SEARCH VEGSOURCE:

 

 

Follow Ups | Post Followup | Back to Discussion Board | VegSource
See spam or
inappropriate posts?
Please let us know.
  




From: TSS ()
Subject: Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N–0273] (formerly Docket No. 02N–0273) RIN 0910–AF46 {MORE BSe}
Date: October 5, 2005 at 8:29 am PST

1

DEPARTMENT OF HEALTH AND HUMAN SERVICES

Food and Drug Administration

21 CFR Part 589

[Docket No. 2002N–0273] (formerly Docket No. 02N–0273)

RIN 0910–AF46

Substances Prohibited From Use in Animal Food or Feed

AGENCY: Food and Drug Administration, HHS.

ACTION: Proposed rule.

SUMMARY: The Food and Drug Administration (FDA) is proposing to amend

the agency’s regulations to prohibit the use of certain cattle origin materials

in the food or feed of all animals. These materials include the following: The

brains and spinal cords from cattle 30 months of age and older, the brains

and spinal cords from cattle of any age not inspected and passed for human

consumption, the entire carcass of cattle not inspected and passed for human

consumption if the brains and spinal cords have not been removed, tallow that

is derived from the materials prohibited by this proposed rule that contains

more than 0.15 percent insoluble impurities, and mechanically separated beef

that is derived from the materials prohibited by this proposed rule. These

measures will further strengthen existing safeguards designed to help prevent

the spread of bovine spongiform encephalopathy (BSE) in U.S. cattle.

DATES: Submit written or electronic comments by [insert date 75 days after

date of publication in the Federal Register]. Submit written comments on the

information collection provisions by [insert date 30 days after date of

publication in the Federal Register].

2

ADDRESSES: You may submit comments, identified by [Docket No. 2002N–0273

or RIN 0910–AF46], by any of the following methods:

SNIP...

124 PAGES OF MORE BSe at the following link;

http://www.fda.gov/OHRMS/DOCKETS/98fr/cv048.pdf

the fda promises us hope at first, then delivers more failures and lies.

promise us anything, and gives us nothing.

the fda is like the usda, bought and paid for by your local cattle dealer.

this is corporate and political science at it's finest hour, nothing, i mean absolutely no 'sound science' here. they just as well have kept on keeping on feeding cattle to cattle with this half @ss approach.

1862 Federal Register / Vol. 69, No. 7 / Monday, January 12, 2004 / Rules and Regulations

DEPARTMENT OF AGRICULTURE

Food Safety and Inspection Service

9 CFR Parts 309, 310, 311, 318, and 319

[Docket No. 03–025IF]

Prohibition of the Use of Specified

Risk Materials for Human Food and

Requirements for the Disposition of

Non-Ambulatory Disabled Cattle

025IF, Room 102, Cotton Annex, 300

12th and C Street, SW., Washington, DC

20250–3700.

snip...

This action will minimize

human exposure to materials that

scientific studies have demonstrated as

containing the BSE agent in cattle

infected with the disease. Infectivity has

never been demonstrated in the muscle

tissue of cattle experimentally or

naturally infected with BSE at any stage

of the disease.

snip...

http://ffas.usda.gov/info/fr/2004/011204bserisk.pdf

FACT

Iwamaru et al. (2005) PrPSc distribution of a natural case of bovine

spongiform encephalopathy. In Prions. Food and Drug Safety. Springer-

Verlag, Tokyo, 2005.

4 Buschmann & Groschup (2005) Highly Bovine Spongiform
Encephalopathysensitive

transgenic mice confirm the essential restriction of infectivity to the

nervous system in clinically disease cattle. J. Infect. Dis. 192, 934-942.

3

BSE cases. SEAC noted the findings were both in single

animals at the clinical stage of disease. The level of infectivity

detected in PNS tissues was considerably lower than in CNS

tissues. Further related research was discussed in the

reserved session.


http://www.seac.gov.uk/minutes/summary89.pdf


PrPSc distribution of a natural case of bovine

spongiform encephalopathy

Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori-

kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa

Priori Disease Research Center, National Institute of Animal Health, 3-1-5

Kannondai, Tsukuba 305-0856 Japan gan@affrc.go.jp

Abstract

Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes

progressive neurodegeneration of the central nervous system. Infectivity

of BSE agent is accompanied with an abnormal isoform of prion protein

(PrPSc).

The specified risk materials (SRM) are tissues potentially carrying BSE

infectivity. The following tissues are designated as SRM in Japan: the

skull including the brain and eyes but excluding the glossa and the masse-

ter muscle, the vertebral column excluding the vertebrae of the tail, spinal

cord, distal illeum. For a risk management step, the use of SRM in both

animal feed or human food has been prohibited. However, detailed

PrPSc distribution remains obscure in BSE cattle and it has caused con-

troversies about definitions of SRM. Therefore we have examined PrPSc

distribution in a BSE cattle by Western blotting to reassess definitions of

SRM.

The 11th BSE case in Japan was detected in fallen stock surveillance.

The carcass was stocked in the refrigerator. For the detection of PrPSc,

200 mg of tissue samples were homogenized. Following collagenase

treatment, samples were digested with proteinase K. After digestion,

PrPSc was precipitated by sodium phosphotungstate (PTA). The pellets

were subjected to Western blotting using the standard procedure.

Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish

peroxidase was used for the detection of PrPSc.

PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal

ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected

in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve).

Our results suggest that the currently accepted definitions of SRM in

BSE cattle may need to be reexamined. ...

179

T. Kitamoto (Ed.)

PRIONS

Food and Drug Safety

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

International Symposium of Prion Diseases held in Sendai, October 31, to

November 2, 2004

http://docket.epa.gov/edkfed/do/EDKStaffAttachDownloadPDF?objectId=090007d480993808

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

I GUESS my next question is about blood from cattle being fed back to cattle. SINCE it has now been proven that nvCJD in humans (which in there terms is the only TSE related to BSE in cattle) that nvCJD in humans transmits to humans via blood, then why no concern about blood from BSE infected cattle being fed back to cattle$ i guess you could trace it back to big business making corporate decisions on scientific matters. BSE tainted blood is just a small part of it. course, if you have no mad cows as Johanns is so sure of himself, you have no problems, unless, the 'fong syndrome' strikes. and we all know how to take care of that, just let the tissue samples sit up on the shelf for 4 months or so in preservative this time...

STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

To minimise the risk of farmers' claims for compensation from feed
compounders.

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by
maintaining the availability of meat and bone meal as a raw
material in animal feeds, and ensuring time is available to make any
changes which may be required.

snip...

THE FUTURE

4..........

MAFF remains under pressure in Brussels and is not skilled at
handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which
contain illegal traces of ruminant protein. More likely, a few positive
test results will turn up but proof that a particular feed mill knowingly
supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed
compounders are free of it. The longer we can avoid any direct
linkage between feed milling _practices_ and actual BSE cases,
the more likely it is that serious damage can be avoided. ...

SEE full text ;

http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf

NO need to worry about the fact that BSE blood transmits to sheep either;

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

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

Commentary
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:
183-89.

http://www.thelancet.com/

From: Terry S. Singeltary Sr. (216-119-130-97.ipset10.wt.net)
Subject: Other Transmission Studies of CJD from Blood and Urine Into Mice...
Date: September 18, 2000 at 2:01 pm PST

In Reply to: Transmission of BSE by blood transfusion in sheep... posted by Terry S. Singeltary Sr. on September 15, 2000 at 9:29 am:

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: BSE-L@uni-karlsruhe.de

######### 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.


>>>>>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 <<<<<<

SEAC

May 2005

1

POSITION STATEMENT

EARLY PHASE OF vCJD INFECTION IN BLOOD TRANSFUSION

RECIPIENTS

Issue

1. The Committee on Microbiological Safety of Blood, Tissue and

Organs has requested advice from SEAC on whether a scientific

distinction can be drawn between historic and recent blood

transfusion recipients in terms of the relative load of the vCJD

agent that may be present in the bone, tissues or organs of the

blood transfusion recipient. In the context of this question, a recent

recipient is defined as having received a blood transfusion within

the week prior to bone, tissue or organ donation. A historic

recipient is defined as having received a blood transfusion in the

more distant past.

Background

2. A pre-symptomatic diagnostic test for vCJD is currently not

available. Therefore, blood, bone, tissue or organ donors with a

sub- or pre-clinical vCJD infection cannot be identified prior to

donation. Two cases of vCJD infection in recipients of blood from

donors that subsequently developed vCJD suggest that the

disease may be transmitted from asymptomatic individuals via

blood transfusion. Epidemiological evidence of iatrogenic

transmission of sCJD suggests there is a potential risk of vCJD

transmission via tissue/organ transplantation.

3. There are no data on the tissue distribution of vCJD infectivity in

humans in the first week following infection by blood transfusion.

There is some, albeit very limited, information from mouse studies

on prion replication and spread in the early phase of infection.

However, these studies used inocula, routes of administration and

prion strains not directly applicable to the human blood transfusion

situation.

2

Early phase tissue accumulation of abnormal prions

4. On the basis of the very limited information available, it is

considered unlikely that significant prion replication would occur in

tissues in the first week following transfusion with infected blood.

Thus, the level of abnormal prions accumulating in a tissue would

probably correlate with the level of vascularisation of that tissue.

Highly vascularised organs such as the liver, lung and spleen, as

well as bone, would be more likely to contain the agent compared

with other organs. At later times in the incubation period (likely to

be well in excess of one week), the accumulation of abnormal prion

protein and infectivity would be expected to correlate with the

ability of various tissues to support prion replication, with the

central nervous system containing the highest levels of infectivity.

Relative risks

5. Data are too limited to allow quantification of the risks of transplant

associated vCJD transmission from donors that have received a

blood transfusion.

6. The number of pre- and sub-clinical vCJD infections in the

population is believed to be small. Therefore, there is a small risk

of vCJD transmission from transplantation of tissues/organs from

all donors, irrespective of whether they have received a blood

transfusion prior to donation. The additional risk resulting from a

tissue/organ donor having received a blood transfusion at any time

prior to donation is likely to be small. Furthermore, the introduction

of precautionary safety measures to protect the blood supply, such

as leucodepletion and exclusion of previously transfused blood

donors, means that, in general, the risk of blood transfusionassociated

transmission of vCJD from tissue/organ donation is, if

anything, likely to be lower if the transfusion is recent rather than

historic. However, it is not possible to define a threshold of lowest

risk in terms of a specific date of, or period of time following, a

blood transfusion.

Possible risk reduction measures

7. Screening cadaveric donors for markers of infection would allow,

depending on the sensitivity of the test used, pre- or sub-clinically

infected donors to be identified prior to the use of the donated

tissues/organs. Retrospective screening of donors would also help

to inform assessment of transmission risks.

3

8. On the basis that tissue/organ infectivity levels in the very early

stage of infection are associated with the blood content of

tissues/organs, washing or perfusing tissues to remove blood could

reduce the infectious load. In this respect, it would be important to

consider processes that efficiently remove bone marrow and blood

from bone.

9. Avoiding the pooling of tissues from different donors to be

transplanted into one individual reduces transmission risks to that

individual.

Summary

10. There is no clinical evidence that vCJD has been transmitted

through tissue/organ transplantation. However, a potential risk of

transmission via this route exists. Relevant data are extremely

limited but suggest that in the early phase of infection, significant

prion replication is unlikely to occur and that, therefore, tissue

levels of abnormal prions following recent transfusions are likely to

be related to the blood supply to each specific tissue.

11. A risk of transplant associated transmission of vCJD exists from

tissue/organ donors that have not received blood transfusions.

The additional risk as a result of a donor having received a recent

blood transfusion is likely to be very small. Post mortem

assessment of donor infection would provide the best method of

risk reduction and enable these risks to be quantified.

12. In assessing and communicating the risks a balance must be

struck between the small risk of vCJD transmission by

transplantation and the benefits to patients receiving a transplant,

especially where tissues/organs are scarce and are required for

(potentially) life-saving procedures.

SEAC

May 2005

http://www.seac.gov.uk/pdf/cjd.pdf

SEAC Statement

7th August 2004

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

Summary of SEAC’s discussion on the second presumed case of blood transfusion-associated infection with vCJD
Background

1. The Department of Health sought advice from the committee on a presumed second instance of blood transfusion-associated transmission of the variant Creutzfeldt-Jakob disease (vCJD) agent. The first case of probable blood transfusion-associated transmission of vCJD1 was considered by SEAC in February 2004.

2. The National CJD Surveillance Unit (NCJDSU) had investigated this second patient after death, as the patient was a known recipient of blood from a donor incubating vCJD. Patient confidentiality and medico-legal issues surrounding the patient at the time of reporting required that the issue was considered in the reserved session of the meeting.

3. The elderly patient died in 2004, showed no clinical signs of vCJD at the time of death, which was from an unrelated cause. The patient had received a single unit of non-leucodepleted blood in 1999 that had been donated by an individual who was confirmed in 2001 as a definite vCJD case. The donor’s disease onset was in 2000.

4. The NCJDSU had investigated the neuropathology, accumulation of prion protein and PrPres in autopsied tissues in the case. The PRPN genotype had also been determined. The following details were reported:

No evidence of a spongiform encephalopathy in an examination of brain material.
Immunohistochemical detection of prion protein accumulation in the spleen and in a cervical lymph node. PrPres was detected by high sensitivity western blotting in the spleen.
No accumulation of prion protein was detected in multiple regions of the central nervous system, tonsils, appendix, large intestine, skeletal muscle or thymus.
Glycotype profile of PrPres in spleen was the same as has been found in clinical cases of vCJD.
Histological pattern of PrP accumulation in the spleen and the lymph node is similar to that in two appendixes reported by Hilton et al (2004)2.
Methionine/valine heterozygosity at codon 129 of PrP gene (PRNP).
5. SEAC was informed that the findings suggested that this might be a preclinical or subclinical case of iatrogenic vCJD associated with blood transfusion. However, UK residency of the patient meant that oral exposure to the BSE agent could not be excluded as a possible cause of infection. Statistical analysis suggested it was extremely unlikely that two cases of infection with the vCJD agent would have been detected by chance in recipients of blood from pre-onset vCJD cases, even if the prevalence of prion protein accumulation in spleen tissue in the UK population was substantially larger than suggested by studies on appendix and tonsil tissue from persons without clinical vCJD.

6. The Department of Health (DH) asked SEAC to assess the data available on this case, and to advise on the implications this finding may have on the risk associated with blood, and on any additional concerns for public health.


Summary of SEAC’s discussion


7. SEAC agreed that the western blot results and glycotype profile suggested it was unlikely that the infection was preclinical sporadic CJD (sCJD). The committee noted that a single study by Glatzel et al (2003) had reported PrPres in the spleen of sCJD clinical cases. However, the levels of PrPres present in sCJD cases were low and detected in patients with a lengthy clinical illness from sporadic CJD.

8. The committee agreed that the statistical analysis suggested that the presence of PrPres in the case was attributable to a vCJD infection acquired via blood transfusion rather than a primary infection resulting from a food borne exposure.

9. SEAC agreed that this second patient with apparent vCJD infection added to the evidence that the vCJD agent can be transmitted by blood. However the committee noted that in this instance, although vCJD infection appeared to have been transmitted, it was not known if clinical vCJD would have developed if the patient had lived longer.

10. SEAC agreed that this case added support to its view on the risk associated with blood transfusion. The finding was consistent with there being a substantial risk associated with receipt of non-leucodepleted blood from a donor incubating vCJD. The extent to which leucodepletion reduces that risk is not known.

11. The committee agreed that it should be a public health priority for all recipients of blood (leucodepleted or not) from donors incubating vCJD to be subject to the kind of careful post-mortem examination that had been possible in this case. This would help to quantify the nature and magnitude of the risks of transmission of the vCJD agent through blood [donated by preclinical cases of vCJD]. The committee re-iterated the continuing importance of the Transfusion Medicine Epidemiology Review (TMER) to identify vCJD cases who have been donors and the recipients of such donations.

12. SEAC noted that the detection of PrPres in lymphoreticular tissues of vCJD cases and the presence of infection in the spleen of this case was compatible with the lymphoreticular system being involved in the early spread of infection before entering the CNS. SEAC agreed that the detection of prion protein in the spleen but not in the tonsil of the case has implications for the national anonymous tonsil archive. The SEAC chair agreed to refer this finding to the DH/MRC steering group overseeing the archive.

13. SEAC noted that the patient was heterozygous at codon 129 of the PRNP gene and that this was the first time infection with the vCJD agent had been reported in an individual not methionine homozygous. This indicated that genotypes other than the methionine homozygous were susceptible to infection with the vCJD agent. Uncertainties remain as to the relative susceptibility of heterozygotes to food borne (or other) infection or the possible outcomes of infection. The committee agreed that the similarities between the western blot band analysis and PrPres glycoprofile seen in this case and in cases of vCJD who were methionine homozygous was reassuring with respect to the ability to make the diagnosis of vCJD in those of genotypes other than methionine homozygous.

14. SEAC stated that, in the interests of public health, this case demonstrates the importance of both in life and in death surveillance of recipients of blood products derived from blood donations from individuals subsequently found to be infected with the vCJD agent. The committee also noted that this case highlighted the importance of obtaining autopsies in such patients and, more generally, the committee reiterated the concern that it had expressed previously, that a mechanism was needed to increase the autopsy rate amongst the UK population to reduce the possibility that cases of vCJD were being missed.

15. SEAC emphasised the importance of the DH-funded sheep transfusion study which is designed to investigate the infectivity of different blood fractions taken from sheep experimentally infected with BSE by transfusing them into ARQ homozygous sheep. The committee noted that the two presumed human cases of blood transfusion-associated vCJD infection indicated the potential infectivity of transfused blood. However, current technology is unable to quantify the levels of infectivity in blood and a rapid diagnostic test remained a key research priority.

SEAC
7th August 2004


1.Llewelyn CA, Hewitt PE, Knight RS, Amar K, Cousens S, Mackenzie J, Will RG. Possible transmission of variant Creutzfeldt-Jakob disease by blood transfusion. Lancet. 2004 Feb 7;363(9407):417-21.

2. Hilton DA, Ghani AC, Conyers L, Edwards P, McCardle L, Ritchie D, Penney M, Hegazy D, Ironside JW. Prevalence of lymphoreticular prion protein accumulation in UK tissue samples. Journal of Pathology: 203 (3).733-739. Published Online: 21 May 2004

http://www.seac.gov.uk/statements/state070804.htm

no need to hurry now that every human on the planet has been needlessly exposed. we all can only hope we outlive the disease, and can remember to tell about it.

seems the uk and the usa have been mirrored in this nightmare from day one;


In relation to animal health, SEAC reviewed the use of dried mammalian blood in animal feed, which is currently permitted under EU legislation. SEAC agreed that there was no evidence to suggest the presence of BSE infectivity in cattle blood. Additionally, the Committee was informed that blood products are rarely used in farm animal feed in the UK and any bovine blood for animal feed would be sourced from animals under 30 months of age. Therefore, SEAC concluded that, although within species recycling should be discouraged, in the case of dried bovine blood, the risks were extremely small and hence there was no compelling need to change previous advice.

Also, because source material for gelatin and tallow was tightly controlled and subject to processing that would reduce any infectivity present, Members were also content for gelatin and tallow to remain exempt from the current feed ban. However, Members considered there was a theoretical possibility that if blood meal derived from a sheep infected with scrapie were included in a sheep ration, this could present a risk to animal health. If so, it may theoretically compromise current efforts to eradicate scrapie from the national flock. SEAC asked that this potential risk and its implications be considered within the context of the national scrapie eradication plan.

http://www.seac.gov.uk/summaries/summ_0900.htm


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://bmj.bmjjournals.com/cgi/eletters/320/7226/8/b#EL1

Race R, Raines A, Raymond GJ, Caughey B, Chesebro B. (2001) Long-term subclinical carrier state precedes scrapie replication and adaptation in a resistant species: analogies to bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease in humans. J Virol. 75(21):10106-12.
(12/24/03)
http://jvi.asm.org/cgi/content/full/75/21/10106
http://jvi.asm.org/cgi/reprint/75/21/10106.pdf

Cattle infected with bovine spongiform encephalopathy (BSE) appear to be a reservoir for transmission of variant Creutzfeldt-Jakob disease (vCJD) to humans. Although just over 100 people have developed clinical vCJD, millions have probably been exposed to the infectivity by consumption of BSE-infected beef. It is currently not known whether some of these individuals will develop disease themselves or act as asymptomatic carriers of infectivity which might infect others in the future. We have studied agent persistence and adaptation after cross-species infection using a model of mice inoculated with hamster scrapie strain 263K. Although mice inoculated with hamster scrapie do not develop clinical disease after inoculation with 10 million hamster infectious doses, hamster scrapie infectivity persists in brain and spleen for the life span of the mice. In the present study, we were surprised to find a 1-year period postinfection with hamster scrapie where there was no evidence for replication of infectivity in mouse brain. In contrast, this period of inactive persistence was followed by a period of active replication of infectivity as well as adaptation of new strains of agent capable of causing disease in mice. In most mice, neither the early persistent phase nor the later replicative phase could be detected by immunoblot assay for protease-resistant prion protein (PrP). If similar asymptomatic carriers of infection arise after exposure of humans or animals to BSE, this could markedly increase the danger of additional spread of BSE or vCJD infection by contaminated blood, surgical instruments, or meat. If such subclinical carriers were negative for protease-resistant PrP, similar to our mice, then the recently proposed screening of brain, tonsils, or other tissues of animals and humans by present methods such as immunoblotting or immunohistochemistry might be too insensitive to identify these individuals.

Ramasamy I, Law M, Collins S, Brooke F (2003). Organ distribution of prion proteins in variant Creutzfeldt-Jakob disease. Lancet Infect Dis. 3(4):214-22.
(2/18/04)

In this article we give an overview of the transmissible spongiform encephalopathies, with emphasis on the evidence for the distribution of abnormal prions in tissues. The normal prion protein is distributed ubiquitously throughout human body tissues. Endogenous expression of the normal prion protein, as well as auxiliary proteins, plays a part in accumulation of the abnormal prion protein. As exemplified by variant Creutzfeldt-Jakob disease (vCJD) the abnormal prion protein can accumulate in the host lymphoid system, in particular the follicular dendritic cells. The route for the disease-related prion neuroinvasion is likely to involve the peripheral nervous system. An alternative route may involve blood constituents. Both animal studies and studies on vCJD patients suggest a potential for abnormal prion distribution in several peripheral tissues other than the lymphoreticular system. In human beings the abnormal prion has been reported in the brain, tonsils, spleen, lymph node, retina, and proximal optic nerve. Infectivity, although present in peripheral tissues, is at lower levels than in the central nervous system (CNS). Animal models suggest that the growth of infectivity in the CNS is likely to be gradual with maximum values during the clinical phase of disease. That tissues may harbour the abnormal prion, at different levels of infectivity, during the incubation period of the disease raises concerns of iatrogenic transmission of the disease either after surgery, blood transfusion, or accidental organ transplantation from donors in the preclinical phase of the disease.


Herzog C, Sales N, Etchegaray N, Charbonnier A, Freire S, Dormont D, Deslys JP, Lasmezas CI. (2004). Tissue distribution of bovine spongiform encephalopathy agent in primates after intravenous or oral infection. Lancet.363(9407):422-8.
(2/18/04)

BACKGROUND: The disease-associated form of prion protein (PrP(res)) has been noted in lymphoreticular tissues in patients with variant Creutzfeldt-Jakob disease (vCJD). Thus, the disease could be transmitted iatrogenically by surgery or use of blood products. We aimed to assess transmissibility of the bovine spongiform encephalopathy (BSE) agent to primates by the intravenous route and study its tissue distribution compared with infection by the oral route. METHODS: Cynomolgus macaques were infected either intravenously or orally with brain homogenates from first-passage animals with BSE. They were clinically monitored for occurrence of neurological signs and killed humanely at the terminal stage of the disease. Brain, lymphoreticular tissues, digestive tract, and peripheral nerves were obtained and analysed by sandwich ELISA and immunohistochemistry for quantitative and qualitative assessment of their PrP(res) content. FINDINGS: Incubation periods after intravenous transmission of BSE were much shorter than after oral infection. We noted that PrP(res) was present in lymphoreticular tissues such as spleen and tonsils and in the entire gut from the duodenum to the rectum. In the gut, PrP(res) was present in Peyer's patches and in the enteric nervous system and nerve fibres of intestinal mucosa. Furthermore, PrP(res) was found in locomotor peripheral nerves and the autonomic nervous system. Amount of PrP(res) ranged from 0.02% to more than 10% of that recorded in brain. Distribution of PrP(res) was similar in animals infected by the intravenous or oral route. INTERPRETATION: Our findings suggest that the possible risk of vCJD linked to endoscopic procedures might be currently underestimated. Human iatrogenic vCJD cases infected intravenously raise the same public-health concerns as primary cases and need the same precautionary measures with respect to blood and tissue donations and surgical procedures.

nope, the fda/usda et al have floundered too long now.

they had there chance, but fumbled the mad cow ball again...

still disgusted in Bacliff, Texas...TSS

Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION


http://docket.epa.gov/edkfed/do/EDKStaffItemDetailView?objectId=090007d480993808

http://docket.epa.gov/edkfed/do/EDKStaffAttachDownloadPDF?objectId=090007d480993808

http://docket.epa.gov/edkfed/do/EDKStaffCollectionDetailView?objectId=0b0007d48096b40d

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

PDF]Freas, William TSS SUBMISSION

File Format: PDF/Adobe Acrobat -

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...

http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf

Asante/Collinge et al, that BSE transmission to the 129-methionine

genotype can lead to an alternate phenotype that is indistinguishable

from type 2 PrPSc, the commonest _sporadic_ CJD;

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm

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 ...


http://www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf

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

# 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


Dockets Entered On October 2, 2003 Table of Contents, Docket #,
Title, 1978N-0301,

OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr.
Vol #: 1, ...

http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm


Daily Dockets Entered on 02/05/03

DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2.
... Vol#: 1.

03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...


http://www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm


Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1


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


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


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


Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...
http://www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003
- Cached


2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 1
Terry S. Singeltary Sr.
Vol #:
1

http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm


2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1

2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1


http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm

TSS





Follow Ups:



Post a Followup

Name:
E-mail: (optional)
Subject:

Comments:

Optional Link URL:
Link Title:
Optional Image URL: