SEARCH VEGSOURCE:

 

 

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




From: TSS ()
Subject: Re: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1)
Date: August 31, 2005 at 2:16 pm PST

In Reply to: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1) posted by TSS on August 31, 2005 at 11:08 am:

Greetings,

I must say, i was much to angry yesterday to put forth a good sound based scientific approach to a thorough critic of the facts.
the reporting by the media of this blunder and the transcripts and remarks from officials at USDA et al, was just too much BSe.
so i thought i might put forth a few more facts below, for whatever scientific facts on TSEs are worth with this administration.
sadly, i think they are starting to believe what they are saying and have said in the past about mad cow in the USA 'no problem',
'triple firewalls', and 'sealed borders' etc.


>>>Now I want to turn to the completion of the epidemiological investigation that was conducted following the BSE detection in Texas in June. Many people worked very hard on the investigation, and I'd like to thank the Veterinary Services employees involved, our colleagues from the Food and Drug Administration, the owners of the animals, along with the Texas Animal Health Commission and the Texas Feed and Fertilizer Control Service for their outstanding work.

This investigation is another great example of federal, state, and local partners cooperating to help protect livestock health in this country. <<<


= = =


>>>But as far as actual poundage, I don't think it's possible for us to give you that actual number. There was two calves of interest that we traced. Due to the lack of appropriate records at the time, we actually traced 213 calves. Of those, it's estimated that 212 of those animals went into the feeding and slaughter channels. Those animals would have been slaughtered likely prior to 30 months of age, which we know that it's extremely small risk of having BSE prior to 30 months of age.

And also internationally and in the research community, while it's never been proven that offspring can get this disease through maternal transmission -- it's never been proven or disproven actually -- but it's thought very much from the international experts and the research it is extremely rare if it does happen.

Both of these calves were born very well prior to this animal being slaughtered. This animal did not show any clinical signs typical of BSE -- sampled and destroyed. This animal did not show any clinical signs or evidence of BSE which would make it even more unlikely that these two offspring would have any risk of having BSE.

The other 200 head that were traced were retraced as a result also of a lack of records. We were looking at cattle of interest over a five-year period of time of which this animal was born. Her approximate age was 12. We expanded one year of that and made her 11 to 13, and then we'd go another year beyond that. So we looked at animals basically in the age range of 10 to 15 years of age to remove those from the herd. And we traced every adult animal that we could from 1990.

Many of those animals would not even be of concern because they would not have received any feed at the time that she was in the herd or would have not been a birth cohort and born at the same time that she was.

So of those, 143 were reported as slaughtered, and we confirmed that 131 were definitely slaughtered; 34 were presumed dead, and 20 of those were untraceable. So again, we feel that the risk is extremely small. We do not feel that the public or our pet food industry should have any concerns relative to this issue. <<<

FACTS;

Maternal transmission

7. There is evidence from animal studies for low level maternal
transmission of prions in cattle and sheep. This transmission may
occur in utero, via milk and/or perinatally. However, the possibility
that this putative maternal transmission might have been due to
another mode of transmission, for example through a contaminated
environment or feed, cannot be ruled out.


http://www.seac.gov.uk/statements/cjdtransmissionfinal.pdf

A BSE case born in September 2001
BSE has been diagnosed in a Holstein cow, born on 28 September 2001.
The case was identified under the current compulsory testing programme for
all animals born after 31 July 1996 slaughtered as cohorts of confirmed BSE
cases. This animal was included in the cohort of the BSE case born on 3
October 2001 on the same farm and confirmed on 1 March 2005. This case
born on 28 September 2001 was born on the same farm in Dyfed and it
remained on this farm until it was submitted for slaughter on 12 May 2005.
Disease was officially confirmed on 27 May 2005. The animal was aged 43
months at slaughter.
Another case born on the same farm on 1 May 2002 has been confirmed on
27 May 2005 in the same cohort. This is the first time that the UK has
confirmed three cases born after July 1996 with the same farm of origin.
Defra will be following up detailed epidemiological analysis of this case.
This case is being drawn to the attention of SEAC and Professor William Hill.
Professor Hill is currently carrying out an independent assessment of the
possible causes of BSE cases born after the reinforced feed ban of August
1996 (BARBs) at the request of Defra.

http://www.defra.gov.uk/animalh/bse/controls-eradication/barbinfo/28-09-2001.pdf


A BSE case born in May 2002
BSE has been diagnosed in a Holstein Friesian cross cow, born on 1 May
2002. The case was identified under the current compulsory testing
programme for all animals born after 31 July 1996 slaughtered as cohorts of
confirmed BSE cases. This animal was included in the cohort of the BSE
case born on 3 October 2001 on the same farm and confirmed on 1 March
2005. This case born on 1 May 2002 was born on the same farm in Dyfed
and it remained on this farm until it was submitted for slaughter on 12 May
2005. Disease was officially confirmed on 27 May 2005. The animal was
aged 36 months at slaughter.
This is the most recently born case of BSE confirmed in the UK. The previous
most recent case was the related case born on 3 October 2001.
Another case born on the same farm on 28 September 2001 has been
confirmed on 27 May 2005 in the same cohort. This is the first time that the
UK has confirmed three cases born after July 1996 with the same farm of
origin. Defra will be following up detailed epidemiological analysis of this
case.
This case is being drawn to the attention of SEAC and Professor William Hill.
Professor Hill is currently carrying out an independent assessment of the
possible causes of BSE cases born after the reinforced feed ban of August
1996 (BARBs) at the request of Defra.


http://www.defra.gov.uk/animalh/bse/controls-eradication/barbinfo/01-05-2002.pdf


>>>I'll now summarize our findings. Our results indicate that the positive animal, called the "index animal." was born and raised on a ranch, termed the "index farm," in Texas. It was a cream-colored Brahma cross, approximately 12 years of age at the time of its death. It was born prior to the implementation of FDA's mandatory ruminant-to-ruminant feed ban in the U.S., and that ban was implemented in August 1997. <<<


FACTS, THE AUGUST 4, 1997 RUMINANT TO RUMINANT FEED BAN WAS ONLY PARTIAL AND VOLUNTARY, it was nothing more than
ink on paper. THE USA cattle have been fed ruminant protein in high concentrations, as proven in TEXAS, where we not only render the falling, stumbling and staggering highly suspect mad cows, we also feed them up documented 5.5 grams each of ruminant protein at the Purina mill, where the FDA again ignores proven and sound science that shows indeed less than a gram, up to one tenth of a gram is lethal. THIS sound science was documented at the time of the Purina feed mill mad cow blunder ;

CATTLE ON FEED IN TEXAS


FOR IMMEDIATE RELEASE
P01-05
January 30, 2001
Print Media: 301-827-6242
Consumer Inquiries: 888-INFO-FDA


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

Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a
cow in Washington state had tested positive for bovine spongiform
encephalopathy (BSE, or mad cow disease). As a result, information on this
Web page stating that no BSE cases had been found in the United States is
now incorrect. However, because other information on this page continues to
have value, the page will remain available for viewing.

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT


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 routinely.

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.

http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html


Risk of oral infection with bovine spongiform encephalopathy agent in
primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa

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


= = =

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


2

6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise
that it

could take as little of 1 gram of brain to cause BSE by the oral route
within the

same species. This information did not become available until the "attack
rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to
ensure

that the actual result was within both a lower and an upper limit within the
study

and the designing scientists would not have expected all the dose levels to
trigger

infection. The dose ranges chosen by the most informed scientists at that
time

ranged from 1 gram to three times one hundred grams. It is clear that the
designing

scientists must have also shared Mr Bradley's surprise at the results
because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram

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


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml

In addition, USDA cannot rely on the Food and Drug Administrations
(FDAs) 1997 BSE feed rule being rigorously enforced. Because of serious
lapses, increased surveillance is needed. The USDA-sponsored Harvard
risk assessment of the risk of BSE in the U.S. noted that compliance
with FDAs 1997 BSE feed rule is the most important factor in preventing
a BSE outbreak. Yet a pair of reports by GAOone published in September
2000 and the other published in January 2002have shown how lax FDA has
been in ensuring compliance with the feed rule. The first report,
published some three years after the BSE feed rule went into effect
found fairly widespread non-compliance: inspection results of the 2,481
firms that were identified as handling prohibited materials . . . 699,
or 28 percent, did not label their products with the required cautionary
statements that the feed should not be fed to cattle or other ruminants.
. . . In addition, of the 1,771 firms that manufacture both prohibited
and non-prohibited material, 361, or 20 percent, did not have a system
in place to prevent commingling and cross contamination, as required by
the regulation (pp. 11-12 in http://www.gao.gov/new.items/rc00255.pdf).

The 2002 GAO report found that, (C)oncerning the feed ban, FDA has not
acted promptly to compel firms to keep prohibited proteins out of cattle
feed and to label animal feed that cannot be fed to cattle. . . .
Moreover, FDAs data on inspections are severely flawed and, as a
result, FDA does not know the full extent of industry compliance. FDA
acknowledges that it has not yet identified and inspected all firms
subject to the ban (pg. 3 in http://www.gao.gov/new.items/d02183.pdf).
The report concludes that federal actions do not sufficiently ensure
that all BSE-infected animals or products are kept out or that if BSE
were found it would be detected promptly and not spread to other cattle
through animal feed or enter the human food chain italics added (pg. 3
in http://www.gao.gov/new.items/d02183.pdf). The failure of FDA to fully
implement the 1997 BSE feed ban should spur USDA to exercise greater
vigilance to ensure that if BSE occurred in the US that it would be
found quickly. USDA should therefore dramatically expand the testing of
cattle to ensure, at a minimum, that all downer cows (e.g. all emergency
slaughter and all fallen stock) are tested for BSE using one of the
rapid tests, preferably the one found to be the most accurate (e.g. with
the lowest rate of false positives and false negatives).

We also believe that USDA should act to ensure that no CNS tissue is
found in meat destined for human consumption. We note that the results
of the Food Safety Inspection Services 2002 AMR survey found that
about 74 percent (25 of 34) of the establishments tested in the AMR
Survey of 2002 had positive laboratory results for CNS tissue in their
final beef AMR products; the other 26 percent had negative laboratory
results (see pg. 2 of http://www.fsis.usda.gov/OA/topics/AMRSurvey.pdf).
The USDA should take appropriate action to ensure that there is zero CNS
contamination of meat destined for human consumption...


GAO says BSE efforts flawed; USDA/FDA respond
2/27/02 - A U.S. General Accounting Office report said there are
weaknesses in import controls, the enforcement of animal feed rules is
not up to par, and inspection records are seriously flawed. "The
continuing absence of [bovine spongiform encephalopathy] in the United
States today cannot be sufficiently ensured by current federal
prevention efforts," the report said. For a copy of the GAO BSE report
see the following web page: GAO Report
http://www.gao.gov/daybook/020226.htm.

B. Investigation of Handling of CNS-Suspect Cow in San Angelo, Texas

Overview

On May 4, 2004, the FSIS Acting Regional Director in Dallas, Texas reported that a cow

identified as having Central Nervous System (CNS) symptoms by an FSIS veterinarian at

Lone Star Beef Processors (Lone Star Beef), a beef processing facility in San Angelo,

Texas was not tested for BSE after it had been slaughtered. The initial decision by the

FSIS Veterinary Medical Officer (VMO) on-site at Lone Star Beef to have the cow tested

for BSE was overturned by a senior APHIS official and the cow’s carcass was sent to a

rendering plant. FSIS regulations at the time of the incident required VMOs to contact

the APHIS Assistant Area Veterinarian in Charge (AAVIC) to allow APHIS to collect a

BSE surveillance sample from suspect cattle.

OIG initiated an investigation to determine if the AAVIC in Austin, Texas, provided a

false statement to USDA FSIS investigators during their inquiry of his decision not to test

the animal at Lone Star Beef. To conduct our investigation, OIG reviewed previously

obtained statements, various documents and USDA regulations, and interviewed APHIS,

FSIS, beef processing facility, and rendering company personnel.

Summary of OIG Findings

The OIG investigation found no substantive evidence that the USDA official(s)

responsible for the decision not to take brain tissue samples from the cow for BSE

testing, or any other USDA personnel, provided false information or engaged in

intentional misconduct. We determined that a misjudgment was made by at least one

USDA veterinary official in the handling of the suspect cow. Sworn statements provided

by the two responsible USDA veterinary officials involved differ as to whether both

concurred in this decision.

The suspect cow’s carcass was sent to a rendering plant in San Angelo on April 27, 2004

for processing as inedible by-product. APHIS then utilized its "Indemnity Plan"

10

procedures to purchase the by-products as a preventative safety measure, and disposed of

it at a local landfill in accordance with applicable environmental standards.

Evidence shows that at the time of this incident, communication problems occurred

between the APHIS and FSIS employees involved. Taken together, the statements of

both APHIS and FSIS personnel and other evidence indicate inconsistencies in their

understanding of procedures for BSE tissue sampling of CNS suspect cattle in certain

circumstances, and the handling of the carcass pending test results. It is apparent from

the sworn statements provided to OIG that APHIS and FSIS personnel and Lone Star

Beef officials could not resolve how best to proceed, and that confusion existed about

how to properly handle the CNS-suspect carcass.

On May 5, 2004, FSIS and APHIS Veterinary Services announced a new joint policy

regarding BSE sampling of condemned cattle at slaughter plants. The policy establishes

protocols for the agencies’ responsibilities to obtain samples from condemned cattle

exhibiting signs of CNS disorders, regardless of age. ...

snip...

http://www.usda.gov/oig/webdocs/Testimony7-2004.pdf

USDA Office of Inspector General Statement on Audit Work Related to the BSE Test

Result Announced on June 10, 2005

In August 2004, the Department of Agriculture’s (USDA) Office of Inspector General

(OIG) issued an audit report on USDA’s BSE Surveillance Program—Phase I. (See

OIG’s website at: http://www.usda.gov/oig/webdocs/50601-9-final.pdf.) OIG made a

number of recommendations to improve the Department’s BSE Surveillance Plan in the

Phase I audit report. Based on our audit findings, we recommended that USDA fully

disclose the assumptions behind its sampling plan, clarify the limitations, and ensure that

all high-risk animals are sampled and tested in accordance with USDA policy and the

2004 Surveillance Plan. We also recommended that USDA expedite development of a

new system to track and report accomplishments, and implement performance measures

and a continuous risk assessment.

Currently, OIG has two audits in progress pertaining to BSE. In our BSE Surveillance

Program—Phase II audit, OIG is monitoring the Department’s implementation of its

BSE Expanded Surveillance Program, involving both APHIS and FSIS. This audit will

evaluate the following: the effectiveness of USDA’s expanded BSE Surveillance

program; the performance of BSE laboratories in meeting their objectives and complying

with program policies and procedures for conducting tests on submitted BSE samples and

reporting test results to APHIS and stakeholders; and the corrective actions taken by

USDA in response to recommendations in the BSE Surveillance Program—Phase I audit

report cited above.

In our Phase III audit, we are evaluating whether the USDA enforcement of the ban on

specified risk materials (SRMs) in meat products and controls to prevent central nervous

system (CNS) tissue in advanced meat recovery (AMR) product have been effectively

implemented. The review also covers FSIS ante mortem condemnation procedures

and procedures for obtaining brain tissue samples from condemned cattle for BSE testing.

In the course of reviewing voluminous records and information gathered during the BSE

Surveillance Program—Phase II audit, OIG auditors noted an unusual pattern of

conflicting test results on one sample and initiated additional testing of that sample. As

announced by USDA on June 10, the sample subsequently rendered a positive result

under the OIE (World Organization for Animal Health) recognized SAF immunoblot test.

OIG’s fieldwork on these audits is ongoing. Once the audits are completed, OIG will

report on the specific BSE Enhanced Surveillance Program issues and procedures we

examined, our corresponding findings and recommendations, and USDA’s response

thereto. We anticipate completing and publicly releasing the reports late this summer.

http://www.usda.gov/oig/webdocs/BSEStatement050615.pdf


January 2002

MAD COW DISEASE

Improvements in the

Animal Feed Ban and

Other Regulatory

Areas Would

Strengthen U.S.

Prevention Efforts

snip...

Results in Brief

While BSE has not been found in the United States, federal actions do not

sufficiently ensure that all BSE-infected animals or products are kept out

or that if BSE were found, it would be detected promptly and not spread to

other cattle through animal feed or enter the human food supply. With

regard to imports, the United States had imported about 125 million

pounds of beef (0.35 percent of total imported) and about 1,000 cattle

(0.003 percent of total imported) from countries that later discovered

BSE—during the period when BSE would have been incubating. In

addition, weaknesses in USDA’s and FDA’s import controls, such as

inspection capacity that has not kept pace with the growth in imports, may

allow BSE-infected products to enter the country. With regard to animal

testing to detect BSE, although USDA has steadily increased the number of

animals it tests, it does not include many animals that die on farms.

Experts consider these animals a high-risk population. Concerning the

feed ban, FDA has not acted promptly to compel firms to keep prohibited

proteins out of cattle feed and to label animal feed that cannot be fed to

cattle. We identified some noncompliant firms that had not been

reinspected for 2 or more years and instances when no enforcement action

had occurred even though the firms had been found noncompliant on

multiple inspections. Moreover, FDA’s data on inspections are severely

flawed and, as a result, FDA does not know the full extent of industry

compliance. FDA acknowledges that it has not yet identified and inspected

all firms subject to the ban. In terms of the public health risk, consumers

do not always know when foods and other products they use may contain

central nervous system tissue, which, according to scientific experts,

could pose a health risk if taken from diseased animals.

The economic impacts of a BSE outbreak in the United States could be

severe, according to federal economists. However, scientific experts

believe the health risks are uncertain. In terms of the economic impacts, if

BSE were discovered in U.S. cattle, beef exports and domestic beef

consumption would drop. The severity and duration of the economic

impact would depend largely on the number of animals affected, the U.S.

response, and the public’s reaction. We could not extrapolate the potential

impact on the U.S. economy by looking at the experiences of countries

Page 3 GAO-02-183 Mad Cow Disease

with BSE because perceptions about food safety risks vary from country

to country, and the economic impacts of BSE on one country might not be

applicable to another. Nonetheless, if BSE were found here, the economic

impact on the $56 billion beef industry could be devastating. Many

consumers might refuse to buy domestic beef; beef exports could decline

dramatically and sales in related industries—such as hamburger chains

and soup and frozen dinner manufacturers—could be similarly affected.

Concerning the health risks, if BSE-infected cattle were to enter the food

supply, some people might develop vCJD. However, experts disagree

about the number of people who would be affected. While many believe

that vCJD is very difficult to contract, so that relatively few people would

develop it, some experts believe that, because of the long incubation

period, no one can predict whether few or many might contract vCJD.

The United States acted as many as 5 years earlier than other countries to

impose controls over imports of animals and animal feed ingredients from

countries that had experienced BSE. Similarly, U.S. surveillance efforts to

test cattle brains for BSE met internationally recommended testing targets

earlier than other countries. However, the United States has a more

permissive feed ban than other countries—one that allows cattle feed to

contain proteins from horses and pigs. FDA is reviewing whether these

ingredients should continue to be allowed in cattle feed. Finally, as in most

countries that are BSE-free, including the United States, cattle brains and

other central nervous system tissue can be sold as human food.

This report makes recommendations to USDA and FDA to, among other

things, strengthen enforcement of the feed ban, develop a coordinated

strategy to identify resources needed to increase inspections of imported

goods, and alert consumers when products may contain central nervous

system tissue. In commenting on a draft of this report, FDA and Customs

concurred with our recommendations. USDA largely concurred but said

that labeling and warning statements should be reserved for known

hazards. ...

snip...full text 63 pages;

http://www.gao.gov/new.items/d02183.pdf

For Release on Delivery

Expected at 3:00 p.m. EST

Tuesday, March 30, 2004

FEDERAL FOOD SAFETY

AND SECURITY SYSTEM

Fundamental Restructuring

Is Needed to Address

Fragmentation and Overlap

Statement of Lawrence J. Dyckman, Director

Natural Resources and Environment

snip...

Page 12 GAO-04-588T

Multiple agencies must respond when serious food safety

challenges emerge. Inconsistent food safety authorities result in the need

for multiple agencies to respond to emerging food safety challenges. This

was illustrated recently with regard to ensuring that animal feed is free of

diseases, such as bovine spongiform encephalopathy (BSE), or mad cow

disease. A fatal human variant of the disease is linked to eating beef from

cattle infected with BSE. As we reported in 2002, four federal agencies are

responsible for overseeing the many imported and domestic products that

6USDA officials report that rulemaking for shell eggs will be separate from rulemaking for

egg products because shell egg packing facilities lack the capacity to respond to a Hazard

Analysis and Critical Control Point (HACCP) rule at present. USDA officials explain that

they will likely propose HACCP and sanitation performance standard regulations for egg

product plants, while shell egg facilities will likely receive guidance and training materials

related to HACCP and sanitation standards.

Page 13 GAO-04-588T

pose a risk of BSE. One, the U.S. Customs and Border Protection, screens

all goods entering the United States to enforce its laws and the laws of 40

other agencies. The second, USDA’s Animal and Plant Health Inspection

Service (APHIS), protects livestock from animal diseases by monitoring

the health of domestic and imported livestock.7 The third, USDA’s FSIS,

monitors the safety of imported and domestically produced meat and, at

slaughterhouses, tests animals prior to slaughter to determine if they are

free of disease and safe for human consumption. Finally, FDA monitors

the safety of animal feed—animals contract BSE through feed that

contains protein derived from the remains of diseased animals. During the

recent discovery of an infected cow in Washington state, FDA investigated

facilities that might have handled byproducts from the infected animal to

make animal feed. Figure 6 illustrates the fragmentation in the agencies’

authorities.

7On March 1, 2003, APHIS’s Agriculture Quarantine and Inspection force became part of the

Department of Homeland Security.

Page 14 GAO-04-588T

Figure 6: Federal Government Agencies Involved in Bovine Spongiform Encephalopathy (BSE) Oversight

When we issued our report in 2002, BSE had not been found in U.S. cattle.

However, we found a number of weaknesses in import controls. Because

of those weaknesses and the disease’s long incubation period—up to 8

years—we concluded that BSE might be silently incubating somewhere in

the United States. Then, in May 2003, an infected cow was found in

Canada, and in December 2003, another was found in the state of

Washington. USDA’s Animal and Plant Health Inspection Service operates

the surveillance program that found the infected U.S. cow, while FDA

must ensure that the disease cannot spread by enforcing an animal feed

ban that prohibits the use of cattle brains and spinal tissue, among other

things, in cattle feed. With regard to the meat from the BSE-infected

Page 15 GAO-04-588T

animal found in Washington state, FSIS conducted a recall of meat

distributed in markets in six states. Both USDA and FDA have reported

that meat from the cow was not used in FDA-regulated foods. However,

had the meat been used, for example, in canned soups that contained less

than 2 percent meat, FDA—not FSIS—would have been responsible for

working with companies to recall those foods. (As app. II shows, the

agencies’ oversight responsibilities for food products vary depending on

the amount of beef or poultry content.) Neither FDA nor USDA has

authority under existing food safety laws to require a company to recall

food products.8 Both agencies work informally with companies to

encourage them to initiate a recall, but our ongoing work shows that each

agency has different approaches and procedures. This can be confusing to

food processors involved in a recall. Overlapping responsibilities in

responding to mad cow disease highlight the challenges that government

and industry face when responding to the need to remove contaminated

food products from the market. As part of work currently underway, we

are looking at USDA and FDA food recalls—including USDA’s oversight of

the BSE-related recall and FDA’s oversight of the feed ban. We are also

monitoring both USDA’s and FDA’s BSE-response activities.

There are undoubtedly other federal food safety activities where overlap

and duplication may occur. For example, in the areas of food safety

research, public outreach, or both FDA, and USDA’s Economic Research

Service, FSIS and the Cooperative State Research, Education and

Extension Service have all received funding to develop food safety-related

educational materials for the public. In addition, responsibility for

regulating genetically modified foods is shared among FDA, USDA, and

the Environmental Protection Agency (EPA). However, we have not yet

examined the extent to which these and other areas of overlap and

duplication impact the efficiency of the food safety system.

8FDA, however, does have legislative authority to require recalls that involve infant

formula.

The fragmented legal and organizational structures of the federal food

safety system are now further challenged by the realization that American

farms and food are vulnerable to potential attack and deliberate

contamination. As we recently reported in a statement for the record

before the Senate Committee on Governmental Affairs,9 bioterrorist

attacks could be directed at many different targets in the farm-to-table

continuum, including crops, livestock, food products in the processing and

Emerging Terrorist

Threats Highlight the

Need to Reorganize

the Federal Food

Safety System

snip...

http://www.gao.gov/new.items/d04588t.pdf


FDA Statement
FOR IMMEDIATE RELEASE
Statement
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.

####


http://www.fda.gov/bbs/topics/news/2004/NEW01061.html

ooops!


>>>DR. SUNDLOF: Thank you again, Mr. Secretary. I don't have the insight to know what the Japanese government is going to do, based on what the feed rule or the proposed feed rule will convey. But the rule is very much risk-based. It uses the Harvard Risk Assessment to actually quantitate the risk and the risk reduction of the proposed measures that we will be publishing soon. And so I would agree with the Secretary that on the basis of science, the science is clearly laid out in the proposed rule and under a risk assessment that has undergone significant peer review by the scientific community. <<<

PLEASE NOTE, the Harvard BSE risk assessment was proven to be a sham, just like the June 2004 Enhanced BSE Surveillance Program was. THOSE 500,000 cattle that were suppose to be tested with proper up to date BSE/TSE testing protocols were terrible flawed. IN essence, the testing was meaningless. some 9,200 of those tests did not even include rapid testing or WB, only IHC, the least likely to find BSE/TSE, as Dr. Detwiler tried to point out in 2003 ;


USDA 2003

We have to be careful that we don't get so set in the way we do things that
we
forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain
stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did
not find lesions or PRP in the area of the obex. They found it in the
cerebellum and the cerebrum. It's a good lesson for us. Ames had to go
back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got
away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS
.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking
only at the brainstem. We may be missing certain things if we confine
ourselves to one area.


snip.............


Dr. Detwiler: It seems a good idea, but I'm not aware of it.
Another important thing to get across to the public is that the negatives
do not guarantee absence of infectivity. The animal could be early in the
disease and the incubation period. Even sample collection is so important.
If you're not collecting the right area of the brain in sheep, or if
collecting lymphoreticular tissue, and you don't get a good biopsy, you
could miss the area with the PRP in it and come up with a negative test.
There's a new, unusual form of Scrapie that's been detected in Norway. We
have to be careful that we don't get so set in the way we do things that we
forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain
stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did
not find lesions or PRP in the area of the obex. They found it in the
cerebellum and the cerebrum. It's a good lesson for us. Ames had to go
back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got
away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS
.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking
only at the brainstem. We may be missing certain things if we confine
ourselves to one area.


snip...


FULL TEXT;


Completely Edited Version
PRION ROUNDTABLE


Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado


THE JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM should be trashed, as with the BSE Minimal Risk Region (MRR) policy.

FACTS ;


GAO says US barriers to mad cow disease are full of holes
Robert Roos News Editor


Note: This story was updated March 1, 2002, to include additional information about recent federal actions to prevent mad cow disease.

Feb 28, 2002 (CIDRAP News) – Congress's General Accounting Office (GAO) concludes in a new report that the United States remains vulnerable to bovine spongiform encephalopathy (BSE), or mad cow disease, because of inadequate import barriers and weak enforcement of rules to contain any BSE-contaminated products that might reach US shores.

"The continuing absence of BSE in the United States today cannot be sufficiently ensured by current federal prevent efforts," states the report, released Feb 26. "The introduction and spread of BSE in the United States could stem from cattle and cattle-derived products from countries that subsequently developed BSE and from gaps in import controls, animal testing, and feed ban enforcement. As a result of these problems, consumers may unknowingly eat foods that contain central nervous system tissue from a diseased animal."

The report says that about 1,000 cattle and 125 million pounds of beef entered the United States from countries that later found cases of BSE. Further, hundreds of firms have violated a ban on putting meat and bone meal in cattle feed, and the Food and Drug Administration (FDA) has done little to enforce the ban, the GAO says.

The GAO investigated the government's BSE prevention efforts at the request of Sens. Tom Harkin, D-Iowa, Richard Lugar, R-Ind., and Dick Durbin, D-Ill. Durbin promised to introduce a bill to strengthen BSE prevention efforts. "We can't have the world's most reliable food supply without an equally reliable system of regulation and oversight," Durbin said in a Feb 26 news release.

Agriculture Secretary Ann Veneman took issue with the report on several counts, saying the GAO didn't fully consider recent actions that federal agencies have taken to strengthen BSE safeguards. She also said the GAO didn't appropriately recognize a Harvard University report issued last year that determined the risk of BSE in the United States to be very low.

Eating meat from animals with BSE is considered a risk factor for variant Creutzfeldt-Jakob disease in humans. BSE prevention steps in the United States began in 1989 with a ban on the importation of live ruminants (cattle, sheep, and goats) and ruminant meat and bone meal from the United Kingdom and other countries with BSE. In 1997 the ban was extended to the rest of Europe, and the FDA banned the use of most mammalian protein in feed for ruminants the same year. In addition, the FDA and the US Department of Agriculture (USDA) screen cattle-derived, FDA-regulated products imported from countries where BSE exists, the GAO report says.

Over the past 20 years, the nation imported about 1,000 cattle, 125 million pounds of beef, and 23 million pounds of inedible meat byproducts from countries where BSE was later found, the GAO determined. Some contaminated animals or products may have entered the country because BSE's incubation period is up to 8 years, the report says.

In particular, the nation imported 242 cattle from Japan between 1993 and 1999. After Japan reported its first BSE cases in September 2001, the USDA managed to locate most of the imported cattle, but 24 animals had already gone to slaughter or rendering.

"In addition to the BSE risk posed by past imports, a small but steady stream of BSE-risk material may still be entering the United States through international bulk mail," the GAO says. USDA inspectors at international bulk mail facilities can spot organic matter with special x-ray scanners, but inspectors are not on duty at all times and they can screen only a fraction of the stream of incoming packages, the report states. In a 6-month period last year, 570 of 116,000 packages screened at one facility contained "at-risk beef or beef-derived products."

Risky items also can slip through federal ports of entry when shipments are inaccurately labeled or through lack of inspection, the GAO reported. For example, sampling by the US Customs Service in fiscal 1999 showed that information on beef shipments was wrong in over 21% of cases. Further, in fiscal year 2000 the FDA inspected only 1% of the 4 million imported food entries under its jurisdiction and less than 1% of the 146,000 shipments of animal drugs and feeds.

BSE prevention efforts also include USDA testing of cattle tissue. The GAO says the USDA has increased its testing program but does not test many cattle that die on farms, which are assumed to pose an increased risk because they are usually older and often die of unknown causes. Some cattle that die on farms are collected and rendered into products that include animal feed, the report says.

The GAO finds serious fault with the FDA's enforcement of the ban on mammalian protein in cattle feed. Since 1997, FDA and state personnel have conducted more than 12,000 inspections at more than 10,576 firms (eg, renderers, feed mills) and found 364 firms in violation, the report states. The FDA estimates that at least another 1,200 firms that should be subject to the ban have not been identified.

"FDA did not take prompt enforcement action to compel firms to comply with the feed ban," the GAO says. By April 2001 (when the GAO investigation began), the agency's only enforcement steps had been to issue two warning letters, though the pace picked up after that. Several firms repeatedly violated the rules but did not receive warning letters. Further, the FDA has no overall enforcement strategy that sets penalties and deadlines.

"Even if FDA were to actively enforce the federal ban, its inspection database is so severely flawed that—until corrected—it should not be used to assess compliance," the report says. It includes a long list of problems with the database; for example, entries for about 45% of all inspections lack information to uniquely identify the firms inspected.

In other findings, the GAO concluded that the United States acted as much as 5 years earlier than other countries to bar imports of animals and animal feed ingredients from countries with BSE cases. However, the nation has a "more permissive" feed ban than other countries in that cattle feed can contain protein from horses and pigs. The FDA is currently reviewing this provision, the report notes.

The report recommends a number of steps to address the problems it describes. Among other things, it suggests that the secretary of agriculture consider using public service announcements or labels to inform consumers that certain beef cuts and products may contain central nervous system (CNS) tissue. The GAO also suggests that the FDA consider requiring labeling of regulated products, including food, cosmetics, and drugs, that contain CNS tissue.

Agriculture Secretary Veneman critiqued the GAO report in a statement released the same day (Feb 26). "The report fails to appropriately recognize the conclusions and recommendations made last year by Harvard University in its comprehensive, 3-year study on BSE," she said. "The Harvard Risk Analysis showed that the risk of BSE occurring in the Untied States is extremely low and that early government protection systems have been largely responsible for keeping BSE out of the United States and would prevent it from spreading if it ever did enter the country."

Veneman also said that despite extensive USDA comments on the draft report, "scientific and technical errors" survived in the final report. Further, the report "does not appropriately consider the additional actions that have been taken by federal agencies to strengthen BSE programs," she added.

The USDA described a number of recent actions related to BSE in a separate news release (see link below). That release says the FDA has "significantly improved" its database on firms' compliance with the animal feed rule. The improved database will be fully operational in April and will allow the FDA to track compliance more effectively, officials said. In addition, the FDA is receiving an extra $15 million for BSE prevention efforts this year, bringing the total to $19 million, and is hiring 115 people this year to help in those efforts.

The USDA also issued a set of responses to the recommendations in the GAO report. The agency rejected the idea of labeling beef and beef products that may contain CNS tissue, stating, "The presence of CNS tissue does not mean that the product is infectious for BSE. Labeling and warning statements should be reserved for known hazards."

In response to another GAO recommendation, the USDA said it is already increasing its testing of tissue samples from animals that die on farms. The agency said that the number of cattle brains tested this year will be more than double last year's total, and that "A focus of this increased surveillance is to obtain more samples from animals that die on farms."

Regarding the Harvard study of BSE risk in the United States, the GAO report says the agency did not try to validate the model or assumptions used by the Harvard researchers. However, the report says the Harvard authors acknowledged that their conclusions "could be influenced by a number of model assumptions that could not be verified with confidence—including assumptions about US measures to prevent the introduction and spread of BSE." The Harvard researchers also noted that compliance with the animal feed ban is the leading source of uncertainty in their assessment, the GAO report states. ...

http://www.cidrap.umn.edu/cidrap/content/other/bse/news/gaorept.html


ANOTHER very important documentation of the facts of the lack of enforcement and knowledge of the 8/4/97 partial and voluntary ruminant to ruminant feed ban was the BSE JAN. 9, 2001 EMERGENCY 50 STATE CONFERENCE CALL, which does not seem to be available on the www. but it happened ;

-------- Original Message --------
Subject: BSE JAN. 9, 2001 EMERGENCY 50 STATE CONFERENCE CALL
Date: Tue, 5 Apr 2005 12:01:37 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@KALIV.UNI-KARLSRUHE.DE


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

Greetings,

I was doing a bit of digging this morning and can not for the life
of me find this transcript of the ;

> BSE JAN. 9, 2001 EMERGENCY 50 STATE CONFERENCE CALL


I know it took place, because I participated in it.

IF you go here ;

http://www.fda.gov/cvm/bse_updates.htm

skroll down to ;

UPDATE ON RUMINANT FEED (BSE) ENFORCEMENT ACTIVITIES
(January 10, 2001 )

http://www.fda.gov/cvm/bseup.htm

YOU will see (above url) the 'day after' report, once the NY TIMES
broke the story, but no 'TRANSCRIPT' of the actual conference
call. WHAT i found most disturbing about the call was that many knew
nothing of the 8/4/97 ruminant-to-ruminant feed ban, some 4 years
after the fact ;

> On Thursday, the Food and Drug Administration reported that hundreds
> of feed manufacturers and rendering companies were not complying with
> regulations intended to ensure the safety of domestically produced feed.


snip...

> On Jan. 9, the F.D.A.'s Center for Veterinary Medicine held a
> nationwide telephone conference with its field officers and 50 state
> agencies responsible for inspecting feed producers. The agency told
> the states that only about 2,700 of the estimated 9,500 feed
> manufacturers had been inspected for compliance, the center's
> director, Dr. Stephen Sundlof, said.


http://muhammadfarms.com/Mad%20Cows%20in%20US.htm#More


I remember old deepthroat mentioning something about this ???


DEEPTHROAT ;

snip...


For you: make sure you have no attachment to my email
or any reference...use at your discretion...the below
info:

IMPORTANT NOTICE: 50 STATE CONFERENCE CALL - BSE

TUESDAY, JANUARY 9, 2001
1:00-2:00 PM EST CALL - (1-888-273-9887)

A special "50 STATE CONFERENCE CALL" to discuss BSE
(Bovine Spongiform Encephalopathy) issues for Food and Drug
Administration (FDA) regulated animal feed products in the United
States and imported animal feeds. The conference call will
discuss the FDA proposed response to the current BSE issue and the
assistance needed from state feed and agriculture programs. THIS
ISSUE MAY IMPACT ALL STATES AND ALL ANIMAL FEED
AND PRODUCTION INDUSTRIES.

The 50 State call is scheduled for Tuesday, January
9, 2001 from 1:00-2:00 pm EST. Any state agency responsible for
animal feed issues wishing to participate should call
1-888-273-9887 and ask to be connected to the "50 State BSE Call". The
conference host operator will explain how to participate, including
asking questions during the call. If possible, please coordinate
within your state to utilize only one phone line per state agency.

We request that you forward this message to your
agency management and feed coordinators or other agencies or departments
who may be responsible for any animal feed issues related to FDA
regulated products.

The agenda will be as follows:

1. Center For Veterinary Medicine (FDA) - Discussion
of the problem related to BSE events in Europe and the impact on US
feed ingredients for animals and feed operations. Discussion of the
proposed actions/ inspections/compliance of licensed and unlicensed feed
mills, commercial feed manufacturers, animal feed imports, renderer's,
protein blenders, on-farm mixers, and ruminant feeders.

2. Office of Regional Operations (FDA) - Discussion
of contracting/ working with states to inspect the universe of feed
mills/industry for "Animal Proteins Prohibited from Use in Animal
Feed". Discussion of working with FDA field offices.

3. Questions and answers.


Richard H. Barnes, Director
Division of Federal-State Relations (HFC-150)
5600 Fishers Lane Room 1207
Rockville, Md. 20857
ph: (301) 827-6906 FAX: (301) 443-2143
Email: RBARNES@ORA.FDA.GOV

____________________________________________________________
>From - Fri Jan 12 08:23:56 2001
Thu Jan 11 21:34:25 2001
Return-Path: snip...
for ; Thu, 11 Jan 2001 21:34:25 -0600

Date: Fri, 12 Jan 2001 03:34:26 +0000 (GMT)
From:
Subject: confidential
To: flounder@wt.net


Sorry did not get back to you. (Ran out of time!!)

Of interest...don't repeat. On Jan 9, was somewhere
and not able to tie into conference call. Was around
an official who should have been on conference
call..another person with me also remembered it and we
both inquired as to how the call went. Was told (to
both of us) that the call had been cancelled!! (Told
us several times that the call was cancelled and they
did not know why!!!) I will try to find out why this
person said that...maybe they got off the call or they
were told to tell everyone that the call was
cancelled.
You need to POST your interaction with the conference
call on a web site....let me know when you do...I will
present this fact to the official who may have lied.
See what they have to say...but need to have the
information POSTED to a web site...send me the address
and make sure you don't mind that I give it to this
very questionable person....There must be a reason for
the lying....??? Surely people who are really
interested will found out what went on? There are
quite a few people who listened in and declined to
identify or acknowledge that they listened in...why
the big secrecy or this person may have been told to
do this. Need to know!!! Something dirty is going
on...some sort of treachery seems to be in the
works...
Not a good situation for me right now...wish I could
tell you more as to what is going on...but too
dangerous right now...got to sort it out.
Later in ....................

snip.......

Another piece of information for you only: Ray
Bradley has been lying throug his teeth for years
(UK). I would not believe one word of what he says.
He has been well paid and taken care of for his SS
role in the BSE nightmare. He will say what he is
supposed to say until his dying day.........don't put
a single ounce of trust in anything he has related or
reported. He will pay the piper for all the misery he
has caused in this life...at the least in the next life....

____________________________________________________________


>From - Sun Jan 21 20:01:42 2001
Received: by sys44.hou.wt.net (mbox flounder)
snip... Sun, 21 Jan 2001 17:50:32 -0600
Date: Sun, 21 Jan 2001 23:50:31 +0000 (GMT)
From: snip...
To: "Terry S. Singeltary Sr."

Confidential:
Budget: let me know what you find out and the
breakdown. There may be some stuff stuffed into it
which is not legit... They may figure some salaries
and such...the real gist of the matter is the shocking
amount of $ that is actually used to "ferret" out the
disease and the $ that are used to P.R. the whole
affair and give appearance of being concerned and
involved...again it was said years ago and it should
be taken seriously....BSE will NEVER be found in the
US!
As for the BSE conference call...I think you did a
great service to freedom of information and making
some people feign integrity...I find it scary to see
that most of the "experts" are employed by the federal
government or are supported on the "teat" of federal
funds. A scary picture!
I hope there is a confidential panel organized by the
new government to really investigate this thing. I
am sure you have seen the whitewash of the Gulf War
Syndrome that was released last Dec. There was a
senate investigation which actually showed the true
extent of the coverup...over 100,000 medical records
missing!!! but it all died down...
There is someone who is rather innovative and free
thinking...a Dr. Rohrer, Roerer, something like that,
who was at Baltimore VA Hospital doing research on
BSE. He was the first to advocate the blood supply
being contaminated. Talk about being shut off...in
the shades of Richard Marsh...he lost some funding,
but seemed to persevere in spite of the attacks. I
saw his names mentioned recently on something through
the FDA. Contact: Baltimore, Maryland, Veteran's
Administration Hospital, Research section, his name
should be there. ......... snip

What a mess! Seems like the time is ripe for everyone
to cover their ass and start screaming...not me, not
me, not my job, etc. etc. We gotta get some big scary
folks more involved in this mess. ............. snip

You need to watch your back........but keep picking at
them.......like a buzzard to the bone...you just may
get to the truth!!!
(You probably have more support than you know. Too
many people are afraid to show you or let anyone else
know. I have heard a few things myself...you ask the
questions that everyone else is too afraid to ask.)

____________________________________________________________


GREETINGS again list members,

MY question I suppose is, WHERE is the official TRANSCRIPT in full, of the
January 9, 2001 50 STATE EMERGENCY CONFERENCE CALL located at ???

WHY is this transcipt not easily available for the public on some URL,
or is it somewhere
I have over looked ???


HERE are my notes of this January 9, 2001 50 STATE EMERGENCY BSE
CONFERENCE CALL


TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########


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

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

Greetings List Members,

I was lucky enough to sit in on this BSE conference
call today and even managed to ask a question.
that is when the trouble started.

I submitted a version of my notes to
Sandra Blakeslee of the New York Times,
whom seemed very upset, and rightly
so.

"They tell me it is a closed meeting and
they will release whatever information
they deem fit. Rather infuriating."

and i would have been doing just fine,
until i asked my question. i was surprised
my time to ask a question so quick.

(understand, these are taken from my notes for now.
the spelling of names and such could be off.)

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

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

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

[host Richard]
could you repeat the question?

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

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

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

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

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

[not sure whom speaking]
NO

from this point, i was still connected, got to listen
and tape the whole conference. at one point someone
came on, a woman, and ask again;

[unknown woman]
what group are you with?

[TSS]
CJD Watch and my Mom died from hvCJD
we are trying to tract down CJD and other
human TSE's world wide. i was invited to
sit in on this from someone inside the USDA/APHIS
and that is why i am here. do you intend on banning
me from this conference now?

at this point the conference was turned back up,
and i got to finish listening. They never answered
or even addressed my one question, or even addressed
the issue. BUT, i will try and give you a run-down
for now, of the conference.

IF i were another Country, I would take heed to my
notes, BUT PLEASE do not depend on them. ask for
transcript from;

RBARNS@ORA.FDA.GOV
301-827-6906

he would be glad to give you one ;-)

Rockville Maryland,
Richard Barns Host

BSE issues in the U.S.,
How they were labelling ruminant feed?
Revising issues.

The conference opened up with the explaining of
the U.K. BSE epidemic winding down with about 30
cases a week.

although new cases in other countries were now
appearing.

Look at Germany whom said NO BSE and now have BSE.

BSE increasing across Europe.

Because of Temporary Ban on certain rendered product,
heightened interest in U.S.

A recent statement in Washington Post, said the
New Administration (old GW) has a list of issues.
BSE is one of the issues.

BSE Risk is still low, minimal in U.S. with a greater
interest in MBM not to enter U.S.

HOWEVER, if BSE were to enter the U.S.
it would be economically disastrous
to the render, feed, cattle, industries,
and for human health.

(human health-they just threw that in cause i was listening. I will now
jot down some figures in
which they told you, 'no need to write them down'.
just hope i have them correct. hmmm, maybe i hope
i don't ???)

80% inspection of rendering

*Problem-Complete coverage of rendering HAS NOT
occurred.

sizeable number of 1st time FAILED INITIAL INSPECTION,
have not been reinspected (70% to 80%).

Compliance critical, Compliance poor in U.K.
and other European Firms.

Gloria Dunason
Major Assignment 1998 goal TOTAL compliance.
This _did not_ occur. Mixed level of compliance,
depending on firm.

Rendering FDA license and NON FDA license

system in place for home rendering & feed
76% in compliance
79% cross contamination
21% DID NOT have system
92% record keeping
less than 60% total compliance

279 inspectors
185 handling prohibited materials

Renderer at top of pyramid, significant
part of compliance.
84% compliance

failed to have caution statement render
72% compliance & cross contamination
caution statement on feed, 'DO NOT FEED TO CATTLE'

56 FIRMS NEVER INSPECTED

1240 FDA license feed mills
846 inspected

"close to 400 feed mills have not been inspected"

80% compliance for feed.

10% don't have system.

NON-FDA licensed mills
There is NO inventory on non licensed mills.
approximately 6000 to 8000 Firms ???
4,344 ever inspected.
"FDA does not have a lot of experience with"

40% do NOT have caution statement 'DO NOT FEED'.

74% Commingling compliance

"This industry needs a lot of work and only half
gotten to"

"700 Firms that were falitive, and need to be
re-inspected, in addition to the 8,000 Firms."

Quote to do BSE inspection in 19 states by end
of January or 30 days, and other states 60 days.
to change feed status??? Contract check and ask
questions and pass info.

At this time, we will take questions.

[I was about the third or fourth to ask question.
then all B.S.eee broke loose, and i lost my train
of thought for a few minutes. picked back up here]

someone asking about nutritional supplements and
sourcing, did not get name. something about inspectors
not knowing of BSE risk??? the conference person assuring that Steve
Follum? and the TSE advisory Committee were
handling that.

Some other Dr. Vet, whom were asking questions
that did not know what to do???

[Dennis Wilson]
California Food Agr.
Imports, are they looking at imports?

[Conference person]
they are looking at imports,
FDA issued imports Bulletin.

[Linda Singeltary ??? this was a another phone in
question, not related i don't think]
Why do we have non-licensed facilities?

(conference person)
other feed mills do not handle as potent drugs???

Dennis Blank, Ken Jackson
licensed 400
non FDA 4400 inspected of a total of 6000 to 8000,

(they really don't know how many non licensed Firms
in U.S. they guess 6000 to 8000??? TSS)

Linda Detwiler
asking everyone (me) not to use emergency BSE number,
unless last resort.
(i thought of calling them today, and reporting the
whole damn U.S. cattle herd ;-) 'not'

Warren-Maryland Dept. Agr.
Prudent to re-inspect after 3 years.
concerned of Firms that have changed
owners.

THE END

TSS

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

FROM New York TIMES

Subject: Re: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA
Posting of cut version...
Date: Thu, 11 Jan 2001 22:02:47 -0700
From: "Sandy Blakeslee"
To: "Terry S. Singeltary Sr."
References: 1

Hi terry -- thanks for all your help. I know it made a difference with
the FDA getting out that release.

----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Thursday, January 11, 2001 2:06 PM
Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA
Posting of cut version...

> http://www.vegsource.com/talk/madcow/messages/8219.html

> http://www.vegsource.com/talk/madcow/messages/8220.html

> http://www.vegsource.com/talk/madcow/messages/8221.html

> http://www.vegsource.com/talk/madcow/messages/8222.html

> http://www.vegsource.com/talk/madcow/messages/8230.html

> hi sandy,

>From the New York Times NYTimes.com, January 11, 2001

Many Makers of Feed Fail to Heed Rules on Mad Cow Disease
By SANDRA BLAKESLEE

Large numbers of companies involved in manufacturing animal feed are not
complying with regulations meant to prevent the
emergence and spread of mad cow disease in the United States, the Food
and Drug Administration said yesterday.

The widespread failure of companies to follow the regulations, adopted
in August 1997, does not mean that the American food supply is unsafe,
Dr. Stephen Sundlof, director of the Center for Veterinary Medicine at
the F.D.A., said in an interview.

But much more needs to be done to ensure that mad cow disease does not
arise in this country, Dr. Sundlof said.

The regulations state that feed manufacturers and companies that render
slaughtered animals into useful products generally may not feed mammals
to cud-chewing animals, or ruminants, which can carry mad cow disease.

All products that contain rendered cattle or sheep must have a label
that says, "Do not feed to ruminants," Dr. Sundlof said. Manufacturers
must also have a system to prevent ruminant products from being
commingled with other rendered material like that from chicken, fish or
pork. Finally, all companies must keep records of where their products
originated and where they were sold.

Under the regulations, F.D.A. district offices and state veterinary
offices were required to inspect all rendering plants and feed mills to
make sure companies complied. But results issued yesterday demonstrate
that more than three years later, different segments of the feed
industry show varying levels of compliance.

Among 180 large companies that render cattle and another ruminant,
sheep, nearly a quarter were not properly labeling their products and
did not have a system to prevent commingling, the F.D.A. said. And among
347 F.D.A.-licensed feed mills that handle ruminant materials - these
tend to be large operators that mix drugs into their products - 20
percent were not using labels with the required caution statement, and
25 percent did not have a system to prevent commingling.

Then there are some 6,000 to 8,000 feed mills so small they do not
require F.D.A. licenses. They are nonetheless subject
to the regulations, and of 1,593 small feed producers that handle
ruminant material and have been inspected, 40 percent
were not using approved labels and 25 percent had no system in place to
prevent commingling.

On the other hand, fewer than 10 percent of companies, big and small,
were failing to comply with the record-keeping
regulations.

The American Feed Industry Association in Arlington, Va., did not return
phone calls seeking comment.

http://www.nytimes.com/2001/01/11/science/11COW.html

Subject:
USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL
Jan. 9, 2001
Date:
Wed, 10 Jan 2001 14:04:21 -0500
From:
"Gomez, Thomas M."
Reply-To:
Bovine Spongiform Encephalopathy
To:
BSE-L@uni-karlsruhe.de


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

USDA/APHIS would like to provide clarification on the following point
from
Mr. Singeltary's 9 Jan posting regarding the 50 state conference call.

[Linda Detwiler asking everyone (me) not to use emergency BSE number,
unless
last resort. (i thought of calling them today, and reporting the whole
damn
U.S. cattle herd ;-) 'not']

Dr. Detwiler was responding to an announcement made during the call to
use
the FDA emergency number if anyone wanted to report a cow with signs
suspect
for BSE. Mr. Singeltary is correct that Dr. Detwiler asked participants
to
use the FDA emergency number as a last resort to report cattle suspect
for
BSE. What Mr. Singeltary failed to do was provide the List with Dr.
Detwiler's entire statement. Surveillance for BSE in the United States
is a
cooperative effort between states, producers, private veterinarians,
veterinary hospitals and the USDA. The system has been in place for
over 10
years. Each state has a system in place wherein cases are reported to
either the State Veterinarian, the federal Veterinarian in Charge or
through
the veterinary diagnostic laboratory system. The states also have
provisions with emergency numbers. Dr. Detwiler asked participants to
use
the systems currently in place to avoid the possibility of a BSE-suspect
report falling through the cracks. Use of the FDA emergency number has
not
been established as a means to report diseased cattle of any nature.

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

Subject:
Re: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE
CALL Jan.9, 2001
Date:
Wed, 10 Jan 2001 13:44:49 -0800
From:
"Terry S. Singeltary Sr."
Reply-To:
Bovine Spongiform Encephalopathy
To:
BSE-L@uni-karlsruhe.de
References:
1


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

Hello Mr. Thomas,

> What Mr. Singeltary failed to do was provide
> the List with Dr. Detwiler's entire statement.

would you and the USDA/APHIS be so kind as to supply
this list with a full text version of the conference
call and or post on your web-site?
if so when, and thank you.
if not, why not?

> The system has been in place for over 10 years.

that seems to be a very long time for a system to be in
place, and only test 10,700 cattle from some 1.5 BILLION head (including
calf crop). Especially since French
are testing some 20,000 weekly and the E.U. as a whole,
are testing many many more than the U.S., with less
cattle, same risk of BSE/TSEs.

Why does the U.S. insist on not doing massive testing
with the tests which the E.U. are using?
Why is this, please explain?

Please tell me why my question was not answered?

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

It was a very simple question, a very important
question, one that pertained to the topic of
BSE/feed, and asked in a very diplomatic way.
why was it not answered?

If all these years, we have been hearing that
pharmaceutical grade bovines were raised for
pharmaceuticals vaccines etc. But yet the
USA cannot comply with feed regulations of
the ruminant feed ban, PLUS cannot even
comply with the proper labelling of the feed,
cross contamination etc.
Then how in the world can you Guarantee the feed
fed to pharmaceutical grade bovine, were actually
non ruminant feed?

Before i was ask to be 'disconnected',
i did hear someone in the background
say 'we can't'-- have him ask the question again.

could you please be so kind, as to answer these
questions?

thank you,
Terry S. Singeltary Sr. Bacliff, Texas USA

P.S. if you will also notice, i did not post that
emergency phone number and do not intend on passing
it on to anyone. I was joking when i said i should
call and report the whole damn U.S. Herd. So please
pass that on to Dr. Detwiler, so she can rest easily.

BUT, they should be reported, some are infected with TSE.
The U.S. is just acting as stupid as Germany and other
Countries that insist they are free of BSE.

TSS

Subject: Report on the assessment of the Georgraphical BSE-risk of the
USA July 2000 (not good)
Date: Wed, 17 Jan 2001 21:23:51 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

Greetings List Members and ALL EU Countries,

Because of this report, and the recent findings
of the 50-state BSE Conference call, I respectfully
seriously suggest that these Countries and the SSC
re-evaluate the U.S.A. G.B.R. to a risk factor of #3.

I attempted to post this to list in full text,
but would not accept...

thank you,
kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA


Report on the assessment of the Geographical BSE-risk of the USA
July
2000

PART II

REPORT ON THE ASSESSMENT OF THE GEOGRAPHICAL BSE
RISK OF THE UNITED STATES OF AMERICA

- 29 -

Report on the assessment of the Geographical BSE-risk of the USA
July
2000

EXECUTIVE SUMMARY

OVERALL ASSESSMENT

The current geographical BSE-risk (GBR) level is II, i.e. it is unlikely
but cannot be excluded that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent.

Stability: Before 1990 the system was extremely unstable because feeding
of MBM to cattle happened, rendering was inappropriate with regard to
deactivation of the BSE-agent and SRM and fallen stock were rendered for
feed. From 1990 to 1997 it improved to very unstable, thanks to efforts
undertaken to trace imported animals and exclude them from the feed
chain and intensive surveillance. In 1998 the system became neutrally
stable after the RMBM-ban of 1997.

External challenges: A moderate external challenge occurred in the
period before 1990 because of importation of live animals from
BSE-affected countries, in particular from the UK and Ireland. It cannot
be excluded that some BSE-infected animals have been imported by this
route and did enter the US rendering and feed production system. The
efforts undertaken since 1990 to trace back UK-imported cattle and to
exclude them from the feed chain reduced the impact of the external
challenge significantly.

Interaction of external challenges and stability: While extremely
unstable, the US system was exposed to a moderate external challenge,
mainly resulting from cattle imports from the UK. It can not be excluded
that BSE-infectivity entered the country by this route and has been
recycled to domestic cattle. The resulting domestic cases would have
been processed while the system was still very unstable or unstable and
would hence have initiated a number of second or third generation cases.
However, the level of the possible domestic prevalence must be below the
low detection level of the surveillance in place.

As long as there are no changes in stability or challenge the
probability of cattle to be (pre-clinically or clinically) infected with
the BSE-agent will remain at the current level.

JUSTIFICATION

1. DATA

The available information was suitable to carry out the GBR risk
assessment.

- 30 -

Report on the assessment of the Geographical BSE-risk of the USA
July
2000

2. STABILITY

2.1 Overall appreciation of the ability to identify BSE-cases and to
eliminate animals at risk of being infected before they are processed

· Before 1989, the ability of the system to identify (and
eliminate) BSE cases was limited.
· Since 1990 this ability is significantly improved, thanks to a
good BSE-surveillance and culling system (contingency plan).
· Today the surveillance should be able to detect clinical
BSE-cases within the limits set by an essential passive surveillance
system, i.e. some cases might remain undetected.

2.2 Overall appreciation of the ability to avoid recycling
BSE-infectivity, should it enter processing

· Before 1997 the US rendering and feed producing system would not
have been able to avoid recycling of the BSE agent to any measurable
extent. If the BSE-agent was introduced the feed chain, it could
probably have reached cattle.
· After the introduction of the RMBM-to-ruminants-ban in August
1997 the ability of the system to avoid recycling of BSE-infectivity was
somewhat increased. It is still rather low due to the rendering system
of ruminant material (including SRM and fallen stock) and the persisting
potential for cross-contamination of cattle feed with other feeds and
hence RMBM.

2.3 Overall assessment of the Stability

· Until 1990 the US BSE/cattle system was extremely unstable as
RMBM was commonly fed to cattle, the rendering system was not able to
reduce BSE-infectivity and SRM were rendered. This means that incoming
BSE infectivity would have been most probably recycled to cattle and
amplified and the disease propagated.
· Between 1990 and 1995 improvements in the BSE surveillance and
the efforts to trace back and remove imported cattle gradually improved
the stability but
the system remained very unstable.
In 1998 the system became unstable because of an RMBM-ban introduced in
1997. After 1998 the ban was fully implemented and the system is
regarded to be neutrally stable since 1998. The US system is therefore
seen to neither be able to amplify nor to reduce circulating or incoming
BSE-infectivity.

3. CHALLENGES

A moderate external challenge occurred in the period 1980-1989 because
of importation of live animals from the UK. imports from other countries
are regarded to have been negligible challenges.
· As a consequence of this external challenge, infectivity could
have entered the feed cycle and domestic animals could have been exposed
to the agent. These domestic BSE-incubating animals might have again
entered processing, leading to an internal challenge since 1991.
· This internal challenge could have produced domestic cases of
BSE, yet prevalence levels could have been below the detection limits of
the surveillance system until now. (According to US calculations, the
current surveillance

-31 -

Report on the assessment of the Geographical BSE-risk of the USA July
2000

system could detect clinical incidence of 1-3 cases per year per million
adult cattle, i.e. in absolute numbers 43-129 cases per year). Between
1990 und 1995, with the exclusion of the imported animals from Europe
from the feed chain, the effect of the external challenges decreased.

4. CONCLUSION ON THE RESULTING RISKS

4.1 Interaction of stability and challenqe

· In the late 80s, early 90s a moderate external challenges met an
extremely unstable system. This would have amplified the incoming
BSE-infectivity and propagated the disease.
· With the exclusion of the imported animals from Europe from the
feed chain between 1990 and 1995 the effect of the external challenge
decreased.
· Before 1998 an internal challenge, if it developed, would have
met a still unstable system (inappropriate rendering, no SRM ban, RMBM
ban only after 1997) and the BSE-infectivity could have been recycled
and amplified.
· After 1998 the neutrally stable system could still recycle the
BSE-agent but due to the RMBM-ban of 1997 the BSE-infectivity
circulating in the system would probably not be amplified.

4.2 Risk that BSE-infectivity enters processing

· A very low processing risk developed in the late 80s when the
UK-imports were slaughtered or died. It increased until 1990 because of
the higher risk to be infected with BSE of cattle imported from the UK
in 1988/89, as these animals could have been processed prior to the
back-tracing of the UK-imports in 1990.
· From 1990 to 1995 a combination of surviving non-traced UK
imports and some domestic (pre-)clinical cases could have arrived at
processing resulting in an assumed constant low but non-negligible
processing risk.
· After 1995 any processing risk relates to assumed domestic cases
arriving at processing.
· The fact that no domestic cases have been shown-up in the
BSE-surveillance is reassuring - it indicates that BSE is in fact not
present in the country at levels above the detection limits of the
country's surveillance system. This detection level has been calculated
according to US-experts to be between 1 & 3 clinical cases per million
adult cattle per year.

Note: The high turnover in parts of the dairy cattle population with a
young age at slaughter makes it unlikely that fully developed clinical
cases would occur (and could be detected) or enter processing. However,
the theoretical infective load of the pre-clinical BSE-cases that
under this scenario could be processed, can be assumed to remain
relatively low.

4.3 Risk that BSE-infectivity is recycled and propagated

· During the period covered by this assessment (1980-1999) the
US-system was not able to prevent propagation of BSE should it have
entered, even if this ability was significantly improved with the
MBM-ban of 1997.
· However, since the likelihood that BSE-infectivity entered the
system is regarded to be small but non-negligible, the risk that
propagation of the disease
took place is also small but not negligible.

- 32 -

Report on the assessment of the Geographical BSE-risk of the USA
July
2000

5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK

5.1 The current GBR

The current geographical BSE-risk (GBR) level is II, i.e. it is unlikely
but cannot be excluded that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent.

5.2 The expected development of the GBR

As long as there are no changes in stability or challenge the
probability of cattle to be (pre-clinically or clinically) infected with
the BSE-agent remains at the current level.

5.3 Recommendations for influencin.q the future GBR

· As long as the stability of the US system is not significantly
enbanced above neutral levels it remains critically important to avoid
any new external
challenges.
· All measures that would improve the stability of the system, in
particular with regard to its ability to avoid recycling of the
BSE-agent should it be present in the cattle population, would reduce,
over time, the probability that cattle could be infected with the
BSE-agent. Possible actions include:
removal of SRMs and/or fallen stock from rendering, better rendering
processes, improved compliance with the MBM-ban including control and
reduction of cross-contamination.
· Results from an improved intensive surveillance programme,
targeting at risk sub-populations such as adult cattle in fallen stock
or in emergency slaughter, could verify the current assessment.

snip...

FULL TEXT about 16 pages

http://www.vegsource.com/talk/madcow/messages/8278.html

http://www.vegsource.com/talk/madcow/messages/8279.html

http://www.vegsource.com/talk/madcow/index.html

to keep up with this epidemic in both humans and animals,
one that will be with us for years to come, and soon will explain the
many demented people in the U.S.,
please go to;

BSE NEWS


http://www.vegsource.com/talk/madcow/index.html


CJD WATCH


http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm


CJD WATCH MESSAGE BOARD


http://disc.server.com/Indices/167318.html


Moms death from hvCJD

http://www.vegsource.com/talk/madcow/messages/7252.html


'MOMS AUTOPSY REPORT'

http://www.vegsource.com/talk/madcow/messages/7548.html


CJD/BSE aka madcow disease in the U.S., please let me count the Ways$$$
PLEASE READ THIS...

http://www.whale.to/v/cjd2.html


SOMETHING TO CHEW ON

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2

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


http://www.vegsource.com/talk/madcow/messages/8278.html


My submission to the MEETING OF PRION GODS,
on Jan. 18/19 2001

http://www.InsideTheWeb.com/messageboard/mbs.cgi?acct=mb172420&MyNum=978977689&P=No&TL=978977689

this message will self destruct in 10 seconds ;-)

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


BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001

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

NOW, just what about that Harvard BSE risk assessment, the IHC gold standard of BSE immunity in the USA (more BSeee) ;

HARVARD PEER REVIEW OF BSE RISK ASSESSMENT

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

Final Report
Prepared for
U.S. Department of Agriculture
Food Safety and Inspection Service
Office of Public Health and Science
Prepared by
RTI
Health, Social, and Economics Research
Research Triangle Park, NC 27709
RTI Project Number 07182.024
RTI Project Number
07182.024
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
RTI
Health, Social, and Economics Research
Research Triangle Park, NC 27709
Contents
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
Emphasized? ..................................................................... 3-4
3.3 Are All Input Data Used in the Model Valid and
Appropriate? ................................................................... 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
iii
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
Appendixes
A Reviewers’ Professional Experience.................................... A-1
B Model Outputs.................................................................. B-1

snip...

Introduction
At the request of the U.S. Department of Agriculture, RTI asked
three experts to review the Bovine Spongiform Encephalopathy
(BSE) risk assessment conducted by the Harvard Center for Risk
Analysis, Harvard School of Public Health, and the Center for
Computational Epidemiology, College of Veterinary Medicine,
Tuskegee University (H-T BSE study).
1.1 REVIEWERS
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.
1-1
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
Analysis.
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
Team”).
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
1-2
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.

snip...

2.2 OVERALL WEAKNESSES OF THE MODEL
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
2-2
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.”

snip...

3.2 HAVE THE DATA BEEN CORRECTLY
INTERPRETED AND EMPHASIZED?
1) The H-T BSE study authors have done their best to
incorporate the existing data in their estimates of the parameters
selected for inclusion in the model. Not much hard data exist that
could be used directly for setting parameter values. Therefore, the
authors used indirect data to justify logical arguments for setting a
parameter to a particular range of values. The authors may have
included some factors in their model simply because some indirect
data could be found.
The reviewers had concerns that the importance of some parameters
has been overestimated and others underestimated.
2) A rather optimistic choice was made in case of doubt or
insufficient hard evidence or data. These concerns relate to overall
model weaknesses in the general comments section. In the
summary section, on Pages 98 and 99, several of the main issues
that involve assumptions that cannot be verified with confidence are
discussed, and several of them could serve as perfect examples of
what has been argued here, that optimistic choices for favorable
3-4
Section 3 — Identification of Data and Critical Evaluation of Evidence
outcome or reassuring nuances are presented (e.g., the
implementation rates, the “remote chance that an infected animal
had been imported from the UK”).
Reviewers commented on the import of MBM.
3) The UK export statistics mention a shipment of 20 tons to
the U.S. in 1989. Such a quantity was enough to spark the Swiss
epidemic. This part of import risk was considered negligible
probably because the U.S. authorities could not corroborate this
figure. The statement (Page 22, second paragraph, last sentence)
that overseas shipping of MBM was economically noncompetitive
seems questionable because at least for the period when MBM was
almost available for free in the UK, it did get all the way to South-
East Asia in large quantities. Figures from Southern State
Cooperative of recent years are moot in this respect.
A reviewer also commented on the import of live cattle from the
UK.
4) Because the USDA reported that about half of the animals
imported in the risk period did not really enter the food chain, these
were considered to carry no risk (Section 3.4.3). The report does
not provide details or evidence to support this statement. Other
arguments regarding the potential risk of import of live cattle from
the UK, such as animals not being from a BSE-infected farm, and
BSE not being a recognized disease (Page iii, last paragraph), are
questionable. Admittedly, not many were imported at the peak of
the risk period.
5) With respect to rendering (Table 3-3, Page 61), two log
reduction for atmospheric continuous rendering with added fat is
optimistic. Also there is a doubt about the statement on Page 25
(Appendix 1, second paragraph, last sentence) that addition of fat
increases the inactivation.
6) In Section 3.1.2.3 on stunning, it is assumed for the base
case that air-injected stunning is not used in the U.S., based on
conversations with involved persons (Page 55, first paragraph,
seventh line). However, it seems that the model is based on
unlikely events such as air-injected stunning. Therefore, the model
may be limited and may become obsolete. In Section 3.1.2.4 (Page
56, second paragraph, last sentence), the assumption that stunners
3-5
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States — Final Report
not using air injection never cause contamination of the blood
(during exsanguination) with brain material needs to be modified.
7) The remark in Section 4.5 in the last line on Page 99 does
not sound very scientific: “exposure could not have been
substantial because we did not see many cases,” having in mind the
German experience. About the level of achieved surveillance, more
will follow.
8) In Section 2.3.9.1 on plate waste, it is said to mainly contain
vegetable material (third paragraph, second sentence), and
vegetable protein must be added to give it the correct nutritional
value. The major question is why one would not add mammalian
protein here instead of vegetable?
9) A reviewer commented on ProbPassAM (Section 2.1.1,
Appendix 1, Page 9). If it is their intent, the authors should specify
that ProbPassAM is the probability that a BSE-infected animal, not
just an animal, passes AM inspection. The authors state that the
probability of an animal passing AM inspection is age dependent.
They provide the references that were used to derive these
estimates. Because BSE evolves slowly, their argument that BSE in
older animals is more likely to be detected makes sense, but the
age-dependent variation is for animals without clinical signs. Thus,
the probabilities really represent the age-dependant chance
occurrence that an infected animal passes. Variations in
probabilities for the three age categories are minute (to third
decimal, Appendix 1, Section 3.1.1, Page 38). The authors do not
specify variation in ProbPassAM in animals with clinical signs by
the actual clinical signs, where variation in the probability among
animals is likely to be higher than variation among age categories.
Therefore, it appears that in one instance the parameter is
overestimated and in the other underestimated.
What is important from an inspection point of view is to pay greater
attention to early signs of disease. The probabilities also do not
reflect improvements in detection over the 20-year time span. If the
0.10 probability chosen by the authors is an average probability of
passing infected animals with early signs and animals with late
signs, perhaps it is appropriate. If it represents the probability of
passing an infected animal in the later stages of disease, then the
3-6
Section 3 — Identification of Data and Critical Evaluation of Evidence
Figure 3-1. Forrester
(rate/state) Diagram to
Depict Relationships
between Population
Parameters
estimate is probably high, because the neurological signs would be
obvious to an inspector.
10) Reviewers commented on the cattle population parameters
(Appendix 3A). The output tables list epidemic statistics such as the
numbers of cattle infected and the numbers infected exhibiting
clinical signs. It appears that cattle population parameters were
included in the model to simulate epidemic statistics, which is also
suggested in Figure 3-1 of the H-T BSE study report. Cattle
population parameters specified in the H-T BSE study report are
ProbBirth, ProbDeath, and InitSize. From an epidemiological point
of view, these variables can be used to estimate the size of the
“national herd,” which can define cattle at risk, and transmission of
prions, for instance between cow and calf, which can define spread.
However, the authors do not define clearly how the population
parameters affect the output. That is, the mathematical
relationships, if there are any, among the population parameters.
Figure 3-1 in the H-T BSE report is not sufficient in describing the
relationships. The authors do not report the density-dependent
process used. They might consider using Forrester (rate/state)
diagrams to depict the relationships in an easy to understand figure.
For instance, a simple way to convey to the reader the factors that
affect the size of the cattle population might be as shown in
Figure 3-1.
Population Birth
Rate
0.0833
at Time t
Death
Rate
A rate that increases the population and a rate that decreases the
population determine the size of the herd at a point in time. Then
the authors can elaborate. For instance, the rate of increase is
affected by the current age-specific size of the population at time t-1
and the birth rate. The rate at which the population decreases is
affected by the death/slaughter rate. The number culled for slaughter
(and other factors) affects the death rate.
3-7
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States — Final Report
In Table 3.4.1, the “natural” death rate is age-specific (Appendix 1,
Page 45). It should be reported that the unit for age is months, and
that the values tabulated are for beef cattle. Overall, the units of
measurement should be included in all tables. Throughout the
report, the stage of production is not considered. For instance, the
death rate is different for stocker cattle on pasture than for feedlot
cattle and varies seasonally and geographically and certainly by
producer. When should details such as these be included in the
model and when should they be excluded? More rationale should
be given for the variables selected and for those omitted.
Population parameters were important in the Great Britain outbreak
because destroying infected animals served to reduce the incidence
rate and disease spread. It is unclear how the population
parameters are used in this model.
11) About maternal transmission, one reviewer noted the
following. The parameters “beginCalving” and “endCalving,” the
beginning and ending age when cows give birth, are defined in
Appendix 1, Pages 10 and 11. They are included presumably to
estimate maternal transmission of prions to offspring or perhaps to
determine the period at which transmission could occur. However,
the actual relationship among the variables is not described.
Therefore, one would have to examine the computer code to
understand the relationships. Again, the authors might consider
depicting the relationship as shown in Figure 3-2.
“ProbTrans” is a probability that a new born calf becomes infected
if the mother is infected and the mother has lived through at least a
fixed fraction of her incubation period and its value is 0.1
(Appendix 1, Section 2.2.2, Page 10). The fixed fraction is specified
by parameter and its value is 0.833
(Appendix 1, Section 3.1.7.3, Page 76). Therefore, it appears that
probTrans is a conditional probability that can take on one of the
two values, which might be depicted by a Warnier-Orr diagram that
the authors could use as a means of making the relationship easier
for the reader to understand:
3-8
Section 3 — Identification of Data and Critical Evaluation of Evidence
Figure 3-2. Forrester
Diagram to Depict
Relationships for
“Begincalving” and
“Endcalving”
Rate
BSE
Calves
BSE
Mom
Transmit
(ProbTrans)
Moms
Time
since
infected
[Fraction of incubation period > 0.833] {ProbTrans = 10%
[Fraction of incubation period < 0.833] {ProbTrans = 0%
If the condition within the square brackets [ ] is true, then the
assignment to the right of the curly brace { is made. Also, the
authors need to specify if the fraction is >0.833 or •0.833.
12) Apparently, the incubation period for BSE is assigned a value
between 0 and >130 months according to the probability
distribution “ClinicalDate” (Appendix 1, Pages 73-76). It is
assumed that although the table indicates >130 months, the highest
value actually used was 130.
13) A few assumptions are based on data extrapolated from
dairy cattle and beef cattle or other animals. Do the results sum
over all “types” of cattle?
14) The number of cattle among which blood meal from a single
slaughtered animal is divided is estimated as described in Section
2.3.1 (Appendix 1, Page 11). Apparently, the blood collected from
individual animals at slaughter establishments is pooled. The
authors calculate the expected amount of blood meal consumed by
a dairy cow to determine the number of animals (88) fed by a single
4,000 lb batch of blood meal. It is not clear how this number is
used along with estimates of blood meal consumption (Table 3.3.3,
Appendix 1, Page 39) by each bovine type, gender, and age
combination to estimate the number of cattle infected by blood.
Also, the value for the number of animals fed by a single batch of
3-9
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States — Final Report
blood meal is reported as 88 in Appendix 1, on Pages 11 and 23,
but 89 in Appendix I, Page 66. Which of these two numbers is
correct? Because the units in the output tables (Appendix 3A) are
not given, it can only be a guess that the value for blood (in mode of
infection) represents cattle numbers infected by blood.
15) One reviewer commented on the lack of emphasis on
exposure routes. It is generally accepted that the highest risk for BSE
is from
Z import of live cattle or MBM from a country with BSE;
Z an internal processing system that is incapable of reducing
infectivity below a certain threshold level (mainly the
rendering system); and
Z exposure of ruminants to the end products of the second
way (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 on
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. This comment is also related to the general
comment on complexity and level of detail.
The study apparently treats the scrapie transmission (Section 2.3.3,
Page 23) and the spontaneous BSE case (Section 2.3.1, Page 21) at
the same level as the above listed priority routes. Below we provide
an example of this inconsistency with what is considered major
risks.
It is stated that from 750,000 up to 2.5 million animals are imported
annually from Mexico and Canada (Section 2.3.2.3, Page 22).
However, the H-T BSE study report does not address what happens
in Mexico in terms of MBM exposure. In general, the report says it
was extremely unlikely that those animals posed a risk of
introducing BSE in the U.S. Perhaps the imported animals do not
pose any risk, but what if they had been fed contaminated starter
ratios as calves in Mexico? Even if such animals would not live
until patent clinical stages, they can introduce infectivity into the
system. The Scientific Study Committee (SCC) concluded that this
was an area for consideration (or concern) in the case of the U.S.
3-10
Section 3 — Identification of Data and Critical Evaluation of Evidence
16) The third paragraph on Page iii discusses the risk presented
by the 334 animals brought into the U.S. from the UK between
1980 and 1989. The text states: “These animals were imported as
breeding stock, not as beef or dairy breeding animals. This fact is
likely to have reduced their potential for exposure to BSE before
their export from the UK” (fifth line). There is a misunderstanding
here as discussed below.
The cattle exported from the UK have carried a greater risk of being
infected by BSE than the other members of their natal cohorts that
were not exported. An assessment based solely on the incidence in
the home-based remnant of the cohort can therefore be misleading.
The reason for this elevated risk is because the exported animals are
more likely to have received commercial concentrate feed,
especially beef breeds that had a much lower exposure to feedstuffs
containing MBM. One reason for this was to ensure that they were
in the best physical condition. Examples of this apparent differential
risk for exported animals are the animals of the Saler breed, which
was exported to Canada, and animals exported to Denmark and
Germany. More generally, at the beginning of the clinical
epidemic, pedigree dairy herds were disproportionally represented.
Their exposure to MBM was relatively greater than for other
commercial herds, because of showing animals and general
traditions of managing such herds. Unfortunately a proportion of
the early affected pedigree herds was the source of Friesian heifers
for export to Portugal to restock after the Contagious Bovine
Pleuropneumonia (CBPP) outbreak there.
17) The second paragraph in Section 2.1.1 on Page 6 describes
transmission of TSE disease in the case of sheep-borne scrapie. It is
stated that TSE transmission has been inked to the use of vaccines.
There is not much evidence that a relatively crudely prepared
louping ill vaccine has been associated with transmission. The
evidence from the Italian outbreak is far from conclusive.
18) It would have been more correct if “at least experimentally”
was inserted after “transmitted” in the second sentence of the
second paragraph of Section 2.1.2.
19) With reference to Anderson et al. (1996), it is stated in
Section 2.1.3, third paragraph, that the susceptibility of animals
peaks at 1.31 years of age and then decreases based on back
3-11
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States — Final Report
calculation of the BSE model. There not only is a slight
misunderstanding of the Anderson paper, but also an error in this
paper that unfortunately has never been amended.
The peak susceptibility quoted is not derived by a back calculation.
However, it is derived from a research institute’s cattle herd that had
a very unusual feeding profile and this is the “error.” In Great
Britain, exposure to feedstuffs containing MBM is relatively rare
between 6 months of age and approximately 2 years when heifers
start to calve. This error is perpetuated in the Woolhouse and
Anderson (1997) paper, which is not a separate investigation (i.e.,
both papers are part of the same investigation). Moreover, it has not
been possible to determine the profile of age-dependent
susceptibility and whether it does occur. This would require a
laboratory-based study because the natural feeding pattern
throughout the first 2 years of the life of cattle in Great Britain
precludes the necessary epidemiological analysis of this putative
age-dependent susceptibility.
The synthesis of the current evidence on this aspect is important to
the risk assessment. If there is an age-dependent susceptibility it is
not absolute. That is, all ages are susceptible. The age at which
cattle are exposed orally and parentally to the BSE agent in
experimental challenges in Great Britain has been 4 months. This is
the age at which calves would have achieved their maximum intake
of commercial concentrate feedstuffs under Great Britain conditions.
The results from the British attack rate study, involving oral exposure
to varying amounts of brain tissue from terminal cases of BSE, has
resulted in an incubation period/age at clinical onset distribution
similar to that observed in naturally occurring cases. The
epidemiological evidence from the epidemic in Great Britain is that
age at exposure does not influence the incubation period.
In the ninth line of the third paragraph, it is hypothesized that agerelated
susceptibility is associated with permeability of the intestine
to large protein. A reference to the hypothesis is required because
the change in permeability of the bovine intestine with age does not
explain the apparent age-dependent susceptibility. The quoted
changes occur too early after birth.
In the second paragraph on Page 12, findings from the attack rate
experiments are discussed for the dose of BSE agent. The
3-12
Section 3 — Identification of Data and Critical Evaluation of Evidence
researchers should have made themselves aware of the attack rate
study conducted in Great Britain. The lowest dose in the original
study (a follow-up study using lower doses is in progress) was 1g.
The results of this study should have been included here. There
appears to be some confusion here and therefore a concern that the
researchers may not have made the best use of the research results
available, which is a “trap” generally advised against in terms of
interpretation and use of the results of the bovine pathogenesis
study. Essentially, the researchers have assumed that all of the
animals in the pathogenesis study, exposed to 100g brain orally,
had an incubation period of 36 months. This is not true and
probably arises from a lack of synthesis of the results from these two
studies; the attack rate study, although initiated at the same time as
the pathogenesis study, was the scoping study for the latter. The
problem is that in the attack rate study the 10 animals were exposed
to 100g brain orally. However, the same exposure dose used in the
pathogenesis study had incubation periods that ranged from 33 to
61 months. It is not correct to assume that all of the pathogenesis
study animals had the same relatively short incubation period.
Therefore, the proportional calculation described in Section 2.10.1,
Appendix 1 will produce conservative estimates of infectivity and
underestimate this value.
20) Section 2.2.1 describes scrapie in sheep as one of the
possible causes of the BSE epidemic in the UK. The section is a
little muddled in that it starts discussing transmission of sheep
scrapie between sheep and then goes on to the sheep scrapie origin.
The latter is a little simplistic and half-hearted. Again, this section is
a little short on primary references and reviews of considerations of
the origin, for example Kimberlin (1997). The comment on the
feeding of concentrates to calves not taking place other than in
Great Britain except Australia (Page 14, last sentence) is not true.
The EU-sponsored Great Britain exercise clearly indicated that the
feeding of concentrates containing MBM to calves was not restricted
to Great Britain/UK. Thus, there is a misquotation regarding the
feeding of concentrates to calves, which needs to be corrected to
make accurate international comparisons. Finally, the last sentence
of Section 2.2.1 could be misinterpreted by the uninformed to mean
that cattle are not susceptible to oral exposure to sheep scrapie.
This is not true.
3-13
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States — Final Report
21) Section 2.2.2 discusses sporadic BSE as one of the possible
causes for the UK epidemic. The first sentence of this section is
rather vague and conflicting. Is this referring to relativity to all other
countries or just to the U.S.? The evidence suggests that this is only
true for the U.S. Occurrence of sporadic BSE according to age of
cattle is discussed in the second paragraph. The age distributions of
the UK animals are specifically mentioned. However, other
European countries certainly have dairy cow populations with
similar age distributions, which needs to be considered here.
22) As discussed in Section 2.2.3, toxic agents and other
hypotheses as a possible cause of the BSE epidemic in the UK are
discussed here. The other hypotheses may not deserve any great
attention in such a risk assessment. They could have been
dismissed either by reference to reviews by others such as the
Spongiform Encephalopathy Advisory Committee (SEAC) in Great
Britain or by the EU’s SSC. As it stands, it is misleading. For
example, the “Organophosphate Pesticides hypothesis” has not
been a singular hypothesis. It has changed significantly throughout
the epidemic by its protagonist. Also, in the last sentence in the first
paragraph of Section 2.2.3.2, it is stated that resulting conditions
from copper deficiency had signs and pathological changes similar
to those of BSE, which is not true. Section 2.2.3.5 discusses
pituitary hormones, but the fact that transmission via hormones
derived from bovine pituitaries was considered in the original
epidemiological study has been ignored.
23) As discussed in Section 2.3.7.1, there is a theoretical risk
that cattle could be exposed to a TSE from porcine-derived protein.
One of the two potential sources of this exposure can be a natural
TSE that infects pigs. Section 2.3.7.1 discusses infectivity in pigs
due to TSE infection. BSE in pigs, as a clinical disease or subclinical
infection, has been 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. This is so specifically for the last part of the
second paragraph and the third paragraph on Page 29. Some
3-14
Section 3 — Identification of Data and Critical Evaluation of Evidence
evidence indicates that subclinical infection is not a problem in
pigs, and this is not presented. Also, some evidence shows that
clinical disease in pigs has not occurred in the pig population in
Great Britain. This has probably got lost in various reports.
However, if one assumes that the incubation period in pigs is the
same as that for BSE in cattle and the surveillance for neurological
disease in pigs in Great Britain is equally effective for such disease
in cattle, then the number of expected cases in the pig population in
Great Britain can be tens of thousands. On the first assumption
there is no evidence to dismiss it. On the second assumption,
evidence indicates that the surveillance of disease, including
neurological disease, in pigs is more effective than in cattle in Great
Britain.
BSE in pigs was detected by a neuropathologist whose specialism
was neurological disease in pigs. Also, during the BSE epidemic
outbreaks of neurological disease in pigs in Great Britain were
detected, brought to the attention of MAFF scientists, and
investigated. The main point is that the third paragraph on Page 29
has a touch of innumeracy. The percentage of pigs slaughtered at
less than 6 months of age is not an important statistic compared to
the number of pigs that reach a potentially susceptible age (~5
years), and this is what the analysis of the pig population referred to
above was concerned with. There is really no evidence that pigs
are important in the epidemiology of BSE, but quoting percentages
rather than absolute numbers is not helpful in such an important risk
assessment.
24) Actions taken in the UK to check BSE are described in
Section 2.4.2, Page 37. The fifth sentence (line 7) indicates that the
ban on specific bovine offal (SBO) as ingredients in feed stuff helps
to identify tissues with the highest infectivity. It should be indicated
that these high risk tissues were identified as a result of research on
sheep scrapie. This sentence also could be more fully referenced.
The last sentence of the paragraph is more accurate if it is moved to
be the penultimate sentence. Because by 1997 the additional ban
on the use of mammalian-derived protein in 1996 could not
possibly have had any effect on the clinical incidence.
To make the second paragraph more realistic, it may be noted that
the SBO ban, with respect to the human food supply, was
introduced in 1989 because of the knowledge that when the
3-15
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States — Final Report
“scrapie agent” successfully crosses to another species, it can have
altered transmission characteristics with respect to other species.
Also, the tissues listed as the SBOs, such as brain and spinal cord
from cattle older than 6 months, are incomplete.
The chronology of events that is suggested in the third paragraph is
not correct. The national surveillance for Creutzfeldt-Jakob Disease
(CJD) was formally instigated in May 1990, which is clear from the
CJD Surveillance Unit’s website. In Table 2-2, the chronology of
BSE-regulated actions in the UK contains errors. For example, there
was no “selective culling” in 1990, and spinal cord in animals older
than 6 months was included in the original SBO ban. There are
perhaps some other important exclusions even though this is a
summary table. For a detailed chronology, refer to the six monthly
progress report on the BSE epidemic published by the Ministry of
Agriculture, Fisheries, and Food (MAFF) (now the Department for
Environment, Food, and Rural Affairs or DEFRA), which is available
on their web site.
The two measures to prevent the BSE epidemic described in the last
two paragraphs of this section are confused as different bans. The
reality was that in March 1996, the SEAC’s recommendation was for
the deboning of carcasses of animals older than 30 months of age
together with the removal of all obvious lymphatic and nervous
tissues. This was not possible because of an insufficient number of
deboning plants. The political decision was therefore made, at the
Prime Ministerial level, to remove all animals over 30 months old
from the human chain. The ban on bone-in-beef was introduced as
a precautionary measure as a result of the later results from the BSE
pathogenesis study (in cattle) conducted in Great Britain that
suggested that infectivity may be present in dorsal root ganglia.
25) In Section 2.4.5, BSE surveillance in the U.S. was evaluated.
The section reads as if there is a little complacency about the
surveillance for BSE, and CJD/vCJD in the U.S. A more critical
evaluation appears to be appropriate. There have clearly been a
number of problems with surveillance for clinical BSE. The first is
the general level of surveillance in the U.S. and other countries.
The second is the fact that at low incidence BSE is clearly a difficult
disease to identify because of its more behavioral, rather than
neurological, clinical presentation in at least the early clinical phase
and the rather variable clinical signs. Thirdly, a concentration on
3-16
Section 3 — Identification of Data and Critical Evaluation of Evidence
suspect rabies cases has not proved to be very effective within
continental Europe; this is mainly because rabies is endemic in the
less cattle-dense areas and such surveillance (on its own) can
therefore exclude a significant proportion of the cattle population.
Fourthly, “downer” cows are probably not the best targets for BSE
surveillance.
The time frame of the BSE risk assessment work is not clear. The
executive summary indicates a starting year of 1998 and the
scientific references section contains some papers published in May
2001. An improved awareness of the extent and magnitude of the
incidence of BSE in EU member states in continental Europe
emerged towards the end of 2000. Any comment on the omission
of what has been learned or stressed from this additional
surveillance in Europe, arising from the use of the more rapid and
economical tests described in Section 2.4.1, may be misplaced.
However, two related aspects emerge. The first is that testing
animals at slaughter improves quite dramatically our knowledge on
the incidence of BSE in countries with a low incidence of clinical
BSE and therefore a relatively poor awareness of the intricacies of
the clinical picture. Secondly, targeting surveillance to the more
general category of fallen stock/casualty slaughter animals, rather
than just “downer” cows is a much more effective method.
A comparison of surveillance for CJD/vCJD in the U.S. with that in
the UK and the more widely based EU funded surveillance project
would have been helpful because there do seem to be some
differences. A lack of change in the observed incidence of CJD in
the U.S. could be interpreted as providing evidence of no increased
intensity in surveillance. This comment is made in light of the
findings from those countries that have participated in the
international project on CJD surveillance.
3.3 ARE ALL INPUT DATA USED IN THE MODEL
VALID AND APPROPRIATE?

snip...


http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf

Mad-Cow Rule Breaches
By Meat Packers Are Noted

By BILL TOMSON
DOW JONES NEWSWIRES
August 19, 2005

WASHINGTON -- Federal documents show U.S. meat packers sometimes failed to follow procedures to prevent the spread of mad-cow disease, including leaving spinal cords in cattle, miscalculating cattle ages and not sanitizing equipment.

Most of the 1,036 "noncompliance records" released by the Department of Agriculture appear to show record-keeping or other paperwork infractions.

And a violation recorded Aug. 3, 2004, said a USDA inspector stopped plant operations after watching employees fail to remove spinal cords from carcasses. Spinal cords are thought to carry the mad-cow disease, or bovine spongiform encephalopathy. The inspector said as a result the facility pledged to retain more than 500 carcasses and inspect them. A "similar" violation for the same establishment had been written up about three months earlier, the report said.

No company's name could be seen on the document that had sections blacked out, but it was accompanied by a letter from Tyson Fresh Meats Inc., a unit of Tyson Foods Inc. Tyson wrote that employees who should have been removing spinal cords were chastised for "poor work performance." Gary Mickelson, a Tyson spokesman, said, "We view this particular incident as more of a procedural issue than a food-safety concern because of the additional measures we take after this point in the production process to make sure nervous-system materials don't enter the food supply."

An unrelated violation said a factory wasn't correctly determining cattle ages. An inspector said when he tried to verify records that four cattle were younger than 30 months, he found three of the animals were older.

USDA maintains that, for the most part, mad-cow infection can only be found in cattle 30 months and older so most tissue capable of carrying the disease -- called specified risk material, or SRM -- only needs to be removed from older animals. If an animal is younger, those parts don't need to be removed. Some parts, such as tonsils and distal ileum, are considered SRM in cattle of all ages and must be removed.

After the first case of mad-cow disease was found in the U.S. in December 2003, USDA began requiring the removal of spinal-cord, brain and other tissues from older cattle. Several other food-safety rules were implemented, including a ban on "downer" or dead animals from the food supply. Humans are believed to be susceptible to the disease through consumption of some beef products if they contain infected tissue.

A slaughterhouse, owned by Smithfield Foods Inc. subsidiary Moyer Packing Co., was written up July 15, 2004, for mishandling an animal that was dead-on-arrival and slated to be tested in USDA's federal BSE surveillance program. The program focuses on downer cattle that are too sick or injured to walk or cattle that died before slaughter. USDA considers those cattle more likely to be infected. The USDA inspector said he observed "abdominal fluids and tissues" from the dead animals "scattered throughout the unloading and livestock scale areas."

Moyer said in a response letter to USDA that the "entire affected area ... was hosed with high-pressure water and debris were removed." Smithfield spokesman Jerry Hostetter said: "The dead animal in question was nowhere near a food-production or processing area. It was in the cattle receiving yards ... prior to being taken into the plant. No parts of the animal got anywhere near the food supply."

Write to Bill Tomson at bill.tomson@osterdowjones.com


http://online.wsj.com/article/0,,SB112440337073117094,00.html?mod=djemHL

From: TSS ()
Subject: 9,200 USA POTENTIAL MAD COWS IN JUNE 2004 ENHANCED COVER-UP SURVEILLANCE PROGRAM NO WB
Date: August 17, 2005 at 7:09 pm PST

Daily Update

On August 17, 2005, no inconclusive test results were reported.

National Veterinary Services Laboratory (NVSL) Immunohistochemistry (IHC) Testing Summary

The BSE enhanced surveillance program involves the use of a rapid screening test, followed by confirmatory testing for any samples that come back "inconclusive." The weekly summary below captures all rapid tests conducted as part of the enhanced surveillance effort. It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing. This was done to ensure that samples inappropriate for the rapid screen test were still tested, and also to monitor and improve upon IHC testing protocols. Of those 9,200 routine tests, one test returned a non-definitive result on July 27, 2005. That sample underwent additional testing at NVSL, as well as at the Veterinary Laboratories Agency in Weybridge, England, and results were negative.
To view the IHC testing numbers from 1990 through 2004, click on the following link: http://www.aphis.usda.gov/lpa/issues/bse/surveillance/figure2f.html

Weekly Summary

Cumulative Total from June 1, 2004: 439,126


http://www.aphis.usda.gov/lpa/issues/bse/surveillance/figure2f.html


http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html


THE USA JUNE 2004 Enhanced BSE program was a sham. it should be totally scrapped and every cow for human and or animal consumption should be retested, with proper protocol annually for 5 years. nothing less should be accepted now. the feed ban was a sham, the testing was a sham, it is exactly as myself and many others have been saying for almost a decade. TSEs are rampant in the USA. THIS is why GW et al force fed everyone this BSe MRR policy, nothing more than a legal pass to trade all TSEs from the USA around the Globe. commodities and futures, to hell with human health.

THE USA BSE GBR RISK ASSESSMENT SHOULD BE IMMEDIATELY REASSESSED TO BSE GBR IV.

>>>"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."<<<

r i g h t ...


>>> The feed history investigation identified 21 products that had been used on the farm since 1990. These feed products were purchased from three retail feedstores and had been manufactured at nine different feed mills.

The investigators visited these establishments to collect information on formulation, shipping invoices, and the use of ruminant meat and bonemeal on the premises, both before the 1997 feed ban and after the 1997 feed ban.

This investigation found no feed products used on the farm since 1997 had been formulated to contain prohibited mammalian protein. The investigation identified one feed which contained an animal protein source that could not be identified and the investigation also found one feed mill that supplied feed to the farm and that used ruminant meat and bonemeal in feed formulations for nonruminant species after the BSE ruminant feed rule went into effect, and this was permitted under the rule.

And there were several feed mills that had used ruminant meat and bonemeal prior to the 1997 feed ban but had ceased to use that material after the 1997 feed ban.

The investigation into the disposition of herd-mates from this farm involved visits to nine slaughter plants and eight rendering plants. The investigation found that all rendering plants were operating in compliance with the BSE ruminant feed rule. A review of the inspection history of each of these rendering firms found no violation. <<<


I DO NOT BELIEVE THIS, and this is why the USDA et al refuse to give out location of this farm. AS long as this secrecy continues, and from the proven
attempted cover-ups in the past (stupidity is not acceptable anymore), millions of animals and humans will become even more exposed to this TSE agent not only in the USA and North America, but also abroad, where many many pontential TSE tainted products will be exported from the USA, Canada and Mexico. Britain did it, got away with it, so why not North America. commodities and futures = GWs BSE MRR policy = millions exposed to TSE.


SOMETHING else i find disturbing is all the reporting that the cow simply went to a pet food plant in Waco (Champion).
IN reality, that mad cow had first gone to a packing plant before going to the pet food plant. therefore, a few days before
IF that cow would had been sent to a packing plant, it would not have been down and could have indeed made it to the
human food supply, as a sub-clinical BSE/TSE cow. see below ;


>>>
The animal
was sold through a livestock sale in November of 2004 and transported to a packing plant. The animal was dead upon arrival. The animal was therefore refused by the packing plant. This refusal was consistent with USDA's safeguards to protect the meat supply from BSE.

The animal was then shipped to a pet food plant where it was sampled for BSE. The plant did not use the animal in its product, and the carcass was destroyed. <<<


BUT HERE, we have just that it arrived at the champion pet food plant;


STATEMENT

by USDA Chief Veterinarian John Clifford Regarding the Epidemiological Investigation into the recently confirmed BSE case

June 29, 2005

"DNA test results have confirmed that we have identified the source herd of the animal determined last week to be positive for BSE. Based on information we have received from the owner, the cow was born and raised in a herd in Texas and was approximately 12 years old. It was sent to a 3D/4D pet food plant in Texas and was selected for sampling on arrival. “The source herd is now under a hold order as we identify animals of interest within the herd. Consistent with OIE guidelines, animals of interest would include any other animals that were born the same year as this animal, as well as any born the year before and the year after. If the age of the animal cannot be pinpointed, then we may expand our inquiry to include all animals in this herd before the feed ban went into place in 1997. We are also interested in any of this animal’s offspring that were born within the last 2 years. “Experience worldwide has shown us that it is highly unusual to find BSE in more than one animal in a herd or in an affected animal’s offspring. Nevertheless, all animals of interest will be tested for BSE. “We are also working with the Food and Drug Administration in an effort to determine the feed history in this herd. Given the animal’s age, we believe it was most likely infected by consuming feed prior to the implementation of the ruminant-to-ruminant feed ban in 1997. “I emphasize that this animal did not enter the human food chain. The plant at which this animal was sampled is a 3D/4D pet food plant that does not handle animals for human consumption and, in this case, did not use the animal in the production of pet food. The animal remains were incinerated.“The testing and traceback efforts may yield further information as to how this animal became infected. The safety of our food supply is not in question. I am very confident that our interlocking safeguards are effective, and this case is evidence of that. USDA bans non-ambulatory cattle from the food supply. USDA bans animal parts that could carry BSE from the food supply. USDA bans slaughter techniques that could introduce BSE into the food supply. These safeguards ensure that American beef is among the safest in the world.”#


http://www.aphis.usda.gov/lpa/issues/bse/bse_statement6-29-05.doc


WHAT about those atypical TSEs ;


NEW STRAIN OF TSE USA CATTLE OR JUST INCOMPETENCE IN TESTING???


DR. CLIFFORD: "Basically the IHC test, besides looking at location of the brain stem you're also doing a staining technique to identify abnormal prion proteins. In this case they had some staining, but the staining did not match up with what they would typically see in a BSE case. It didn't have the normal distribution it would see within the samples. So basically that's why the request for doing additional testing, and that's why we're sending it to Weybridge as well."


DR. CLIFFORD: "There was some staining present. But it did not match a normal pattern, and we're taking through that to do additional tests in additional parts of the brain stem to try to see if we can find a normal staining pattern as well as sending that sample to Weybridge to run against their IHC."

http://www.usda.gov/wps/portal/usdahome?contentidonly=true&contentid=2005/07/0280.xml

IN CONFIDENCE

PERCEPTION OF UNCONVENTENTIONAL SLOW VIRUS DISEASES OF ANIMALS IN THE USA

1985 The Stetsonville outbreak (farmer's name: Brecke). In addition to the downer cows and horses Brecke's mink recieved a cereal supplement. Hartsough's view was that this would contain bone meal and would be from a commercial source. If this were so and it was contaminated with a TME agent why were no other ranches affected?

Many mink ranches now feed a commerical pelleted diet. Brecke was equipped to process LARGE CARCASSES USING A CRUSHER/MIXER WHICH COULD ACCOMMODATE A WHOLE COW!

snip...

Dead mink go for rendering but are used only in poultry feed.


A commercial mink ranch was visited. This was Johny Werth's, Capitol Fur Farm comprising 1400 breeding females. The feed is bought in from a commercial supplier in the form of frozen packs of ''poultry'', ''fish'', ''dried egg'' or ''tripe''. A commercial mink cereal supplement is used and contains ''animal meat meal'' which was said to contain material mainly from poultry or fish origin but OCCASIONALLY FROM BEEF SOURCES. the partially thawed packs were tipped into an augur mixer which has a fully loaded capacity of 6000lb and this would be approximately 15000 mink per day.

In the fall at pelting time the skinned carcasses of the mink are placed in large barrels which are left in the open to freeze. When full, a renderer collects ''for use in poultry feeds''.

Sections from the brains of the two Brecke TME inoculated cattle were examined and Marsh provided all the blocks from the 2nd steer for study at CVL and comparison with BSE. In general the vacuolar changes were more severe than in most cases of BSE but very similar in distribution. Unfortunately material aken fro histopathology from those anials omitted representaion of most of the brain stem. ...........

Wilbur Clarke (reference the Mission, Texas scrapie transmission transmission to cattle study) is now the State Veterinarian for Montana based at Helena.

I was given confidential access to sections from the Clarke scrapie-cattle transmission experiment. Details of the experimental design were as supplied previously by Dr. Wrathall (copy of relevant information appended). Only 3 animals (2 inoculated with 2nd pass Suffolk scrapie and 1 inoculated with Angora goat passaged scrapie) showed clinical signs. Clinical signs were characterised by weakness, ''a stilted hindlimb gait'', disorientation, ataxia and, terminally, lateral recumbency. The two cattle from which I examined material were inocluated at 8 months of age and developed signs 36 months pi (goat scrapie inoculum) and 49 months pi (one of the Suffolk scrapie inoculated) respectively. This latter animal was killed at 58 months of age and so the clinical duration was only 1 month. The neuropathology was somewhat different from BSE or the Stetsonville TME in cattle. Vacuolar changes were minimal, to the extent that detection REQUIRED CAREFUL SEARCHING. Conversely astrocyte hypertrophy was a widespread and prominent feature. The material requires DETAILED NEUROPATHOLOGICAL ASSESSMENT BUT WHETHER OR NOT THIS WILL BE DONE REMAINS A QUESTION.

Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases

{the following was written but with a single line marked through it ''first passage (by this route)}...TSS

resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest
incubation period in the ferret.

snip...

Appendix 3

VISIT TO USA - DR A E WRATHALL - INFO OH BSE AND SCRAPIE

1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The
experimental results have not been published but there are plans to do
this. This work was initiated in 1978. A summary of it is:-

Expt A
6 Her x Jer calves born in 1978 were inoculated as follows with
a 2nd Suffolk scrapie passage:-


i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BSE-like disease.

Expt B
6 Her or Jer or HxJ calves were inoculated with angora Goat
virus 2/6 went down similarly after 36 months.

Expt C
Mice inoculated from brains of calves/cattle in expts A • B
were resistant, only 1/20 going down with scrapie and this was the
reason given for not publishing.

Diagnosis in A, B, C was by histopath. No reports on SAT were given.

2. Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally- (and naturally) infected sheep by ET.
He had found difficulty in obtaining embryos from naturally infected
sheep (cf SPA).

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.
BSE was not reported in USA.


4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control Scheme was started
there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.

5. Scrapie agent was reported to have been isolated from a solitary
fetus.

6. A western blotting diagnostic technique (? on PrP) shows some promise.

7. Results of a questionnaire sent to 33 states on the subject of the
national sheep scrapie programme survey indicated


17/33 wished to drop it

6/33 wished to develop it

8/33 had few sheep and were neutral


Information obtained from Dr Wrathall's notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.

33

end...TSS


>> Differences in tissue distribution could require new regulations
>> regarding specific risk material (SRM) removal.


snip...end

full text 33 PAGES ;


http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf


It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.

http://www.bseinquiry.gov.uk/

1: J Infect Dis. 1994 Apr;169(4):814-20.


Intracerebral transmission of scrapie to cattle.

Cutlip RC, Miller JM, Race RE, Jenny AL, Katz JB, Lehmkuhl HD, DeBey BM, Robinson MM.

USDA, Agriculture Research Service, National Animal Disease Center, Ames, IA 50010.

To determine if sheep scrapie agent(s) in the United States would induce a disease in cattle resembling bovine spongiform encephalopathy, 18 newborn calves were inoculated intracerebrally with a pooled suspension of brain from 9 sheep with scrapie. Half of the calves were euthanatized 1 year after inoculation. All calves kept longer than 1 year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis, general weakness, and permanent recumbency. The incubation period was 14-18 months, and the clinical course was 1-5 months. The brain from each calf was examined for lesions and for protease-resistant prion protein. Lesions were subtle, but a disease-specific isoform of the prion protein was present in the brain of all calves. Neither signs nor lesions were characteristic of those for bovine spongiform encephalopathy.

MeSH Terms:
Animals
Brain/microbiology*
Brain/pathology
Cattle
Cattle Diseases/etiology*
Cattle Diseases/pathology
Encephalopathy, Bovine Spongiform/etiology*
Encephalopathy, Bovine Spongiform/pathology
Immunoblotting/veterinary
Immunohistochemistry
Male
Motor Neurons/physiology
Prions/analysis
Scrapie/pathology
Scrapie/transmission*
Sheep
Sleep Stages
Time Factors

Substances:
Prions

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8133096&dopt=Citation


Intracerebral transmission of scrapie to cattle FULL TEXT PDF;

SNIP...


Discussion


WE conclude that American sources of sheep scrapie are transmissible to cattle by direct intracerebral inoculation but the disease induced is NOT identical to BSE as seen in the United Kingdom. While there were similarities in clinical signs between this experimental disease and BSE, there was no evidence of aggressiveness, hyperexcitability, hyperesthesia (tactile or auditory), or hyperemetria of limbs as has been reported for BSE (9). Neither were there extensive neurologic lesions, which are primary for BSE, such as severe vacuolation of neurons and neuropil or neuronal necrosis and gliosis. Although some vacuolation of neuropil, chromotolysis in neurons, and gliosis were seen in the brains of some affected calves, these were industinguishable from those of controls. Vacuolated neurons in the red nucleus of both challenged and normal calves were considered normal for the bovines as previously described (50).


PrP-res was found in ALL CHALLENGED CALVES REGARDLESS OF CLINCIAL SIGNS, and the amount of PrP-res positively related to the length of the incubation. ...


snip...


WE also conclude from these studies that scrapie in cattle MIGHT NOT BE RECOGNIZED BY ROUTINE HISTOPATHOLOGICAL EXAMINATION OF THE BRAIN AND SUGGEST THAT DETECTION OF PrP-res by immunohistochemistry or immunoblotting is necessary to make a definitive diagnosis. THUS, undiagnosed scrapie infection could contribute to the ''DOWNER-COW'' syndrome and could be responsible for some outbreaks of transmissible mink encephalopathy proposed by Burger and Hartsough (8) and Marsh and harsough (52). ...


snip...


Multiple sources of sheep affected with scrapie and two breeds of cattle from several sources were used inthe current study in an effort to avoid a single strain of either agent or host. Preliminary results from mouse inoculations indicate multiple strains of the agent were present in the pooled inoculum (unpublished data). ...


Transmission of the sheep scrapie to cattle was attempted in 1979 by using intracerebral, intramuscular, subcutaneous, and oral routes of inoculation of 5, 8- to 11-month old cattlw with a homologous mixture of brain from 1 affected sheep (61, 62). ONE of the 5 cattle develped neurologic signs 48 months after inoculation. Signs were disorientation, incoordination, a stiff-legged stilted gait, progressive difficulty in rising, and finally in terminal recumbency. The clinical course was 2.5 months. TWO of the 5 cattle similarly inoculated with brain tissue from a goat with scrapie exhibited similar signs 27 and 36 months after incoluation. Clinical courses were 43 an 44 days. Brain lesions of mild gliosis and vacuolation and mouse inoculation data were insufficient to confirm a diagnosis of scrapie. This work remained controversial until recent examination of the brains detected PrP-res in all 3 cattle with neurologic disease but in none of the unaffected cattle (62). Results of these studies are similar to ours and underscore the necessity of methods other than histopathology to diagnose scrapie infection in cattle. We believe that immunologic techniques for detecting PrP-res currently provide the most sensitive and reliable way to make a definitive diagnosis...


http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf


Visit to USA ... info on BSE and Scrapie

http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf


http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=12;t=000385

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

snip...

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

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

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

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

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

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

snip...

76/10.12/4.6

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

sCJD in a young Dutch valine homozygote: atypical molecular
Sat Aug 13, 2005 15:06
70.110.89.34


1: Ann Neurol. 2001 Aug;50(2):258-61.

Sporadic Creutzfeldt-Jakob disease in a young Dutch valine homozygote:
atypical molecular phenotype.

Head MW, Tissingh G, Uitdehaag BM, Barkhof F, Bunn TJ, Ironside JW,
Kamphorst W, Scheltens P.

Department of Pathology, University of Edinburgh, Western General Hospital,
UK. m.w.head@ed.ac.uk

A case of sporadic Creutzfeldt-Jakob disease (sCJD) is described in a young
Dutch protein prion gene (PRNP) codon 129 valine homozygote. Certain
clinical and molecular features of this case overlap those of variant CJD.
The case highlights possible difficulties in the differential diagnosis of
vCJD and the more rare sCJD subtypes based on molecular features alone.

Publication Types:
Case Reports

PMID: 11506411 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11506411&dopt=Abstract


IN light of Asante/Collinge et al findings 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;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:
"'flounder@wt.net'"

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.

Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:

e.asante@ic.ac.uk (until 9/12/02)

New e-mail: e.asante@prion.ucl.ac.uk (active from now)

____________________________________

snip...

full text ;

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


AND 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


http://www.pnas.org/cgi/content/abstract/0305777101v1


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;

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

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

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama

BRITISH MEDICAL JOURNAL

SOMETHING TO CHEW ON

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2

BMJ

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


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 ...


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, ...

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. ...


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 ...
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

ALL animals for human/animal consumption must be tested for TSE.


ALL human TSEs must be made reportable Nationally and Internationally, OF ALL AGES.


THE infamous USA SPORADIC CJDs, something to ponder;


IF ALL USA TSE in cattle does not look like UK BSE, why would ALL USA human TSE look like UK nvCJD???


THE UK BSE nvCJD only and everything else is o.k. theory should be trashed once and for all.


THE TSE nightmare is far more reaching than that. ...TSS

From: TSS ()
Subject: TRANSCRIPT OF JOHANNS ABOUT THE TEXAS BSe Release No. 0339.05
Date: August 30, 2005 at 6:48 pm PST

Release No. 0339.05
Contact:
USDA Press Office (202) 720-4623


TRANSCRIPT OF TECHNICAL BRIEFING WITH AGRICULTURE SECRETARY MIKE JOHANNS, USDA CHIEF VETERINARY OFFICER DR. JOHN CLIFFORD (ANIMAL AND PLANT HEALTH INSPECTION SERVICE), AND CENTER FOR VETERINARY MEDICINE DIRECTOR DR. STEVE SUNDLOF (FOOD AND DRUG ADMINISTRATION), UPDATE ON NATIONAL ANIMAL IDENTIFICATION SYSTEM AND BSE EPIDEMIOLOGY INVESTIGATION, WASHINGTON, DC -- AUGUST 30, 2005

SEC. MIKE JOHANNS: Thank you very much, and good afternoon everyone, and thank you for joining us. I will begin today with an announcement about the National Animal Identification System, and then what I'd like to do from there is ask Dr. John Clifford to report on the conclusion of the investigation related to the cow that tested positive for BSE in June of this year.

Many of you have heard me say before that I am deeply committed to the spirit of public service that involves listening, really listening, to the people whom we serve. We may not always agree with each other, but as public servants it is important that we listen. That's why I've been traveling around the country doing a Farm Bill listening tour to hear from the entire ag community about what's on their mind, what we're doing right, and what we might do better.

Well, today I'd like to tell you about some of the listening we've done on the National Animal Identification System. That's a good place for me to start. The system is one of the most important infrastructure initiatives in animal agriculture today. Our goal is to work hand-in-hand with producers and the states to enhance our collective ability to quickly identify animals that may be of concern in a disease outbreak.

When this system is fully implemented, we expect to be able to identify all potentially affected animals and premises within 48 hours of a disease detection.

You'd be hard-pressed to find anyone working in animal agriculture today who doesn't believe that's a worthy objective and an important investment for us to make. After all, the faster we identify affected animals and premises, the faster we are able to contain the disease.

But as with any major initiative touching so many segments of the industry, there are differing views on some pretty fundamental questions like whether data in the system should be publicly or privately held, how can we protect confidentiality of the data, and whether the data collection should be a voluntary system or a mandatory system.

Last year the USDA held a series of listening sessions around the country, some 16 in all as a matter of fact, to hear what folks around the country had to say. We also formed a special subcommittee under the Secretary's Advisory Committee on Foreign Animal and Poultry Diseases that has widespread producer representation.

And in May as you know we published a detailed thinking paper outlining our proposed strategy for getting a mandatory system in place and framing some additional questions for stakeholders to contemplate.

In their responses, producers expressed concern about confidentiality when it comes to animal movement information. Without question, the participation of producers is absolutely essential to the success of an animal identification system. That's why we paid attention when producers asked that animal movement data be privately held.

Based on the feedback, I'm putting forth guiding principles today that allow animal movement data to be maintained in a private system that can be readily accessed when necessary by state and federal animal health authorities. This allows the industry to continue developing databases that house animal movement information, and we envision those databases feeding a single, privately-held animal tracking repository that we can access.

This initiative, or innovative approach, addresses producers' concerns while at the same time enabling federal and state officials to access information that we may need for disease control purposes.

There are a number of concepts being discussed in the private sector about how this should work and how it should be funded. USDA is not favoring any one of them over the other. USDA will be scheduling a stakeholder meeting this fall to clarify expectations for the private tracking system and discuss user requirements in system specifications.

In the meantime, USDA will be finalizing and releasing the program standards that were presented in the thinking paper. Beyond that, we will be looking to industry to come together to drive this leg of the journey.

I believe strongly this is the right approach. This system has always been about government and private partnership. USDA has invested a great deal, nearly $19 million in 2004, to get the infrastructure started. Most of that went to cooperative agreements with states and with tribes. For Fiscal Year 2005, we've invested another $33 million with about half of that going to additional cooperative agreements. And there's another $33 million in the President's 2006 Budget for additional infrastructure building.

We are making great progress in the area of premise registration with 100,000 premises now registered and plans to begin later this year allocating blocks of animal identification numbers to tag manufacturers.

With today's announcement, we begin work on the next step in developing the animal identification system, tracking animal movements. The only way the system will work is if stakeholders have a role in designing it, if all are truly, fully invested. The piece of the system that is the most producer-dependent is this piece dealing with tracking animal movements, and so it simply makes good sense for producers to design and to maintain that piece of the system.

Ultimately we know we will end up with a system that embodies the best that the private system and government have to offer.

I would be happy to answer your questions about the National Animal Identification System in just a moment.

But just briefly while we're speaking of tracing animals, I did want to mention that we've completed our epidemiological investigation related to the BSE animal identified in June. This very thorough investigation has been a tremendous example of partnership at the federal, state, and, I might add, the industry level. And we appreciate that.

It's worth nothing that this investigation would have taken far less than two months if we had the National Animal Identification System in place. That delay is not significant in terms of human or animal health because BSE is not a contagious disease. But the time it has taken to identify, locate, and test animals of interest is significant to our efforts to reopen export markets, because a number of trading partners have been reluctant to make decisions until the investigation is complete.

I am pleased that we are now in a position to close the investigation, communicate this information to our trading partners, and then move forward. I have with me today Dr. John Clifford, our chief veterinarian, along with Dr. Steve Sundlof of the Food and Drug Administration, to provide you with information about their conclusions. So I'll now turn the microphone to Dr. Clifford.

DR. JOHN CLIFFORD: Thank you, Mr. Secretary. As you said, the announcement of the guiding principles for the future of a public/private partnership for animal ID is a giant step forward for a national animal identification system. Because it was developed through the integration of premises registration, animal registration, and animal tracking, the NAIS has always been viewed as a government/industry partnership. Today's announcement affirms our commitment and eagerness to work with the industry to achieve the goals of the NAIS.

Now I want to turn to the completion of the epidemiological investigation that was conducted following the BSE detection in Texas in June. Many people worked very hard on the investigation, and I'd like to thank the Veterinary Services employees involved, our colleagues from the Food and Drug Administration, the owners of the animals, along with the Texas Animal Health Commission and the Texas Feed and Fertilizer Control Service for their outstanding work.

This investigation is another great example of federal, state, and local partners cooperating to help protect livestock health in this country.

I'll now summarize our findings. Our results indicate that the positive animal, called the "index animal." was born and raised on a ranch, termed the "index farm," in Texas. It was a cream-colored Brahma cross, approximately 12 years of age at the time of its death. It was born prior to the implementation of FDA's mandatory ruminant-to-ruminant feed ban in the U.S., and that ban was implemented in August 1997.

The animal was sold through a livestock sale in November of 2004 and transported to a packing plant. The animal was dead upon arrival. The animal was therefore refused by the packing plant. This refusal was consistent with USDA's safeguards to protect the meat supply from BSE.

The animal was then shipped to a pet food plant where it was sampled for BSE. The plant did not use the animal in its product, and the carcass was destroyed.

APHIS's epidemiological investigation attempted to trace all adult animals that left the index farm after 1990. The investigation also attempted to trace all progeny born within two years of the index animal's death.

Together these animals are called "animals of interest." These steps are consistent with the guidance for epidemiological investigations and to detections of BSE issued by the International Animal Health governing body or the OIE.

During the course of this investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE.

A total of 200 additional adult animals of interest were determined to have left the index farm. Of these 200, APHIS determined that 143 animals were slaughtered, 2 animals were found alive but one was determined not to be of interest because of its age, and the other tested negative for BSE. 34 animals were presumed dead, 1 is known dead, and the remaining 20 are classified as "untraceable."

In addition to the adult animals, we also looked for two calves born to the index animal. Due to record-keeping and identification issues, we had to trace 213 calves. Of these 213, 208 entered feeding and slaughter channels, 4 are presumed to have entered feeding and slaughter channels, and 1 calf was untraceable.

As you know, BSE is not a contagious animal disease. This disease is spread through contaminated feed. To determine whether contaminated feed could have played a role in the index animal's infection, FDA and the Texas Feed and Fertilizer Control Service conducted a thorough feed investigation.

For a summary of the findings of the feed investigation, we have Dr. Steve Sundlof here from the FDA.

Before I turn things over, though, I will say that we are extremely pleased with the results of the epidemiological investigation. It shows there was no widespread problem associated with the index herd, and as you will hear more about in a moment, that the ruminant feed ban in the United States is solid. It also affirms that USDA's interlocking system of safeguards to prevent BSE from entering the food chain is working as it should.

We remain vigilant, as well, as in our efforts to determine the prevalence of BSE in the United States. To date there have been only 2 BSE-positive animals found in this country in more than 452,000 animals tested in the last 14 months.

All evidence is that the prevalence is extremely low and continues to decline given the length of time the ruminant feed ban has been in effect.

With that, I will turn things over to Dr. Steve Sundlof from the Food and Drug Administration.

DR. STEVE SUNDLOF: Thank you, Dr. Clifford. I will read an opening statement as well.

On June 24, 2005, the USDA informed the FDA that a cow in Texas tested positive for bovine spongiform encephalopathy. The animal was disposed of by incineration and did not enter the human food or animal feed chains. Although the animal posed no risk to the animal feed supply, FDA, along with USDA's Animal and Plant Health Inspection Service, the Texas Animal Health Commission, and the Texas Feed and Fertilizer Control Service conducted a feed investigation with two main objectives.

The first objective was to identify all protein sources in the animal's feed history that could potentially have been the source of the BSE agent.

The second objective was to verify that cattle of interest leaving the herd after 1997 were rendered at facilities that were in compliance with the 1997 regulation that prohibits most mammalian protein in the feed for ruminants, which hereafter we will call the BSE Ruminant Feed Rule.

The feed history investigation identified 21 products that had been used on the farm since 1990. These feed products were purchased from three retail feedstores and had been manufactured at nine different feed mills.

The investigators visited these establishments to collect information on formulation, shipping invoices, and the use of ruminant meat and bonemeal on the premises, both before the 1997 feed ban and after the 1997 feed ban.

This investigation found no feed products used on the farm since 1997 had been formulated to contain prohibited mammalian protein. The investigation identified one feed which contained an animal protein source that could not be identified and the investigation also found one feed mill that supplied feed to the farm and that used ruminant meat and bonemeal in feed formulations for nonruminant species after the BSE ruminant feed rule went into effect, and this was permitted under the rule.

And there were several feed mills that had used ruminant meat and bonemeal prior to the 1997 feed ban but had ceased to use that material after the 1997 feed ban.

The investigation into the disposition of herd-mates from this farm involved visits to nine slaughter plants and eight rendering plants. The investigation found that all rendering plants were operating in compliance with the BSE ruminant feed rule. A review of the inspection history of each of these rendering firms found no violation.

And those are my prepared comments.

SEC. JOHANNS: Very good. Thank you, both of you. And with that I think we're ready to open it up to some questions.

OPERATOR: Thank you. If you have a question you can do so by pressing *1 on your touchtone phone. Anytime you wish to cancel your question you can do so by pressing *2. Please be mindful to record your name as well as your affiliation when announced.

First question comes from Libby Quaid.

REPORTER: Hi. Thank you. A question for Dr. Sundlof with FDA. Your agency promised more than a year and a half ago to close loopholes in the feed ban. When will FDA act on that promise, and what will FDA do to close the loopholes?

DR. SUNDLOF: Thank you. Yes, we have been working on the proposed rule. We announced July 14 of 2004, in an advanced notice of proposed rulemaking, that we intended to move forward with a modification of the feed rule that would prohibit specified risk materials in all animal feeds. I can report that there's been quite a great deal of progress on that, and that we hope that a rule will be forthcoming within the next month or two.

REPORTER: Can you say what that rule will entail? Will it be different from what the ANPR was?

DR. SUNDLOF: It will -- well, the ANPR dealt with a whole lot of issues. And so I can't say it will be different, but I think you'll find it's consistent with what we announced in the ANPR.

MR. JIM ROGERS: Next question, please?

OPERATOR: Next question comes from Daniel Goldstein of Bloomberg News.

REPORTER: Yeah, hi. This question is for the Secretary. Last month or earlier this month the USDA released about 1,000 incidents where there was a case of meat plants not following the rules or violations for specified risk materials. And you spoke of some reluctance on the part of trading partners to reopen trade while there was a BSE investigation happening.

Has there been any reluctance on the part of these trading partners to reopen because of some of these violations?

SEC. JOHANNS: There hasn't been. They've asked for information. We supply that information, we answer whatever questions they have. There's an interest in it, I can say that, but I haven't had any trading partner say, 'We're not going to open the border,' or 'We're considering closing the border if they've opened it already.'

So at least at this stage it's been more of a situation where they were interested and we provided the information.

MR. ROGERS: Next question, please?

OPERATOR: Next question comes from Ron Hays of Clear Channel.

REPORTER: Yes. I guess my question is regards to some of the comments that have been made by the Japanese in recent days, Japanese Food Safety Commission. Seemingly some of their panel members questioning our feed ban and saying they're fearful that we might have as "bad of a situation as they had in Britain" is one quote we saw from the Japanese media. You know. Can anybody address-- what assurances can we make to them and to folks in this country that we are effective on our feed ban and right across the board?

SEC. JOHANNS: I'll ask Dr. Sundlof to address that in just a second, but I would just offer a thought.

That's just simply not the case. I mean, it just simply is not, not the case. We've worked very intensely, as you know, with the Japanese over many, many months now to deal with their questions and to address whatever concerns they raised. With the Japanese we've even gone beyond what international rules require. We agreed that we would start trading with animals at 20 months and under, and even the international standards don't require that.

In 452,000 animals tested in the last 14 months we've had two BSE-positive animals. So again, we'll respectfully address their question, but quite honestly I don't see any scientific basis for the issue they're raising.

Doctor, you can offer a thought if you would.

DR. SUNDLOF: Thank you, Mr. Secretary.

Well, let me just say that we've had a very effective feed ban in place since 1997. It's been over eight years now this month. And we have really focused our efforts on enforcing the ban and making sure that compliance with the feed ban was high.

And we reported on several occasions that compliance when we go out and investigate -- we did over 6,800 inspections in the last year and are projecting to do even more in the upcoming years -- that their physical inspections, where inspectors go out and do a physical examination of the feed plants or the renderers, in all cases we find the compliance by the industries affected is greater than 99 percent. So it's an extremely high compliance rate. It's hard to get any better than that.

The fact that both of these cattle that were BSE-positive in the United States were born at or before the feed ban and probably very likely consumed contaminated feed well before 1997-- there's just no indication the feed rule is not effective.

MR. ROGERS: Our next question, please?

OPERATOR: Next question comes from Steve Kay of Cattle Buyers Weekly.

REPORTER: Gentlemen, I want to go back to the proposed rule by AFDA because the question of Ron Hayes mentioned what members of Japan's Prion Subcommittee were referring to in part, and one of their concerns that we were still, we the U.S. are still allowing meat and bonemeal to be fed to nonruminants.

Now the advanced notice by FDA Dr. Sundlof suggests or proposes a ban on SRMs from all animal feed. Can you tell me, if you proceed with that, is that going to satisfy Japan, do you think? How is USDA going to convey to Japan that we might be moving in this way, because if this rule becomes a final rule but doesn't take effect for another year or more is Japan going to say, Well, we'll reopen our border in a year when this takes effect? I mean, how is all this going to play out?

SEC. JOHANNS: Well, I'll offer another thought and then Dr. Sundlof, I'd ask you to offer your thoughts.

Japan would not be justified under any science, any view of the world, to adopt that viewpoint. Again I point out with Japan we at the USDA, actually before I arrived, but made a decision to agree with Japan that we would start with the trade of animals 20 months and under.

In the history of the world we haven't found an animal that tested positive for BSE 20 months and under. They just simply have no risk here. So that approach would not be justified by international standards, it would not be justified by scientific standards. It really is time for Japan, in my opinion, to step up here and go through a science-based process and reopen the border, and hopefully we're nearing the end of that very kind of process.

Doctor, any thoughts?

DR. SUNDLOF: Thank you again, Mr. Secretary. I don't have the insight to know what the Japanese government is going to do, based on what the feed rule or the proposed feed rule will convey. But the rule is very much risk-based. It uses the Harvard Risk Assessment to actually quantitate the risk and the risk reduction of the proposed measures that we will be publishing soon. And so I would agree with the Secretary that on the basis of science, the science is clearly laid out in the proposed rule and under a risk assessment that has undergone significant peer review by the scientific community.

So I think if the decisions are going to be based in science then I think we will have a very defensible position.

MR. ROGERS: Next question, please.

OPERATOR: Next question comes come from Kerry Young of Bloomberg.

REPORTER: Hi. I just had a question on why it's taking so long to get the revised feed ban out there.

SEC. JOHANNS: Dr. Sundlof, if you could address that?

DR. SUNDLOF: Okay, thank you again. Well, one of the reasons was -- there's actually a number of reasons. Back in January 2004 when, within a month after the first case in the U.S. was reported, the Secretary of Health and Human Services at that point made a statement that the FDA would propose modifications to the feed rule that would eliminate plate waste, poultry litter, cattle blood and require that all facilities that manufacture with ruminant meat and bonemeal be dedicated to non-ruminants and not prepare any ruminant feed in those mills.

Within a week after the Secretary's announcement, the International Review Team that was advisory to the Secretary of Agriculture made recommendations that were very much different than that which the Secretary had announced the week prior. Based on that, we decided at that point to go through an advanced notice of proposed rulemaking to get all the information out, all the recommendations that the International Review Team has made, and discuss those from a risk basis.

And as a result of that, we are now into rulemaking.

One other thing that was a reason for the delay is that during this time USDA was in the middle of their intense surveillance activity to try and determine the prevalence of BSE in U.S. cattle. And that was done, the questions that were before us were--the International Review Team based their recommendations on assumptions that there was significant infectivity in the U.S. cattle herd. The results of the USDA surveillance tend to cast doubt on that assumption, and so it had a major effect on which was the correct regulation or what were the correct measures that would be commensurate with the real risk?

So those are some of the reasons it has been delayed. It's a complicated regulation. It involves a lot of material that will have to be disposed of in some environmentally friendly way, and so we have to be very thoughtful about how we propose a rule that has minimal environmental impacts but yet does the greatest amount to reduce the actual risk to BSE in cattle.

SEC. JOHANNS: If I could just add something that obviously is very, very relevant and very important. Again, that's to point out that in the last 14 months we've tested 452,000 high-risk animals. These are the animals, that present themselves for testing, that experience would show from other countries would have the highest chance of being a BSE situation. We've had two out of that identify as positive. And both of those animals were born before the feed ban.

So it's obviously the decision, some years ago now, to impose the first generation of feed ban was the right decision.

MR. ROGERS: Next question, please.

OPERATOR: Next question comes from Sally Schuff from Feedstuffs.

REPORTER: Yes. This is Sally Schuff at Feedstuffs. Thank you for taking the question.

The question is a two-part question for Dr. Clifford and Dr. Sundlof. Dr. Clifford, you said when the second case was announced the test results were more similar to the Western blot test, was more similar to results found in France than in the United Kingdom, leading to some question about what strain of BSE she might have. My question to you is, has that been resolved yet? Do you have any more positive identification on the strain?

My question for Dr. Sundlof is, have you identified the source of the meat and bonemeal that was fed prior to the feed ban? Was it domestic or imported?

DR. CLIFFORD: This is John Clifford. I'll answer the first part. From a regulatory standpoint, this is a case of BSE. Looking from a molecular standpoint, there's further work that's being done internationally on some of these cases. And--but from our standpoint, this is a case of traditional BSE that we would find. So that's the way we're approaching this.

OPERATOR: Next question comes from Karen Robinson of Dallas Morning News.

REPORTER: Hello, this is Karen Robinson Jacobs with the Dallas Morning News. I wanted to go back to the Texas cow, and if you could tell us maybe a little more slowly how much cattle or meat from this particular index ranch got into the human food chain, how much got into the pet food chain, and how concerned should consumers be that they may have eaten something already before the test even began?

DR. CLIFFORD: This is John Clifford. I'd begin by saying if you look at what we know internationally, it's not very common at all. In fact it's rare to have more than one single case of BSE found within a herd. So from that standpoint alone, the risk is extremely small. In addition you have other safeguards in place. We have had a feed ban in place since 1997. It's been in place for 8 years, and then there's other cross-cutting protections as well from the food safety side that Dr. Ken Peterson's on if he wants to address as well.

But as far as actual poundage, I don't think it's possible for us to give you that actual number. There was two calves of interest that we traced. Due to the lack of appropriate records at the time, we actually traced 213 calves. Of those, it's estimated that 212 of those animals went into the feeding and slaughter channels. Those animals would have been slaughtered likely prior to 30 months of age, which we know that it's extremely small risk of having BSE prior to 30 months of age.

And also internationally and in the research community, while it's never been proven that offspring can get this disease through maternal transmission -- it's never been proven or disproven actually -- but it's thought very much from the international experts and the research it is extremely rare if it does happen.

Both of these calves were born very well prior to this animal being slaughtered. This animal did not show any clinical signs typical of BSE -- sampled and destroyed. This animal did not show any clinical signs or evidence of BSE which would make it even more unlikely that these two offspring would have any risk of having BSE.

The other 200 head that were traced were retraced as a result also of a lack of records. We were looking at cattle of interest over a five-year period of time of which this animal was born. Her approximate age was 12. We expanded one year of that and made her 11 to 13, and then we'd go another year beyond that. So we looked at animals basically in the age range of 10 to 15 years of age to remove those from the herd. And we traced every adult animal that we could from 1990.

Many of those animals would not even be of concern because they would not have received any feed at the time that she was in the herd or would have not been a birth cohort and born at the same time that she was.

So of those, 143 were reported as slaughtered, and we confirmed that 131 were definitely slaughtered; 34 were presumed dead, and 20 of those were untraceable. So again, we feel that the risk is extremely small. We do not feel that the public or our pet food industry should have any concerns relative to this issue.

MR. ROGERS: Next question, please.

OPERATOR: Next question comes from Chuck Abbott of Reuters.

REPORTER: Good afternoon. I'm curious -- what, Mr. Secretary, what you're going to do about the downer ban which is still now a preliminary rather than a permanent rule. When will you decide on the downer ban? How sweeping will it be? And what's going to happen to the surveillance testing program? It has run some months beyond its originally envisioned lifetime. I'll stop there.

SEC. JOHANNS: The surveillance program, as you know, was really open-ended. So I might debate with you a little bit on your last thought there. But here's what I would say. I am not prepared to bring the surveillance program to a conclusion, have not made a final decision on the downer ban. As you know, we've started now with the testing of the 20,000 healthy animals. We hope to have that done in the next 60 days.

Dating from the time of my confirmation hearing really until now, my view was to get the surveillance program in the kind of shape that we wanted, make sure that we'd touched all the bases. And then, in addition to that, do the additional testing of the 20,000 healthy animals and then, once we have all the information together, make a decision on some of those pending issues.

So that's where it's at.

MR. ROGERS: All right. I'd like to thank everyone for calling today. If you have further questions for the U.S. Department of Agriculture, you can call me, Jim Rogers, at 202-690-4755. If you have questions for the Food and Drug Administration, please contact my counterpart Ray Jones at 301-827-6246. This concludes the call for today, and I thank you all for participating.


Last Modified: 08/30/2005


http://www.usda.gov/wps/portal/usdahome?contentidonly=true&contentid=2005/08/0339.xml


>>>
All evidence is that the prevalence is extremely low and continues to decline given the length of time the ruminant feed ban has been in effect.
<<<


HOW much longer can this buffoonery go on???

I only pray that the world does not buy into this phony BSE MRR policy and June 2004 Enhanced BSE surveillance program. none of it was based on sound science.
THE June 2004 Enhanced BSE/TSE surveillance program was a terrible failure, other than to prove just how bad the situation is in the USA, and how out of control the Federal Government is in trying to cover it up. THE OIG should hold an inquiry into this program. THE BSE MRR policy should be dismantled, and the USA BSE GBR risk assessment should be immediately raised to BSE GBR IV.
THE International guidelines for trade in animal and animal products which are developed by the World Organization for Animal Health (formerly known as the Office International des Epizooties (OIE)), is and has been terrible flawed. ALL one has to do is to look at the countries that have gone by there very minimal guidelines, most all went on to develop BSE. IT would be nice if the OIE et al would define “controlled BSE-risk country” or “effectively enforced ban”. The USA and North America have neither. THIS has been proven time and time again via the GAO, OIG and the European EFSA BSE-risk assessments of North American countries. Many Countries have not even reported there first case of BSE yet, and many countries have not even produced a risk analysis for BSE. A fine example is Mexico, which is also a BSE GBR III country. IN Mexico, they are NOT even required to remove SRM;

Working Group Report on

the Assessment of the Geographical BSE-Risk (GBR) of

MEXICO

2004


Specified Risk Material (SRM) and fallen stock

There is no SRM-ban. SRM is normally destined for human consumption. According

to the CD, fallen stock from pasture and diseased animals are incinerated and not

rendered.

Conclusion on the ability to avoid recycling

In light of the above information, it has to be assumed that the BSE agent, should it

have entered Mexico, could have been recycled and potentially amplified.


snip...


In view of the above - described consideration the combination of the very / extremely

high external challenges with a very unstable system makes the occurrence of an

internal challenge likely in Mexico from approximately 1993 onwards.

4.2 Risk that BSE infectivity entered processing

It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’

MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late

1990’s). The high level of external challenge is maintained throughout the reference

period, and the system has not been made stable, leading to increased internal

4.3 Risk that BSE infectivity was recycled and propagated

It is likely that BSE infectivity was recycled and propagated from approximately

1993. The risk has since grown consistently due to a maintained internal and external

challenge and lack of a stable system.

5. CONCLUSION ON THE GEOGRAPHICAL BSE - RISK

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 likely but not confirmed

that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.

snip...end


http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/scr_annexes/566/sr04_biohaz02_mexico_report_annex_en1.pdf


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)

Report

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 increases.

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/573_en.html


From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Tuesday, July 29, 2003 1:03 PM
To: fdadockets@oc.fda.gov
Cc: ggraber@cvm.fda.gov; Linda.Grassie@fda.gov; BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

Greetings FDA,

snip...

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 decisions
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


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


Gerald Wells: Report of the Visit to USA, April-May 1989

snip...

The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...

snip...

It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...

snip...

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_...

snip...

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

WITH all said, the following is probably the most ignoramus statement about the Texas mad cows and
BSE/TSE surveillance as a whole in the USA. really, it's very frightening to me, because i think
they are starting to believe in there lies and deciet ;


>>>
Before I turn things over, though, I will say that we are extremely pleased with the results of the epidemiological investigation. It shows there was no widespread problem associated with the index herd, and as you will hear more about in a moment, that the ruminant feed ban in the United States is solid. It also affirms that USDA's interlocking system of safeguards to prevent BSE from entering the food chain is working as it should. <<<


there must be some kind of hearing or congressional investigation into this continued blunder by the USDA et al about BSE/TSE in the USA and all of North America. ...


TSS

----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Wednesday, August 31, 2005 1:19 PM
Subject: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1)


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

From: TSS ()
Subject: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1)
Date: August 31, 2005 at 11:08 am PST

Texas BSE Investigation

Final Epidemiology Report

August 2005

2

Table of Contents

Executive Summary............................................................................................................. 3

Background of the Investigation......................................................................................... 3

BSE Response Plan .............................................................................................................. 3

Definition of At-Risk Cattle.................................................................................................... 3

Definition of Cattle of Interest ............................................................................................... 4

Definition of Feed Cohort...................................................................................................... 4

Definition of Birth Cohort...................................................................................................... 4

Definition of At-Risk Progeny................................................................................................ 4

Epidemiology Investigation of Index Herd: Farm A....................................................... 5

Background........................................................................................................................... 5

Progeny................................................................................................................................. 6

Birth Cohort ........................................................................................................................... 6

Feed Cohort ........................................................................................................................... 6

Removal of Cattle from the Index Farm............................................................................ 7

Tracing of Progeny .............................................................................................................. 7

Tracing of Birth Cohorts..................................................................................................... 8

Tracing of Cattle of Interest................................................................................................ 9

Calculation of Minimum Estimated Ages .............................................................................. 9

Trace Herds ........................................................................................................................ 10

Trace Herd 1........................................................................................................................ 10

Trace Herd 2........................................................................................................................ 10

Trace Herd 4........................................................................................................................ 11

Trace Herd 5........................................................................................................................ 11

Trace Herd 6........................................................................................................................ 11

Trace Herd 7........................................................................................................................ 12

Trace Herd 8........................................................................................................................ 12

Analysis of Data on Presumed Dead and Untraceable Animals.................................... 12

Appendix 1 – Final Trace-Out Diagram.............................................................................. 13

3

Executive Summary

In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from

November 2004, that had originally been classified as negative on the

immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot).

The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow

in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation

with the Texas Animal Health Commission (TAHC), established an incident command post

(ICP) and began response activities according to USDA’s BSE Response Plan of

September 2004. Response personnel removed at-risk cattle and cattle of interest (COI)

from the index herd, euthanized them, and tested them for BSE; all were negative. USDA

and the State extensively traced all at-risk cattle and COI that left the index herd. The

majority of these animals entered rendering and/or slaughter channels well before the

investigation began. USDA’s response to the Texas finding was thorough and effective.

Background of the Investigation

On June 10, 2005, USDA announced that the November 2004 inconclusive BSE sample

tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s National

Animal Disease Center (NADC) upon the recommendation of USDA’s Office of the

Inspector General. Samples were sent to a World Organization for Animal Health (OIE)

reference laboratory for BSE in Weybridge, England, for confirmatory tests. Farm A,

located in Texas, was the suspected farm of origin for the index cow and was placed under

hold order on June 20, 2005 pending confirmation of the positive results and DNA analysis

of the herd. Weybridge confirmed the BSE positive on June 24, 2005. The carcass of the

index cow had been disposed of by incineration in November 2004. Cattle from several

units on Farm A were bled for DNA testing (a unit is a part of the business entity of a farm.

For example, a pasture on which a group resides may be a unit). Farm A was confirmed as

the farm of origin for the index cow on June 29, 2005, and an ICP was established in Texas

to coordinate the response. Removal of at-risk cattle from the index herd, and tracing of atrisk

cattle and COI that had left the index herd, commenced immediately.

BSE Response Plan

The September 2004 BSE Response Plan outlines the necessary tracing and removal of atrisk

cattle and, in some cases, COI, in response to the identification of a BSE-positive

animal. Response personnel removed at-risk animals from the index farm and traced atrisk

animals and COI in accordance with the response plan.

Definition of At-Risk Cattle

At-risk cattle were cattle that were confirmed to be: part of the birth cohort; part of the feed

cohort; or progeny of the positive cow born within 2 years prior to the positive test.

Response personnel removed at-risk cattle from the herd, euthanized them, and tested them

for BSE; all were negative.

4

Definition of Cattle of Interest

In many cases, at-risk cattle could not be definitively identified. Response personnel then

analyzed herd inventories and herd records to identify a group of cattle that include all

potential at-risk cattle and any other cattle that could not be distinguished from at-risk

cattle. All of these cattle (at-risk cattle and any additional cattle as necessary) were defined

as COI. COI that fell into the appropriate age range and could be part of the birth or feed

cohort were removed from the herd, euthanized, and tested for BSE; all were negative.

Definition of Feed Cohort

The feed cohort consisted of all cattle which, during their first year of life, were reared with

the positive animal during its first year of life and consumed the same feed during that

period. In the index herd, this definition applied to cattle in any unit that were weaned and

fed with calves from the other units for a short period of time and then later returned to

their respective units of origin from 1991-1995 (the range of years that could have

coincided with the first year of life of the index cow).

Definition of Birth Cohort

In most cases, it was impractical or impossible to definitively determine which cattle were

exposed to a feed source. Accordingly, response personnel used a birth cohort to determine

which cattle to consider at-risk. The birth cohort included all cattle born on the positive

animal’s birth premises within 1 year before or after the BSE-positive animal’s date of

birth.

Since the index cow was approximately 12 years of age, but an exact date of birth did not

appear in the herd records, response personnel used a potential age range of 12 years with 1

year added to each end of that age (age 11 to 13) to sufficiently cover the most likely age

range of the animal. In addition, if the positive animal moved from the birth premises to

any other premises during its first year of life, all cattle of less than 1 year of age that were

present on such additional premises were also considered to be at-risk. Using the age range

of the index animal, all cattle born on the index premises from 1990-1995 were part of the

birth cohort of the index animal.

Definition of At-Risk Progeny

Since the index cow was not confirmed to have been exhibiting clinical signs of BSE prior

to her positive test results, the at-risk progeny as defined by the OIE were those offspring

that were born within the 2 years prior to the positive test result. Those 2 years prior to the

positive test result would have included her calves from 2002, 2003, and 2004. According

to the owner, the index cow produced her last calf either in Fall 2003 or Spring 2004, and

the calf prior to that was born either in Fall 2002 or Spring 2003. Tracing activities

focused on these two calves as at-risk progeny.

5

Epidemiology Investigation of Index Herd: Farm A

Background

The index cow was an approximately 12-year-old yellow or cream-colored Brahma cross

that originated from Farm A located in Texas. The cow was sold through a livestock sale

on 11/11/04, purchased by an order buyer, and was transported to a packing plant on

Monday, 11/15/04. When the truck arrived at the packing plant during the late afternoon of

11/15/04, the index cow and one other were found dead on the truck and were transported

to a pet food plant later that day where they were sampled for BSE testing as part of the

enhanced BSE surveillance.

DNA analysis of blood samples taken from five of the six units of cattle that comprise

Farm A yielded four animals from two different units that were genetically related to the

index cow and confirmed Farm A as her herd of origin.

The herd on Farm A consisted of mixed breed beef cattle that are traditionally not used as

seedstock replacement animals. Market records and preliminary tracing indicated that most

animals that left the index herd either went to slaughter within a few days of sale or, in the

case of younger animals, entered into known rendering and slaughter channels immediately

following sale. There were only 11 cows identified during the investigation that were

traced from Farm A into other herds where they had been used as replacement cows.

The owner of Farm A raised this cow from birth and stated that the cow had never been off

the premises prior to its sale. She was marketed because of poor body condition (the

animal’s condition had not improved despite the early weaning of her 2003/2004 calf). The

owner stated that the cow had always been excitable and had fallen while she was being

loaded to go to the market, but that this was not unusual behavior for her in his opinion. In

addition there was a report of this cow being down in the alley at the livestock market on

11/11/04, but she apparently got up again and was able to be loaded onto the truck to go to

the packing plant. When questioned about any previous history of neurological signs in

cattle on the farm, the owner reported that no cattle on the farm had ever shown any

neurological signs, nor had there been any cases of rabies on the index farm.

Index Herd Census

Farm A consisted of 6 units (Units A through F) containing a total of about 217 adult cattle

and approximately 100 to 120 calves. Early in the investigation, response personnel

discovered that an additional unit belonging to the owner’s son and located adjacent to Unit

F could also contain COI. This group, Unit G, contained 16 adult cattle and made a

seventh unit that became included in the investigation.

On 6/22/05, the first three of the original six units were sampled for DNA testing to

confirm the herd of origin of the index cow. Those first three units consisted of: Unit A

contained 62 head with some older cattle (more likely than the other units to provide a

DNA match); Unit B with 28 head (3-year-old unit); and Unit C with 25 head (2-year-old

unit). Two additional units were sampled for DNA on 6/23/05; Unit D with 31 head and

Unit E with 30 head, both of which contained older animals.

6

The sixth unit, Unit F, containing 41 head, was purchased in 1993 from another source.

Because it did not have animals that were genetically related to the other 5 units, this unit

was not sampled for DNA testing. Unit F, and adjacent Unit G, contained COI because the

weaned heifers from those units were commingled and fed with weaned heifers from the

other units for a short period of time before they were returned to their respective units of

origin. This practice of weaning and feeding together fit the definition of a feed cohort.

Progeny

The owner did keep some replacement heifers and, although he was relatively sure that he

had not kept any offspring from the yellow cow because of her excitable demeanor, DNA

analysis of the herd revealed several animals in the herd that may have been older offspring

of the index cow. While the owner sold 12 calves at the sale with the index cow on

11/11/04, her last calf was not in that group. According to the owner, the index cow’s last

calf was born either in Fall 2003 or Spring 2004, weaned early, and sold through the

livestock market some time between February and October 2004. The calf prior to that

would have been born either in Fall 2002 or Spring 2003 and was sold at the livestock

market sometime between January and December 2003.

Birth Cohort

The owner of Farm A kept very few herd records; this made finding documentation on this

cow’s birth cohort difficult. The birth cohort, by definition, included all cattle born on the

positive animal’s birth premises within 1 year, before or after, the positive animal’s date of

birth. The index cow was approximately 12 years of age in November 2004, but there was

no exact birth date in the herd records. A potential age range of 11 to 13 years was used to

sufficiently cover the animal’s most likely age. Using this range, all cattle born on the

index premises between 1990 and 1995 were considered part of the birth cohort.

In lieu of the owner’s records, herd records from Veterinary Services’ Generic Database

(GDB) were used to compile a list of brucellosis calfhood vaccination (CV) tag numbers

from the index herd that corresponded to animals to be included in the birth cohort. There

were 121 animals identified through GDB as having been calfhood vaccinated on the index

farm between 1991 and 1994. The owner of Farm A did not calfhood vaccinate after 1994.

Moreover, calfhood vaccinates include only heifers. Therefore, the list of 121 animals was

not a complete list of all birth cohorts. However the tracing that response personnel

conducted on other COI was designed to account for the remainder of the birth cohorts.

Feed Cohort

Animals in Units A, D, and E, that were weaned and fed with the positive cow between

1991-1995, were already considered at-risk as part of the defined birth cohort. Animals in

Units B and C were 3-year-olds and 2-year-olds, respectively, and were too young to be

either birth or feed cohorts. Although Unit F was purchased separately and did not contain

animals genetically related to the other units, calves from Unit F were weaned and fed for a

short period of time with weaned calves from other units and all calves were later returned

to their respective units of origin. Since Unit F was not purchased until 1993, the feed

cohort consisted of those animals in Unit F that could have been weaned and fed with the

index cow in 1993 or 1994. Additionally, Unit G contained possible feed cohorts that

could have been weaned and fed with the index cow between the years of 1991 and 1995.

7

Feed

The feeding regimen for the cattle in this herd consisted of natural pasture, hay, mineral

supplement, syrup tubs occasionally, and a breeder’s supplement (predominantly a name

brand manufactured breeder’s cube). The Food and Drug Administration (FDA)

investigated all sources of feed and supplements used on Farm A. In-depth investigations

and site visits were conducted by FDA involving retail feed stores, feed manufacturers,

slaughter plants, renderers, and brokers. A more detailed account of the investigation is

contained in FDA’s final report.

Removal of Cattle from the Index Farm

Any animal still present within the index herd that could have been a possible birth cohort

or feed cohort of the index cow was targeted for removal as an at-risk animal. Units A, D,

E, F, and G, all of which were known to contain older animals, were inventoried.

Identification tags, tattoos, and brands were recorded, and all animals were aged based on

their dentition and any man-made identification. Cattle whose estimated age indicated that

they could have been part of the index cow’s birth or feed cohort were removed from the

herd, euthanized, and tested for BSE; all were negative.

Units B and C were exempt from the cohort removal process because they contained only

3-year-old and 2-year-old animals respectively. Although the DNA analysis of animals in

Units A through E determined that there were 2 animals present that could have been

offspring of the index cow, their estimated age by dentition revealed that they were not of

the appropriate age to be at-risk progeny. This verified the owner’s claim that he had sold

the index cow’s last two calves at the livestock market and they were not currently present

in the index herd.

After sorting by age, response personnel identified and removed the following numbers of

cows from the herd on 7/6/05: Unit A, 11 cows; Unit D, 11 cows; Unit E, 7 cows. The

same process was applied to Units F and G and the following numbers of cows were

identified and removed from the herd on 7/7/05: Unit F, 28 cows; Unit G, 10 cows.

Of the 67 animals removed from the herd as possible birth cohorts and/or feed cohorts of

the index cow, 42 were definitively identified as belonging to the birth cohort due to the

presence of a calfhood vaccination tag or tattoo that corresponded to the appropriate birth

cohort years. All 67 animals were euthanized on 7/6/05 and 7/7/05 and samples were

subsequently sent to USDA’s National Veterinary Services Laboratories (NVSL) for BSE

testing. All samples were run on the ELISA test and confirmed negative on 7/8/05 and

7/9/05. Upon confirmation of negative results, disposal of carcasses was completed by

burial in an approved landfill facility. The index farm was released from hold order on

7/11/05.

Tracing of Progeny

The 2003/2004 progeny of the index cow was known to have left the farm through a

specific livestock market sometime between February and October 2004. The 2002/2003

progeny of the index cow left the farm through the same market sometime between January

8

and December 2003. Response personnel learned early in the investigation that animals

from the index farm were sold not only under the index farm owner’s name and that of his

wife, but also by other members of the owner’s immediate family. Additionally, there were

no herd records to indicate the gender of the two at-risk progeny. Therefore, market

records for February through October 2004 and January through December 2003 were

obtained for all calves sold both by Farm A’s owner and by members of his immediate

family; response personnel traced all such calves to determine their disposition.

With the index herd being composed of mixed breed beef cattle, the calves that left the

farm were genetically unsuitable for use as replacement animals or for sale as breeding

stock, a fact that was confirmed by the trace work and the documentation of the final

disposition of the calves of interest.

Response personnel ultimately identified 213 calves of interest to be traced. Of these, 208

were confirmed to have entered known rendering/slaughter channels, 4 were presumed to

have entered rendering/slaughter channels, and 1 was purchased in cash through a livestock

market with no buyer name or contact information (this animal was classified as

untraceable. See Appendix 1). A calf was categorized as presumed to have entered

rendering/slaughter channels if it passed through at least one livestock market subsequent

to its original sale and could not be individually traced due to unknown resale date and new

backtag, but all calves resold matching that description during an appropriate date range

were purchased by known rendering/slaughter order buyers.

It was not possible to DNA test the calves that entered known rendering and slaughter

channels – most were of an age in which they were likely to have been slaughtered prior to

the time of the investigation. There were no calves traced to farms outside of rendering and

slaughter channels.

Tracing of Birth Cohorts

Since there were essentially no records maintained on the index farm, it was necessary to

compile the list of known birth cohorts using brucellosis CV tag numbers for this herd from

the period 1991 to 1994. The calves vaccinated during that time period were part of the

index cow’s birth cohort and tracing activities centered on finding those animals.

There were 121 animals whose CV tag number and/or tattoo included them as part of the

birth cohort. Of those 121 animals, 67 animals were definitively accounted for (42 were

found in the index herd, removed, and tested BSE negative; 25 were identified as having

left Farm A through the market system and were traced, 11 of those were reported

slaughtered, 13 were classified as presumed dead, and 1 was found alive, euthanized, and

tested BSE negative). Of the remaining 54 animals from the birth cohort, there may have

been several that died within the index herd, but the majority likely left the herd without

identification and would have been either re-tagged at the livestock market or consigned

directly to slaughter without identification. To account for these remaining birth cohorts,

all adult cattle that left the index farm since 1990 were traced as COI.

9

Tracing of Cattle of Interest

The investigation revealed that many animals left Farm A, arrived at markets without any

identification tags, and were subsequently re-tagged at the market. Due to lack of farm

records, it is unknown which of these re-tagged animals may have belonged to the birth

cohort. As a result, all animals that may have left Farm A since 1990 were traced as COI.

Additionally, animals from the index farm were sold not only under the index farm owner’s

name and that of his wife, but also by other members of the owner’s immediate family;

therefore, cattle sold from the index farm by all pertinent family members were traced.

There were some older animals that left the index farm but were able to be excluded from

further trace work because they were known not to have been part of the birth cohort or

feed cohort of the index cow despite their being of the appropriate age. The index farm

owner’s late father had maintained a herd of cattle separate from the index farm but which

was added to the index farm in 1997. Complete herd test data and CV data from the GDB

was obtained for the father’s herd and those animals were excluded from the tracing

activities.

There were a total of 200 COI traced: 143 were reported to have been slaughtered (131 of

those were confirmed as having been slaughtered), 1 is known to have died previously and

was buried, 2 were found alive (1 was a known birth cohort that tested negative, 1 was

determined not to be one of the cattle of interest due to her young age), 34 were classified

as presumed dead, 20 were classified as untraceable. (See Appendix 1). Animals were

confirmed at slaughter using GDB slaughter testing data or the hard copies of slaughter

testing Form 4-54.

An animal was classified as presumed dead if records that could be used to advance the

tracing of the animal were exhausted or did not exist, and the age of the animal at the time

of the investigation was estimated to be at least 11 years old or older. Since the index herd

was not a purebred or seedstock operation, and animals leaving the herd were unlikely to

be purchased as replacement cattle, standard industry practices indicated that most adult

animals that had left the herd would have been culled and slaughtered by the time they

were in this age group. Additionally, this age cutoff was arrived at through review of

market records and the specific years in which Farm A sold cattle through the market. An

animal was classified as untraceable if all records to advance the tracing of the animal were

exhausted or did not exist, and the age of the animal at the time of the investigation was

estimated to be less than 11 years of age (the animal, therefore, could not be presumed

dead).

Calculation of Minimum Estimated Ages

Throughout the tracing process, personnel used minimum estimated ages of the 200 COI to

evaluate whether those individuals could be old enough to be part of the birth or feed

cohort of the index cow. Since Farm A’s owner maintained no records on the ages of

animals, GDB data assisted in assigning minimum estimated ages. Animals that were

wearing brucellosis CV eartags could be aged quite accurately because the exact CV date

was recorded in the GDB and those animals would have been vaccinated between 4 to 12

months of age. The GDB also contained lists of individual eartags for all animals on the

10

index farm that were included in complete herd brucellosis testing in 1991, 1993, and 1994.

Cattle included in those herd tests would have been at least 18 months of age at the time of

the test and their minimum age today could be extrapolated from that data. Finally, the

GDB also contained livestock market testing data that could also be used to assign a

minimum age because the animal would have been at least 18 months of age on date the

earliest brucellosis market test was conducted. The minimum ages calculated for the cattle

of interest were used later in an analysis by USDA’s Centers for Epidemiology and Animal

Health (CEAH) to determine the probable disposition of untraceable and presumed dead

animals based on their age.

Trace Herds

Response personnel made every attempt to trace COI to their final dispositions (which, in

most cases, was slaughter). If an animal was traced to a herd owner and the owner could

not provide information that indicated that the animal of interest was not currently present

within his/her herd, the owner’s herds were placed under hold order pending a herd

inventory to determine whether or not the animal of interest had been retained. There were

eight herds identified as the last traceable location of the animal of interest and were,

therefore, subjected to herd inventories in an attempt to locate the animal.

When an animal of interest was located within a herd, the age of the animal was estimated

using dentition and any man-made identification. If the animal fell into the appropriate age

range to be a possible birth cohort or feed cohort of the index cow, the animal was removed

from the herd and tested. If an animal of interest was located within the herd and fell into

the appropriate age range to be a possible at-risk progeny of the index cow, the animal was

sampled for DNA testing.

Trace Herd 1

The owner of Trace Herd 1 was identified as having received one of the adult COI from the

index herd. Trace Herd 1 contained 909 head of cattle in multiple pastures and was placed

under hold order on 7/21/05. Upon completion of herd inventory, the animal of interest

was not found within the herd. A GDB search of all recorded herd tests conducted on

Trace Herd 1 and all market sales by the owner failed to locate the identification tag of the

animal of interest and she was subsequently classified as untraceable. The hold order on

Trace Herd 1 was released on 8/8/05.

Trace Herd 2

Trace Herd 2 was identified as having received one of the adult COI from the index herd.

Trace Herd 2 contained 19 head of cattle on one pasture and was placed under hold order

on 7/25/05. The owner of Trace Herd 2 identified the animal of interest by her eartag while

he was feeding his cattle out of a bucket and individually penned her for inspection by field

personnel. While the cow was identified as one of the animals that had left the index farm,

her age by dentition was estimated to be only 5 years old, which was too young to have

placed her as part of the birth or feed cohort of the index animal. She was classified as

found alive but determined not to be one of the COI; the hold order on Trace Herd 2 was

released on 7/26/05.

11

Trace Herd 3

The owner of Trace Herd 3 was identified as possibly having received an animal of

interest. The herd was placed under hold order on 7/27/05. The herd inventory was

conducted on 7/28/05. The animal of interest was not present within the herd, and the hold

order was released on 7/28/05. The person who thought he sold the animal to the owner of

Trace Herd 3 had no records and could not remember who else he might have sold the cow

to. Additionally, a search of GDB for all cattle sold through the markets by that individual

did not result in a match to the animal of interest. The animal of interest traced to this herd

was classified as untraceable because all leads were exhausted.

Trace Herd 4

The owner of Trace Herd 4 was identified as having received one of the COI through an

order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd

inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were

examined individually by both State and Federal personnel for all man-made identification

and brands. The animal of interest was not present within the herd. Several animals were

reported to have died in the herd sometime after they arrived on the premises in April 2005.

A final search of GDB records yielded no further results on the eartag of interest at either

subsequent market sale or slaughter. With all leads having been exhausted, this animal of

interest has been classified as untraceable. The hold order on Trace Herd 4 was released on

8/23/05.

Trace Herd 5

The owner of Trace Herd 5 was identified as having received two COI and was placed

under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple

pastures. During the course of the herd inventory, the owner located records that indicated

that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was

subsequently found alive. Upon completion of the herd inventory, the other animal of

interest was not found within the herd. A GDB search of all recorded herd tests conducted

on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of

the animal of interest and she was subsequently classified as untraceable due to all leads

having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.

Trace Herd 6

The owner of Trace Herd 6 was identified as possibly having received an animal of interest

and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on

two pastures. A herd inventory was conducted and the animal of interest was not present

within the herd. The owner of Trace Herd 6 had very limited records and was unable to

provide further information on where the cow might have gone after he purchased her from

the livestock market. A search of GDB for all cattle sold through the markets by that

individual did not result in a match to the animal of interest. Additionally, many of the

animals presented for sale by the owner of the herd had been re-tagged at the market

effectually losing the traceability of the history of that animal prior to re-tagging. The

animal of interest traced to this herd was classified as untraceable due to all leads having

been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.

12

Trace Herd 7

The owner of Trace Herd 7 was identified as having received an animal of interest and was

placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple

pastures in multiple parts of the State, including a unit kept on an island. The island

location is a particularly rough place to keep cattle and the owner claimed to have lost 22

head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the

animal of interest was not found present within Trace Herd 7. A GDB search of all

recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to

locate the identification tag of the animal of interest. The cow was subsequently classified

as untraceable. It is quite possible though that she may have died within the herd,

especially if she belonged to the island unit. The hold order on Trace Herd 7 was released

on 8/8/05.

Trace Herd 8

Trace Herd 8 received an animal of interest, which happened to be a known birth cohort of

the index cow, from Trace Herd 5. Trace Herd 8 consists of 146 head of cattle that were

placed under hold order on 8/4/05. A herd inventory was conducted, the birth cohort was

found alive in the herd, and she was purchased and euthanized. The hold order on Trace

Herd 8 was released on 8/4/05. The cow was sampled on 8/5/05 and BSE tested by ELISA

at NVSL. Results were negative (as reported on 8/6/05); carcass disposal was completed

by alkaline digestion.

Analysis of Data on Presumed Dead and Untraceable Animals

CEAH performed an analysis of the minimum estimated ages of those COI that were

classified as either presumed dead or untraceable to determine the likely disposition of

those animals based on their ages. Moreover, CEAH performed an analysis of the likely

disposition of the one calf that was classified as untraceable during the investigation.

13

Appendix 1 – Final Trace-Out Diagram


http://www.aphis.usda.gov/lpa/issues/bse/epi-updates/bse_final_epidemiology_report.pdf

TSS


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




Follow Ups:



Post a Followup

Name:
E-mail: (optional)
Subject:

Comments:

Optional Link URL:
Link Title:
Optional Image URL: