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From: TSS ()
Subject: Urine from Scrapie-Infected Hamsters Comprises Low Levels of Prion Infectivity
Date: September 11, 2006 at 12:32 pm PST

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

Original Paper

Urine from Scrapie-Infected Hamsters Comprises Low Levels of Prion Infectivity

Zehavit Kariv-Inbala, Tamir Ben-Hura, Nikolaos C. Grigoriadisb, Roni Engelsteina, Ruth Gabizona

aDepartment of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah University Hospital, Jerusalem, Israel;
bDepartment of Neurology, Laboratory of Experimental Neurology, AHEPA University Hospital, Thessaloniki, Greece

Address of Corresponding Author

Neurodegenerative Diseases 2006;3:123-128 (DOI: 10.1159/000094770)


Key Words

Light chain



The question of whether prion diseases can be transmitted by body fluids has important epidemiological, environmental and economical implications. In this work, we set to investigate whether urine collected from scrapie-infected hamsters can transmit fatal or subclinical infectivity to normal hamsters. After prolonged incubation times ranging from 300 to 700 days, a small number of animals inoculated with scrapie urine succumbed to scrapie disease, and several asymptomatic hamsters presented low levels of PrPSc in their brains. In addition, most of the asymptomatic hamsters inoculated with scrapie urine, as opposed to those inoculated with normal urine, presented extensive gliosis as well as protease-resistant light chain IgG in their urine, a molecule shown by us and others to be a surrogate marker for prion infection. Our results suggest that urine from scrapie-infected hamsters can transmit a widespread subclinical disease that in some cases develops into fatal scrapie.

Copyright © 2006 S. Karger AG, Basel


Author Contacts

Dr. Ruth Gabizon
Department of Neurology
Hadassah University Hospital
Jerusalem 91120 (Israel)
Tel. +972 2 677 7858, Fax +972 2 642 9441, E-Mail


Article Information

Received: February 2, 2006
Accepted after revision: April 12, 2006
Number of Print Pages : 6

Number of Figures : 3, Number of Tables : 1, Number of References : 29


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

FURTHER into this study ;

Original Paper

Urine from Scrapie-Infected Hamsters Comprises Low Levels of Prion Infectivity

Zehavit Kariv-Inbala, Tamir Ben-Hura, Nikolaos C. Grigoriadisb, Roni Engelsteina, Ruth Gabizona

aDepartment of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah University Hospital, Jerusalem, Israel;
bDepartment of Neurology, Laboratory of Experimental Neurology, AHEPA University Hospital, Thessaloniki, Greece



The experiments presented in this work suggest that

inoculation of urine from scrapie-infected hamsters may

induce a widely distributed subclinical prion disease that

in some cases develops into fatal scrapie. If true for additional

prion-infected animals, such as bovine and sheep,

these findings may explain the unexpected outbreaks of

prion disease in the field even after the implementation

of eradication programs which included slathering of infected

flocks [25, 26] . It also explains the sporadic appearance

of chronic wasting disease in North America and

the transmission of the disease over long distances [27,

28] .

Renal inflammation, such as the one present in mice

suffering from lymphocytic nephritis, resulted in excretion

of infectious prions into urine [15] . Such an inflammation

process may also be present in apparently healthy

animals, especially at older age, therefore increasing the

possibility of disease transmission by infectious urine. In

addition, it is possible that experiments performed in the

past to look for infectivity in body fluids such as blood

and urine may have produced subclinical prion disease,

which was overlooked in view of the negative appearance

of clinically scrapie-sick animals.

The presence of protease-resistant LC in scrapie urine

is very intriguing. LC Ig is known to be a beta sheet protein,

although it was never shown to be protease-resistant

even in diseases where it is present in large concentrations

such as multiple myeloma [17, 29] . If this is so, then the

presence of protease-resistant LC in urine may constitute

a surrogate marker for the presence of secreted prion


The accumulating data on subclinical prion infection

suggests it is possible that apparently healthy individuals

may harbor prions without showing overt clinical disease.

These individuals would represent a reservoir of infectivity

for the potential infection of others. The results

shown in this work suggest that scrapie urine may represent

such a reservoir. While the exposure of animals to

scrapie urine will reflect mostly as subclinical disease,

environmental- or human-induced changes may change

the outcome to more virulent prion diseases.

Kariv-Inbal /Ben-Hur /Grigoriadis /Engelstein /Gabizon

Neurodegenerative Dis 86 6


WHICH brings to mind ;

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

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


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

######### 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


Volume 356, Number 9234 16 September 2000

BSE and transmission through blood

Lancet 2000; 356: 955 - 956
Download PDF (55 Kb)
Wether the outbreak of variant Creutzfeldt-Jakob disease
(vCJD) in the UK will ultimately
affect hundreds, or tens of thousands of people,
cannot yet be predicted.1 If large numbers of
apparently healthy people are now silently incubating
infections with bovine spongiform
encephalopathy (BSE), the implications for public
health include the possiblity that blood from
such individuals may be infectious. Established facts
about infectivity in the blood of human
beings and animals with transmissible spongiform
encephalopathies (TSEs) are as follows:2-4

Blood, especially the buffy-coat component,
from animals experimentally infected with
scrapie or CJD and from either a clinical or
preclinical incubation phase, is consistently infectious
when bioassayed by intracerebral or intraperitoneal
inoculation into the same species;

In naturally infected animals (sheep and goats
with scrapie, mink with transmissible mink
encephalopathy, and cows with BSE), all attempts
to transmit disease through the inoculation of
blood have failed;

Blood from four of 37 human beings with
clinically evident sporadic CJD has been reported
to transmit the disease after intracerebral inoculation into guineapigs,
mice, or hamsters. But each
success has been questioned on technical grounds
and has not been reproducible; and

Epidemiological data have not revealed a
single case of CJD that could be attributed to the
administration of blood or blood products among
patients with CJD, or among patients with
haemophilia and other congenital clotting or
immune deficiencies who receive repeated doses of
plasma concentrates.

No comparable information about vCJD is available.
However, since lymphoreticular organs,
such as tonsils have been shown to contain the
prion protein (which is an excellent index of
infectivity), whereas it is not detectable in
patients with sporadic CJD, there is some reason to
worry that blood from individuals incubating
vCJD might be infectious.5 Data from studies into
the ability of blood from experimentally infected
rodents and primates with vCJD to transmit the
disease will not be available for months or years.

In this issue of The Lancet, F Houston and co-workers
report convincing evidence that blood
from a seemingly healthy sheep incubating BSE
(infected by the oral route with brain from a
diseased cow) was able to cause the disease when
transfused into another sheep. This
observation is entirely consistent with past
experience in experimentally infected rodents. It
extends current knowledge about blood infectivity
in experimental models to a host/TSE strain
pair that is closer to the human vCJD situation
than the earlier rodent studies. It is also the first
successful transfusion of BSE from blood taken
during the all-important incubation period of
infection. This result is part of a larger study
(n=19) that includes both positive and negative
control animals, all still healthy and in various
early stages of the incubation period.

Is it appropriate to publish an experimental
result from a single animal in a study that is not far
enough along even to have validated its positive
controls? Especially a result that does not in any
fundamental way change our current thinking about
BSE and vCJD and which would not seem
to have any practical consequences for public
health? The UK National Blood Transfusion
Service has already implemented leucodepletion
of donated blood, and imports all plasma and
plasma derivatives from BSE-free countries. No
further measures would seem possible--short
of a draconian decision to shut down the whole
UK blood-donor system. What, therefore, is the
rationale for this publishing urgency? The
answer, evidently, is a perceived need to "defuse", by
an immediate and accurate scientific report,
public reaction to possibly inaccurate media
accounts. The full study, when it appears, will
be an important addition to our knowledge of
TSEs, but science should not be driven to what
in certain medical quarters might be termed a
premature emission through fear of media misrepresentation.

Paul Brown

Laboratory of Central Nervous System Studies,
National Institutes of Health, Bethesda,
MD 20892, USA

1 Ghani AC, Ferguson NM, Donnelly CA, Anderson RM.
Predicted vCJD mortality in Great
Britain. Nature 2000; 406: 583-84 [PubMed].

2 Brown P. Can Creutzfeldt-Jakob disease be
transmitted by transfusion? Curr Opin Hematol
1995; 2: 472-77 [PubMed].

3 Brown P, Cervenáková L, McShane LM, Barber P,
Rubenstein R, Drohan WN. 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 1999; 39: 1169-78 [PubMed].

4 Rohwer RG. Titer, distribution, and transmissibility
of blood-borne TSE infectivity. Presented
at Cambridge Healthtech Institute 6th Annual Meeting
"Blood Product Safety: TSE, Perception
versus Reality", MacLean, VA, USA, Feb 13-15, 2000.

5 Hill AF, Butterworth RJ, Joiner S, et al. Investigation
of variant Creutzfeldt-Jakob disease and
other human prion diseases with tonsil biopsy samples. Lancet 1999; 353:

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).

although 176 products do _not_ conform to the CSM/VPC





was quite prepared to believe in unofficial pituitary hormones, also in the
1970's, whether as described by Dr. Little, or in other circumstances, for
animal use. snip... The fact that there were jars of pituitaries (or
extract) around on shelves is attested by the still potent 1943 pituitaries,
described in Stockell Hartree et al. (J/RF/17/291) which had come from the
lab. at Mill Hill. Having taken the trouble to collect them, they were not
lightly thrown out...

more on the 1968 medicine act, they forgot to follow

Draft cover letter to product licence holders (considered by Human and Vet
Medicines including deer)

(It was noted with concern that hormone extracts could be manufactured by a
veterinary surgeon for administration to animals under his care without any
Medicines Act Control.)




Prion infections, blood and transfusions Aguzzi and Glatzel
Sat Jul 8, 2006 12:18

Prion infections, blood and transfusions

Adriano Aguzzi* and Markus Glatzel;article=2948;title=CJD%20WATCH;pagemark=60

Freas, William

Terry S. Singeltary Sr. []

Monday, January 08,200l 3:03 PM


CJDIBSE (aka madcow) Human/Animal TSE's--U.S.--Submission To Scientific
Advisors and

Consultants Staff January 2001 Meeting (short version)

Greetings again Dr. Freas and Committee Members,

I wish to submit the following information to the

Scientific Advisors and Consultants Staff

2001 Advisory Committee (short version).


I am beginning to think that the endless attempt to track

down and ban, potential victims from known BSE Countries

from giving blood will be futile. You would have to ban

everyone on the globe eventually? AS well, I think we

MUST ACT SWIFTLY to find blood test for TSE's,

whether it be blood test, urine test, eyelid test,

anything at whatever cost, we need a test FAST. ,

DO NOT let the incubation time period of these TSEs fool you.

To think of Scrapie as the prime agent to compare CJD,

but yet overlook the Louping-ill vaccine event in 1930's

of which 1000's of sheep where infected by scrapie

from a vaccine made of scrapie infected sheep brains,

would be foolish. I acquired this full text version of the

event which was recorded in the Annual Congress of 1946

National Vet. Med. Ass. of Great Britain and Ireland.

From the BVA and the URL is posted in my (long version).

U.S.A. should make all human/animal TSE's notifiable at all ages,

with requirements for a thorough surveillance and post-mortem

examinations free of charge, if you are serious about eradicating

this horrible disease in man and animal.

There is histopathology reports describing o florid plaques"

in CJD victims in the USA and some of these victims are getting

younger. I have copies of such autopsies, there has to

be more. PLUS, sub-clinical human TSE's will most definitely

be a problem.

THEN think of vaccineCJD in children and the bovine tissues

used in the manufacturing process, think of the FACT that

this agent surviving 6OO*C.

PNAS -- Brown et al. 97 (7): 3418 scrapie agent live at 600*C

Then think of the CONFIDENTIAL documents of what was known of

human/animal TSE and vaccines in the mid to late 8Os, it was all about

depletion of stock, to hell with the kids, BUT yet they knew.


full text ;

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR)
of the United States of America (USA)
Last updated: 19 July 2005
Adopted July 2004 (Question N° EFSA-Q-2003-083)

Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group
on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE)
Risk (GBR) were asked by the European Commission (EC) to provide an
up-to-date scientific report on the GBR in the United States of America,
i.e. the likelihood of the presence of one or more cattle being infected
with BSE, pre-clinically as well as clinically, in USA. This scientific
report addresses the GBR of USA as assessed in 2004 based on data covering
the period 1980-2003.

The BSE agent was probably imported into USA and could have reached domestic
cattle in the middle of the eighties. These cattle imported in the mid
eighties could have been rendered in the late eighties and therefore led to
an internal challenge in the early nineties. It is possible that imported
meat and bone meal (MBM) into the USA reached domestic cattle and leads to
an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle imports
from BSE risk countries were slaughtered or died and were processed (partly)
into feed, together with some imports of MBM. This risk continued to exist,
and grew significantly in the mid 90's when domestic cattle, infected by
imported MBM, reached processing. Given the low stability of the system, the
risk increased over the years with continued imports of cattle and MBM from
BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is likely
but not confirmed that domestic cattle are (clinically or pre-clinically)
infected with the BSE-agent. As long as there are no significant changes in
rendering or feeding, the stability remains extremely/very unstable. Thus,
the probability of cattle to be (pre-clinically or clinically) infected with
the BSE-agent persistently increases.

Publication date: 20 August 2004

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR)
of the United States of America (USA)

Adopted July 2004 (Question N° EFSA-Q-2003-083)

[Last updated 08 September 2004]
[Publication Date 20 August 2004]

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle


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

03-025IF 03-025IF-631 Linda A. Detwiler [PDF]

Specified Risk Materials (SRMs)

I am in full support of the interim final rule which prohibits SRMs from

being included in food for human consumption. In addition to the list of

tissues published in this rule, I am requesting that additional tissues be

added to the list. These would include dura

("sheath") covering the spinal cord and the ENTIRE INTESTINE (from pylorus

to rectum). The scientific justification is provided below. THESE SRMs

should also be prohibited from ANY FDA regulated food or product intended

for human consumption, including but not limited to flavorings, extracts,

etc. ...

Dr. Linda Detwiler comments in full;


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