##################### Bovine Spongiform Encephalopathy #####################
From: TSS ()
Subject: Re: Texas BSE Investigation Final Epidemiology Report August 2005
(PART 1)
Date: August 31, 2005 at 2:16 pm PST
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:
[email protected]
www.thelancet.com Published online January 27, 2005
http://image.thelancet.com/extras/05let1056web.pdf 1
Risk of oral infection with bovine spongiform
encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,
Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown,
Jean-Philippe Deslys
The uncertain extent of human exposure to bovine spongiform encephalopathy
(BSE)—which can lead to variant
Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about
the efficiency of oral infection
and the magnitude of any bovine-to-human biological barrier to transmission.
We therefore investigated oral
transmission of BSE to non-human primates. We gave two macaques a 5 g oral
dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60
months after exposure, whereas the
other remained free of disease at 76 months. On the basis of these findings
and data from other studies, we made a
preliminary estimate of the food exposure risk for man, which provides
additional assurance that existing public
health measures can prevent transmission of BSE to man.
B
C
E
A
Dilution
D
3·215
1·989
0·984
0·302
0·131
0·065
0·052
1/10
1/30
1/100
1/300
1/1000
1/3000
Neg
36 kDa
36 kDa
22 kDa
22 kDa
16 kDa
1 2 3 4
ELISA detection of PrPres (absorbance units)
Figure: PrPres content of brain homogenate and histopathological assessment
of macaque tissues
(A) Results of in-vitro testing for PrPres in BSE-infected inoculum by ELISA
and western blot. Neg=normal bovine
brain material. (B) Typical florid plaque in the occipital cortex of the
macaque that developed disease.
PrPres detected by proteinase K treatment with SAF32 anti PrP monoclonal
antibody (kindly provided by Jacques
Grassi, CEA Saclay). The dense core of PrPres is surrounded by several
vacuoles in a fibrillar proteinaceous corona;
bar=10 m. (C) Positive PrPres staining in tonsil (80% of follicules
stained positive) of the macaque that developed
disease; bar=50 m. (E) Negative PrPres staining in tonsil of the macaque
that did not develop disease; bar=50 m.
(D) Western blot showing similar PrPres patterns in samples from a patient
with vCJD (lane 1), the macaque that
developed disease (lane 3), and the bovine BSE inoculum (lane 4). By
contrast, a macaque inoculated intracerebrally
with material from a patient with sporadic CJD showed a different PrPres
pattern (lane 2).
For personal use. Only reproduce with permission from Elsevier Ltd
Research Letters
longer than that of intraspecies transmission (60 months
vs 44 and 47 months, representing 36% and 28%
increases, respectively). The interval between the period of
peak exposure to infectious BSE tissue and the hitherto
peak incidence of vCJD is about 10–15 years, but
incubation periods of up to 40 years have followed oral
infection with kuru between human beings.5 Therefore,
maximum incubation periods might exceed 50 years in
cases of oral transmission of BSE from cattle to man.
The present data do not provide a definitive minimum
infective dose for transmission of cattle BSE to primates,
but they do give enough information for a preliminary
assessment of the adequacy of existing measures to
protect the human food chain. Results of ongoing
experiments provide a rough estimation of the intraspecies
transmission rates in cattle. The BSE brain
inoculum to which the cattle were exposed had an
infectivity titre of 103·5 mouse infectious (intracerebral
and intraperitoneal) units ID50 per g (ID50 is the dose at
which 50% of animals become infected). Interim results
at 6 years after exposure suggest that the oral ID50 in
cattle may be between 100 mg and 1 g (table 1; S A C
Hawkins, T Konold, G A H Wells, unpublished data).
Since the brain of a cow weighs 500 g and a spinal cord
200 g, CNS tissues from a cow with clinical signs of BSE
could contain enough infective agent to transmit disease
orally to 490–1400 cows (70% of 700 g if 1g is needed, or
20% of 700 g if 100 mg is sufficient), or to 70 primates
(50% of 700 g if 5 g represents the oral ID50).
The accuracy of estimates of the oral ID50 for man will
not be improved until completion, several years from
now, of a large dose-response European study (QLK1-
2002-01096) in macaques, in which the minimum dose
is 50 mg. However, because similar inocula were used in
both the cattle and macaque studies,6 a tentative comparison
can be made between the efficiency of oral infection
in cattle and that in primates. On this basis, a factor of
7–20 could be considered as the range of magnitude of a
bovine-to-primate species barrier for oral BSE infection
(70 primates infected compared with 490 or 1400 cows,
with a similar dose).
Elimination from the human food chain of CNS
tissues from cows with clinical BSE is estimated to have
reduced the risk of human exposure to the disease by
about 90%.7 Risk was further reduced in continental
Europe by systematic screening for the diagnostic
presence of PrPres in the brainstem of all cattle older than
30 months, and in the UK by the total interdiction of
cows older than 30 months. In an oral exposure study to
assess the pathogenesis of BSE in cattle, in which the
same European Union-evaluated test as we used in the
present study was applied to CNS tissues, some
preclinical cases of the disease were diagnosed.8
Using the same test, pooled brainstem from cows with
clinical BSE has yielded a endpoint titre of PrPres
corresponding to a 1-in-300 to 1-in-1000 dilution of
positive brainstem.6,9 If people were to eat CNS tissues
from a cow with preclinical BSE with a concentration of
PrPres just below the test detection limit of 1 in 300, they
would need to ingest at least 1·5 kg to reach the degree
of exposure equivalent to that in the 5 g of brain used for
oral transmission to the macaque in the present study. If
the oral ID50 for man was one log below this dose (ie,
similar to that in cattle, and not accounting for any
species barrier between cattle and man; see table), 150 g
of CNS tissue that tested falsely negative could represent
an infective dose. Because use of cattle brain and spinal
cord for human consumption is prohibited, and in view
of the existing mechanically recovered meat regulations,
a person would be very unlikely to ingest this amount of
cattle CNS tissue.
The minimum sensitivity of screening tests to detect
100% of BSE-infected animals has yet to be ascertained.
However, our results provide reassurance that BSE
screening procedures combined with CNS removal are
effective measures to protect the human food chain.
Contributors
J-P Deslys, C Lasmézas, and E Comoy were responsible for design and
management of this study. G Wells, S Hawkins, and T Konold were
responsible for the pathogenesis study in ruminants. C Lasmézas,
C Herzog, and N Lescoutra-Etchegaray were in charge of the primate
experiments. F Auvré undertook the biochemical analyses. N Salès was
responsible for the immunohistochemical analyses, which were done
by E Correia. C Lasmézas, E Comoy, F Mouthon, G Wells, P Brown, and
J-P Deslys drafted the manuscript.
Conflict of interest statement
Commissariat à l'Energie Atomique owns a patent covering the BSE
diagnostic test commercialised by Bio-Rad. All authors had full access to
all data and had responsibility to submit for publication. The funding
sources had no role in the collection, analysis, and interpretation of
data, writing of the report, or decision to submit the paper for
publication.
2 www.thelancet.com Published online January 27, 2005
http://image.thelancet.com/extras/05let1056web.pdf
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)
RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log.
icip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula
For personal use. Only reproduce with permission from Elsevier Ltd
Research Letters
Acknowledgments
We gratefully acknowledge the expert care of the primate animals
provided by René Rioux, Sébastien Jacquin, and Anthony Fort, and the
technical expertise of Dominique Marcé, Capucine Dehen,
Sophie Freire, and Aurore Jolit Charbonnier. This work has received
financial support from the French Ministry of Research (GIS Prion). It is
now continued within the framework of the EU consortium QLK1-2002-
01096 and the European network of Excellence NeuroPrion. Ongoing
studies by the Veterinary Laboratories Agency in cattle are funded by the
UK Department for Environment, Food, and Rural Affairs.
References
1Anderson RM, Donnelly CA, Ferguson NM, et al. Transmission
dynamics and epidemiology of BSE in British cattle. Nature 1996;
382: 779–88.
2 Lasmézas CI, Deslys JP, Demaimay R, et al. BSE transmission to
macaques. Nature 1996; 381: 743–44.
3 Lasmézas CI, Fournier JG, Nouvel V, et al. Adaptation of the bovine
spongiform encephalopathy agent to primates and comparison with
Creutzfeldt-Jakob disease: implications for human health. Proc Natl
Acad Sci USA 2001; 98: 4142–47.
4 Herzog C, Salès N, Etchegaray N, et al. Tissue distribution of bovine
spongiform encephalopathy agent in primates after intravenous or
oral infection. Lancet 2004; 363: 422–28.
5 Klitzman RL, Alpers MP, Gajdusek DC. The natural incubation
period of kuru and the episodes of transmission in three clusters of
patients. Neuroepidemiol 1984; 3: 3–20.
6 Deslys JP, Comoy E, Hawkins S, et al. Screening slaughtered cattle
for BSE. Nature 2001; 409: 476–78.
7 European Commission. Opinion of the Scientific Steering
Committee on the Human Exposure Risk via food with respect to
BSE. Adopted on 10 December 1999. http://europa.eu.int./comm/
food/fs/sc/ssc/out67_en.pdf (accessed Jan 17, 2004).
8 Grassi J, Comoy E, Simon S, et al. Rapid test for the preclinical
postmortem diagnosis of BSE in central nervous system tissue.
Vet Rec 2001; 149: 577–82.
9 Moynagh J, Schimmel H. Tests for BSE evaluated. Bovine
spongiform encephalopathy. Nature 1999; 400: 105.
www.thelancet.com Published online January 27, 2005
http://image.thelancet.com/extras/05let1056web.pdf 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.
suppressed peer review of Harvard study October 31, 2002
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
TSS
