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From: Terry S. Singeltary Sr. (
Subject: Senate Committee Hearing Impact of Mad Cow Disease on Imports 2/3/05
Date: February 3, 2005 at 11:11 am PST

-------- Original Message --------
Subject: Senate Committee Impact of Mad Cow Disease on Imports 2/3/05
Date: Thu, 3 Feb 2005 13:08:59 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

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


SOUND SCIENCE is not in the vocabulary of USDA.

THE just of the meeting had absolutely nothing to do with
science and the real risk to the consumer. THE just of the
meeting was nothing more than get the borders back opened
and sooner rather than later. THE science issues were not
even discussed. THEY mentioned the OIE guidelines,
but fail to mention that every BSE documented country
went by those same guidelines. THIS tells me they were
terribly flawed. THEY mention the Harvard study, but
fail to mention to you what the PEER REVIEW of the
HARVARD STUDY found. AND they never mention
the EFSA re-assessment of the USA, Canada and Mexico
to a BSE GBR risk assessment of III, and what that means.
NOPE, just like it never happened. ALL in all the hearing
was a joke. ALL in all it really does not matter. YOU have
Mexico, Canada and the USA having a moderate risk of BSE.
THIS should tell the world not to import beef, sheep, goat,
deer and or elk from the North America, due to the free trading
of TSEs. THEY speak of the 8/4/97 R-TO-R feed ban as
LAW. IT was nothing more than a voluntary gesture no one
adhered to. VERY few complied with the ban.

NOW, lets talk science, this hearing refused to speak of it;

1st let us look at the infamous Harvard Risk assessment of BSE,
which was bought and paid for by the very industry it was investigating.
THEY always fail to mention the PEER REVIEW of
the Harvard study;

132 pages
October 31, 2002
Review of the Evaluation of the
Potential for Bovine Spongiform
Encephalopathy in the United States
Conducted by the Harvard Center for Risk Analysis,
Harvard School of Public Health and Center for
Computational Epidemiology, College of Veterinary
Medicine, Tuskegee University

Final Report
Prepared for
U.S. Department of Agriculture
Food Safety and Inspection Service
Office of Public Health and Science
Prepared by
Health, Social, and Economics Research

Review of the Evaluation of the
Potential for Bovine Spongiform
Encephalopathy in the United States
Conducted by the Harvard Center for Risk Analysis,
Harvard School of Public Health & Center for
Computational Epidemiology, College of Veterinary
Medicine, Tuskegee University
Final Report
October 31, 2002
Prepared for
U.S. Department of Agriculture
Food Safety and Inspection Service
Office of Public Health and Science
Prepared by
Health, Social, and Economics Research
Research Triangle Park, NC 27709

1. Introduction 1-1
2. General Comments 2-1
2.1 Overall Strengths of the Model
.......................................... 2-1
2.2 Overall Weaknesses of the
Model...................................... 2-2
2.3 Clarity of Model
Structure.................................................. 2-3
2.4 Complexity and the Level of Details
.................................. 2-4
2.5 Omission of Exposure
Routes............................................. 2-5
2.6 Presentation of Model Outputs
.......................................... 2-7
2.7 A Basic Aspect of
BSE........................................................ 2-7
2.8 Treatment of Literature and Expert Knowledge ................... 2-8
3. Identification of Data and Critical Evaluation of
Evidence 3-1
3.1 Have All Key Studies and Data Been Identified?................. 3-1
3.2 Have the Data Been Correctly Interpreted and
..................................................................... 3-4
3.3 Are All Input Data Used in the Model Valid and
................................................................... 3-17
4. Overarching Logical Structure of the Risk
Assessment 4-1
5. Biological Plausibility of the Assumptions 5-1
6. Are the Mechanics of the Model Consistent
With Known Biology? 6-1
7. Appropriateness of Modeling Techniques
(Model Mathematics and Equations) 7-1
8. Appropriate Characterization of the Risks 8-1
9. Identification and Characterization of
Variability, Uncertainty, Critical Assumptions,
and Data Gaps 9-1
9.1 Key Sources of Variability and Uncertainty ........................ 9-1
9.2 Critical
Assumptions.......................................................... 9-5
9.3 Important Data Gaps
......................................................... 9-6
10. Usefulness of the Results for Risk Management 10-1
11. User Friendliness of the Model 11-1
12. Editorial Comments 12-1
References R-1
A Reviewers’ Professional Experience.................................... A-1
B Model

RTI recruited two European reviewers who are experts on different
aspects of BSE, one U.S. reviewer who is an expert in U.S. beef
cattle production and processing systems, and a team of two U.S.
reviewers who are experts in risk assessment methods and
modeling. We contracted with the experts to perform the reviews,
sent them the H-T BSE study and model, and provided the experts
with guidelines for conducting the reviews.
The reviewers’ training and experience represent several areas of
expertise relevant to the BSE risk assessment model. Their full
biographies and resumes are included in Appendix A of this
document. Below, we present brief biographical sketches of the
reviewers’ relevant experience:
Z Dr. H. Christopher Frey is an associate professor at North
Carolina State University, Raleigh. He specializes in
uncertainty and variability analysis, exposure and risk
assessment, process modeling, air pollution characterization,
and other related fields. He is developing methods for
sensitivity analysis of food safety risk models. He has been
involved in numerous risk assessment modeling exercises.
Review of the Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States — Final Report
Dr. Frey’s contributions have been recognized by national
awards, including a Faculty Early Career Development grant
from the National Science Foundation in 1997, and the
1999 Chaucey Staff Award from the Society for Risk
Z John C. Galland has a Ph.D. in ecology from the University
of California-Davis and is a full professor in the Departments
of Clinical Sciences and Diagnostic Medicine/Pathobiology,
College of Veterinary Medicine at Kansas State University.
He is co-coordinator of Public Health and Epidemiology
courses in the professional curriculum. He has worked with a
number of animal diseases, modeled distribution and
movement of large animal groups, and has done extensive
research on E. coli. At Kansas State, Dr. Galland created a
microbiology laboratory to conduct research under the Good
Laboratory Practices (GLP) Act to undertake government and
industry contract work. From 1994 to 2000 he was
Corporate President of Animal Health Systems, Inc., a
software development company specializing in custom large
database applications, voice recognition, and electronic
identification systems.
Z Dr. Zheng Junyu is a post-doctoral associate who works with
Dr. H.C. Frey. His research involves uncertainty and
variability analysis and air pollution. Dr. Junyu is also
experienced in risk assessments and developing computer
models using C++. Dr. H.C. Frey and Dr. Junyu were the
reviewers for the modeling aspects of the BSE risk
assessment (henceforth, they are referred to as the “NCSU
Z Dr. Bram E. C. Schreuder is a senior scientist at the DLOInstitute
for Animal Science and Health (ID-Lelystad),
Department of Statutory Tasks, in the Netherlands. He is a
trained veterinarian, specializing in small ruminant diseases,
and is specifically involved in BSE and scrapie research. In
1990, he became project coordinator of the
multidisciplinary BSE/scrapie research project of the IDDLO.
He received his Ph.D. in 1998; his thesis studied the
epidemiological aspects of scrapie and BSE, including a risk
assessment study.
Z Dr. John William Wilesmith is a visiting professor in the
Department of Infectious and Tropical Diseases, London
School of Hygiene and Tropical Medicine, University of
London; and Veterinary Head, Epidemiology Team, State
Veterinary Services, Department for Environment, Food and
Rural Affairs. Since 1987, his research efforts have
concentrated on BSE in cattle and other TSEs in animals and
man and foodborne zoonotic infections. This work has
Section 1—Introduction
involved developing effective collaborations with colleagues
involved in the medical epidemiological aspects of the
diseases, and until 2000 he was the Veterinary Laboratories
Agency’s TSE R&D and Surveillance Programme Manager.
This report is a compilation of the reviewers’ comments. The
opinions expressed in this report do not necessarily represent
RTI’s views on the H-T BSE study report.


1) To the extent that the model identifies factors that might
affect risk, the model has utility in a heuristic sense. However, the
lack of data to support the assumptions, but more importantly, the
lack of data on other factors that could have a greater effect on risk,
limits the predictive value of the model. After all, the outbreak in
Great Britain was because of an unforeseen event—a change in the
rendering process that resulted in a prolonged period of exposure to
many animals. Because of the long incubation period of the
disease, the impact of this change was not detected for years
following the change in rendering practices. The model should
explore the effects of such events.
The authors state that the U.S. Department of Agriculture asked
them to evaluate, should BSE arise in this country, the robustness of
U.S. measures to prevent the spread of BSE among animals and
between animals and humans (page i). Therefore, the deliverable to
USDA requires that the contractor begin with the given that an
introduction has occurred. People (animal), place, and time factors,
such as the source of infection, the level of infectivity introduced,
the location or locations of introduction, temporal aspects of the
Section 2 — General Comments
introduction, and factors of the feed distribution system that would
spread contamination after an introduction, should be considered.
A model is relevant if it leads or might lead to a different conclusion
or reaffirms a previous conclusion. This model tells us no more
than our current experience tells us. The nature of the disease and
the means of infection tell us that the risk is low, so why is a model
needed? No BSE has been detected in the U.S. currently, nor is it
likely to occur given existing practices, so it is not surprising that
results of the simulations reveal that the risk is low, especially when
the assumptions are based on events that occur with low frequency
and low volumes of “infectivity.”


The authors have insufficiently specified or omitted parameters that
may be more likely to affect BSE infection.
1) Spatial considerations are not considered in the model. The
model does not consider the distribution system for feed. If
contamination occurred in a specific area, how widespread would it
2) Perhaps because the model was constructed before the
events of September 11, 2001, the model does not include the
possibility of an intentional introduction of BSE into the U.S. The
model includes scenarios that are highly unlikely to occur, and if
they did occur, they would be mitigated by existing production and
processing practices. The model ignores the more likely scenario of
an unexpected introduction, such as bioterrorism or a breakdown or
alteration of practices that destroy prions or the spread of prions.
The change in rendering practices that was largely responsible for
the Great Britain outbreak was an unexpected scenario. If the
authors began with the assumption that the “experimental unit” is
the prion (“infectivity”) and not an infected animal, then scenarios
that test the effectiveness of practices that destroy prions and spread
of prions could be evaluated.
3) It is generally accepted that the highest risk for BSE is from
(1) import of live cattle or MBM from a country with BSE, (2) an
Review of the Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States — Final Report
internal processing system that is incapable of reducing infectivity
below a certain threshold level (mainly the rendering system), or (3)
exposure of ruminants to the end products of (2), be it purposely or
accidental, by cross contamination.
Although it is commendable that all possible routes and potential
risks are addressed, the emphasis could have been placed more on
the above limited number of priority routes, instead of dwelling into
sometimes highly theoretical routes. In other words, some of the
reported unlikely infection routes are easily dismissed by the model
with a simple statement, whereas others are investigated to a
surprisingly deep level.
The study concerned lists as three main routes, also the scrapie
transmission and the spontaneous BSE case, at the same level of
ranking as the above listed priority routes.
Just one example of this inconsistency with what we consider major
risks: It has not been addressed what happens in Mexico in terms of
MBM exposure, whereas it is stated that from 750,000 up to 2.5
millions of animals are imported annually (p. 22) from Mexico (and
Canada). More or less only a conclusion is presented “that it is
extremely unlikely that these animals pose a risk of introducing BSE
in the USA”. Maybe they don’t pose any risk, but what if they had
been fed contaminated starter ratios as calves in Mexico? Even if
they would not live until patent clinical stages, they could introduce
infectivity into the system, which is, as we concluded in the SSC, in
the case of the US, not very stable.
4) A recent study has shown that prions can be found in the
muscle of BSE-infected mice. Such a finding in cattle would
dramatically alter the structure of the model and the risk estimates.
5) One is naturally concerned that the risk assessment ignores
the importation of BSE through contaminated feedstuffs, other than
MBM as a specific commodity. There is, perhaps arguably,
disproportionality in the whole exercise. On the one hand it
considers the risk of emboli, a relatively low phenomenon, but there
happens to be some limited research on this aspect. On the other
hand, the risk of importation from contaminated fish meal which is
known to be both adulterated with MBM illegally and have MBM
added legitimately to produce fish meal with a known protein
content (because fish meal has a variable protein content depending
Section 2 — General Comments
on its source) is ignored. The same is true for the contamination of
other feed ingredients. This may have been considered and
dismissed, but it deserves some consideration and comment.


1) The feeling one obtains from reading this report is that the
primary objective was to construct a relatively complex quantitative
simulation model. This approach ignores some basic aspects of
BSE. The overriding one is that if a cattle population becomes
infected and MBM is fed to cattle, then no rendering system is
capable of effectively inactivating the BSE agent. Transmission to
and amplification by cattle is therefore possible. There is a lack of
discussion on and assessment of the probability of the introduction
of the BSE agent into the U.S. cattle population from imported
animals, animal products, and animal feedstuffs. This is somewhat
Review of the Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States — Final Report
fundamental and would have provided additional basis for the risk



1) Judging from the impressive list of references at the end of
the main text, the authors did not miss many key studies. However,
a few references in the text of the Appendices (e.g., the ones
mentioned on Pages 4 and 5 of Appendix 2) are not explicitly listed.
These Appendices did not contain a list of references, nor were the
individual references included in the overall list starting at Page
Review of the Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States — Final Report
All known key data seem to have been identified, but some simple
tables showing the input data would have been useful: for example,
the numbers of imported risk animals, by country and birth cohort
(the latter could not be retrieved from the report, although they were
listed in SSC [2000d]), and tonnage and origin of imported MBM,
by country and year. In many cases, data on the above examples
are in the text, but tables could have been helpful.
2) Since completion of the Harvard/Tuskegee report, a new
study could have a profound effect on the risk assessment of BSE.
The study, “Prions in Skeletal Muscle,” was published in the
proceedings of the National Academy of Science (NAS, 2002). The
study’s authors (Bosque et al.) report that mouse skeletal muscle can
propagate prions. The concern is that meat could be a source of
infection, “…even if it is largely free of neural and lymphatic
tissue….” Although, the accumulation of prions in muscle has been
demonstrated only in mice, to meet the requirements of the
statement of work (to assess the robustness of production and
processing practices to prevent spread), the possibility of prions in
meat should be addressed. For instance, how effective would
testing biopsied tissue in asymptomatic animals be in detecting
infected animals? How effective would practices such as steam
pasteurization and irradiation, designed to reduce bacteria, be in
deactivating prions?
3) It is perhaps unusual to comment on the Executive
Summary, but in the second sentence on Page iv, third paragraph, it
would have been helpful to include the time when the prohibition
of the rendering of animals that die on the farm was introduced.
The actual timing of the introduction of this intervention remains
mysterious throughout the text.
4) With respect to Section 2.1.3, third paragraph, one reviewer
said the following:
Z One of the original publications on the epidemiology of BSE
(Wilesmith et al., 1988) is not quoted here or elsewhere in
this report. This paper describes the first evidence of agedependent
Z In the third paragraph, fifth line, on Page 12, it is uncertain
whether the studies attributed to a personal communication
from Dr. Linda Detwiler are the studies in progress in Great
Britain. If so, a little detail on their design would have been
Section 3 — Identification of Data and Critical Evaluation of Evidence
appropriate, together with a discussion of the possible effects
of the results on this risk assessment.
5) With respect to Section 2.2, one reviewer said the following:
Z In the fifth sentence of the first paragraph, additional
references would have been appropriate that would have
confirmed the quoted author’s initial assessment, for
example, papers by Ferguson and Donnelly (2000).
Z The first sentence of the second paragraph would have
benefited from the appropriate references, such as Wilesmith
and Ryan (1992, 1993); Hoinville (1994); Stevenson,
Wilesmith et al. (2000), and the Ferguson and Donnelly
(2000) papers. A number of these are not quoted at all. The
quantitative estimates of the reduction in risk provided by
the analyses that are reported in these papers seem
appropriate to any risk assessment. In the third sentence
onwards, the paragraph is also somewhat deficient in
quoting primary references. For example, the paper by
Wilesmith, Ryan, and Atkinson (1991) appears to be the
primary paper on changes in rendering practices. There are
other important observations on changes in rendering
practices such as the work of Taylor (1995) and observations
by Paul Brown (Brown, 1998) in the Lancet.
6) With reference to Section, BSE in pigs, as a clinical
disease or subclinical infection, has presented a concern
worldwide. They were clearly of potential importance in Great
Britain because of the inclusion rate of MBM. In simple terms, pigs
could represent an effective “sump” for the BSE agent, in which the
BSE agent is effectively removed from the feed system, or at the
other extreme they could represent a means of amplification. The
evidence from Great Britain could have perhaps been used to
strengthen this section, specifically the last part of the second
paragraph on page 29 and the third paragraph on this page.
Evidence indicates that subclinical infection is not a problem in
pigs, and this is not presented. In addition, evidence suggests that
clinical disease in pigs has not occurred in the pig population in
Great Britain. This has probably gotten lost in various reports.
7) One reviewer notes that Section 2.4.3 does not refer to
papers on the risks of the introduction of infection via infected
animals exported from the UK to other EU member states (Schreuder
et al., 1997) nor on the introduction of infection into Switzerland
via MBM (see, for example, papers by Hörnlimann).
Review of the Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States — Final Report
8) With respect to Section, one reviewer mentioned the
Z In the first paragraph, more discussion of the incubation
period distribution would be useful because the model
outputs do not provide very precise estimates of the
incidence of the clinical incidence. The confidence bounds
are very large.
Z One major concern is that the risk assessment ignores the
importation of BSE through contaminated feedstuffs, other
than MBM as a specific commodity. This, perhaps arguably,
underlines disproportionality in the risk assessment. On the
one hand it considers the risk of emboli, a relatively low
phenomenon, but there happens to be some limited research
on this aspect. On the other hand, the risk of importation
from contaminated fish meal, which is known to be both
adulterated with MBM illegally and have MBM added
legitimately to produce fish meal with a known protein
content (because fish meal has a variable protein content
depending on its source), is ignored. The same is true for
the contamination of other feed ingredients. This may have
been considered and dismissed, but it deserves some
consideration and comment. Also, see the general comment
on basic aspects of BSE.


1) In Section 3.2 of the H-T BSE study report, the authors list 15
sources of uncertainty that they evaluated individually for influences
on the model predictions for two outcomes:
Z the total number of cattle that become infected after the
introduction of 10 infected animals at the beginning of the
period, and
Z the amount of BSE infectivity (quantified in terms of the
number of cattle oral ID50s) in food produced for human
consumption over that period.
In addition to varying the parameters to reflect a best case and
worse case, the authors considered the impact of different sources
of infection on the model’s predictions, described in Section 3,
Pages 71-79 and compared the model’s predictions with alternative
Review of the Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States — Final Report
scenarios. The parameters evaluated in the sensitivity (uncertainty)
analysis are listed in detail in the synopsis.
2) The method used for evaluating the contributions of
uncertainty in inputs to uncertainty in model predications has key
shortcomings. The chosen method in the BSE risk assessment model
is to evaluate the influence of one individual uncertainty source
while setting all of the other assumptions or uncertainty sources to
their base-case values. For example, when considering the impact
of the uncertainty in maternal BSE transmission rate on the model
prediction, the other 14 uncertainty sources are set to their basecase
point estimates. This kind of analysis should be referred to as
“sensitivity analysis,” not as “uncertainty analysis” as described in
the report. Although uncertainty analysis and sensitivity analysis are
closely related, they are two different disciplines. Uncertainty
analysis assesses the uncertainty in model outputs that derives from
uncertainty in all inputs when simulated simultaneously. Sensitivity
Analysis assesses the contributions of the inputs to the total
uncertainty in analysis outcomes (Cullen and Frey, 1999).
Therefore, the results from the BSE model “uncertainty analysis” do
not represent the full range of uncertainty in the risk of animal or
human exposed to BSE associated with simultaneous contributions
from all uncertainty inputs. Instead, what is reported is an
individual contribution of one uncertainty input to the partial
uncertainty in the model output, the risk such as associated with
animal or human exposure to BSE.
3) Variability refers to the heterogeneity of values with respect
to time, space, or a population. For example, in exposure
assessment, variable quantities include the rate at which individuals
consume specific dietary items and the body weights of the
individuals (Cullen and Frey, 1999). Variability can be represented
by a frequency distribution showing the variation in a characteristic
of interest over time, space. Uncertainty arises due to lack of
knowledge regarding the true value of a quantity. For example,
there may be uncertainty regarding the proportion of animals that
die on the farm that are rendered. Uncertainty can be quantified as
a probability distribution representing the likelihood that the
unknown quantity falls within a given range of values (Frey, 1997).
Although the BSE model evaluates the impact of how comparison of
various uncertainty sources influences the model predication, there
Section 9 — Identification and Characterization of Variability, Uncertainty,
Critical Assumptions, and Data Gaps
is no distinction between variability and uncertainty in the model
inputs or outputs. In typical practice, in an exposure or risk
assessment model, the model inputs can be divided into those that
are variable, those that are uncertain, and those with some aspects
of each (Bogen and Spear, 1987; IAEA, 1989; Morgan and Henrion,
1990; Finkel, 1990; Frey, 1992). For example, in the BSE model,
maternal BSE transmission rate is variable across different mothers,
but it is also uncertain because there is no knowledge regarding its
true value. It is not possible to determine whether there are
variables that are misspecified as uncertain that instead should have
been arranged distribution for variability because there is not
enough description of the characteristics of most of the input
variables. Therefore, based upon the information presented in the
model documentation, it is not possible to determine which inputs
should be arranged distributions for variability and/or uncertainty.
Variability and uncertainty have different ramifications for decisionmakers
(Cullen and Frey, 1999). Uncertainty forces decisionmakers
to judge how probable it is that risks will be overestimated
or underestimated for every member of the exposed population,
whereas variability forces them to cope with the certainty that
different individuals will be subjected to risks both above and below
any reference point one chooses (NRC, 1994). Therefore, it is
recommended that both sources of variability and uncertainty be
identified and distinguished and that variability and uncertainty
analysis be done in the BSE risk assessment model.
4) In Section 2, at the beginning of Page 26, the authors state
the uncertainty in ascertaining the potential risk posed by oral
exposure to Chronic Wasting Disease (CWD):
Ascertaining the potential risk posed by oral
exposure to CWD is further complicated by the
following sources of uncertainty. First, there are no
accurate statistics documenting the number or type
of deer and elk killed by hunters. Second, the type
of deer and elk that can be hunted in different
geographic areas varies. Third, the disposition of
deer and elk remains after slaughter is uncertain.
Finally, the prevalence of the disease in all but the
highest risk areas is unknown.
The authors have found no data for key sources of uncertainty.
Review of the Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States — Final Report
5) On Page 55 at the end of the first paragraph, the authors
state, “Our base case assumes that clinical BSE cases would be
detected at AM inspection 90 percent of the time. Because this
value is highly uncertain, our uncertainty analysis evaluates the
impact of using a wide range of values on the results of our
simulation (see Section 3.2.2).” However, it was found that only
two values were evaluated.
6) Table 2.18-1 (Appendix 1, Page 31) specifies joint
probability as a percentage but Table (Appendix 2, Page 8)
specifies it as a probability. (Also, the reviewers wonder if the
decimal point is in the correct place.) Consistency among the units
or measures of the probability would be nice.
7) The authors have done a sensitivity analysis where they
altered the parameter values one at a time to determine the effect on
the model’s predictions, varied values defining the source of
infectivity to determine the effect on the model’s predictions, and
compared the model’s prediction for other scenarios. These are all
important means to determine the model’s behavior and reliability.
The sources of variability are largely only considered individually,
so synergistic effects cannot be assessed. The authors have been
careful to select “reasonable” values for the best and worst cases,
but allowing a greater range of variability would provide a better
understanding of the behavior of the model and its stability.
8) Key sources of variability that have been omitted are
accidents that can sometimes happen and the intentional
introduction of prions to feed or water; and a long-term change in
practices by producers, processing establishments, and/or renderers
that might result in prolonged exposure. Because of these
omissions, one may wonder whether a more parsimonious model
might be as predictive.
9) In the case of variability and uncertainty, the risk of infection
through imported animals is addressed in a defensible manner, even
though the probability of this incursion is not estimated. However,
the age at infection ignores the information and the uncertainty of
the incubation period and is not addressed. The summary of these
aspects, perhaps somewhat harshly, is that the synthesis and critical
review of the literature needs more attention.
Section 9 — Identification and Characterization of Variability, Uncertainty,
Critical Assumptions, and Data Gaps
10) Little information regarding the distributions of BSE model
inputs and simulation techniques was provided for the so-called
“uncertainty analysis.” Therefore, key questions that should be
addressed include the following: (1) How was the value of an input
altered? (2) What sampling techniques were used? It is necessary to
clearly list the distribution assumptions and parameters (if used) and
to clearly describe related simulation techniques when doing
uncertainty analysis. The description in the report regarding the
“uncertainty analysis” of the BSE model is not clear enough for users
or reviewers to understand how the “uncertainty analysis” (if any) is
1) Surveillance efficiency, recognition rate of “clinical cases,”
and level of inactivation by local rendering are overestimated. Also,
with respect to recognition rate (where only the very typical cases
will be recognized), it is assumed that 90 percent (in the case of
worst case, 50 percent) of the BSE clinical cases will be detected in
the ante-mortem inspection, which is way off from the general
feeling in the EU on this topic.
2) In discussing fracContaminate on Page 16, Appendix 1, the
authors state that flushing and cleaning leave only 0.1 percent of the
prohibited material behind. This cross-contamination as compared
to European demonstrated rates is grossly underestimated, unless
flushing and cleaning are done in a very different (and probably
uneconomical) way.
3) The readability of the report could be improved by
tabulating all assumptions, as was done for the slaughter process
assumptions (Table 3-8, Page 68) and the render and feed
production assumptions (Table 3-9, Page 69). On Page 67 (second
paragraph, first line), the authors refer to 15 sets of assumptions, but
present only seven bullets (does a bullet represent a set?). If each
item within a bullet is summed, 17 assumptions can be identified.
Also, the authors set parameters to three values: base case, best
case, and worst case. But the justification for the specific values
assigned is weak, because little data are available. Without hard
data, the detailed list of assumptions for this process has heuristic
Review of the Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States — Final Report
value but does not particularly strengthen the predictive value of the
4) The authors assume that “conditions affecting the spread of
BSE in the U.S. would remain unchanged for the 20 years following
its introduction” (Executive summary, Page i, third paragraph, sixth
line). This is a huge assumption and probably unrealistic. As with
most agents of disease, especially newly discovered agents
(emerging diseases), prevalence increases over time largely because
of more and improved testing over time. This has not been
incorporated into the model. Often, agents, once thought rare, are
found to be ubiquitous (e.g., E. coli O157:H7). The public health
goal then is to prevent the agents from spreading or accumulating in
critical locations, including animals, during critical periods of time.
1) The authors state, “There exist considerable data gaps for
many important model assumptions” (Page 87). The authors have
done a commendable job of incorporating the available data, but
this also has limited the scope of the model and/or has resulted in
giving certain factors more weight (a larger contribution to the
results) than perhaps is warranted.
2) On Pages 22 and 23 the introduction risks are discussed.
The import of risk material from the UK is assessed properly, but the
import of risk material from third countries seems largely ignored.
The EU concluded long ago that lots of risk material from the UK
was transported via third countries. Switzerland, for example,
mainly got infected via France not directly from the UK. Thus, the
introduction risk is probably underestimated, although it is plausible
that this risk still remains very low.
3) An analysis of all imported MBM and feed in the 1980s
would be welcomed. Confirming evidence that imported MBM was
only used in pet food would also be useful.
4) “Tallow” at least deserves some more comments (Page 34),
given the fact that traces of protein are certainly in there and that
international flow of these products is even more difficult to



NOW, let us look at the findings from the most recent
BSE GBR risk assessment of USA, Canada and Mexico
by experts in the field of TSEs at the EFSA ;

Working Group Report on
the Assessment of the Geographical BSE-Risk (GBR) of


Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the
Geographical BSE Risk of Canada
- 13 -
On the basis of the available information, it has to be concluded that
the country's
BSE/cattle system was extremely unstable until today, i.e., it would
have recycled and
amplified BSE-infectivity very fast, should it have entered the system.
The stability of the
BSE/cattle system in Canada overtime is as given in table 5 above.
4.1 Interaction of stability and challenges
In conclusion, the stability of the Canada BSE/cattle system in the past
and the external
challenges the system has coped with are summarised in the table 6.
Period Stability External Challenge Internal challenge
1980 to 1990 Low Unlikely but not excluded
1991 to 1995 High
1996 to 2000 Extremely high
Likely and rapidly growing
2001 to 2003
Very high Confirmed at a lower level
Table 6: Internal challenge resulting from the interaction of the
external challenge and stability. The
internal challenge level is determined according to guidance given in
the SSC-opinion on the GBR of
July 2000 (as updated in 2002).
From the interaction of the two parameters "stability" and "external
challenge" a
conclusion is drawn on the level of "internal challenge" that emerged
and had to be met
by the system, in addition to external challenges that occurred.
An external challenge resulting from cattle import could only lead to an
challenge once imported infected cattle were rendered for feed and this
feed reached domestic cattle. Cattle imported for slaughter would
normally be
slaughtered at an age too young to harbour plenty of BSE infectivity or
to show signs,
even if infected prior to import. Breeding cattle, however, would
normally live much
longer and only animals having problems would be slaughtered younger. If
being 4-6
years old when slaughtered, they could suffer from early signs of BSE,
approaching the end of the BSE-incubation period. In that case, they
would harbour,
while being pre-clinical, as much infectivity as a clinical BSE case.
Hence cattle imports
could have led to an internal challenge about 3 years after the import
of breeding cattle
(that are normally imported at 20-24 months of age) that could have been
infected prior
to import. In case of Canada this implies that cattle imported in the
mid eighties could
have been rendered in the late eighties and therefore led to an internal
challenge in the
early 90s.
On the other hand imports of contaminated MBM would lead to an internal
challenge in
the year of import, if fed to cattle. The feeding system is of utmost
importance in this
context. If it could be excluded that imported, potentially contaminated
feed stuffs
reached cattle, such imports might not lead to an internal challenge at
all. In case of
Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the
Geographical BSE Risk of Canada
Canada this implies that it was possible that imported MBM reached
domestic cattle and
lead to an internal challenge in the early 90s.
4.2 Risk that BSE infectivity entered processing
A certain risk that BSE-infected cattle entered processing in Canada,
and were at least
partly rendered for feed, occurred in the early 1990s when cattle
imported from UK in
the mid 80s could have been slaughtered. 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.
4.3 Risk that BSE infectivity was recycled and propagated
A risk that BSE-infectivity was recycled and propagated exists since a
processing risk
first appeared; i.e. in the early 90s. Until today this risk persists
and increases fast
because of the extremely unstable BSE/cattle system in Canada.
5.1 The current GBR as function of the past stability and challenge
The current geographical BSE-risk (GBR) level is III, i.e. it is
confirmed at a lower level
that domestic cattle are (clinically or pre-clinically) infected with
the BSE-agent.
This assessment deviates from the previous assessment (SSC opinion,
2000) because at
that time several exporting countries were not considered a potential risk.
into account.

- 14 -
5.2 The expected development of the GBR as a function of the past and
present stability and challenge
. As long as the system remains unstable, it is expected that the GBR
continues to
grow, even if no additional external challenges occur.
. Since recent improvements in the safety of MBM production in many
countries or
significant recent reductions in the incidence of BSE are not taken into
account for
the assessment of the external challenge, the external challenge
assessed after 2001
could be overestimated and is the worst case assumption. However all
current GBR
conclusions are not dependent on these assumptions in any of the
countries assessed.
For future assessments and when the impact of the production,
surveillance and true
incidence changes has been fully quantified, these developments should
be taken
5.3 Recommendations for influencing the future GBR
. Enhancing the stability of the system, in particular by ensuring that
cattle have no
access to mammalian MBM in combination with appropriate rendering and
exclusion of
SRM and fallen stock from any feed chain could lead, over time, to a
reduction of the
. Improved passive and active surveillance, i.e. sampling of animals not
signs compatible with BSE from "at-risk" cattle populations, such as
adult cattle in
Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the
Geographical BSE Risk of Canada



EFSA Scientific Report on the Assessment of the Geographical BSE-Risk
(GBR) of the United States of America (USA)
Publication date: 20 August 2004

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

* 167 kB Report

* 105 kB Summary

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




From: Terry S. Singeltary Sr. []
Sent: Tuesday, July 29, 2003 1:03 PM
Cc:;; BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

Greetings FDA,


PLUS, if the USA continues to flagrantly ignore the _documented_ science
to date about the known TSEs in the USA (let alone the undocumented TSEs
in cattle), it is my opinion, every other Country that is dealing with
BSE/TSE should boycott the USA and demand that the SSC reclassify the
USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the
SSC to _flounder_ any longer on this issue, should also be regarded with
great suspicion as well. NOT to leave out the OIE and it's terribly
flawed system of disease surveillance. the OIE should make a move on CWD
in the USA, and make a risk assessment on this as a threat to human
health. the OIE should also change the mathematical formula for testing
of disease. this (in my opinion and others) is terribly flawed as well.
to think that a sample survey of 400 or so cattle in a population of 100
million, to think this will find anything, especially after seeing how
many TSE tests it took Italy and other Countries to find 1 case of BSE
(1 million rapid TSE test in less than 2 years, to find 102 BSE cases),
should be proof enough to make drastic changes of this system. the OIE
criteria for BSE Country classification and it's interpretation is very
problematic. a text that is suppose to give guidelines, but is not
understandable, cannot be considered satisfactory. the OIE told me 2
years ago that they were concerned with CWD, but said any changes might
take years. well, two years have come and gone, and no change in
relations with CWD as a human health risk. if we wait for politics and
science to finally make this connection, we very well may die before any
or changes are made. this is not acceptable. we must take the politics
and the industry out of any final decisions of the Scientific community.
this has been the problem from day one with this environmental man made
death sentence. some of you may think i am exaggerating, but you only
have to see it once, you only have to watch a loved one die from this
one time, and you will never forget, OR forgive...yes, i am still very
angry... but the transmission studies DO NOT lie, only the politicians
and the industry do... and they are still lying to this day...TSS


Vet Pathol 42:107108 (2005)
Letters to the Editor
Absence of evidence is not always evidence of absence.
In the article Failure to detect prion protein (PrPres) by
immunohistochemistry in striated muscle tissues of animals
experimentally inoculated with agents of transmissible spongiform
encephalopathy, recently published in Veterinary
Pathology (41:7881, 2004), PrPres was not detected in striated
muscle of experimentally infected elk, cattle, sheep, and
raccoons by immunohistochemistry (IHC). Negative IHC,
however, does not exclude the presence of PrPSc. For example,
PrPres was detected in skeletal muscle in 8 of 32
humans with the prion disease, sporadic Creutzfeldt-Jakob
disease (CJD), using sodium phosphotungstic acid (NaPTA)
precipitation and western blot.1 The NaPTA precipitation,
described by Wadsworth et al.,3 concentrates the abnormal
isoform of the prion, PrPres, from a large tissue homogenate
volume before western blotting. This technique has increased
the sensitivity of the western blot up to three orders
of magnitude and could be included in assays to detect
PrPres. Extremely conspicuous deposits of PrPres in muscle
were detected by IHC in a recent case report of an individual
with inclusion body myositis and CJD.2 Here, PrPres was
detected in the muscle by immunoblotting, IHC, and paraf-
fin-embedded tissue blot. We would therefore caution that,
in addition to IHC, highly sensitive biochemical assays and
bioassays of muscle are needed to assess the presence or
absence of prions from muscle in experimental and natural
TSE cases.
Christina Sigurdson, Markus Glatzel, and Adriano Aguzzi
Institute of Neuropathology
University Hospital of Zurich
Zurich, Switzerland
1 Glatzel M, Abela E, et al: Extraneural pathologic prion
protein in sporadic Creutzfeldt-Jakob disease. N Engl J
Med 349(19):18121820, 2003
2 Kovacs GG, Lindeck-Pozza E, et al: Creutzfeldt-Jakob
disease and inclusion body myositis: abundant diseaseassociated
prion protein in muscle. Ann Neurol 55(1):
121125, 2004
3 Wadsworth JDF, Joiner S, et al: Tissue distribution of protease
resistant prion protein in variant CJD using a highly
sensitive immuno-blotting assay. Lancet 358:171180,

and started cherry picking there cows to test.
course when they did find one, they simply ;

May 13, 2004

Failure To Test Staggering Cow May Reflect Wider Problems
Rep. Waxman raises concerns that the recent failure of USDA to test an
impaired cow for BSE may not be an isolated incident, citing the failure
of USDA to monitor whether cows condemned for central nervous system
symptoms are actually tested for mad cow disease.

- Letter to USDA

May 4, 2004

Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms

On Friday, April 30 th , the Food and Drug Administration learned that a
cow with central nervous system symptoms had been killed and shipped to
a processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately
began an investigation. On Friday and throughout the weekend, FDA
investigators inspected the slaughterhouse, the rendering facility, the
farm where the animal came from, and the processor that initially
received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over
the weekend FDA was able to track down all the implicated material. That
material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known
as "mad cow disease," can exhibit such symptoms. In this case, there is
no way now to test for BSE. But even if the cow had BSE, FDA's animal
feed rule would prohibit the feeding of its rendered protein to other
ruminant animals (e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and
informing the firm that FDA will not object to use of this material in
swine feed only. If it is not used in swine feed, this material will be
destroyed. Pigs have been shown not to be susceptible to BSE. If the
firm agrees to use the material for swine feed only, FDA will track the
material all the way through the supply chain from the processor to the
farm to ensure that the feed is properly monitored and used only as feed
for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the
U.K. showed that the disease spreads by feeding infected ruminant
protein to cattle.

Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action
specifying that the material go only into swine feed means also that it
will not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates
closely with the U.S. Department of Agriculture on all BSE issues. The
animal feed rule provides crucial protection against the spread of BSE,
but it is only one of several such firewalls. FDA will soon be improving
the animal feed rule, to make this strong system even stronger.




January 30, 2001
Print Media:
Broadcast Media:
Consumer Inquiries:


Today the Food and Drug Administration announced the results of tests
taken on feed used at a Texas feedlot
that was suspected of containing meat and bone meal from other domestic
cattle -- a violation of FDA's 1997
prohibition on using ruminant material in feed for other ruminants.
Results indicate that a very low level of
prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams -
approximately a quarter ounce -- of prohibited material. These animals
weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in
origin (therefore not likely to contain infected
material because there is no evidence of BSE in U.S. cattle), fed at a
very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even
if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy
Commissioner, "The challenge to regulators
and industry is to keep this disease out of the United States. One
important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined
with other steps, like U.S. Department
of Agriculture's (USDA) ban on the importation of live ruminant animals
from affected countries, these steps
represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless
announcing that it is voluntarily purchasing all 1,222
of the animals held in Texas and mistakenly fed the animal feed
containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA
believes any cattle that did not consume
feed containing the prohibited material are unaffected by this incident,
and should be handled in the beef supply
clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first
reporting the human error that resulted in the
misformulation of the animal feed supplement and then by working closely
with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food
supply and that continued vigilance needs to be taken, by all concerned,
to ensure these rules are followed

FDA will continue working with USDA as well as State and local officials
to ensure that companies and
individuals comply with all laws and regulations designed to protect the
U.S. food supply.

NOW we know that .1 gram is lethal.

COURSE, who knows about these other 500 cows;

No mad cow results for nearly 500 cows

By Steve Mitchell
United Press International
Published 8/11/2004 11:23 AM

WASHINGTON, Aug. 11 (UPI) -- The U.S. Department of Agriculture failed
to test for mad cow disease or collect the correct portion of the brain
on nearly 500 suspect cows over the past two years -- including some in
categories considered most likely to be infected -- according to agency
records obtained by United Press International.

The testing problems mean it may never be known with certainty whether
these animals were infected with the deadly disease. Department
officials said these animals were not included in the agency's final
tally of mad cow tests, but the records, obtained by UPI under the
Freedom of Information Act, indicate at least some of them were counted...



Steve Mitchell is UPI's Medical Correspondent. E-mail
Copyright © 2001-2004 United Press International

Congress of the United States Washington, DC 20515
January 5, 2005 The Honorable Michael Johanns Governor State of Nebraska
Office of the Governor P.O. Box 94848 Lincoln, NE 68509-4848 Dear
Governor Johanns: On January 4, 2005, the U.S. Department of Agriculture
announced that it would lift the ban on cattle imports from Canada,
effective on March 7. A principal rationale for USDA's decision is that
Canada has a "rigorous" and "effective" feed ban in place, which
prevents the spread of "mad cow disease" by preventing protein derived
from cattle from being fed to cattle. It appears, however, that USDA has
failed to review significant evidence that calls into question the
effectiveness of the Canadian feed ban. If, as expected, you are
confirmed as Secretary of Agriculture, we urge you to assess this new
information carefully before proceeding with the plan to reopen the U.S.
border to the importation of millions of Canadian cattle. We have
learned that: " U.S. regulators have discovered animal muscle, hair,
blood and bone in Canadian feed. Over the last 15 months, the U.S. Food
and Drug Administration (FDA) has issued "import alerts" blocking the
importation of products from 17 Canadian companies, including two of the
largest feed manufacturers in the country. FDA found muscle tissue in 15
products, animal hair in five, blood in eight, and bone in two. Eight
"import alerts'' on Canadian feed are still active today. " Recent tests
have shown that Canadian feed often contains unanticipated animal
protein. Over two-thirds of samples of vegetarian animal feed
manufactured in Canada and recently tested by the Canadian regulators
contained "undeclared animal materials." In an internal memo, a senior
regulator called the test results "worrisome." " Major noncompliance
with Canadian feed rules persists. Recent inspections have revealed that
seven Canadian feed mills had "major non-compliance" issues, and three
were failing "to prevent contamination of... feeds." In one recent case,
potentially contaminated feed was consumed by cattle. " Canada
recognizes gaps in its own feed ban. On December 10, 2004, Canadian
regulators concluded that "the current framework provides opportunities
for prohibited proteins to be accidentally included in or
cross-contaminate feeds." Canada then proposed changes to its feed ban.
The Honorable Michael Johanns January 5, 2005 Page 2 These findings,
which are discussed in detail in the attachments to this letter, have
significant implications. The recent discovery of another case of mad
cow disease in Canada underscores the potential risk of inadequate
measures to prevent the spread of the disease. If Canada's feed ban is
not effective, then Canada does not qualify as a "minimal risk" country
under the new definition put forward by USDA, and the importation of
Canadian cattle cannot resume. It is imperative that these issues be
thoroughly investigated before authorizing Canadian imports. For these
reasons, we urge you to consult with FDA about the "import alerts"
against Canadian feed suppliers and assess their implications for the
effectiveness of the Canadian feed ban. We also urge you to review the
Canadian documents questioning industry's compliance with the feed ban
and to talk to Canadian officials about the limitations of their current
feed ban. After undertaking this investigation, we urge you to appear
before Congress to communicate your findings. Sincerely, Henry A. Waxman
Ranking Minority Member Committee on Government Reform U.S. House of
Representatives Kent Conrad Senator U.S. Senate


"If the science doesn't fit what the White House wants it to be, it
distorts the science."

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


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

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



File Format: PDF/Adobe Acrobat -

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

Sr. [] Monday, January 08,200l 3:03 PM freas ...

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;

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

[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. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
TSS 1/27/03 (0)

Docket Management

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

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, ...

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. ...

Docket Management

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

Comment Number: EC -1

Accepted - Volume 1

Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ... - 05-20-2003
- Cached

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

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

i simply disagree...

3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...


AND THEY MEANT IT, God save the industry at all cost,
including human health. simply has nothing to do with science anymore...


NO mention of these studies either;

Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions

Mathias Heikenwalder,1* Nicolas Zeller,1* Harald Seeger,1* Marco
Prinz,1* Peter-Christian Klöhn,2 Petra
Schwarz,1 Nancy H. Ruddle,3 Charles Weissmann,2 Adriano Aguzzi1!

1Institute of Neuropathology, University Hospital of Zürich, CH-8091
Zürich, Switzerland. 2Medical Research Council Prion
Unit, Department of Neurodegenerative Diseases, Institute of Neurology,
Queen Square, London WC1N 3BG, UK. 3Department
of Epidemiology and Public Health and Section of Immunobiology, Yale
University School of Medicine, New Haven, CT
06520, USA.

*These authors contributed equally to this work.
Present address: Institute of Neuropathology, Georg-August-Universität,
D-37073 Göttingen, Germany.
!To whom correspondence should be addressed. E-mail:

Prions typically accumulate in nervous and lymphoid
tissues. Because proinflammatory cytokines and immune
cells are required for lymphoid prion replication, we
tested whether inflammatory conditions affect prion
pathogenesis. We administered prions to mice with five
inflammatory diseases of kidney, pancreas or liver. In all
cases, chronic lymphocytic inflammation enabled prion
accumulation in otherwise prion-free organs.
Inflammatory foci consistently correlated with
lymphotoxin upregulation and ectopic induction of PrPCexpressing
FDC-M1+ cells, whereas inflamed organs of
mice lacking lymphotoxin-? or its receptor did not
accumulate PrPSc nor infectivity upon prion inoculation.
By expanding the tissue distribution of prions, chronic
inflammatory conditions may act as modifiers of natural
and iatrogenic prion transmission.


The above results indicate that chronic follicular
inflammation, induced by a variety of causes, specifies prion
tropism for otherwise prion-free organs. In most instances
infectivity tended to rise with time, suggesting local prion
replication. Organ-specific expression of one single proinflammatory
cytokine (LT?) or chemokine (SLC) sufficed to
establish unexpected prion reservoirs, suggesting
differentiation of ubiquitous stromal constituents into prionreplication
competent cells. In several instances, prion
concentration in individual inflamed organs approached that
of spleen long before any clinical manifestation of scrapie.
Inflamed non-lymphoid organs not only accumulated PrPSc,
but transmitted bona fide prion disease when inoculated into
healthy recipient mice.

Knowledge of the distribution of prions within infected
hosts is fundamental to consumer protection and prevention
of iatrogenic accidents. Based on the failure to transmit BSE
infectivity from any tissue but central nervous system,
intestinal, and lymphoid tissue (35), the risk to humans of
contracting prion infection from other organs has been
deemed small even in countries with endemic BSE. It may be
important now to test whether superimposed viral, microbial
or autoimmune pathologies of farm animals trigger
unexpected shifts in the organ tropism of prions. Conversely,
the lack of infectivity in burned out postinflammatory
pancreases suggests that anti-inflammatory regimens may
abolish ectopic prion reservoirs.

References and Notes snip...END



Human Prion Protein with
Valine 129 Prevents Expression
of Variant CJD Phenotype

Jonathan D. F. Wadsworth, Emmanuel A. Asante,
Melanie Desbruslais, Jacqueline M. Linehan, Susan Joiner,
Ian Gowland, Julie Welch, Lisa Stone, Sarah E. Lloyd,
Andrew F. Hill,* Sebastian Brandner, John Collinge

Variant Creutzfeldt-Jakob disease (vCJD) is a unique and highly distinctive
clinicopathological and molecular phenotype of human prion disease
associated with infection with bovine spongiform encephalopathy (BSE)-like
prions. Here, we found that generation of this phenotype in transgenic mice
required expression of human prion protein (PrP) with methionine 129.
Expression of human PrP with valine 129 resulted in a distinct phenotype
remarkably, persistence of a barrier to transmission of BSE-derived
prions on
subpassage. Polymorphic residue 129 of human PrP dictated propagation of
distinct prion strains after BSE prion infection. Thus, primary and
human infection with BSE-derived prions may result in sporadic CJD-like or
novel phenotypes in addition to vCJD, depending on the genotype of the
source and the recipient.


Although caution must be exercised in
extrapolating from animal models, even
where, as here, faithful recapitulation of
molecular and pathological phenotypes is
possible, our findings argue that primary
human BSE prion infection, as well as sec-
ondary infection with vCJD prions by iatro-
genic routes, may not be restricted to a single
disease phenotype. These data, together with
the recent recognition of probable iatrogenic
transmission of vCJD prions to recipients of
blood {21, 22), including a PRNP codon 129
Met/Val heterozygous individual (22), re-
iterate the need to stratify all human prion
disease patients by PrPSc type. This surveil-
lance will facilitate rapid recognition of novel
PrPSc types and of any change in relative
frequencies of particular PrPSc subtypes in
relation to either BSE exposure patterns or
iatrogenic sources of vCJD prions.

References and Notes snip...END

THE new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic Creutzfeldt-Jakob disease

Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human
health THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy
Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François
Lamoury*, Nicolas Kopp [Dagger ] , Jean-Jacques Hauw§, James Ironside¶,
Moira Bruce [||] , Dominique Dormont*, and Jean-Philippe Deslys* et al,
that 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;

Characterization of two distinct prion strains derived from bovine
spongiform encephalopathy transmissions to inbred mice

still deeply disgusted in Bacliff, Texas USA

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

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