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From: TSS ()
Subject: BSE USA, CANADA, AND JAPAN comparing apples to oranges
Date: August 17, 2007 at 1:51 pm PST

K. Hagiwara1, Y. Nakamura1, Y. Yamakawa1, Y. Sato2, M. Tobiume2, T. Sata2
and the Expert Committee for
BSE Diagnosis, Ministry of Health, Labour and Welfare (MHLW) 3
Dep. Biochemistry and Cell Biology1 and Pathology2, Natl. Inst. Infectious
Diseases, Shinjuku, Tokyo 162-8640,
Japan, and MHLW, Tokyo 100-8916, Japan 3
An ELISA (Plateria, BioRad) positive specimen of a 14 year-old Japanese
Black cow (beef cattle)
slaughtered in an abattoir was examined by western-blot (WB) and
(IHC) analyses for the confirmation of BSE. Dysstasia had been reported as a
clinical symptom.
Histological examination of the medulla oblongata at the level of obex
showed severe vacuolations in
dorsal nucleus of the vagus, nucleus of the solitary tract and nucleus of
the spinal tract. Granular and
linear deposition of PrPSc was also detected in these areas by IHC analysis.
Thus, histological and
IHC data were compatible with the histopathology of the typical BSE. In the
WB analysis, however,
the amount of the di-glycosylated PK-resitant PrPP
Sc was found to be at approx.35% of the total PrPSc,
and the mono-glycosylated PrPSc was at approx.40%. The WB analyses showed
that PrPSc
distributed widely in the brain with the unchanged glycosylation ratio. Such
a glycosylation-ratio is
distinct from that of the typical BSE agent in which the di-glycosylated
form is dominant (approx.70%)
but, intriguingly, similar to that of the type-2 sporadic CJD agent. No DNA
mutation was detected in
the PrP coding region, except polymorphisms of the codons for Gln78 and
Asn192 being determined
as CAG and AAT, respectively. Judging from the glycosylation-ratio, BSE
prion herein is different
from the typical BSE prion, and the atypical BSE prion found previously in a
Holstein steer in Japan
(ref. 1). Instead, its molecular feature is close, if not identical, to
PrPSc found in the cattle succumbed
to bovine amyloidtic spongiform encephalopathy (ref. 2), and to the sporadic
CJD-like PrPSc in the
mice inoculated with BSE agent (ref. 3).
References: 1) Y. Yamakawa, Jpn.J.Infect.Dis. (2003), 56, 221. 2) C.
Casalone, PNAS (2004), 101, 3065. 3) S.E.
Lloyd, J.Gen.Virol. (2004), 85, 2471.


RA- 07
J.Montag1, G.Hunsmann1, W.Schulz-Schaefer2, and D.Motzkus1
1German Primate Center (DPZ), Dept. of Virology and Immunology, Kellnerweg
4, 37077 Göttingen, Germany
2Georg-August University Göttingen, Dept. of Neurology, Robert-Koch-Str. 40,
37075 Göttingen, Germany
According to biochemical and epidemiological findings bovine spongiform
encephalopathy (BSE) was transmitted
to humans causing variant Creutzfeldt Jakob disease (vCJD). Previous studies
have shown intracerebral (i.c.)
transmission of BSE affected brain from cattle can cause TSEs in cynomolgus
macaques (M. fascicularis). The
lesion profile resembles that of vCJD. Recently, oral infection of M.
fascicularis with macaque-adapted BSE
material was reported.
In cooperation with five European partners a quantitative study for the
transmission of the BSE agent to M.
fascicularis was initiated to assess the risk of vCJD infection in humans
through contaminated food products.
Titration was performed orally and intracerebrally to determine the minimal
infectious dose for cynomolgus
Here we report the outcome of the intracerebral infection with 50 mg BSE
brain homogenate in six non-human
primates. All animals showed clinical symptoms of TSE after an average of
1100 days. Using immunohistological
and biochemical methods prion protein (PrP) deposits were confirmed in the
brains of all animals. Using Western
blot analysis the glycosylation pattern was compared to the inoculum and to
the pattern of different CJD
subtypes. The glycopattern TSE infected cynomolgus macaques resembles human
CJD type 2. Simian PrPres
was detected with the monoclonal anti prion antibody 11C6, which revealed a
higher sensitivity in comparison to
12F10 and 3F4. We further analysed the distribution of PrPres by
microdissection of seven different brain regions
of all infected macaques. High concentrations of PrPres were found in
central brain regions, as gyrus cinguli,
nucleus caudatus, vermis cerebelli and basis pontis. In contrast, in the
peripheral regions gyrus frontalis, gyrus
parietalis and gyrus occipitalis PrPres was hardly detectable.
Thus, the incubation period related to the life expectancy, the PrPres
glycosylation pattern as well as the
distribution in certain brain regions resemble those in vCJD patients. The
relative abundance of PrPres in
macaques will be compared to that of orally infected animals.


Transmission of BSE to cynomolgus macaques

J Montag1, G Hunsmann1, W Schul-Schaeffer2, D Motzkus1
1 German Primate Centre, Department of immunology and virology, Göttingen,
Germany; 2 Georg-August-Universität
Göttingen, Dept. of Neurology, Robert-Koch-Str. 40, 37075 Göttingen, Germany

The risk of transmitting transmissible spongiform encephalopathies (TSEs)
from animal to
humans is still an important question in TSE research. There are scientific
indications that bovine
spongiform encephalopathy (BSE) is transmitted to humans causing variant
Creutzfeldt Jakob
disease (vCJD). Previous studies have shown that infectious material from
cattle can cause TSEs
in cynomolgus macaques (M. fascicularis) resembling the lesion profile of
vCJD. Recently, oral
infection using macaque-adapted brain homogenate was successful in the same
animal model.
In cooperation with five European partners a quantitative study for the
transmission of the BSE
agent to M. fascicularis was initiated to assess the risk of vCJD infection
in humans through
contaminated of BSE-infected material. Infection was performed orally and,
as a control,
intracerebrally with non adapted BSE material. As the first result we report
the successful
intracerebral transmission of BSE to M. fascicularis. 6/6 have died of TSE.
The analysis of one
animal is exemplified here. By immunohistology, amyloid plaques with PrP
depositions were
detected in different brain sections. The Western Blot analysis revealed
PrP-specific bands
between 26 and 39 kDa. After PK-digestion of the infected macaque brain
homogenate this
pattern shifted to three bands between 17 - 36 kDa. The bandshift was also
detected after PNGase
digestion. These data confirm the clinical diagnosis of vCJD.


Experimental oral BSE infection of cattle - German Pathogenesis Study -2,5
after infection
Ute Ziegler1, Artur Weber1, Baerbel Wagenschwanz1, Chris Hoffmann1, Anne
Martin H Groschup1
1 Institute for Novel and Emerging Infectious Diseases at the
Friedrich-Loeffler-Institute Federal Research Institute for
Animal Health, Germany
Since January 2003 the Institut for Novel and Emerging Infectious Diseases
is carrying out a
pathogenesis study of BSE in cattle. A total of 56 calves (two groups of 28
animals each) was
infected orally with a macerate of BSE positive brainstem (100g per animal).
Another 18 animals
received noninfected cattle brain stem homogenate to serve as mock controls.
All animals are bled and urine is taken every eight weeks as well as
cerebrospinal fluid every four
months (under sedation). In the course of serial kills, every four month 4-5
animals are
euthanised and necropsied under TSE steril conditions to collect an
extensive number of tissue
and bodily fluid samples (i.e. more than 1.400 samples of more than 150
tissues from each
euthanised animal).
Selected samples will subsequently be inoculated into transgenic mice, that
overexpress the
bovine PrP (Tgbov XV mice) and which are about 10.000 times more sensitive
than wild type
mice to cattle derived BSE prions. Using this novel bioassay, the spread of
infectious agent from
the alimentary tract to the CNS in bovines is analysed.
Immunohistological staining and immunoblotting examination of samples
already demonstrated
the accumulation of PrPSc in the distal ileum (Peyer's Patches) in the
challenged animals, which
were dissected 12 months p.i., 16 months p.i. and 20 months p.i. Therefore,
the oral challenge
was successful. Further immunochemical and immunochemical studies on the
tissue samples
more proximal to the CNS are currently under way.
Samples, which are taken at selected time points during the incubation
period are of utmost
importance for the development and the evaluation of new BSE diagnostic
assays and in
particular for the development of a live animal test.


Pathological Prion Protein in Muscles of Rodents Infected with BSE or vCJD
Achim Thomzig1, Franco Cardone2, Dominique Krüger1, Maurizio Pocchiari2,
Paul Brown3,
Michael Beekes1
1 Robert Koch-Institut, P24; 2 Instituto Superiore di Sanità, Depatment of
Cell Biology and Neurosciences, Rome, Italy;
3 Bethesda, Maryland, USA
Recently, pathological prion protein PrPTSE was detected in muscles from
sheep infected with
scrapie, the archetype of transmissible spongiform encephalopathies (TSEs).
This finding has
highlighted the question of whether mammalian muscle may potentially also
provide a reservoir
for TSE agents related to Bovine Spongiform Encephalopathy (BSE) and variant
Jakob Disease (vCJD). We here report results from studies in hamsters and
mice which provide
direct experimental evidence, for the first time, of BSE- and
vCJD-associated PrPTSE deposition
in muscles. Our findings emphasize the need for further assessment of
possible public health
risks from TSE involvement of skeletal muscle.


Adaptation of the Bovine Spongiform Encephalopathy to the Primate Microcebus
murinus by Oral Route
1 INSERM U710-EPHE-University Montpellier 2, France; 2 CNRS UPR1142, IGH,
Montpellier, France; 3 INSERM
U592, Paris, FRANCE; 4 EA1784-IFR PMSE 112, University Aix -Marseille,
Experimental transmission of BSE through oral route to mice or to non-human
primates such as
Cynomolgus macaca have been reported in several studies. Here, we report on
the investigation
of oral transmission of BSE to a small non-human primate, the lesser-mouse
lemur (Microcebus
murinus). Seven microcebes were contaminated by bovine brain or
bovine-adapted macaca brain.
Only the three microcebes that received BSE-macaca brain develop a
neurological disease after
long incubation periods (44 months). The duration of clinical stage was 2
months. The symptoms
begin by nervousness evolving rapidly to agressivity, visual troubles,
imbalance then
incoordination of movements, myoclonic jerks and later on, the microcebes
became ataxic,
turning round on itself.
The spongiform extent was related with the duration of illness. It ranged
from small discrete
vacuoles randomly dispersed throughout the neuropil to large confluent
cystic spaces traversed
by thin septae. Spongiform changes were most pronounced in the thalamus, the
basal ganglia, the
hypothalamus and the brainstem. The neocortex was relatively spared by
spongiosis: small sparse
vacuoles were seen in the frontal and occipital lobes whereas the
hippocampus showed larger
vacuoles. Spongiform changes were accompanied by important astrocytic
Proteinase K resistant-prion protein was detected by western blot as well as
immunocytochemistry. PrPres accumulation was observed in all the microcebes
clinical signs. The prion immunostaining was more intense in thalamus, basal
ganglia and
brainstem. Focal deposits or plaques were seen in the cortex. In the
cerebellum, some plaques
were evidenced in the molecular layer.
In conclusion, BSE agent does not seem to be directly pathogenic to
microcebe by oral route, but
necessitates an adaptation of the strain to macaca.


A special form of PrPSc in muscles of a BSE-infected cow
I Schiller1, J Duss1, F Kuhn1, J Schmid1, M Glatzel2, F Ehrensperger2, M
Hilbe2, K Zlinszky2, B
Stierstorfer3, B Oesch1, A.J. Raeber1
1 Prionics AG, Switzerland; 2 Universitiy of Zurich, Switzerland; 3
Ludwig-Maximilians-Universitaet Muenchen,
PrPSc, the abnormal form of the prion protein, has been detected in muscles
of patients with
sporadic Creutzfeldt-Jakob disease, in natural and experimental scrapie in
sheep and in ro-dent
adapted scrapie but not in cattle with bovine spongiform encephalopathy
In this study we have analyzed 60 muscle samples originating from 7 Swiss
and 6 Bavarian cows
with confirmed BSE by 3 different methods: (1) phosphotungstic acid
precipitation fol-lowed by
proteinase K digestion, (2) phosphotungstic acid precipitation followed by
with the PrPSc conformation specific antibody 15B3, and (3)
ultracentrifugation followed by
immunoprecipitation with the antibody 15B3. Analysis of PrP was performed by
blotting with the antibody 6H4. Here we report for the first time the
detection of a special form of
PrPSc in muscles of a clinical BSE case. This form of PrPSc is
protease-resistant yet the
protease-resistant fragment detected on Western blot differs from that
typi-cally found in BSE
positive brains. In 1 of 7 Swiss BSE cases, we detected PrPSc in
sem-itendinous muscle, triceps
muscle, sternocephalicus muscle and in the tongue but not in two other
muscles analysed. Our
findings show that low levels of a special form of PrPSc are present in a
small percentage of
muscles from BSE affected cattle. Whether this type of PrPSc in muscle of
cattle with BSE is
associated with infectivity remains to be established.




Order Code RL32199
Bovine Spongiform Encephalopathy
(BSE, or “Mad Cow Disease”):
Current and Proposed Safeguards
Updated May 18, 2007

Bovine Spongiform Encephalopathy
(BSE, or “Mad Cow Disease”):
Current and Proposed Safeguards
Through mid-May 2007, the United States had confirmed three cases of bovine
spongiform encephalopathy (BSE, or “mad cow disease”): the first in December
2003 in a Canadian-born cow found in Washington state, the second in June 2005 in
cow in Texas, and the third in March 2006 in a cow in Alabama.
Shortly after the first case, U.S. Department of Agriculture (USDA) and other
officials announced measures to improve existing safeguards against the introduction
and spread of BSE. Previously, the major safeguards were: (1) USDA restrictions
on imports of ruminants and their products from countries with BSE; (2) a ban on
feeding most mammalian proteins to cattle and other ruminants, issued by the Food
and Drug Administration (FDA); and (3) a targeted domestic surveillance program
by USDA’s Animal and Plant Health Inspection Service (APHIS), the agency
responsible for animal health monitoring and disease control.
Some argued that these safeguards were inadequate, as evidenced by findings
of BSE here and subsequent federal efforts to bolster protections. Most new actions
announced by USDA on December 30, 2003, were under the purview of USDA’s
Food Safety and Inspection Service (FSIS), responsible for the safety of most U.S.
meat and poultry. These actions took effect in January 2004 and included (1) holding
tested carcasses until BSE-negative results are obtained; (2) banning nonambulatory
(“downer”) cattle from human food; and (3) banning certain additional animal parts
from human food. USDA also increased work and spending on a national animal
identification and tracking system, and undertook an enhanced BSE surveillance
program, among other activities. On January 26, 2004, FDA announced planned
changes to its safeguards, including additional bovine materials banned from the
human foods and cosmetics it regulates; a ban on poultry litter, restaurant waste, and
ruminant blood products from ruminant feed; and stricter oversight of feed manufacturing.
In lieu of these changes, FDA on October 6, 2005, proposed a ban, in all types
of animal feed, of some higher-risk cattle parts. A final rule is pending.
Many Members of the 110th Congress continue to closely follow these BSE
developments; hearings and legislative proposals on various aspects of the issue are
possible. Among the policy questions have been whether expanded agency actions
have provided further protections against BSE, whether they are scientifically sound,
and what costs they may have imposed on consumers, taxpayers, and industry. Also
at issue have been whether USDA and FDA have effectively implemented and
enforced the current safeguards; whether these safeguards will be sufficient to rebuild
foreign markets’ confidence in the safety of U.S. beef; and whether other types of
actions should be considered, among other questions. Additional U.S. BSE cases
could affect these policy deliberations.
This report will be updated if significant developments occur.


U.S. Beef Recall
First U.S. Case: On December 23, 2003, upon the announcement of a BSE-positive
cow in Washington state, FSIS requested a voluntary recall of 10,410 pounds of meat
traced to the affected animal and 19 others slaughtered and processed along with it.2 The
agency announced that upon reviewing slaughter records for the BSE-positive cow, it had
determined that high-risk materials — the animal’s brain, spinal cord and lower intestine
(“distal ileum”) — had been removed at slaughter, and that the muscle meats that passed
inspection posed an “extremely low likelihood that the beef contained the infectious agent
that causes BSE.” The agency stated that the tissues of highest infectivity are the brain,
spinal cord, and distal ileum, and all were removed from the rest of the carcass at
slaughter. “Therefore, the meat produced were cuts that would not be expected to be
infected or have an adverse public health impact. The recall is being conducted out of
an abundance of caution.”3
Most of the recalled product was distributed to stores in the West, and primarily in
Oregon and Washington, according to various news reports. These reports indicated that
some individuals already had consumed meat from the affected production lot, consisting
of the positive cow and others slaughtered with it on December 9, 2003. USDA’s
February 9, 2004 release observed that additional beef was mixed in with the originally
recalled beef products at several points in the distribution network. This caused the
department to expand the recall to approximately 38,000 pounds.
Second and Third U.S. Cases: Material from the second and third U.S. cases did
not enter the food or feed supply, according to USDA. The Texas cow had been
delivered to a Texas plant where its remains would have been processed into pet food,
according to USDA officials. However, these remains were held during testing for BSE
and ultimately were incinerated. The Alabama cow was buried on the farm. So no beef
recall was necessary in either case.

2 USDA, “FSIS Update Of Recall Activities,” release, February 9, 2004, on the Internet at
[]. A Class II recall “is
a health hazard situation where there is a remote probability of adverse health consequences
from the use of the product,” according to the release. USDA does not have explicit
statutory authority to mandate meat recalls or to initiate recalls on its own. However, some
believe that because USDA has the power to withdraw inspection, effectively keeping meat
from the food supply, such mandatory authority is implied. For more information about
meat inspection and slaughter practices, see CRS Report RL32922, Meat and Poultry
Inspection: Background and Selected Issues, by Geoffrey S. Becker.
3 “FSIS Update Of Recall Activities.”

4 USDA, Final BSE Update — Monday, February 9, 2004. Included in the 255 were 28 of
the 80 cattle that had entered the United States with the cow that tested positive for BSE.
Because of a lack of records, only 28 of these 80 other imports were positively identified,
contributing to the need for the wider investigation and destruction of more animals. For
a timeline, see CRS Report RL32932, Bovine Spongiform Encephalopathy (BSE, or “Mad
Cow Disease”) in North America: A Chronology of Selected Events, by Geoffrey S. Becker.
5 USDA Texas BSE Investigation — Final Epidemiology Report, August 2005. For recent
USDA information, see [].
U.S. Cases of BSE
In the first U.S. case, USDA stated that virtually no risk to public health existed.
However, the department announced a voluntary recall of thousands of pounds of
beef that had entered the food supply as a precautionary measure (see box), and also
conducted an extensive epidemiological investigation into how the cow likely
contracted BSE and whether other animals also might have the disease. During this
investigation, which was officially concluded on February 9, 2004, more than 700
cattle at 11 facilities were destroyed and 255 of those were tested for BSE, all with
negative results. The 255 were deemed “of interest” because they could have been
from the source herd in Alberta, Canada.4
In the second U.S. case, USDA said that no material from the animal entered the
food or feed supply. The epidemiological investigation, completed in late August
2005, attempted to trace all adult animals that left the index farm (the Texas ranch)
after 1990 and all progeny born within two years of the BSE cow’s death. Sixtyseven
animals still on the index farm were killed and tested, all negative for BSE.
USDA determined that 200 animals of interest had left the farm, 143 of which were
slaughtered. Only two others were found alive; one was not tested because its age
ruled it out as a suspicious animal, and the other tested negative. Of the rest, 34 were
presumed dead, one was known dead, and 20 were untraceable. USDA also was
interested in two calves born to the BSE cow, but due to recordkeeping gaps, it had
to trace a total of 213 calves to try to eliminate the calves of interest. None were
found alive to test (most were fed and slaughtered for beef).5
Regarding the third U.S. case, in which no material entered the food or feed
supply (the animal had been euthanized and buried on the farm), APHIS and
Alabama State officials investigated 36 farms and five auction houses, and conducted
DNA testing on herds that may have included relatives of the BSE case. However,
they were unable to determine the cow’s herd of origin or to find any related animals
of interest, except for the two most recent calves of the infected animal. One calf
was still on the farm of the infected cow and being held by APHIS for observation;
the other had died the year before.
Officials also conducted investigations into the source of the feed consumed by
the infected animals, because feed containing infective ruminant material (i.e., meat
and bone meal from rendered cattle) is considered the most likely source of BSE
infection. Of concern to some scientists, however, was that several of the Canadian
BSE cases were born after 1997, when both the United States and Canada instituted
similar but separate bans on the use of most mammalian proteins in cattle feed. This
6 Bill Tomson, “Much Still Unknown About Two US BSE Cases,” Dow Jones Newswires,
June 8, 2006.
led some to question the effectiveness of such a feed ban in general, and/or the
effectiveness of its implementation in Canada. (Both native-born U.S. cases were
born before 1997.)
In June 2006, a USDA official reported that the two native-born U.S. cattle had
“atypical” BSE, not the type seen in cattle in Europe or in the other North American
cases.6 The implications of this finding, including whether atypical BSE could be
spread by novel means, or whether existing controls are appropriate, are unclear at
this time. The USDA official stated at the time that there were no plans to change
existing controls, and the department was already in the process of ramping down its
domestic BSE surveillance activity.
The North American BSE cases prompted widespread debate over the
effectiveness of U.S. (and Canadian) safeguards against BSE. These safeguards
generally have been implemented incrementally over a number of years, not only as
a response to its emergence in Great Britain and spread to other countries, but also
to evolving scientific evidence about this relatively new disease, its causes, and
means of transmission. Many animal health experts inside and outside of
government assert that these regulatory developments have not constituted a
“piecemeal” approach to addressing the BSE threat but rather an increasingly unified
system of overlapping and complementary safeguards.
Some critics, nonetheless, have questioned whether these safeguards are
providing adequate protection against BSE. Also at issue have been whether their
costs to taxpayers and industry are justified; whether such steps are defensible
scientifically and will fully restore foreign markets’ markets’ confidence in the safety of U.S.
cattle and beef; and whether other types of regulatory and/or legislative actions
should be considered, among other questions.


Following the first U.S. BSE case, the FDA in January 2004 announced
imminent plans to expand feed ban restrictions. The agency published an advance
notice of proposed rulemaking (ANPR) in 2004 and a proposed rule in 2005, each
with provisions that varied from the other and from the 2004 announcement. The
regulation had yet to be altered as of mid-May 2007. An analysis of these rulemaking
proposals follows.


The OIE continues to state, as it always has, that bovine blood and blood
products in feed do not present a risk for BSE transmission.47 But in its rationale for
proposing a blood ban in January 2004, FDA noted recent concerns about human
transmission of vCJD by blood transfusion, which suggested that infectious prions
could be present in blood, while also noting that transfusion would likely pose a
greater risk from minute exposures than would feeding.48 In its July 2004 ANPR, the
agency requested comment on the evidence of a transmission risk from blood in feed.


As of mid-May 2007, FDA had not finalized any proposed changes to the feed
ban. An FDA official was quoted in September 2006 as saying that the agency may
have underestimated the impacts that the ban of SRM in all feeds could have on the
rendering industry. He said that FDA continued to review the proposal, and that
publication of a final rule would be pushed back to “later this year” or beyond.55


GAO Evaluations. GAO issued reports on FDA’s oversight of the feed ban,
in 2002 and 2005, in which it noted a number of problems with administrative
procedures, inspection, and enforcement.67 In its February 2005 report, GAO
commented that FDA’s 99% reported compliance rate may be misleading because
the rate was based on inspections of only about 570 firms. GAO added that FDA
does not include all serious violations in its calculations because it reclassifies firms
as being in compliance once they correct violations, no matter how long a problem
existed. For this and other reasons GAO said that FDA did not have sufficient
information to calculate a compliance rate and recommended instead that the agency
report enforcement information in its complete context.
Also in its 2005 report, GAO concluded that FDA had made improvements in
its management of the feed ban since the 2002 GAO report, but that “various
program weaknesses continue to undermine the nation’s firewall against BSE.” One
of the weaknesses cited was the lack of a uniform approach to identify all the
additional feed manufacturers, on-farm mixers, and other feed industry businesses
beyond the approximately 14,800 firms the agency had identified at the time. Among
other concerns, GAO also commented that FDA had not reinspected approximately
2,800 firms for several years and therefore did not know whether they use prohibited
materials in their feed, that the agency had not required a warning label on feed for
export that is not intended for cattle and other ruminants, and that it had not always
alerted USDA and the states when it learns that cattle may have been given
prohibited feed.


On April 27, 2004, a cow showing signs of a central nervous system disease at
a Texas slaughter plant was condemned for human food use by FSIS, and the FSIS
veterinarian on site recommended that it be tested for BSE. However, a higher-level
APHIS official determined that it should not be tested, so the animal’s carcass was
sent to a rendering plant for processing into inedible byproducts. This led some
critics to charge that the department had “covered up” a possible case of BSE.
Such concerns became the subject of investigation by USDA’s Inspector
General (IG). She presented her preliminary findings at a joint hearing held July 14,
2004, by the House Government Reform and Agriculture Committees. The IG told
the committees that in the case of the Washington state cow, her office had “... found
no instances where USDA personnel knowingly conveyed false or misleading
information, or engaged in intentional misconduct.” The investigation, however, “...
did reveal procedural errors and inconsistent descriptions that gave rise to some of
the public concerns that the identification of the BSE-positive cow may have been
The IG testified that her office also found “no substantive evidence” that USDA
officials provided any “false information or engaged in intentional misconduct” in
the Texas case. However, the IG cited inconsistencies in officials’ understanding of
BSE sampling and carcass handling procedures. As a result, FSIS and APHIS on
May 5, 2004, had announced a new joint policy to clarify these procedures and
responsibilities, she observed.86
The IG also presented the preliminary results of an audit of the department’s
expanded surveillance plan, finding a number of inconsistences. For example, the
IG stated that surveillance findings may be unreliable because the plan: is not truly
random since participation is voluntary; assumes that BSE is confined only to the
high-risk cattle population while other studies show that healthy-looking animals
could have BSE; does not include a process for obtaining animals that die on farms;
cannot obtain a statistically appropriate geographical representation of the cattle
population; and does not allow APHIS to find and test enough cattle in the high-risk
population. The final OIG report, issued in late August 2004, generally paralleled the
preliminary findings.87
The Secretary of Agriculture and other USDA officials at the July 2004 hearing
defended the surveillance program, noting among other things that the OIG
observations were based on the plan before it was implemented and that many of the
88 A fuller statistical and descriptive picture of the surveillance conducted, such as the types
of sites where samples were taken, their geographical locations, and clinical signs observed,
is available in APHIS documents on the web, i.e., Summary of Enhanced BSE Surveillance
in the United States, prepared by APHIS’ Veterinary Services Centers for Epidemiology and
Animal Health National Surveillance Unit, April 27, 2006 at [
report’s recommendations had already been addressed. APHIS was receiving a
representative mix of samples from all locations, reaching deeply into the higher-risk
cattle population, and the statistical basis for the sampling was sound, officials
asserted.88 They added that adjustments had been made as the result of ongoing
assessments of the program. The OIG has continued to assess the testing program.
It was at the IG’s insistence that APHIS researchers re-tested tissue from a cow that
first was determined to be negative, and then ultimately positive for BSE (see below).


full text 59 pages ;

compare to

Bovine Spongiform Encephalopathy
(BSE, or “Mad Cow Disease”):
Current and Proposed Safeguards
Updated September 20, 2006

sporadic cjd

Colorado Surveillance Program for Chronic Wasting Disease
Transmission to Humans (TWO SUSPECT CASES)

An evaluation of scrapie surveillance in the United States
From: Terry S. Singeltary Sr.
Date: Sun, 5 Aug 2007 13:05

SEAC New forms of Bovine Spongiform Encephalopathy 1 August 2007
From: Terry S. Singeltary Sr.
Date: Sun, 5 Aug 2007 13:09:38 -0500

Owens, Julie
From: Terry S. Singeltary Sr. []
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
Page 1 of 98

Greetings FSIS,

I would kindly like to comment on the following ;

[Federal Register: July 12, 2006 (Volume 71, Number 133)]
[Page 39282-39283]
From the Federal Register Online via GPO Access []
Food Safety and Inspection Service
[Docket No. FSIS-2006-0011]
Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Update; Notice of Availability and Technical Meeting


MY comments/questions are as follows ;

1. SINCE the first Harvard BSE Risk Assessment was so flawed and fraught
with error after the PEER REVIEW
assessment assessed this fact, how do you plan on stopping this from
happening again, will there be another peer
review with top TSE Scientist, an impartial jury so-to-speak, to assess this
new and updated Harvard BSE/TSE risk
assessment and will this assessment include the Atypical TSE and SRM issues

*** Suppressed peer review of Harvard study October 31, 2002 ***

that consisted of
some 10,878.06 TONS, then another Mad Cow feed ban warning letter in May, IT
should seem prudent to ask why our
feed bans continue to fail in 2006, and continue to fail today ?


full text 98 pages ;

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

Terry S. Singeltary

Page 1 of 17

From: Terry S. Singeltary Sr. []

Sent: Thursday, September 08, 2005 6:17 PM


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

Greetings FSIS,

I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS
Prohibition of the Use of Specified
Risk Materials for Human Food and Requirements for the Disposition of
Non-Ambulatory Disabled Cattle
THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle Broken bones and
such may be the first
signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;



Issued: Monday, 28 August 2000



A team of researchers led by Professor John Collinge at the Medical

Research Council Prion Unit1 report today in the Proceedings of the

National Academy of Sciences, on new evidence for the existence of a

"sub-clinical" form of BSE in mice which was unknown until now....

full text 17 pages ;

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


No. 04-047-l

No. 04-021ANPR

No. 2004N-0264


Federal Measures to Mitigate BSE Risks: Considerations for Further Action

Greetings FDA, USDA and APHIS et al,

I would kindly like to comment on the continued delay of the regulations
that have been proposed for years to reduce the risk of BSE/TSE in the
USA. Each day that is wasted debating this issue allows this agent to
and many many more humans and animals become needlessly exposed to
this agent via a multitude of potential routes and sources right here in the
USA. TO continue to ignore the new findings from several scientists
about the fact that BSE is not the only strain of TSE in cattle, the fact
new atypical strains of TSE are showing up in not only cattle, but
sheep and the fact that the new strain of TSE in cattle seems to be
more similar to sporadic CJD as opposed to the nv/v CJD, to continue
to ignore these findings will only further spread this agent. ..............

full text ;

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


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

Terry S. Singeltary Sr.
Vol #:

Docket Management Docket: 02N-0276 - Bioterrorism Preparedness ...
General Comments, Subject: Docket No: 02-088-1 RE-Agricultural ...
From: Terry S. Singeltary Sr.


Docket No: 02-088-1 Title: ...

Greetings FDA and public,

if you go to the below site, and search all BSE known countries and check
out their air traffic illegal meat they have confiscated, and check out the
low number checked, compared to actual passenger traffic, would not take too
much for some nut to bring in FMD/TSEs into the USA as a 'suitcase bomb'.

[[Under APHIS-PPQ's agricultural quarantine inspection monitoring, 284 air
passengers from Israel were sampled for items of agricultural interest in
fiscal year 2001. Seven of these passengers, or 2 percent, carried a total
of 11 kg of meat items that could potentially harbor the pathogen that
causes BSE. None of these passengers from whom meat items were confiscated
reported plans to visit or work on a ranch or farm during their visit to the

if they were to have questioned the terrorist that bombed the Twin Towers
with jets, if they were to have questioned them at flight school in the USA,
i am sure that they would have said they did not intend to visit the Twin
Towers as a flying bomb either. what am i thinking, they probably did ask
this? stupid me. ...

full text ;


File Format: PDF/Adobe Acrobat -

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

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

Greetings again Dr. Freas and Committee Members,

I wish to submit the following information to the
Scientific Advisors and Consultants Staff
2001 Advisory Committee (short version).

I understand the reason of having to shorten my submission,
but only hope that you add it to a copy of the long version,
for members to take and read at their pleasure,
(if cost is problem, bill me, address below).
So when they realize some time in the near future
of the 'real' risks i speak of from human/animal TSEs and
blood/surgical products. I cannot explain the 'real' risk
of this in 5 or 10 minutes at some meeting,
or on 2 or 3 pages, but will attempt here:

remember AIDS/HIV, 'no problem to heterosexuals in the U.S.?
no need to go into that, you know of this blunder.

DO NOT make these same stupid mistakes again with
human/animal TSE's aka MADCOW DISEASE. I lost my Mom to hvCJD,
and my neighbor lost his Mother to sCJD as well (both cases
confirmed). I have seen many deaths, from many diseases.
I have never seen anything as CJD, I still see my Mom laying helpless,
jerking tremendously, and screaming "God, what's wrong
with me, why can't I stop this". I still see this, and will
never forget. Approximately 10 weeks from 1st of symptoms to death.
This is what drives me. I have learned more in 3 years about not only
human/animal TSE's but the cattle/rendering/feeding industry/government
than i ever wished to.

I think you are all aware of CJD vs vCJD, but i don't think
you all know the facts of human/animal TSE's as a whole,
they are all very very similar, and are all tied to the
same thing, GREED and MAN.

I am beginning to think that the endless attempt to track
down and ban, potential victims from known BSE Countries
from giving blood will be futile. You would have to ban
everyone on the Globe eventually? AS well, I think we
MUST ACT SWIFTLY to find blood test for TSE's,
whether it be blood test, urine test, eyelid test,
anything at whatever cost, we need a test FAST.

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

full text 6 pages ;

1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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





MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported 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. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?

Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam


Answering critics like Terry Singeltary, who feels that the U.S. under-
counts CJD, Schonberger conceded that the current surveillance system
has errors but stated that most of the errors will be confined to the older

Copyright © 2003 Published by Elsevier Ltd.

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003.

Volume 3, Issue 8, August 2003, Page 463

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD)
and have been searching for answers ever since. What I have found is that we
have not been told the truth. CWD
in deer and elk is a small portion of a much bigger problem.”


see history of cjd questionnaire

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

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