Such studies
underlie the search for improved diagnostics and therapies. The researchers
also will seek to better understand the entire spectrum of disease
transmission and under what circumstances chronic wasting disease might
"jump" to other species. In addition, scientists at the center are working
on a possible vaccine to prevent the spread of chronic wasting disease in
deer and elk.

To assist investigators in obtaining needed materials to study TSE diseases,
NIAID has created a TSE repository with joint funding from the National
Institute of Neurological Disorders and Stroke. The repository will help
researchers obtain standard biochemical reagents and animals with genetic
modifications for use in prion protein research.

Cross-Species Transmission

At RML, studies are ongoing to understand the mechanisms by which TSE
infections cross species. Experiments have demonstrated that species once
thought to be resistant to certain TSE strains can be life-long carriers of
the infection without ever becoming sick.

RML scientists are also investigating whether chronic wasting disease can be
transmitted from deer or elk to monkeys if monkeys eat brain matter from
deer or elk that are infected with chronic wasting disease. That knowledge
would provide valuable insight into whether chronic wasting disease could be
transmitted to humans.

Therapeutic Approaches

Although there are no known ways to treat TSE diseases, scientists around
the world are working to develop treatments. Using infected tissue culture
cells for fast initial screening, NIAID researchers have tested thousands of
compounds and identified hundreds of molecules that inhibit the formation of
the abnormal form of prion protein. Further testing of the most potent of
these inhibitors has revealed several that can prolong the lives of rodents
if treatments are begun near the time of infection. Researchers at RML, and
at Utah State University through a contract with NIAID, are testing these
compounds in animals. Other groups are further testing two of the inhibitors
in Creutzfeldt-Jakob disease patients. However, no compounds have proven to
have therapeutic effects after the onset of clinical signs of disease.

RML researchers have also identified antibodies and short synthetic protein
molecules (fragments of prion protein) that can block the conversion of
normal prion protein to the abnormal form. If successful, these
investigations will lead to safe and effective methods to prevent prion
infections as well as therapies that work in either the pre-symptomatic or
symptomatic phases of disease.

Diagnostics

Improved diagnostic tests for TSE diseases are critical for the success of
both therapeutic strategies and eradication programs. NIAID scientists are
exploring various approaches to creating new tests. In addition, NIAID has
provided funds to the CDC for better monitoring of TSE disease incidence and
to improve collection of tissue specimens for TSE disease-related
diagnostics.

Related Information

Other federal agencies work on prion issues from standpoints of research,
public health, food supply safety, and animal health. The following links
provide more information.

http://www.niaid.nih.gov/factsheets/priondis.htm

TSS


----- Original Message -----
From: "Terry S. Singeltary Sr." <[email protected]>
To: <[email protected]>
Sent: Sunday, August 28, 2005 6:03 PM
Subject: Detection of prions in blood Joaquín Castilla1, Pau la Saá1, 2 &
Claudio Soto1


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


From: TSS ()
Subject: Detection of prions in blood Joaquín Castilla1, Paula Saá1, 2 &
Claudio Soto1
Date: August 28, 2005 at 3:53 pm PST

Public release date: 28-Aug-2005


Contact: Jim Kelly
[email protected]
409-772-8791
Media Hotline: 409-772-6397
University of Texas Medical Branch at Galveston

'Mad cow' proteins successfully detected in blood
Biochemical technique expected to yield new, more effective test for
disease-causing prions in cattle and humans
GALVESTON, Texas -- Researchers at the University of Texas Medical Branch at
Galveston (UTMB) have found a way to detect in blood the malformed proteins
that cause "mad cow disease," the first time such "prions" have been
detected biochemically in blood.
The discovery, reported in an article scheduled to appear online in Nature
Medicine Aug. 28, is expected to lead to a much more effective detection
method for the infectious proteins responsible for brain-destroying
disorders, such as bovine spongiform encephalopathy (BSE) in cattle and
variant Creutzfeldt-Jakob disease (vCJD) in humans. The blood test would
make it much easier to keep BSE-infected beef out of the human food supply,
ensure that blood transfusions and organ transplants do not transmit vCJD,
and give researchers their first chance to figure out how many people may be
incubating the disease.

"The concentration of infectious prion protein in blood is far too small to
be detected by the methods used to detect it in the brain, but we know it's
still enough to spread the disease," said UTMB neurology professor Claudio
Soto, senior author of the Nature Medicine paper. "The key to our success
was developing a technique that would amplify the quantity of this protein
more than 10 million-fold, raising it to a detectable level."

Soto and the paper's other authors, UTMB assistant professor of neurology
Joaquin Castilla and research assistant Paula Saá, applied a method they
call protein misfolding cyclic amplification (PMCA) to blood samples taken
from 18 prion-infected hamsters that had developed clinical symptoms of
prion disease. PMCA uses sound waves to vastly accelerate the process that
prions use to convert normal proteins to misshapen infectious forms.

Successive rounds of PMCA led to the discovery of prions in the blood of 16
of the 18 infected hamsters. No prions were found in blood samples that were
taken from 12 healthy control hamsters and subjected to the same treatment.

"Since the original publication of a paper on our PMCA technology, we've
spent four years optimizing and automating this process to get to this
point," Soto said. "The next step, which we're currently working on, will be
detecting prions in the blood of animals before they develop clinical
symptoms and applying the technology to human blood samples."

Tests for infectious prions in cattle and human blood are badly needed.
Because current tests require post-slaughter brain tissue for analysis, in
the United States only cattle already showing clinical symptoms of BSE
(so-called "downer cows") are tested for the disorder. This is true even
though vCJD potentially can be transmitted by animals not yet showing
symptoms of the disease. (Only two cases of BSE have been found in American
cows so far.) And although British BSE cases have been in decline since
1992, scientists believe the British BSE epidemic of the 1980s could have
exposed millions of people in the UK and Europe to infectious prions. The
extent of the vCJD epidemic is yet unknown. So far the disease has killed
around 180 people worldwide, but numbers could reach thousands or even
hundreds of thousands in the coming decades. Prions have also been shown to
be transmissible through blood transfusions and organ transplants.

"Who knows what the real situation is in cattle in the United States? And
with people, we could be sitting on a time bomb, because the incubation
period of this disease in humans can be up to 40 years," Soto said. "That's
why a blood test is so important. We need to know the extent of the problem,
we need to make sure that beef and the human blood supply are safe, and we
need early diagnosis so that when scientists develop a therapy we can
intervene before clinical symptoms appear--by then, it's too late."


###
For more information or to schedule an interview request a digital photo or
arrange a taped or live television interview via UTMB's satellite services,
please call the media hotline.


----------------------------------------------------------------------------
----


http://www.eurekalert.org/pub_releases/2005-08/uotm-cp082505.php


Published online: 28 August 2005; | doi:10.1038/nm1286
Detection of prions in blood
Joaquín Castilla1, Paula Saá1, 2 & Claudio Soto1

1 Departments of Neurology, Human Biological Chemistry & Genetics and
Neuroscience & Cell Biology, University of Texas Medical Branch, 301
University Boulevard, Galveston, Texas, 77555-0646, USA.

2 Centro de Biología Molecular, Universidad Autónoma de Madrid, Madrid
28409, Spain.

Correspondence should be addressed to Claudio Soto [email protected]





Prion diseases are caused by an unconventional infectious agent termed
prion, composed mainly of the misfolded prion protein (PrPSc)1. The
development of highly sensitive assays for biochemical detection of PrPSc in
blood is a top priority for minimizing the spread of the disease2. Here we
show that the protein misfolding cyclic amplification (PMCA) technology3 can
be automated and optimized for high-efficiency amplification of PrPSc. We
show that 140 PMCA cycles leads to a 6,600-fold increase in sensitivity over
standard detection methods. Two successive rounds of PMCA cycles resulted in
a 10 million-fold increase in sensitivity and a capability to detect as
little as 8,000 equivalent molecules of PrPSc. Notably, serial PMCA enables
detection of PrPSc in blood samples of scrapie-afflicted hamsters with 89%
sensitivity and 100% specificity. These findings represent the first time
that PrPSc has been detected biochemically in blood, offering promise for
developing a noninvasive method for early diagnosis of prion diseases.


http://www.nature.com/nm/journal/vaop/ncurrent/abs/nm1286.html


TSS

#################### https://lists.aegee.org/bse-l.html
####################

#################### https://lists.aegee.org/bse-l.html ####################
 
EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Scientific Steering Committee
OPINION ON
ORGANOPHOSPHATE (OP) POISONING AND
HYPOTHETICAL INVOLVEMENT IN THE ORIGIN OF BSE
Background
In its opinion on possible links between BSE and Organophosphates adopted on 25-26 June
1998 and in its opinion on Hypotheses on the origin and transmission of BSE adopted on 29-
30 November 2001 the SSC concluded that there is no scientific evidence in support of the
hypothesis of an OP origin of BSE.
The issue of organophosphate poisoning has not been dealt with by the SSC so far. The
concerns expressed in the enquiries cover mainly intoxication by occupational exposure of
shepherds and farmers to OPs upon use against ecto-parasites, especially in sheep dipping and
treatment of cattle against Warble Fly infestation. Risks from residues are addressed to a
lesser extend.
In early 2003, a large number of additional enquiries on the issue have been addressed to
European Commission’s Health and Consumer Directorate General. Four of these with
substantial enclosures were by one person. Most of them are addressing both issues: chronic
organophosphate (OP) poisoning and the origin of BSE.
Information provided with the enquiries
In addition to numerous newspaper and magazine articles the enclosures to the enquiries
provide the Material Safety Data Sheet on diazinon, the OHSA Occupational Safety and
Health Guideline for Tetraethylpyrophosphate (TEPP), an US agency Hazardous Substances
Fact Sheet on crufomate, company safety information sheets, some correspondence with UK
authorities including their activities to improve safe use of these chemicals. The information
regarding claimed OP chronic poisoning of cases presented does not provide evidence, neither
for OPs being the cause for diseases nor for their exclusion (i.e., “very lowâ€￾ bloodcholinesterase
levels, provided without data or comparison with the normal distribution of
values; successful treatment of a patient for OP clearance without giving any OP data). It
C:\WINNT\Temporary Internet Files\SSC_Last_OP_Final.doc 2
seems however, that due to insufficient, non-prudent use of the safety requirements undue
exposures of shepherds and farmers have occurred.
There is no additional information on the claimed involvement of OPs in the origin of BSE.
This applies for both, the hypotheses on the direct effect of OPs as well as on their
hypothetical role for Cu-deficiency to be involved in the origin of BSE (Cu binding of prion
protein is known). New publications are mentioned in one enquiry but they have not yet been
provided. In an Internet search no recent scientifically valid publications were traceable. The
SSC had been informed that research would be launched on this hypothesis, but no
information has been provided so far on its status or on results.
Conclusions
a) As regards the involvement of organophosphates in the origin of BSE, no new scientific
information providing evidence or supporting the hypothesis by valid data became
available after the adoption of the last opinion of the SSC on this issue. Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for registration of
plant protection products and veterinary medicines â€" addressed in the enquiries â€" provide
the basis for safe use of registered compounds and their formulations. Regarding the
alleged intoxication cases reported and OP exposure it must be concluded that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf

transmission studies do not lie, amplification and transmission!!!

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


Docket Management
Docket: 02D-0073 - Guidance: Validation of Procedures for Processing of Human Tissues Intended for Transplantation
Comment Number: EC -4
Accepted - Volume 1
TSS


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html

Docket Management Docket: 02D-0371 - Class II Special Controls Guidance Document: Human Dura Mater
Comment Number: EC -1
Accepted - Volume 1
TSS

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html


-----Original Message----- From: Terry S. Singeltary Sr. [ ... <http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.pdf>
... FULL STORY>> my name is Terry S. Singeltary Sr., and i lost my mother ... Scrapie has
increased significantly, and CWD is spreading. with the titre ...
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.pdf - Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fac%2F03%2Fslides%2F3923s1_OPH%2Epdf+CWD%20TERRY%20S.%20SINGELTARY%20SR.> -

http://www.fda.gov/ohrms/dockets/dailys/00/mar00/030100/emc0597.rtf
... BSe. To be continued... Terry S. Singeltary Sr. PO Box 42 Bacliff, Texas USA. ... batch?
CWD is just a small piece of a very big puzzle. I have seen. ...
Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fdailys%2F00%2Fmar00%2F030100%2Femc0597%2Ertf+CWD%20TERRY%20S.%20SINGELTARY%20SR.> -

Freas, William <http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf>
... From: Sent: To: Subject: Terry S. Singeltary Sr. [[email protected]] Monday ... easily
amplify TSE's: Have we increased ... long version) and CWD and transmission to ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf - Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fac%2F01%2Fslides%2F3681s2_09%2Epdf+CWD%20TERRY%20S.%20SINGELTARY%20SR.> -

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec ...
Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fdailys%2F03%2FJan03%2F012403%2F8004be11%2Ehtml+CWD%20TERRY%20S.%20SINGELTARY%20SR.> - 17k

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec ...
Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fdailys%2F03%2FJan03%2F012403%2F8004bdfe%2Ehtml+CWD%20TERRY%20S.%20SINGELTARY%20SR.> - 17k

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec ...
Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fdailys%2F03%2FJan03%2F012403%2F8004bdfc%2Ehtml+CWD%20TERRY%20S.%20SINGELTARY%20SR.> - 17k

-----Original Message----- <http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm>
... FULL STORY>>. my name is Terry S. Singeltary Sr., and i lost my mother. ... Scrapie has
increased significantly, and. CWD is spreading. with the titre ...
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm - Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fac%2F03%2Fslides%2F3923s1_OPH%2Ehtm+CWD%20TERRY%20S.%20SINGELTARY%20SR.> - 51k

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec ...
Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fdailys%2F03%2FJan03%2F012403%2F8004be09%2Ehtml+CWD%20TERRY%20S.%20SINGELTARY%20SR.> - 56k

http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec ...
Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fdailys%2F03%2FMar03%2F031403%2F96N%2D0417%2DEC%2D2%2Ehtm+CWD%20TERRY%20S.%20SINGELTARY%20SR.> - 61k

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
... 2002 12:07:02 -0700 >>From: Terry S. Singeltary Sr. Reply-To: BSE-L >> >>so ... how many
dead road-kill CWD infected carcasses >>were rendered into ...
Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fdailys%2F03%2FJan03%2F012403%2F8004be07%2Ehtml+CWD%20TERRY%20S.%20SINGELTARY%20SR.> - 68k


LegaI Basis for Animal-Derived Legal Basis for Animal-Derived <http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_07.pdf>
... From: Sent: To: Subject: Terry S. Singeltary Sr. [[email protected]] Monday ... easily
amplify TSE's: Have we increased ... long version) and CWD and transmission to ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_07.pdf - Cached <http://fdagov.sitesearch.google.com/fdagov?client=fdagov&q=cache%3Ahttp%3A%2F%2Fwww%2Efda%2Egov%2Fohrms%2Fdockets%2Fac%2F01%2Fslides%2F3681s2_07%2Epdf+CWD%20TERRY%20S.%20SINGELTARY%20SR.> -

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

Wednesday 20 July 2005 13:15
Department of Health (National)

NOTIFICATION EXERCISE BEGINS TO REDUCE RISK OF VCJD TRANSMISSION


An extension to the precautionary measures to reduce the risk of transmitting vCJD through blood transfusion and surgical procedures, began today. Around 100 people who donated blood to three people who later developed vCJD, are being told that they may have a greater chance of carrying the vCJD agent, compared with the general population.

They will be asked not to donate blood, tissue or organs and to inform health professionals so extra precautions can be taken should they have surgery or other invasive procedures.

Although it is not known whether the source of vCJD in these patients is related to the blood that they received, precautionary steps are being taken to inform and provide support to the individuals as well as safeguard public health. This is being done on the advice of two expert committees and a detailed risk assessment exercise.

Notification of donors is taking place via letters from the National Blood Service who are working closely with the Health Protection Agency to identify the people involved. The letters that people receive will provide the telephone number for a dedicated helpline staffed by senior transfusion experts from the National Blood Service, and will also advise them to contact their GP for more information, advice and support.

The likelihood of a person who may be infected with vCJD going on to develop symptoms of the disease is uncertain. It is possible that an infected person may never develop symptoms.

The Chief Medical Officer, Sir Liam Donaldson said:

"We need to ensure that appropriate action is taken on any new information that becomes available on the risk of transmission of vCJD, to protect the public as much as possible. When a recipient of a blood transfusion goes on to develop vCJD, we have to consider the possibility that the infection could have been passed on through the transfusion.

"Until a reliable blood screening test becomes available, it is sensible to proceed with highly precautionary measures such as this to rule out any possibility of onward transmission of the disease. We are committed to further research to help us understand this disease and diagnose infection at an early stage.

"Following the identification of vCJD, we introduced a number of measure to reduce the possible risk that infection could be transmitted through the blood supply. Since the announcement in December 2003 of the first case of possible transfusion-associated transmission of vCJD, we have further strengthened these preventative measures.The decisions taken so far have been based on the principles of caution and openness. This announcement today is a continuation of the process."

Dr Angela Robinson from the National Blood Service said:

"Blood donors are highly committed to helping other people and we greatly value their contribution. The NHS depends upon their continued commitment in order to be able to save lives.

"This notification exercise will affect in the order of 100 donors. If you have donated blood in the last five years and are not contacted shortly, you can be assured that you are not involved in this new safety measure and need to take no further action.

"For those people who are involved, this information may be difficult to absorb. That is why we have set up the National Blood Service helpline and are working with their doctors and other clinicians, to ensure that they have the information and support they need."

Notes to editors:

1. This notification exercise has been done after a detailed risk assessment by the Department of Health and reviewed by its relevant expert committees. The risk assessment can be found at http://www.dh.gov.uk

2. The degree of increased risk for any individual donor depends on many factors, including how many other donors' blood went to the infected recipient. This varies very widely between these three recipients. Individual donors will be able to find out more if they wish.

3. Of the 156 cases of vCJD to date, 4 have been confirmed as having had blood transfusions that experts believe could be linked with their vCJD. For one of these cases, the probable source of infection has already been identified, as one of the donors went on to develop vCJD. For three cases, transfusion remains a possible source of the recipient's infection.

4. The blood donors involved in England, all gave blood during 1993.

5. The two expert committees advising this course of action were the CJD Incidents Panel and the Committee on the Microbiological Safety of Blood Tissues and Organs.

6. Previous measures taken to improve the safety of blood in relation to vCJD include the following:

- From December 1997, blood components, plasma products or tissues obtained from any individual who later develops vCJD, have been withdrawn/recalled.
- In July 1998, we announced that plasma for the manufacture of blood products, such as clotting factors, would be obtained from non-UK sources.
- From November 1999, white blood cells (which may carry a significant risk of transmitting vCJD) have been removed from all blood used for transfusion.
- In August 2002 we announced that fresh frozen plasma for treating babies and young children born on or after 1 January 1996 would be obtained from the USA.
- The report of the first possible case of transmission of vCJD by blood transfusion was in December 2003. Following this, we announced in April 2004 that individuals had themselves received a transfusion of whole blood components since January 1980, would be excluded from donating blood. (In July 2004, the second possible case of transmission of vCJD by blood transfusion was reported.)
- On July 2004, the exclusion criteria for blood donation were extended to include two new groups, who had received transfusions of whole blood components since 1980:
- Previously transfused platelet donors
- Donors who were unsure if they had previously had a blood transfusion.

This means that for blood donation the full exclusion criteria are:
- Recipients of dura mater grafts.
- Recipients of corneal or scleral grafts.
- Recipients of human pituitary derived extracts such as growth hormone or gonadotrophins.
- Individuals at familial risk of prion-associated diseases. This includes individuals who have had two or more blood relatives develop a prion -associated disease and individuals who have been informed they are at risk following genetic counselling.
- Individuals who had themselves received a transfusion of whole blood. components since January 1980 are excluded from donating blood.
- Individuals identified as 'at risk' by CJD Incidents Panel.
- Previously transfused platelet donors.
- Donors who were unsure if they had previously had a blood transfusion.

- In September 2004, the Department of Health announced further precautionary measures for patients who had received certain batches of plasma products.
- In July 2005 the use of USA sourced fresh frozen plasma (FFP) was extended to all children up to the age of 16.

7. There is currently no validated diagnostic test that can be used before the onset of clinical symptoms to diagnose whether someone has contracted vCJD. Since 1995, the Department has contributed over £30 million into CJD research, including research for the development of an effective test.




HOUSE OF COMMONS

Notice of Written
Ministerial Statement




Title of Secretary of State/Ministerial
head of department: The Under Secretary of State (Public Health)




Subject of Statement: Secondary Transmission of Variant CJD
Recommendations for Further Health Precautions




1. Notice of written Statements for the following day will be placed on the effective Orders of the Day. Otherwise, the notices will be placed on Future Business E (written ministerial statements). Notices may be given of written statements to be made not later than 5 sitting days after the day on which notice was given.

WRITTEN MINISTERIAL STATEMENT

DEPARTMENT OF HEALTH

20 July 2005

The Under Secretary of State (Public Health): Written Ministerial Statement on secondary transmission of vCJD

The Under Secretary of State (Public Health): (Ms Caroline Flint)

Further to the statements made to the House by the then Secretary of State (Dr John Reid) on 17 December 2003 and 16 March 2004 (and the written statements of 22 July 2004 and 9 September 2004) concerning variant Creutzfeldt-Jakob disease (vCJD) and blood, I wish to provide a further update on this subject.

Following cases of possible transmission of vCJD by blood transfusion, we have already put in place a series of precautionary public health measures. These include:
- In December 2003 we put in place arrangements for contacting recipients of blood from donors who went on to develop vCJD so that any necessary action could be taken;
- Since April 2004 we have excluded anyone who has received a blood transfusion since January 1980 from donating blood.
- In September 2004 we announced arrangements to identify and notify patients who had received certain batches of UK manufactured plasma products.

In the light of further advice I have received from two of my Department's expert committees, the CJD Incidents Panel (CJDIP) and the Committee on Microbiological Safety of Blood, Tissues and Organs (MSBTO), I am now announcing further public health precautions in relation to a small group of blood donors whose blood has been transfused to people who later developed vCJD.

The Chief Medical Officer, Sir Liam Donaldson, had asked the expert committees to consider the implications for donors where a recipient of their blood had developed vCJD. The recommendations of the committees are based on an assessment of risk undertaken by the Department of Health's analysts. The risk assessment is being published on the Department's website.

There are 110 donors in the UK whose blood was given to three people who later developed vCJD and for whom this blood might be a possible source of their infection. The advice of the committees is that, although we do not know whether these cases of vCJD could be related to the blood that they received, we should take precautionary steps to inform and support the individual blood donors concerned and to safeguard public health.

As an extension to the current precautionary measures, these people are being contacted by the National Blood Service and advised not to donate blood, tissues or organs. Current donors from this group of 110 are being contacted today and offered expert advice and support. The National Blood Service will contact the GPs of lapsed donors, that is those who have not donated blood during the last five years, and make arrangements to contact these people as soon as practicable.

The committees have also advised that the donors in question should be considered at risk of vCJD for wider public health purposes and that the donors and their clinicians should be informed of their risk status and asked to implement the public health precautions currently specified by the CJD Incidents Panel. This means that they should inform doctors, nurses and dentists of their status if they present for surgery or other invasive medical procedures.

These public health precautionary measures are the same as those applied to any patients considered by the CJDIP to be at risk of vCJD, including the individuals notified following the previous statements to the House.

There is another group of people for whom further public health precautions may need to be considered. This group is all the other recipients of blood from the currently identified group of 110 donors (estimated to be up to 3,000 individuals). At present, these people are already excluded from blood donation themselves by the measures implemented in April 2004. I have asked for additional expert advice on this group and I will take further action if necessary.

Blood donors should be assured that it is not possible to contract vCJD by giving blood. Blood donors are highly committed to helping others and we greatly value their contribution. The NHS depends on their continued commitment to donating blood which saves lives every day in this country.

The vast majority of the over two million current blood donors will not be involved in this new safety measure and need take no action. However, current and past blood donors who are concerned can contact the National Blood Service helpline on 0845 7711 711.

People who have received blood donations and other members of the public who are concerned should contact NHS Direct on 0845 850 9850.

As with our actions to date on the possible transmission of vCJD, we continue to follow a highly precautionary approach.










Client ref 2005/0256

GNN ref 118433P



http://www.gnn.gov.uk/content/detail.asp?NewsAreaID=2&ReleaseID=164111



TSS

#################### https://lists.aegee.org/bse-l.html ####################


Similar levels of infectivity in the blood of mice infected with
human-derived vCJD and GSS strains of transmissible spongiform
encephalopathy
Larisa Cervenakova, Oksana Yakovleva, Carroll McKenzie, Svetlana
Kolchinsky, Lisa McShane, William N. Drohan, and Paul Brown

BACKGROUND:

The possible transmission of variant CJD (vCJD) through blood
transfusion or use of plasma-derived products prompted this study
comparing infectivity in murine models of vCJD and
Gerstmann-Sträussler-Scheinker (GSS) disease, a non-vCJD form of
transmissible spongiform encephalopathy (TSE).

STUDY DESIGN AND METHODS:

RIII/Fa/Dk (RIII) or Swiss-Webster (Swiss) mice were inoculated
intracerebrally (IC) with mouse-adapted strains of vCJD or GSS
(Fukuoka-1) of similar infectivity. Groups of RIII mice were euthanized
17 weeks after inoculation (during the incubation period), and another
23 weeks after inoculation (when symptomatic). Blood was collected,
separated into components, and inoculated into groups of healthy mice;
brains and spleens from all mice were harvested and tested for the
presence of PrPres by Western blot using 6H4 MoAb.

RESULTS:

Levels of 20-30 infectious doses per mL were present in buffy coat and
plasma during both the incubation and symptomatic stages of disease; PLT
pellet infectivity was lower (10 ID/mL) and RBCs were not infectious.
The disease was transmitted more efficiently by IV than IC inoculation
of plasma, but there was no difference observed with inoculation of
buffy coat. The incubation period was shorter after IC inoculation of
GSS- than vCJD-brain inocula. The amount of PrPres in spleens was
similar for both TSE agents, but was slightly lower in brains of vCJD
than GSS mice.

CONCLUSION:

Infectivity was detected in blood components of mice infected with a
human-derived strain of vCJD during both the preclinical and clinical
phases of disease in a similarly low range of concentrations as in mice
infected with a human-derived nonvariant strain (GSS, Fukuoka-1). Other
measures of virulence, including brain infectivity titers, incubation
periods, and the accumulation of PrPres in spleens and brains, were also
comparable in both experimental models.

http://www.blackwell-synergy.com/servlet/useragent?func=synergy&synergyAction=showAbstract&doi=10.1046/j.0041-1132.2003.00586.x&area=production&prevSearch=allfield%3A%28cjd%29



Transmission of Creutzfeldt-Jakob Disease from Blood and Urine Into Mice

The Lancet, November 9, 1985

Sir,--Professor Manuelidis and his colleagues (Oct 19, p896) report
transmission to animals of Creutzfeldt-Jakob disease (CJD) from the
buffy coat from two patients. We also transmitted the disease from
whole blood samples of a patient (and of mice) infected with CJD.1
Brain, Cornea, and urine from this patient were also infectious, and
the clinicopathological findings2 are summarised as follows.

A 70-year-old man was noted to have a slowing of speech and writing
and some disorientation, all of which progressed rapidly. Decorticate
rigidity, forced grasping, positive snout reflex, and myoclonus
appeared within 2 months. Electroencephalogram revealed typical
periodic synchronous discharge, and he died of pneumonia and upper
gastrointestinal haemorrhage, about 3 months after onset of the
symptoms. The Brain weighed 1290g and showed severe histological
changes diagnostic of CJD, including spongiform change, loss of
nerve cells, and diffuse proliferation of astrocytes. There were no
inflammatory cells, microglia, neurofibrillary tangles, and
amyloid plaques, although virus-like particles were detected by
electron microscopy.

Results of innoculation in Mice

Inocula NO* Incubation period (days)+
Brain 7/10 (4) 789 (+ or - 112)
Cornea 1/6 (0) 1037
Blood 2/13 (0) 1080 (+ or - 69)
Urine 5/10 (1) 880 (+ or - 55)
CSF 0/10

* Number of mice with CJD change/number examined histologically.
Number with amyloid plaques shown in parentheses.

+ means + or - SD

Samples were taken aseptically at necropsy. 10% crude homogenates
of brain and cornea in saline, whole blood (after crushing a clot),
and untreated CSF and urine were innoculated intracerebrally into
CF1 strain mice (20 ul per animal). Some mice showed emaciation,
bradykinesia, rigidity of the body and tail, and sometimes tremor
after long incubation periods. Tissues obtained after the animal
died (or was killed) were studied histologically (table). Animals
infected by various inocula showed common pathological changes,
consisting of severe spongiform changes, glial proliferation, and
a moderate loss of nerve cells. A few mice inoculated with brain
tissue or urine had the same amyloid plaques found in patients and
animals with CJD.3

In our long-term experiments, inoculating materials taken from
twenty patients with CJD or Gerstmann-Straussler-Scheinker's
disease (GSS) into rodents, positive results were obtained in
seventeen cases, including this patient. Brain tissue transmitted
the disease most frequently within the shortes incubation period,
except for one case where the lymph node was the most infectious.
Transmission through the cornea has been noted in man4 and in
guineapigs.5 Whole blood samples taken from three patients were
inoculated and a positive transmission occured only in the case
recorded here. Mouse-to-mouse transmission through blood
inoculation was successful after a mean incubation period of 365
days.1 Transmission through urine was positive in this patient
only, and negative in one other patient and in many infected animals.
Transmission through the CSF from eight patients was negative, yet
transmission via the CSF of infected rats was positive.1

As viraemia has been proved in guineapigs,6 mice,1,7 and lately
in patients with CJD, blood for transfusion or blood products for
medical use must be tested for unconventional pathogens. For this
purpose, we inoculated blood products inot rodents.8 The CJD
pathogen was not found in the products examined. However, this
approach takes too long to be of practical value. More efficient
methods must be developed to detect pathogens and to eliminate
them from blood. One proposal9 is to apply membrane filtration to
the pruification protocol of human growth hormone suspected of
being contaminated with CJD. Similar methods are needed for blood
contamination.

Department of Neuropathology,
Neurological Institute,
Faculty of Medicine,
Kyushu University,
Fukuoka812, Japan

JUN TATEISHI

1. Tateishi J, Sato Y, Kaga M. Doi H, Ohta M. Experimental transmission
of human subacute spongiform encephalopathy to small
rodents 1: Clinical and histological observations.
Acta Neuropathol (Berl) 1980; 51: 127.

2. Shibayama Y, Sakaguchi Y, Nakata K, et al, Creutzfeldt-Jakob
disease with demonstration of virus-like particles.
Acta pathol Jpn 1982;32: 695.

3. Tateishi J, Nagara H, Hikita K, Sato Y. Amyloid plaques in the
brains of mice with Creutzfeldt-Jakob disease.
Ann Neurol 1984; 15: 278.

4. Duffy P, Wolf J, Colings G, DeVoe AG, Streeten B, Cowen D.
Possible person-to-person transmission of Creutzfeldt-Jakob disease.
N Engl J Med 1974; 290: 692.

5. Manuelidis EE, Angelo JN, Gorgacz EJ, Kim JH, Manuelidis L.
Experimental Creutzfeldt-Jakob disease transmitted via the eye
with infected cornea. N Engl J Med 1977; 296: 1334.

6. Manuelidis EE, Gorgacz EJ, Manuelidis L. Viremia in experimental
Creutzfeldt-Jakob disease. Science 1978: 200: 1069.

7. Kuroda Y, Gibbs CJ Jr, Amyx HL, Gajdusek DC.
Creutzfeldt-Jakob disease in mice. Persistent viremiam and
preferential replication of virus in low-density lymphocytes.
Infect Immun 1983; 41: 154.

8. Tateishi J, Tsuji S. Unconventional pathogens causing spongiform
encephalopathis absent in blood products. J Med Virol 1985; 15: 11.

9. Tateishi J, Kitamoto T, Hiratani H. Creutzfeldt-Jakob disease
pathogen in growth hormone preparations is eliminatable.
Lancet (in press).


========================================================
also, this from the Her Majesty's Government...TSS

Subject: Transmission of TSEs through blood
Date: Tue, 28 Mar 2000 14:48:35 +0100
From: Ralph Lucas
Reply-To: Bovine Spongiform Encephalopathy
To: [email protected]

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

The Lord Lucas asked Her Majesty's Government:

Whether there is any evidence that any Transmissible Spongiform
Encephalopathy in any species can be transmitted through blood; and whether they will place in the Library of the House copies of the principal relevant scientific papers. (HL1545)


The Parliamentary Under-Secretary of State, Department of Health (Lord Hunt of Kings Heath):

Some animal studies have shown that certain transmissible spongiform
encephalopathies can be experimentally transmitted from animal to animal through blood components. However, the Spongiform Encephalopathy Advisory Committee at its February meeting reviewed recent research undertaken in this area and did not consider any measures were necessary, in addition to those already in place, to reduce any potential risk to public health from human blood and blood products.

Copies of the following relevant scientific papers are being placed in the Library.

Brown P, 1995, "Can Creutzfeldt-Jakob Disease be transmitted by
Transfusion?" Haematology 2: 472 - 477.

Brown et al 1999, Further studies of blood infectivity in an experimental model of transmissible spongiform encephalopathy, with an explanation of why blood components do not transmit Creutzfeldt - Jakob disease in humans.

Transfusion Vol. 39, November/December 1169 - 1178.


Research letters
Volume 356, Number 9234 16 September 2000

Transmission of BSE by blood transfusion
in sheep


Lancet 2000; 356: 999 - 1000
Download PDF (1 Mb)


F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock

See Commentary

We have shown that it is possible to transmit
bovine spongiform encephalopathy (BSE)
to a sheep by transfusion with whole blood
taken from another sheep during the
symptom-free phase of an experimental BSE
infection. BSE and variant
Creutzfeldt-Jakob disease (vCJD) in human
beings are caused by the same infectious
agent, and the sheep-BSE experimental model
has a similar pathogenesis to that of
human vCJD. Although UK blood transfusions
are leucodepleted--a possible protective
measure against any risk from blood
transmission--this report suggests that blood
donated by symptom-free vCJD-infected human
beings may represent a risk of spread
of vCJD infection among the human population
of the UK.

The demonstration that the new variant of
Creutzfeldt-Jakob disease (vCJD) is caused by the
same agent that causes bovine spongiform
encephalopathy (BSE) in cattle1 has raised concerns
that blood from human beings in the symptom-free
stages of vCJD could transmit infection to
recipients of blood transfusions. There is no
evidence that iatrogenic CJD has ever occurred as a
result of the use of blood or blood products,
but vCJD has a different pathogenesis and could
present different risks. CJD is one of the
transmissible spongiform encephalopathies (TSEs)
characterised by the deposition of an abnormal
form of a host protein, PrPSc; the normal
isoform (PrPC) is expressed in many body tissues.
Available evidence, based on detection of
infectivity in blood in rodent models, and absence
of infectivity in naturally occurring TSEs, adds
to the uncertainty in risk assessments of the
safety of human blood. PrPSc has been reported in
blood taken from preclinical TSE-infected sheep,2
but it does not follow that blood is infectious.
Bioassays of human blood can only be carried out
in non-human species, limiting the sensitivity
of the test. One way of avoiding such a species
barrier is to transfer blood by transfusion in an
appropriate animal TSE model. BSE-infected sheep
harbour infection in peripheral tissues3 and
are thus similar to humans infected with vCJD.4
BSE infectivity in cattle does not have
widespread tissue distribution.

We report preliminary data from a study
involving blood taken from UK Cheviot sheep
challenged orally with 5 g BSE-affected cattle
brain and transfused into Cheviot sheep from a
scrapie-free flock of New Zealand-derived animals
(MAFF/SF flock). MAFF/SF sheep do not
develop spontaneous TSE and the transfused
animals are housed separately from other sheep.
All sheep in the study have the PrP genotype
AA136QQ171 which has the shortest incubation
period of experimental BSE in sheep.5 19 transfusions from
BSE-challenged sheep have been
done, mostly with whole blood. Sheep have
complex blood groups and only simple
cross-matching can be done by mixing recipient
serum and donor erythrocytes and vice versa.
Therefore single transfusions only were made
between sedated cross-matched animals to
minimise the risk of severe reactions. Negative
controls were MAFF/SF sheep transfused with
blood from uninfected UK Cheviot sheep. As a
positive control, MAFF/SF sheep were
intravenously injected with homogenised BSE-affected
cattle brain.

We have seen BSE clinical signs and pathological
changes in one recipient of blood from a
BSE-infected animal, and we regard this finding
as sufficiently important to report now rather
than after the study is completed, several years
hence. The blood donation resulting in
transmission of BSE to the recipient was 400 mL
of whole blood taken from a healthy sheep
318 days after oral challenge with BSE. BSE subsequently
developed in this donor animal 629
days after challenge, indicating that blood was taken
roughly half way through the incubation
period. 610 days after transfusion, the transfused
sheep (D505) itself developed typical TSE
signs: weight loss, moderate pruritus, trembling
and licking of the lips, hind-limb ataxia, and
proprioceptive abnormalities. This is the first
experimental transmission of BSE from sheep to
sheep and so we have nothing with which to compare
this incubation period directly. In
cross-species transmissions, bovine BSE injected
intracerebrally gives incubation periods of
about 450 days in these sheep,5 and the donor animal
had an oral BSE incubation period of 629
days (see above). There are no similar data
available on other infection routes.
Immunocytochemistry with the antibody BG4 on tissues
taken from sheep D505 showed
widespread PrPSc deposition throughout the brain and
periphery. Western blot analysis of brain
tissue with the antibody 6H4 showed that the PrPSc
protein had a glycoform pattern similar to
that of experimental BSE in sheep and unlike that
of UK natural scrapie (figure), indicating that
the TSE signs resulted from transmission
of the BSE agent. All other recipients of transfusions
and positive and negative controls are
alive and healthy. The positive controls, which involve a
species barrier, are expected to have
lengthy incubation periods. With one exception, all
transfused animals are at earlier stages
post-transfusion than was D505. The exception is a
sheep which is healthy 635 days after transfusion
with BSE-blood donated at less than 30% of
the BSE incubation period of the donor sheep.

PrPSc (proteinase K treated) analysed by SDS-PAGE,
immunoblotted with 6H4, and
visualised with a chemiluminescent substrate

All lanes are from the same gel with different
exposure times. Size markers are to the left of
lane 1. Lane1: natural scrapie sheep brain,
3 min exposure. Lane 2: as lane 1, 10 min exposure.
Lane 3: sheep D505, blood-transfusion
recipient, 10 min exposure. Lane 4: experimental
BSE-affected sheep brain, 30 s exposure.
Lane 5: as lane 4, 10 min exposure. Each lane
loaded with amount of protein extracted from
0·1 g wet weight of brain, except lane 3 which
was extracted from 0·2 g brain.


Although this result was in only one animal, it
indicates that BSE can be transmitted between
individuals of the same species by whole-blood
transfusion. We have no data on blood fractions
or on levels of infectivity in blood of preclinical
vCJD cases, but whole blood is not now used in
UK transfusions. The presence of BSE infectivity
in sheep blood at an early stage in the
incubation period suggests that it should be
possible to identify which cells are infected, to test
the effectiveness of leucodepletion, and to
develop a diagnostic test based on a blood sample.

We thank Karen Brown, Moira Bruce, Calum
McKenzie, David Parnham, Diane Ritchie, and
the Scottish Blood Transfusion Service. The
project is funded by the Department of Health.

1 Bruce ME, Will RG, Ironside JW, et al.
Transmissions to mice indicate that 'new variant' CJD
is caused by the BSE agent. Nature 1997;
389: 488-501 [PubMed].

2 Schmerr MJ, Jenny A, Cutlip RC. Use of
capillary sodium dodecyl sulfate gel electrophoresis
to detect the prion protein extracted from
scrapie-infected sheep. J Chromatogr B Biomed
Appl 1997; 697: 223-29 [PubMed].

3 Foster JD, Bruce M, McConnell I, Chree A,
Fraser H. Detection of BSE infectivity in brain
and spleen of experimentally infected sheep.
Vet Rec 1996; 138: 546-48 [PubMed].

4 Hill AF, Zeidler M, Ironside J, Collinge J.
Diagnosis of new variant Creutzfeldt-Jakob disease
by tonsil biopsy. Lancet 1997; 349: 99-100.

5 Goldmann W, Hunter N, Smith G, Foster J,
Hope J. PrP genotype and agent effects in
scrapie: change in allelic interaction with
different isolates of agent in sheep, a natural host of
scrapie. J Gen Virol 1994; 75: 989-95 [PubMed].


Institute for Animal Health, Compton, Newbury,
UK (F Houston PhD, CJ Bostock
PhD); and Institute for Animal Health, Neuropathogenesis Unit,
Edinburgh, EH9
3JF, UK (N Hunter PhD, JD Foster BSc, Angela Chong BSc)


Correspondence to: Dr N Hunter

tss
 
Floundering flatulence, flounder, you got anything to say or do you expect these copied articles to teach everyone something.

At least R2 and Mike shorten them down a bit.

Got something to prove, let's chat. That's what this site is all about.
 
i think i have said enough, you apparently have not read it.
this is the problem. once again, transmission studies do not lie,
only politicians and industry do. they have for years. they are the
problem. the amplification and transmission of this agent are the results
of the Govs and industry. but one must read and understand the science.
GWs BSE MRR policy was nothing more than a legal tool to trade many
documented USA strains of TSE globally. ...tss
 
British Medical Journal 2000

In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.

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




http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1
 
>>>Floundering flatulence, flounder, you got anything to say or do you expect these copied articles to teach everyone something. <<<


yes indeed there rkaiser, this is indeed what i am hoping. hell, i have wasted almost 8 years of my life daily on this. i am hoping to educate a few, simply with the rest of the story. i tried to do this on several of the CWD boards for hunters. i think more appreciate it, than don't. but you will always have the ones that just dont want to believe in sound science, and others that never will. you only have to see it once for it to profoundly change your life, then to have them tell you it's not here. it's a spontaneous mutation of a chance happening of bad luck in 85%+ of all cases and only in one part of the globe there is the UKBSE=nvCJD only theory, when ..............


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

Veterinary Services
Centers for Epidemiology and Animal Health March 2004
____________________________________________________________________________
_____________________________________________
Highlights of Phase II: Scrapie:
Ovine Slaughter Surveillance
Study 2002-2003
The purpose of the SOSS study was to estimate
the regional and national prevalence of scrapie in
mature cull sheep in the United States.
Phase I of SOSS was conducted from February
2001 through March 2002 and included refinement
of the study design and sample collection training.
The purpose of Phase I was to develop and modify
the sample collection and testing processes,
without emphasizing statistical results.
SOSS Phase II is similar to Phase I in that
sample collection procedures and testing were
used, along with a representative sample
allocation. Beginning April 1, 2002, and continuing
through March 31, 2003, Phase II included the
collection of tissue samples from 12,508 sheep
from 22 slaughter plants throughout the United
States (21 FSIS inspected, 1 State plant) and 1
large livestock market in Texas. The 21 FSIS plants
represented approximately two-thirds of the total
FSIS mature sheep slaughtered during the study
period. The livestock market represented
approximately one-half of the live sheep exported
to Mexico. All sample data were statistically
weighted to reflect the population from which the
sample was selected. The number of samples
collected from each plant on a specific day was
statistically weighted to represent the volume of
mature sheep slaughtered (sold) through each
plant (market) that specific day. This weight was
adjusted for the total volume of mature sheep
through the plant (market) from April 2002 through
March 2003. Within each facility sample collectors
were instructed to collect samples using systematic
sampling. Overall, the samples collected from the
22 plants and the livestock market represented
299,000 sheep (54 percent of the cull sheep
population, estimated at 550,000 head).
Sheep were traced to State of origin based on
ear tags and/or other information obtained by the
collector at the plant or market. For analysis
purposes, samples identified to individual States
were assigned to one of four defined regions.
Sometimes only a listing of multiple States could be
obtained for a group of sheep (e.g., market animals
accumulated across numerous States). These
samples were assigned to the Multiregion category
if the States they came from were not all in the
same region. In cases where a trace State was not
identified by the collector (n = 2,020), a region was
assigned based on their official identification
information. The 2001 NAHMS Sheep study
showed that at least 95 percent of cull sheep
movement was within the region of origin. Out of
the 12,508 samples submitted, all but 2,127 were
identified to a unique region (Table 1).
Table 1. Number of Samples Submitted, by Face Color
and By Region.
Samples Submitted
Region
Face
Color West Mountain Central East
Multiregion
Total
Black 100 535 680 1,023 453 2,791
White 493 2,997 1,993 1,283 1,472 8,238
Mottled 71 305 413 404 194 1,387
Unknown 6 32 4 42 8 92
Total 670 3,869 3,090 2,752 2,127 12,508
Obex, tonsil, and lymph-node tissues from each
sheep were tested using the immunohistochemistry
(IHC) technique at the National Veterinary Services
Laboratory. A positive case was defined as having
a positive test result on any tissue.
United States Department of Agriculture • Animal and Plant Health Inspection
Service • Safeguarding American Agriculture
Prior to the SOSS study, the estimated
pre as 0.07
p '96
spected
'96
hlights were excerpted from
Pha
revalence estimates
Of the 12,508 mature sheep sampled, valid (at
itive
0.20
s
.
Three tissue types (obex, tonsil, and
llected
in
s
valence of scrapie in the United States w
percent (based on unpublished data from the
NAHMS Sheep '96 study). However, the Shee
estimate was based on a mail-in survey of
producers who reported the presence of su
or confirmed cases of scrapie in their flock over a
period of 5 years, including lambs and mature
sheep. The flock estimate was then expanded
based on flock size to generate the animal-leve
prevalence estimate. The results of the SOSS
study cannot be directly compared to the Sheep
prevalence estimate because of differences in
study design, reference population, and data
collection methods.
The following hig
l
se II: Scrapie: Ovine Slaughter Surveillance
Study 2002-2003.
P

least one testable tissue) test results were
obtained from 12,491 (99.9 percent). A pos
result was recorded for any animal that tested
positive by IHC on one or more of the tissues
sampled. The overall weighted national
prevalence of scrapie in mature sheep is
percent. Estimates could not be made in the
West region due to the low number of sample
obtained. However, national estimates include
samples collected in the West region (Figure 1)

retropharyngeal lymph node) were co
from each sheep head for IHC testing. As
expected, each tissue type differed slightly
the number tested as well as the number of
positive results; however, the prevalence wa
similar for the three tissue types (Figure 2).
0.0
0.2
0.4
0.6
Figure 2. Percent of Sheep That Tested Positive for Scrapie,
by Tissue Type
Percent
Tissue Type
Obex Tonsil Retropharyngeal
lymph node
0.18 0.19 0.20
Scrapie prevalence (one or more tissue
lack-
ot

samples tested positive) was highest in b
faced sheep (0.84 percent). White-faced sheep
were far less likely to test positive for scrapie
(less than 0.01 percent). Some animals were
presented for sample collection with the skin
removed. Therefore, face color could not be
determined on these animals and they were n
included in these estimates (Figure 3).
West Mountain Central East
United States Department of Agriculture • Animal and Plant Health Inspection
Service • Safeguarding American Agriculture
0.0
0.2
0.4
0.6
0.8
1.0
Percent
Face Color
Figure 3. Percent of Sheep That Tested Positive for Scrapie,
by Face Color
0.00
0.84
0.12
White Black Mottled
p
t of
,
Age was determined based on the number of
•• visible permanent incisors. Four-year-old shee
tested positive (one or more tissue samples
tested positive) most frequently (0.49 percen
sheep tested). Scrapie prevalence increased
with age until the animals reached 4 years old
then decreased (Figure 4).
0.0
0.5
1.0
1.5
2.0
Black-faced sheep
National
Figure 4. Percent of Sheep That Tested Positive for Scrapie
(National and Black-faced Sheep), by Age
Percent
Age
0.11
0.00
0.21
0.54 0.49
1.77
0.13
0.69
1 and 2 years 3 years 4 years 5 years or more
enetics
ue samples from the 33 sheep that tested
pos
e at
______________________________
or more information, contact:
E7
G
Tiss
itive for scrapie were submitted for genetic
testing. All 33 samples were of the QQ genotyp
codon 171. This genotype has been characterized
as the least resistant to scrapie.
__
F
SDA:APHIS:VS:CEAH U
NRRC Building B, M.S. 2
2150 Centre Avenue
-8117 Fort Collins, CO 80526
970.494.7000
[email protected] E-mail: NAHMS
www.aphis.usda.gov/vs/ceah/cahm
N421.0304 #
____________________________________
) prohibits discrimination in
plaint of discrimination, write USDA, Director, Office of
yer.
ention of companies or commercial products does not imply
s nor
he U.S. Department of Agriculture (USDA T
all its programs and activities on the basis of race, color, national
origin, sex, religion, age, disability, political beliefs, sexual
orientation,
or marital status or family status. (Not all prohibited bases apply to all
programs.) Persons with disabilities who require alternative means for
communication of program information (Braille, large print, audiotape,
etc.) should contact USDA's TARGET Center at (202) 720-2600 (voice
and TDD).
o file a com T
Civil Rights, Room 326-W, Whitten Building, 1400 Independence
Avenue, SW, Washington, DC 20250-9410 or call (202) 720-5964
(voice and TDD). USDA is an equal opportunity provider and emplo
M
recommendation or endorsement by the U.S. Department of
Agriculture over others not mentioned. USDA neither guarantee
warrants the standard of any product mentioned. Product names are
mentioned solely to report factually on available data and to provide
specific information.
United States Department of Agriculture • Animal and Plant Health Inspection
Service • Safeguarding American Agriculture


http://www.aphis.usda.gov/vs/ceah/ncahs/nahms/sheep/SOSS_highlights.pdf


Animal and
Plant Health
Inspection
SOSS
Phase II: Scrapie: Ovine Slaughter Surveillance
Study 2002-2003

snip...

Section I: Prevalence Estimates
A. Weighted Test
Results
1. Overall prevalence
Of the 12,508 mature sheep sampled, valid (at least one testable tissue)
test
results were obtained from 12,491 (99.9 percent). A positive result was
recorded for any animal that tested positive by immunohistochemistry (IHC)
on
one or more of the tissues sampled. The overall weighted national
prevalence of scrapie in mature sheep is 0.20 percent. Estimates could not
be
made in the West region due to the low number of samples obtained. However,
national estimates include samples collected in the West region.
a. Percentage of sheep that tested positive for scrapie, by region*:
Percent Sheep
Region
Mountain Central East Multiregion National
Pct.
Std.
Error Pct.
Std.
Error Pct.
Std.
Error Pct.
Std.
Error Pct.
Std.
Error
0.14 (0.06) 0.21 (0.10) 0.52 (0.15) 0.13 (0.07) 0.20 (0.04)
*Because of the low number of samples obtained in the West region, results
for the
West region are included in the National estimates but are not listed
individually.

snip...


http://www.aphis.usda.gov/vs/ceah/ncahs/nahms/sheep/SOSSphase2.pdf


TSS

----- Original Message -----
From: "Terry S. Singeltary Sr." <[email protected]>
To: <[email protected]>
Sent: Wednesday, August 24, 2005 9:11 PM
Subject: SCRAPIE USA UPDATE MARCH - JUNE 2005


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

From: TSS ()
Subject: SCRAPIE USA UPDATE MARCH - JUNE 2005
Date: August 24, 2005 at 7:03 pm PST

SCRAPIE USA MONTHLY REPORT 2005

AS of March 31, 2005, there were 70 scrapie infected source flocks (Figure
3). There were 11 new infected and source flocks reported in March (Figure
4) with a total of 51 flocks reported for FY 2005 (Figure 5). The total
infected and source flocks that have been released in FY 2005 are 39 (Figure
6), with 1 flock released in March. The ratio of infected and source flocks
released to newly infected and source flocks for FY 2005 = 0.76 : 1. IN
addition, as of March 31, 2005, 225 scrapie cases have been confirmed and
reported by the National Veterinary Services Laboratories (NVSL), of which
53 were RSSS cases (Figure 7). This includes 57 newly confirmed cases in
March 2005 (Figure 8). Fourteen cases of scrapie in goats have been reported
since 1990 (Figure 9). The last goat cases was reported in January 2005. New
infected flocks, source flocks, and flocks released or put on clean-up plans
for FY 2005 are depicted in Figure 10. ...

FULL TEXT ;

http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.htm
l


SCRAPIE USA JUNE 2005 UPDATE


AS of June 30, 2005, there were 114 scrapie infected and source flocks
(Figure 3). There were 14 new infected and source flocks reported in June
(Figure 4) with a total of 123 flocks reported for FY 2005 (Figure 5).


snip...


In addition, as of June 30, 2005, 448 scrapie cases have been confirmed and
reported by the National Veterinary Services Laboratories (NVSL), of which
106 were RSSS cases (Figure 7). This includes 81 newly confirmed cases in
June 2005 (Figure 8). Fifteen cases of scrapie in goats have been reported
since 1990 (Figure 9). The last goat case was reported in May 2005.


snip...end


http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.htm
l


USDA/APHIS

SOSS

Phase II: Scrapie: Ovine Slaughter Surveillance

Study 2002-2003


http://www.aphis.usda.gov/vs/ceah/ncahs/nahms/sheep/SOSSphase2.pdf


12/10/76
AGRICULTURAL RESEARCH COUNCIL
REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
Office Note
CHAIRMAN: PROFESSOR PETER WILDY

snip...

A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all
countries.

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human
dementias"

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer
grievously.

snip...

76/10.12/4.6

http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf


Like lambs to the slaughter
31 March 2001
Debora MacKenzie
Magazine issue 2284
What if you can catch old-fashioned CJD by eating meat from a sheep infected
with scrapie?
FOUR years ago, Terry Singeltary watched his mother die horribly from a
degenerative brain disease. Doctors told him it was Alzheimer's, but
Singeltary was suspicious. The diagnosis didn't fit her violent symptoms,
and he demanded an autopsy. It showed she had died of sporadic
Creutzfeldt-Jakob disease.

Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number
of campaigners who say that some sCJD, like the variant CJD related to BSE,
is caused by eating meat from infected animals. Their suspicions have
focused on sheep carrying scrapie, a BSE-like disease that is widespread in
flocks across Europe and North America.

Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in ...

The complete article is 889 words long.

full text;

http://www.newscientist.com/article.ns?id=mg16922840.300



Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*,, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*,
Domíníque Marcé*, François Lamoury*, Nicolas Kopp, Jean-Jacques Hauw§, James
Ironside¶, Moira Bruce, Dominique Dormont*, and Jean-Philippe Deslys*
* Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction
des Sciences du Vivant/Département de Recherche Medicale, Centre de
Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc,
BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Hôpital Neurologique Pierre
Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; § Laboratoire de
Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital,
75013 Paris, France; ¶ Creutzfeldt-Jakob Disease Surveillance Unit, Western
General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and
Institute for Animal Health, Neuropathogenesis Unit, West Mains Road,
Edinburgh EH9 3JF, United Kingdom

Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)


Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
Conclusions
References
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.


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



TSS

#################### https://lists.aegee.org/bse-l.html
####################

#################### https://lists.aegee.org/bse-l.html ####################
:mad:


THEN you have 4.5 million demented and dying from alzheimer's with a guesstimate of 20 million by 2050. NOT to go into the science of TSE and Alzheimer's similarity, and only sticking to the 4 university studies, the Mexican study, the Duke, the Yale, and the PA study, where it is shown that from 3 to 33 % of those elderly diagnosed with Alzheimer's, AFTER autopsy actually had CJD. but i suppose that is for another board. so yes
indeed there rkaiser i am just going to drop a few lines here and mooove on. folks can take the data with how ever many grains of salt they wish.
but it's not going away, and you cannot ignore it. and i think really it's better to have all the data made available to the public. ...
 
Who says anyone is ignoring anything flounder. My point, and the point of a few other here on ranchers is that the world is following a lost leader. The key to dealing with TSE's is to discuss and concern ourselves with the sporatic, the spontaneous, or the environmentally affected.

I believe that is what some of your postings have eluded to, but most still deal with infection and transmission.

Supporting a fear based theory in which less than 200 humans have "supposedly" died makes very little sense to me. Looking into the truth behind these deaths, and the deaths of hundreds of thousands of others with TSE difficulties seems more practical. The relation of these diseases is obvious. Yet for some profound reason, the world has focused on"MAD COW" to the point of ruining the livelyhood of millions of ranchers around the world.

Study flounder, and show us more. Show us real studies on real issues, rather than going back and following the one man who coined this infectious prion crap.
 
Hello Terry S. Singeltary Sr.,

I see you have been called in as reinforcement.

Well, I would take more time to read your thoughts at "vegsource.com" if it weren't for the fact that your site downloads all types of nasty adware, etc.

Please read about oxidative stress apoptosis. The presence of prion fibrils is not necessarily the be all, end all of nerve cell death. Many cases diagnosed as BSE did not show accummulation of the prion or vacuoles, yet still they were animals with the very same symptoms and resulting disease process.

Research on OPs, done by Purdey and Whatley clearly showed that exposure to OPs caused the upregulation of PrPC. By looking at all the available evidence, Purdey has pointed to the truths of TSEs, that they require more than one causal agent (natural exposure, of course). The present use of sonication and other forms of energy, such as heat to amplify the prion are vindicating his hypothesis that sound energy could help lead to the tertiary change. The role of copper in the activities of superoxide dismutase, an important enzyme that handles oxidative free radicals of superoxide, has also been verified by Dr. D. Brown. More and more evidence is accummulating,that the disruption of copper's normal functions in the brain is involved with the death of nerve cells. Also see University of Calgary video on this. Effects of Mercury on brain neuronal death.

Please read more on the damage of oxidate stresses, such as the newly published:

"Copper binding is the governing determinant of prion protein turnover", Haigh Cathryn L., et al.

"Reactive oxygen species-mediated bata-cleavage of the prion protein in the cellular response to oxidative stress", Watt NT, et al.

"Is there a role for copper in neurodegenerative disease?", Cerpa W, et al

The homogenate transmission experiments clearly show a strong link to the iatrogenic transmission of the disease agent(s). However they are not equivical to natural TSE, as in natural cases the presence of PrPC is more limited. Humans and mammals may carry "proteon nucleated centres" as Dr. Vitaly Vodyanoy calls them; but that does not mean that they will definitively develop TSEs or other brain disorders. However, exposure to other factors such as OPs, radiation, and other reactive oxidative stress initiators, could be the major trigger mechanism in the brain, and eye, that causes the formation of the first seeds of the prion disease. The subsequent further exposure, or lack thereof, is likely also a contributing factor. Of course, some forms of oxidative stress have a longer life than others, ie: nuclear radiation.

Other research just out: "Effective levels of tetanus toxin can be made in a production medium totally lacking both animal (eg. brain, heart infusion) and dairy proteins or digests (eg. casein hydrolysates)", Demain AL et al.

this article, though I have not seen it yet, is appearing to link the spread of TSE to tetanus innoculation. Although the UK science does not admit an epidemiological link to vaccination, the possibility of one (fear of one) will aid in the advancement of these nonanimal protein products. Isn't that what you want, master of vegsource.com.
 
hello kathy,

kathy writes;


>>> I see you have been called in as reinforcement. <<<

just surfed in by accident. nobody called my in from anywhere.
i knew i would be wasting my time here. it took years for the deer hunters to finally come around, i dont think there is enough time in my life to get all the farmers and ranchers to come around. i have ignored my family too long. i simply will put the data here, some will read the science and learn, the others will ignore it as in the past, because they are not brave enough to accept the truth and try and do anything about it. but i had to at least put the studies here for the ones that did want the truth and accept the change, i had do do that. give you something to think about;-) much BSe was being posted here. i have debated OPs theory before with UK BSE farmer. they do not even believe it;



1) None of our animals that contracted BSE were treated with OP's, even
in utero.
2) My kids were treated with OP's as infants to control head lice. This
seems to be endemic as infection waves in UK primary schools (and
possibly elsewhere).
3) One might argue if the continued use of british beef in the UK was
ethical, none the less it happened. We have a duty to learn from it, not
least a duty to learn on behalf of those people who died so horribly....



Kathy,

I have agreed before that OPs might increase the susceptibility to the prion agent by altering the levels of accessible PrP i.e. Whatley et al;


1: Neuroreport. 1998 May 11;9(7):1391-5.


Phosmet induces up-regulation of surface levels of the cellular prion protein.

Gordon I, Abdulla EM, Campbell IC, Whatley SA.

Department of Neuroscience, Institute of Psychiatry, London, UK.

Chronic (2 day) exposure of human neuroblastoma cells to the organophosphate pesticide phosmet induced a marked concentration-dependent increase in the levels of PrP present on the cell surface as assessed by biotin labelling and immunoprecipitation. Levels of both phospholipase C (PIPLC)-releasable and non-releasable forms of PrP were increased on the plasma membrane. These increases appear to be due to post-transcriptional mechanisms, since PrP mRNA levels as assessed by Northern blotting were unaffected by phosmet treatment. These data raise the possibility that phosmet exposure could increase the susceptibility to the prion agent by altering the levels of accessible PrP.




BUT, this is a far cry from believing in the OP theory. again, amplification and transmission, transmission studies do not lie.
we have floundered to long. the 8/4/97 ruminant to ruminant partial and voluntary feed ban was and still is a joke.
same as with the surveillance of BSE/TSE in the USA. these are both fact.


>>>Well, I would take more time to read your thoughts at "vegsource.com" if it weren't for the fact that your site downloads all types of nasty adware, etc. <<<


i agree. i have complained about that before, but not my site. one of many i simply document TSE data on for the public.


>>>> this article, though I have not seen it yet, is appearing to link the spread of TSE to tetanus innoculation. Although the UK science does not admit an epidemiological link to vaccination, the possibility of one (fear of one) will aid in the advancement of these nonanimal protein products. Isn't that what you want, master of vegsource.com. <<<<


LIKE so many others that cannot prove the OP theory, or disprove the TSE transmission studies, you try to find something that would bring people to tarnish my credibility by bringing up vegsource URL for where i post my research of this nightmare. this happens everytime. but the facts and science generally prevail in the end. takes time for the science to digest. dont blame me, i am only the messenger. fact is, i was and am very thankful to jeff et al there for letting me post my research of the different transmission studies. they gave me a place to document these studies when your federal gov and these journals would not let the normal lay person have access to them. for that i am very grateful to them. the only problem to your approach kathy is that i am still a meat eater. however my consumption is not near the consumption it was. my goal was to simply make it better. give the public _all_ the facts. the OPs and this new/old theory of the human mbm in the lancet last week are about as possible as martians planting the agent here, compared to the scrapie amplification and transmission via mbm via ruminant feed and factory farm practices. the tranmission studies speak for themselves. the USA and N. America are very unique. the many different TSEs in many different species that have been rendered for decades. time will tell here, once only science is left to deal with it.


about the vaccines route you mention, only one of many. i am very much aware of the iatrogenic CJD from the surgical and medical arena, and i have always said this goes far far beyond the mad cow hamburger. dont let the vegsource urls scare you too bad, look at the source of the data. i am not making this stuff up here.

another disturbing likely route and source, the nutritional supplements industry and SRMs to humans here. the cosmetics another potential source of human TSEs.

no, you don't want to hear it, i don't want to hear it, but these are the facts. take um or leave um. ...



From: TSS <mailto:[email protected]> (216-119-163-253.ipset45.wt.net)
Subject: MAD COW DISEASE, SMALLPOX VACCINE (Dried Calf Lymph Type) and TSEs
Date: December 15, 2002 at 9:52 am PST

Subject: MAD COW DISEASE, SMALLPOX VACCINE (Dried Calf Lymph Type)
and TSEs
Date: Sun, 15 Dec 2002 11:37:55 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: [email protected]

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

Greetings,

with the threat of terrorism and the recent news of the SMALLPOX
vaccine being distributed, and the fact we may all be faced with
the real possibility of having to make a decision whether or not
to take this vaccine, i got to thinking of what the ingredients
in the smallpox vaccine might be. never could really get a clear
picture of what the actual ingredient might be from start of process
to end product. with more and more _bad_ news of other tissues having
the potential to carry enough infectivity to be lethal, i thought
it would be nice to know what we are really getting ourselves into.
i found a little about smallpox vaccine and posted below. i am not sure
if any of this is still in use, but i would be most curious to know;

what the ingredients of the smallpox vaccine the USA is going to be
distributing from start to end product might be?

the source country of those ingredients?

the process or processes used to kill the TSE agent from start to finish?

or (without trying to be sarcastic), under the new Bush anti terrorism
plan (re-USA mad cow feed ban warning letters via F.O.I.A. only now),
do i have to go through the F.O.I.A. act to find this out as well???

thank you,
kind regards,

Terry S. Singeltary Sr.

8. The Secretary of State has a number of licences. We understand that
the inactivated polio vaccine is no longer being used. There is a stock
of smallpox vaccine. We have not been able to determine the source
material. (Made in sheep very unlikely to contain bovine ingredients).

http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf

http://www.bseinquiry.gov.uk/report/volume7/chapted2.htm

http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf

although 176 products do _not_ conform to the CSM/VPC
guidelines.

http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf

5.23 This alerted Sir Donald Acheson to the fact that concerns about the
safety of vaccines had not yet been resolved. He contacted Dr Pickles,
and their conversation led him to ask Dr Harris to look into the matter:
My attention has been drawn to a sentence in Dr Pickles' draft of a
submission to the Secretary of State on this matter. It reads: 'At the
present time we can't give any complete guarantee of safety for human
medicines that use bovine materials in manufacture such as most
vaccines.' Having looked at the report I am not able to find any
statement which supports this statement of concern. I have, however,
therefore spoken to Dr Pickles on the telephone and she reports to me
that for some considerable time she has had serious concern about the
safety of bovine-based vaccines in the light of the fact it has been
discovered that contamination with placental material (which is known to
be heavily infected with the BSE particle) is a distinct possibility in
the preparation of material for human vaccines derived from foetal
serum. This matter as described to me by Dr Pickles gives me sufficient
cause for concern to ask you to look into it urgently together with
Medicines Division. I shall amend the submission to indicate that the
question of the safety of vaccines derived from bovine material is a
matter which has not been dealt with directly by Southwood's group, but
is one in which I am making urgent enquiries. 22

http://www.bseinquiry.gov.uk/report/volume7/chapted2.htm

WHO/CDS/CSR/APH/2000.2

3.5 Animal vaccine-related Transmissible Spongiform Encephalopathy risks:

Scrapie outbreak in Italy

Maurizio Pocchiari:

Historically, Italy has had a low incidence of scrapie; however, in 1997
there was a dramatic increase in the number of reported flocks. This
increase in reports included a relatively high proportion of goat
flocks, generally considered more resistant to natural scrapie than
sheep. Details of the timing of the flock outbreaks, composition of the
flocks and vaccination status were provided. It was noted that
vaccination for Mycoplasma agalactiae was provided to a large proportion
of the flocks developing scrapie, and that this vaccine is made from
sheep brain and mammary gland. Small batches of brain and mammary glands
are mixed, and given subcutaneously to adult and young animals,
providing considerable possible exposure to contaminated material. Some
flocks receiving this vaccine did not develop scrapie, and western blot
and transmission experiments are underway. However, the consultation
agreed that the epidemiologic evidence points toward a vaccine origin
for the scrapie disease seen in some of the flocks.

snip...

7.6 Could vaccines prepared from animal brain tissue pose a risk of
transmission of Transmissible Spongiform Encephalopathies to humans?
François Meslin:

Over 40,000 deaths due to rabies are reported annually worldwide and
each year seven to eight million people receive antirabies vaccine
treatment following dog bites. Dog rabies poses a significant public
health problem in Asia, as 85% of the human deaths due to rabies
reported worldwide and 80% of the vaccine doses applied in
developing countries come from this part of the world.
In many Asian countries such as Bangladesh, India, Nepal and Pakistan,
sheep-brain based Semple vaccine 15 is the only vaccine available free
of cost. It represents 50 to 95% of all vaccine doses used for rabies
post-exposure treatment, depending upon the country. A complete
treatment consists of 10 subcutaneous daily injections
of 2 to 5 ml (depending mainly on patient size and nature of the
exposure) plus booster doses; that is a total of 25 to 50 ml of the 5 %
sheep brain suspension injected over a 10-day period.
According to the literature, the reported rate of neuroparalytic
complications following the use of this vaccine varies from 1:600 to
1:1575 administrations, and 20-25% of these lead to death. The exact
incidence of neuroparalytic complications throughout India or other
countries in the area is not known. However, in the State of
Karnataka, India, 112 cases of neuroparalytic accidents were admitted in
the past 20 years following Semple vaccine administration. In contrast,
the newly developed cell culture or embryonating egg vaccines are
effective and safe, with lower and less severe complication rates.
In many Asian countries, Semple type vaccine has been used for the past
90 years. In India forty million ml of this vaccine are produced in this
country to treat at least 500 000 persons each year. In Pakistan 450 000
and in Bangladesh 60 000 people receive Semple type vaccine after
possible exposure to rabies. There is a theoretical risk of TSE
transmission to humans through parenteral administration of
these products. Although there is to date no evidence of such
occurrences in human medicine, recent events in the TSE field have
demonstrated that an animal TSE agent could affect human beings.
The situation is very similar regarding rabies vaccines for animal use.
For example various Indian veterinary vaccine institutes prepare 100
million ml of Semple vaccine for use in both rabies pre-and
post-exposure prophylaxis in dogs and food production animals each year.
Scrapie could be theoretically transmitted to animal vaccine recipients,
especially ruminants, through sheep-brain based vaccines such as
Semple type vaccine. This could happen because scrapie infectivity, if
present, would not be inactivated by the manufacturing process. In this
connection, a recent 15 Ãx-propiolactone inactivated or phenolized
antirabies vaccine containing 5% suspension of sheep brain infected with
a fixed strain of rabies virus.

WHO/CDS/CSR/APH/2000.2

34 WHO Consultation on Public Health and Animal TSEs
Epidemiology, Risk and Research Requirements

publication strongly suggests that scrapie was transmitted to sheep and
goats through the administration of a veterinary vaccine whose method of
preparation is similar to the Semple type vaccine. In addition, various
Asian countries have begun to use animal tissues as feed supplement for
intensive sheep and dairy cattle production. This introduces an
additional, though still theoretical, possibility that scrapie, or even
BSE, could spread among the sheep population and enter the sheep flocks
that are used as a source of rabies vaccine production for human or
animal use. In areas where the status of animal TSE is not well
documented, this risk cannot be totally ruled out, though it may be
remote, as there is no test available at present to detect
pre-clinical cases of prion disease in sheep.

snip...

Recommendation 25

Human vaccines prepared from whole ruminant brains may carry the risk of
transmission of animal TSE agents, because the inactivation processes
usually applied to these products do not inactivate TSE agents. In
particular, considering the recent emergence of vCJD in humans related
to BSE in cattle, the consultation recommends that the use of these
vaccines should be avoided if suitable alternatives can be made
available. The Consultation strongly supported the recommendation made
by WHO Expert Committee on Rabies, which states:

"The (Expert) Committee reiterated, as stated in its 1983 report, its
support for the trend to limit or abandon completely - where
economically and technically possible - the production of
encephalitogenic brain-tissue vaccines, and strongly advocated the
production and use of inactivated cell-culture rabies vaccines in both
developed and developing countries."

Recommendation 26

The use of veterinary vaccines prepared from whole ruminant brains, for
use in ruminants, should be avoided unless the process ensures TSE
inactivation and/or removal, or the source animals have been
demonstrated to be free of any TSE.

snip...

http://www.who.int/emc-documents/tse/docs/whocdscsraph20002.pdf

http://216.239.37.100/search?q=cache:ha1lZiMaWG4C:www.who.int/emc-documents/tse/docs/whocdscsraph20002.pdf+Acquisition+of+spongiform+encephalopathies+in+India+through+sheep-brain+rabies+vaccination.&hl=en&ie=UTF-8

55
III.3. IATROGENIC TRANSMISSION
Iatrogenic transmission of BSE has not been reported, or even suspected,
in cattle but there are some definite occurrences of scrapie in sheep
that have been reliably attributed to the use of non-commercial vaccines
containing ovine starting materials. For this reason, the issue is
discussed below. Other forms of iatrogenic transmission of TSE have been
restricted to humans and human tissues. For the sake of completeness and
convenience, these subjects are briefly discussed below.

III.3.1 VACCINES
Reference has already been made to the occurrence of at least several
hundred cases of scrapie in British sheep as a direct result of the use
of a vaccine against the tick transmitted, viral disease, louping-ill
(Gordon, Brownlee and Wilson, 1939, Gordon, 1946 and Greig, 1950). This
occurrence resulted from the accidental use of scrapie-infected source
material and processing methods that did not inactivate the scrapie
agent that was unknowingly present. A more recent possible occurrence of
possible iatrogenic scrapie has recently been reported in Etna Silver
crossbred goats in Italy by Cappucchio et al., (1998). The goats were
kept at grass and concentrate rations were not fed, thus eliminating a
source of infection from feed via mammalian proteins. Animals over two
months old were annually vaccinated against contagious agalactia caused
by Mycoplasma agalactiae. The vaccine included central nervous system
from pathogen-free sheep. The mortality rate in the goats reached
28% in 1 herd, 60% in the second and 5.5% in a third herd. About half
the 56 goats were between 2.5 - 3 years old. Only 1.15% of sheep that
were kept with the goats developed scrapie. Scrapie was confirmed by
microscopic examination of the brain and by detection of PrPSc including
by immunocytochemistry. PrPSc was widespread in the brain and beyond
sites of vacuolar change. The high mortality, severe loss of weight and
simultaneous appearance in the three herds were distinctly unusual
features in this outbreak. The source of infection remains uncertain and
unproven but iatrogenic transmission must be considered.
A larger epidemic involving 20 outbreaks of scrapie in sheep and goats,
also in Italy, has been even more recently reported by Agrimi et al.,
(1999). The annual incidence ranged from 1% to 90% with a mean incidence
for goats of 26% and for sheep of 10%. The total number of cases in
sheep and goats together was 1040. The clinical disease was confirmed by
microscopic examination of the brain and PrP immunocytochemistry or
Western blotting. The high incidence in goats, the high
within-flock/herd incidence, the temporal clustering, absence of
commercial concentrate feeding in eight flocks and association with the
use of a sub-cutaneously administered M. agalactiae vaccine, prepared
locally using brain and mammary tissue from clinically healthy sheep,
strongly suggests an iatrogenic origin. Scrapie appeared between 23 and
35 months after the vaccine was administered. A third outbreak in
southern Italy attributed also to the same vaccine has been described by
Caramelli et al, (2001) in a mixed flock of Comisana sheep and half-bred
goats in an upland area of southern Italy. High crude mortality and
scrapie incidence occurred in both species and a large proportion of
aged animals were affected. The neuropathology was similar to that in
other sheep in Italy with iatrogenic disease but different from
conventional natural scrapie. Affected sheep were all of the most
susceptible genotype (Codon 171 QQ). It is stressed that the vaccines
incriminated in the transmission of scrapie in all these incidents are
not commercially produced. They have been prepared and distributed
locally within the country. Dr Subash Arya has repeatedly drawn
attention to the possible risk of transmitting CJD to humans vaccinated
with sheep-brain derived vaccines in India, e.g. Arya, (1994). However,
neither Dr Arya nor any of his colleagues has yet found any such case.
The episodes of scrapie resulting from the use of vaccines prepared from
infected sheep tissues emphasises the need for caution and mandatory
selection of safe sources for starting materials used in the manufacture
of vaccines. Such vaccines could theoretically at least, be used in
cattle thus creating a potential risk, though it is most unlikely that
they would be licensed for this purpose in Europe. Vaccines have not
been incriminated in the transmission of BSE (Wilesmith et al., 1988,
J.W.Wilesmith, personal communication). Furthermore, large numbers of
doses of commercially produced vaccines that have used bovine starting
materials, have been inoculated by parenteral and oral routes into
cattle throughout the world and a substantial proportion have been
produced in Europe, but no incident of BSE has been attributed to their
use. This is important because, since there is no species barrier, any
chink in the armour protecting vaccines from contamination would have
been revealed, but none has.

III.3.2.OTHER MEDICINAL PRODUCTS DERIVED FROM TSE-SUSCEPTIBLE SPECIES
Animal sources of material used in medicinal products vary, but mostly
are derived from cattle. There is thus at least a possibility that
unless strict precautions are taken, disease could be transmitted in
this way. It cannot be ruled out that no case ever arose by this means,
but it is clear that the majority did not, even at the very beginning of
the BSE epidemic before publication of information on BSE, and before
any legislation was in place (Wilesmith et al., 1988). The highest risk
tissue is bovine brain from a clinically affected animal or one in the
immediate pre-clinical phase. Posterior pituitary extract (now prepared
biosynthetically), was available and used in veterinary practice mainly
in adult female cattle at the time of parturition, to assist treatment
of retained placenta or to assist in milk let down. However, no
association was found between its use and the occurrence of BSE
(Wilesmith et al., 1988).

http://europa.eu.int/comm/food/fs/sc/ssc/out236_en.pdf

Indian J Pediatr 1991 Sep-Oct;58(5):563-5

Arya SC.

Centre for Logistical Research and Innovation, Greater Kailash, New Delhi.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1813404&dopt=Abstract

BMJ 1996 Nov 30;313(7069):1405

Comment on:

* BMJ. 1996 Aug 24;313(7055):441.


Blood donated after vaccination with rabies vaccine derived from
sheep brain cells might transmit CJD.

Arya SC.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8956737&dopt=Abstract

BMJ 1996;313:1405 (30 November)
Letters
Blood donated after vaccination with rabies vaccine derived from sheep
brain cells might transmit CJD
EDITOR,--Janet Morgan reports that the National Blood Authority in
Britain has decided to tighten the donor screening programme to exclude
transmission of Creutzfeldt-Jakob disease or its variant through blood
donations.1 Prospective donors will be prevented from donating blood if
they have a history of treatment with human growth hormone or if one of
their siblings, parents, or grandparents developed the disease. I would
point out that similar care should also be taken when immigrants from
Asia and Africa offer to donate blood, in case they received rabies
vaccine derived from culture of sheep brain cells when they were living
in their country of origin.

In many countries in Asia and Africa limited supplies of imported rabies
vaccines derived from culture of human cells have been available. Many
people continue to be offered indigenously produced sheep brain vaccine
after exposure to a rabid animal. Scrapie is known to exist in sheep
around many centres where the vaccine is produced. In the mountain sheep
of the Kumaon foothills in the Himalayas, for example, scrapie was
established more than four decades ago and 1-10% of the flock was
reported to have the disease in 1961.2 In the Himalayan foothills the
Central Research Institute continues to produce four to five million
doses of sheep brain vaccine annually. Transmission of abnormal prion
protein, PrPsc, in sheep brain vaccine might have occurred in some of
the 30 documented cases of Creutzfeldt-Jakob disease in different
regions in India.3 Because Creutzfeldt-Jakob disease has a latency of
about 20 years, many recipients of sheep brain rabies vaccine could
emigrate to Britain before becoming ill.

Before accepting blood donations from immigrants it would be desirable
to ask the potential donors whether they were exposed to a rabid animal
and immunised with sheep brain rabies vaccine in their country of
origin. Furthermore, indirect assessment should be possible through, for
example, assay looking for antibodies specific to rabies.

Clinical microbiologist Centre for Logistical Research and Innovation,
M-122 (of part 2), Greater Kailash-II, New Delhi-110048, India

Subhash C Arya

http://bmj.com/cgi/content/full/313/7069/1405/a

: Neuroepidemiology 1991;10(1):27-32

Creutzfeldt-Jakob disease in India (1971-1990).

Satishchandra P, Shankar SK.

Department of Neurology, National Institute of Mental Health and
Neurosciences (NIMHANS), Bangalore, India.

Thirty cases including 20 definite and 10 probable cases of
Creutzfeldt-Jakob disease (CJD) seen in India between 1971 and 1990 are
reported. Demographic analysis has shown similarities to the previously
published reports from other parts of the world. Though 21 (70%) of
cases were from two centers--Bombay and Bangalore-, suggesting
clustering, this seems to be more apparent than real. One subject worked
in the medical field, where possibility of iatrogenic transmission could
not be ruled out. None of the cases had positive family history of CJD.
There is no epidemiological data of CJD from India so far and hence this
report is one such pilot study.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2062414&dopt=Abstract

i recieved the 1947 report of the Louping-ill vaccine
incident and posted on www here;

Louping-ill vaccine (scrapie transmission by vaccine)

THE VETERINARY RECORD
516 No 47. Vol. 58
November 23rd, 1946

NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND

ANNUAL CONGRESS, 1946

snip...

The enquiry made the position clear. Scrapie was developing in
the sheep vaccinated in 1935 and it was only in a few instances
that the owner was associating the occurrence with louping-ill
vaccination. The disease was affecting all breeds and it was
confined to the animals vaccinated with batch 2. This was clearly
demonstrated on a number of farms on which batch 1 had been
used to inoculate the hoggs in 1935 and batch 2 to inoculate
the ewes. None of the hoggs, which at this time were three-
year-old ewes. At this time it was difficult to forecast whether all
of the 18,000 sheep which had received batch 2 vaccine would
develop scrapie. It was fortunate, however, that the majority of
the sheep vaccinated with batch 2 were ewes and therfore all
that were four years old and upwards at the time of vaccination
had already been disposed of and there only remained the ewes
which had been two to three years old at the time of vaccination,
consequently no accurate assessment of the incidence of scrapie
could be made. On a few farms, however, where vaccination was
confined to hoggs, the incidence ranged from 1 percent, to 35 percent,
with an average of about 5 percent. Since batch 2 vaccine
had been incriminated as a probable source of scrapie infection,
an attempt was made to trace the origin of the 112 sheep whose
tissues had been included in the vaccine. It was found that they
had been supplied by three owners and that all were of the
Blackface or Greyface breed with the exception of eight which
were Cheviot lambs born in 1935 from ewes which had been in
contact with scrapie infection. Some of these contact ewes
developed scrapie in 1936-37 and three surviving fellow lambs to
the eight included in the batch 2 vaccine of 1935 developed
scrapie, one in September, 1936, one in February, 1937, and one
in November, 1937. There was, therefore, strong presumptive
evidence that the eight Cheviot lambs included in the vaccine
althought apparently healthy were, in fact, in the incubative stage
of a scrapie infection and that in their tissues there was an
infective agent which had contaminated the batch 2 vaccine,
rendering it liable to set up scrapie. If that assumption was
correct then the evidence indicated that:-

(1) the infective agent of scrapie was present in the brain, spinal
cord and or spleen of infected sheep:
(2) it could withstand a concentration of formalin of 0-35 percent,
which inactivated the virus of louping-ill:
(3) it could be transmitted by subcutaneous inoculation;
(4) it had an incubative period of two years and longer.

Two Frenchmen, Cuille & Chelle (1939) as the result of experiments
commenced in 1932, reported the successful infection of
sheep by inoculation of emulsions of spinal cord or brain material
by the intracerebral, epidural, intraocular and subcutaneous routes
The incubation period varied according to the route employed,
being one year intracerebrally, 15 months intraocularly and 20
months subcutaneously. They failed to infect rabbits but succeeded
in infecting goats. Another important part of their work
showed that the infective agent could pass throught a chamberland
1.3 filter, thus demonstrating that the infective agent was a
filtrable virus. It was a curious coincidence that while they
were doing their transmission experiments their work was being
confirmed by the unforeseeable infectivity of a formalinized tissue
vaccine.

As a result of this experience a large-scale transmision experiment
involving the ue of 788 sheep was commenced in 1938 on a
farm specially taken for the purpose by the Animal Diseases
Research Association with funds provided by the Agricultural
Research Council. The experiment was designed to determine the
nature of the infective agent and the pathogenesis of the disease.
It is only possible here to give a summary of the result which
showed that (1) saline suspensions of brain and spinal cord tissue
of sheep affected with scrapie were infective to normal sheep
when inoculatted intracerebrally or subcutaneously; (2) the incubation
period after intracerebral inoculation was seven months and
upwards and only 60 percent of the inoculated sheep developed
scrapie during a period of four and a half years; (3) the incubation
period after subcutaneous inoculation was 15 months and upwards
and only about 30 percent of the inoculated sheep developed
the disease during the four and a half years: (4) the infective
agent was of small size and probably a filtrable virus.

The prolonged incubative period of the disease and the remarkable
resistance of the causal agent to formalin are features of
distinct interest. It still remains to determine if a biological test
can be devised to detect infected animals so that they can be
killed for food before they develop clinical symptoms and to
explore the possibilities of producing an immunity to the disease...

http://www.vegsource.com/talk/madcow/messages/7634.html



USA IMPORTS VACCINE PRODUCTS FROM BSE COUNTRIES

http://www.mad-cow.org/00/may00_news.html

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).

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

Human vaccine prepared in animal brains

http://www.mad-cow.org/00/nov00_late_news.html#fff

http://www.whale.to/v/singeltary7.html

http://www.mad-cow.org/00/may00_news.html

http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh

STUDY DESIGN AND METHODS: BSE was passaged through macaque monkeys and
then adapted to the prosimian microcebe (Microcebus murinus ). Brain
homogenate and buffy coat from an affected microcebe were separately
inoculated intracerebrally into three healthy microcebes (two animals
received brain and one received buffy coat).

RESULTS: All three inoculated microcebes became ill after incubation
periods of 16 to 18 months. Clinical, histopathologic, and
immunocytologic features were similar in each of the recipients.

CONCLUSION: Buffy coat from a symptomatic microcebe infected 17 months
earlier with BSE contained the infectious agent. This observation
represents the first documented transmission of BSE from the blood of an
experimentally infected primate, which in view of rodent buffy coat
infectivity precedents and the known host range of BSE is neither
unexpected nor cause for alarm.

http://www.blackwell-synergy.com/servlet/useragent?func=synergy&synergyAction=showAbstract&doi=10.1046/j.1537-2995.2002.00098.x

Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy BSE-L
To: BSE-L

snip...

[host Richard Barns]
and now a question from Terry S. Singeltary of
CJD Watch.

[TSS]
yes, thank you,
U.S. cattle, what kind of guarantee can you
give for serum or tissue donor herds?

[no answer, you could hear in the back ground,
mumbling and 'we can't. have him ask the question
again.]

[host Richard]
could you repeat the question?

[TSS]
U.S. cattle, what kind of guarantee can you
give for serum or tissue donor herds?

[not sure whom ask this]
what group are you with?

[TSS]
CJD Watch, my Mom died from hvCJD and we are
tracking CJD world-wide.

[not sure who is speaking]
could you please disconnect Mr. Singeltary

[TSS]
you are not going to answer my question?

[not sure whom speaking]
NO

snip...

http://vegancowboy.org/TSS-part1of8.htm

Meanwhile, health officials with the Food and Drug Administration say
the method of manufacturing the old vaccine, called Dryvax, which was
made by Wyeth using calf skin, is "no longer considered optimal."
Instead, the agency says the new smallpox vaccine "will be prepared in
MRC-5 cells" a line of aborted fetal cells dating back to 1966
because that method is more efficient.

"The MRC-5 line was developed & from lung tissue taken from a 14-week
fetus aborted for psychiatric reasons from a 27-year-old physically
healthy woman," said a description of the cell tissue by the Coriell
Institute for Medical Research at the University of Medicine and
Dentistry of New Jersey, where the line is maintained. The institute
further describes it as "normal human fetal lung fibroblast."

http://www.worldnetdaily.com/news/article.asp?ARTICLE_ID=25362

SMALLPOX VACCINE, Dried, Calf Lymph Type
Summary of Package Insert

Dryvax, Wyeth Laboratories, Marietta, PA (1960)

Ingredients
brilliant green:

calf lymph

chloriatracycline hydrochloride;
dihydrostreptomycin sulfate;
glycerin;
neomycin sulfate;
phenol;
polymixin B sulfate.

http://www.vaccineawareness.org/IllinoisIssues/SmallpoxInsert.htm

TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

http://www.vegsource.com/talk/madcow/messages/9912194.html

From: TSS <mailto:[email protected]> (216-119-163-199.ipset45.wt.net)
Subject: HUMANS MAY CATCH MAD COW FROM SHEEP !!!
Date: December 16, 2002 at 6:37 am PST

In Reply to: MAD COW DISEASE, SMALLPOX VACCINE (Dried Calf Lymph Type) and TSEs <http://www.vegsource.com/talk/madcow/messages/9912194.html> posted by TSS on December 15, 2002 at 9:52 am:

Humans may catch mad cow from sheep

December 13 2002 at 07:41PM
Quickwire

London - The number of people with a human form of mad-cow disease could be much higher than originally thought, according to a new study.

Since 1990, there have been 117 confirmed deaths in Britain from the variant CJD, which until now was assumed to be the only disease linked to eating BSE-infected beef.

But scientists at the Medical Research Council's Prion Unit in London believe they have identified links between BSE and a second type of the human brain disease - sporadic CJD.

The government's latest figures show that from 1990 to November this year, 588 people died from sporadic CJD, including 28 in 1990, 63 in 1998, and 53 last year.

'Some patients with sporadic CJD may have a disease arising from BSE exposure'
The scientists, led by Professor John Collinge, cast further doubt on the safety of sheep meat by suggesting that more animals - including humans -could carry and transmit the diseases than previously thought.

The researchers wrote: "It remains of considerable concern whether BSE has transmitted to, and is being maintained in, European sheep flocks".

They said that given the widespread infection of sheep breeds with scrapie, it was possible some had contracted BSE but that this infection had been hidden by the other disease.

A full study is needed of all the tonsils surgically removed over a 12-month period - around 80 000 - to map the extent of CJD infection in the population, the Medical Research Council argued.

The British Department of Health is thought to be considering such a plan. The research team used a series of experiments on mice that had been genetically altered so they would display the human effects of a prion - an infectious protein. The "transgenic" mice were then exposed to BSE-infected material and the changes in the prion protein were monitored.

As expected, some developed vCJD, but the researchers wrote that, surprisingly, other mice showed effects of sporadic CJD. "These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with sporadic CJD may have a disease arising from BSE exposure," they wrote.

The researchers said their findings were important when considering the present sporadic CJD outbreak in Switzerland, which had the highest incidence of cattle BSE in Europe over the past 12 years.

There was a two-fold increase in sporadic CJD in the last 18 months in Switzerland, while cases of vCJD remain low, a spokesman for the MRC said. - Sapa-DPA

http://iol.co.za/index.php?click_id=143&art_id=iol103980126094S532&set_id=1



Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7

http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm


[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML
Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of
those who provided comments in response to Docket No. ...
Meager 8/18/01 Terry S. Singeltary Sr ...



# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] -
TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305
Comment Number: EC-254 [TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm






TSS
 
Dear Terry,

I suppose we must agree to disagree on many matters, not all, though.

I am glad to hear you are not the master of vegsource. But their site causes way to many problems on my computer.

I will read what research I can. We will some day meet, I'm sure. And we will hopefully have a better understanding of how all this came to be.

Discounting the damaging effects of OPs and chemicals will be more of a problem than the lack of regulations pertaining to BSE and nutraceuticals and cosmetics.

The simple fact is that PrPC has a very important role in protecting our nerve cells from oxidative stress, and other factors I am sure we will soon understand. Elimination of this gene, or rendering it dormant, will cause one hell of a lot more trouble than keeping it.

This old phrase, comes to mind: use it or lose it. Keeping our minds sharp, is probably the best medicine.
 
##################### Bovine Spongiform Encephalopathy #####################

From: TSS ()
Subject: FDA Amends Interim Final Rule "Use of Materials Derived from Cattle in Human
Date: September 6, 2005 at 8:54 am PST

FOR IMMEDIATE RELEASE
Media Inquiries: Michael Herndon
P05-58
301-827-6242
September 6, 2005
Consumer Inquiries: 888-INFO-FDA


FDA Amends Interim Final Rule "Use of Materials Derived from Cattle in Human
Food and Cosmetics"

The U.S. Food and Drug Administration today published several amendments to
the July 2004 interim final rule, "Use of Materials Derived from Cattle in
Human Food and Cosmetics," that will allow the use of certain cattle-derived
material in human foods and cosmetics.

The rule prohibits the use of cattle-derived materials that can carry the
infectious agent for bovine spongiform encephalopathy (BSE), or mad cow
disease, in human foods, dietary supplements, and in cosmetics. Based on
the scientific information provided during the interim final rule's comment
period, which demonstrates that a part of the cow's digestive tract called
the distal ileum can be consistently and effectively removed from the other
sections of the small intestine, it is no longer necessary to designate the
entire small intestine as a prohibited cattle material.

As a result, FDA is amending the rule to allow use of the small intestine in
human food and cosmetics, provided that the distal ileum has been removed.
The U.S. Department of Agriculture is publishing today a similar amendment
to its interim final rule on BSE.

The amendments also clarify that milk and milk products, hides and
hide-derived products, and tallow derivatives are not prohibited for use in
human food and cosmetics.

Finally, FDA has reconsidered the recommended method for determining
insoluble impurities in a type of solid fat known as tallow, in response to
information submitted to the agency, to cite a method that is less costly to
use and requires less specialized equipment.

FDA issued the interim final rule to minimize human exposure to materials
that studies have demonstrated are highly likely to contain the BSE agent in
cattle with the disease. The amended interim final rule provides the same
level of protection against the agent that causes BSE as the original
provisions.

The amendments to the interim final rule are effective on October 7, 2005
and comments are being are accepted on the amendments through November 7,
2005.

###

http://www.fda.gov/bbs/topics/news/2005/NEW01229.html


2003 - 2004 Product Catalog

Standard Process Inc.


NATURAL COCOA STANDARDBAR (mad cow candy bar)
(i will just list animal organs)
bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...

NATURAL PEANUT BUTTER STANDARDBAR

bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...

USF (MAD COW) OINTMENT (RUB A DUB DUB, KURU ETC) ;

bovine orhic glandular extract

UTROPHIN PMG

bovine uterus PMG

VASCULIN

bovine heart PMG extract, veal bone PMG extract, bovine liever, porcine
duodenum,
bovine adrenal Cytosol extract, bovine spleen, ovine spleen (some yummy
stuff)

IPLEX (neighbors mom died from CJD while taking these pills for years)

bovine eye PMG extract, veal bone PMG, bovine liver, porcine stomach,
bovine adrenal,
bovine kidney, bovine adrenal Cytosol extract, BOVINE BRAIN, bovine
bone, veal bone
meal

MYO-PLUS

bovine heart PMG, bovine liver, porcine stomach, bovine orchic extract,
bovine
spleen, ovine spleen, bovine adrenal Cytosol extract, BOVINE BRAIN

NEUROPLEX

bovine orchic Cytosol extract, bovine spleen, BOVINE BRAIN PMG EXTRACT,
BOVINE ANTERIOR PITUITARY, bovine liver, BOVINE PITUITARY PMG EXTRACT,
AND MORE BOVINE BRAIN... HOLY MAD COW IN A PILL !!!

NEUROTROPHIN PMG

BOVINE BRAIN PMG

NIACINAMIDE B6 VM

bovine liver, porcine stomach, bovine spleen ovine spleen,
BOVINE BRAIN

OCULOTROPHIN PMG
BOVINE EYE PMG

ORCHEX

bovine liver, bovine orchic Cytosol extract, porcine stomch,
bovine spleen, ovine spleen, BOVINE BRAIN

OSTARPLEX

veal bone PMG extract, veal bone PMG extract, bovine liver,
porcine stomach, bovine adrenal, bovine spleen, ovine spleen,
BOVINE BRAIN

PARAPLEX

bovine pancreas PMG extract, porcine duodenum, bovine adrenal PMG,
BOVINE PITUITARY PMG EXTRACT, bovine thyroid PMG extract

PITUITROPHIN PMG

RUMAPLEX

BOVINE BRAIN, veal bone PMG extract, bovine adrenal, bovine prostate
Cytosol extract, veal bone meal, bovine liver PMG extract, bovine spleen,
ovine spleen, bovine liver

SENAPLEX

bovine liver PMG extract, bovine adrenal, BOVNE BRAIN, veal bone meal,
bovine
kidney, bovine orchic extract, bovine spleen, ovine spleen ..........

THESE are just a few of MANY of just this ONE COMPANY...TSS

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7

http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm


TSS


#################### https://lists.aegee.org/bse-l.html ####################


here, the oral dose of BSE in primates--look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE. ...TSS


Published online
January 27, 2005
http://image.thelancet.com/
extras/05let1056web.pdf
Commissariat à l'Energie
Atomique/Direction des
Sciences du Vivant/Départment
de Recherche Médicale,
18 Route du Panorama, 92265
Fontenay-aux-Roses, France
(C I Lasmézas DrMedVet,
E Comoy DrMedVet,
Risk of oral infection with bovine spongiform
encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,
Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant
Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the efficiency of oral infection
and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral
transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the
other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a
preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public
health measures can prevent transmission of BSE to man. ...

SNIP...

For personal use. Only reproduce with permission from Elsevier Ltd
longer than that of intraspecies transmission (60 months
vs 44 and 47 months, representing 36% and 28%
increases, respectively). The interval between the period of
peak exposure to infectious BSE tissue and the hitherto
peak incidence of vCJD is about 10–15 years, but
incubation periods of up to 40 years have followed oral
infection with kuru between human beings.5 Therefore,
maximum incubation periods might exceed 50 years in
cases of oral transmission of BSE from cattle to man.
The present data do not provide a definitive minimum
infective dose for transmission of cattle BSE to primates,
but they do give enough information for a preliminary
assessment of the adequacy of existing measures to
protect the human food chain. Results of ongoing
experiments provide a rough estimation of the intraspecies
transmission rates in cattle. The BSE brain
inoculum to which the cattle were exposed had an
infectivity titre of 103·5 mouse infectious (intracerebral
and intraperitoneal) units ID50 per g (ID50 is the dose at
which 50% of animals become infected). Interim results
at 6 years after exposure suggest that the oral ID50 in
cattle may be between 100 mg and 1 g (table 1; S A C
Hawkins, T Konold, G A H Wells, unpublished data).
Since the brain of a cow weighs 500 g and a spinal cord
200 g, CNS tissues from a cow with clinical signs of BSE
could contain enough infective agent to transmit disease
orally to 490–1400 cows (70% of 700 g if 1g is needed, or
20% of 700 g if 100 mg is sufficient), or to 70 primates
(50% of 700 g if 5 g represents the oral ID50).
The accuracy of estimates of the oral ID50 for man will
not be improved until completion, several years from
now, of a large dose-response European study (QLK1-
2002-01096) in macaques, in which the minimum dose
is 50 mg. However, because similar inocula were used in
both the cattle and macaque studies,6 a tentative comparison
can be made between the efficiency of oral infection
in cattle and that in primates. On this basis, a factor of
7–20 could be considered as the range of magnitude of a
bovine-to-primate species barrier for oral BSE infection
(70 primates infected compared with 490 or 1400 cows,
with a similar dose).
Elimination from the human food chain of CNS
tissues from cows with clinical BSE is estimated to have
reduced the risk of human exposure to the disease by
about 90%.7 Risk was further reduced in continental
Europe by systematic screening for the diagnostic
presence of PrPres in the brainstem of all cattle older than
30 months, and in the UK by the total interdiction of
cows older than 30 months. In an oral exposure study to
assess the pathogenesis of BSE in cattle, in which the
same European Union-evaluated test as we used in the
present study was applied to CNS tissues, some
preclinical cases of the disease were diagnosed.8
Using the same test, pooled brainstem from cows with
clinical BSE has yielded a endpoint titre of PrPres
corresponding to a 1-in-300 to 1-in-1000 dilution of
positive brainstem.6,9 If people were to eat CNS tissues
from a cow with preclinical BSE with a concentration of
PrPres just below the test detection limit of 1 in 300, they
would need to ingest at least 1·5 kg to reach the degree
of exposure equivalent to that in the 5 g of brain used for
oral transmission to the macaque in the present study. If
the oral ID50 for man was one log below this dose (ie,
similar to that in cattle, and not accounting for any
species barrier between cattle and man; see table), 150 g
of CNS tissue that tested falsely negative could represent
an infective dose. Because use of cattle brain and spinal
cord for human consumption is prohibited, and in view
of the existing mechanically recovered meat regulations,
a person would be very unlikely to ingest this amount of
cattle CNS tissue.
The minimum sensitivity of screening tests to detect
100% of BSE-infected animals has yet to be ascertained.
However, our results provide reassurance that BSE
screening procedures combined with CNS removal are
effective measures to protect the human food chain.
Contributors
J-P Deslys, C Lasmézas, and E Comoy were responsible for design and
management of this study. G Wells, S Hawkins, and T Konold were
responsible for the pathogenesis study in ruminants. C Lasmézas,
C Herzog, and N Lescoutra-Etchegaray were in charge of the primate
experiments. F Auvré undertook the biochemical analyses. N Salès was
responsible for the immunohistochemical analyses, which were done
by E Correia. C Lasmézas, E Comoy, F Mouthon, G Wells, P Brown, and
J-P Deslys drafted the manuscript.
Conflict of interest statement
Commissariat à l'Energie Atomique owns a patent covering the BSE
diagnostic test commercialised by Bio-Rad. All authors had full access to
all data and had responsibility to submit for publication. The funding
sources had no role in the collection, analysis, and interpretation of
data, writing of the report, or decision to submit the paper for
publication.
2 www.thelancet.com Published online January 27, 2005 http://image.thelancet.com/extras/05let1056web.pdf


Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument

Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA


https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed


Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html



PART 2


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html



Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

TSS
 
TimH was so kind as to post this website. Perhaps if you read it, especially R2, you will understand what was in the Meat and bone meal that was so dangerous. It is all starting to add up and fit the puzzle. A defining document, and well said.

www.gerryparish.co.uk/research/bse/
 
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

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

Vet. Res. 36 (2005) 615-628
DOI: 10.1051/vetres:2005020

Poultry, pig and the risk of BSE following the feed ban in France - A spatial analysis
David Abriala, Didier Calavasb, Nathalie Jarrigeb and Christian Ducrota

a Unité d'Épidémiologie Animale, INRA Theix, 63122 Saint-Genès-Champanelle, France
b Unité Épidémiologie, AFSSA Lyon, 31 avenue T. Garnier, 69364 Lyon Cedex 07, France

(Received 24 September 2004; accepted 16 December 2004)

Abstract - A spatial analysis was carried out in order to analyse the reason why the risk of Bovine Spongiform Encephalopathy (BSE) was spatially heterogeneous in France, during the period following the feed ban of Meat and Bone Meal to cattle. The hypothesis of cross-contamination between cattle feedstuff and monogastric feedstuff, which was strongly suggested from previous investigations, was assessed, with the assumption that the higher the pig or poultry density is in a given area, the higher the risk of cross-contamination and cattle infection might be. The data concerned the 467 BSE cases born in France after the ban of meat and bone meal (July 1990) and detected between July 1st, 2001 and December 31, 2003, when the surveillance system was optimal and not spatially biased. The disease mapping models were elaborated with the Bayesian graphical modelling methods and based on a Poisson distribution with spatial smoothing (hierarchical approach) and covariates. The parameters were estimated by a Markov Chain Monte Carlo simulation method. The main result was that the poultry density did not significantly influence the risk of BSE whereas the pig density was significantly associated with an increase in the risk of 2.4% per 10 000 pigs. The areas with a significant pig effect were located in regions with a high pig density as well as a high ratio of pigs to cattle. Despite the absence of a global effect of poultry density on the BSE risk, some areas had a significant poultry effect and the risk was better explained in some others when considering both pig and poultry densities. These findings were in agreement with the hypothesis of cross-contamination, which could take place at the feedstuff factory, during the shipment of food or on the farm. Further studies are needed to more precisely explore how the cross-contamination happened.


Key words: BSE / bovine / poultry / pig / spatial analysis

Corresponding author: David Abrial [email protected]

© INRA, EDP Sciences 2005


http://www.edpsciences.org/articles/vetres/pdf/2005/04/v4072.pdf



TSS

#################### https://lists.aegee.org/bse-l.html ####################
 
flounder said:
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

TSS

What's your point, Flounder??
You post 25 year old research that only SEEMS to show that CJD,Srapie and Kuru would seem to have an incubation period of less than 4 years.(Much less than the "estimated" 20 to 30 year incubation period of vCJD that some claim in HUMAN-primate cases.)
Also, there is no mention of what method was used to determine that the monkeys had actually contracted these diseases.....only that they remained "asymptomatic" for various periods of time.
There was also no mention of BSE or vCJD.

If there was a point to your post, I must have missed it. Please forgive my ignorance and explain your point, if you would be so kind.... Thanks!!
 

Latest posts

Top