Replacement of soybean meal in compound feed by European protein
sources
Effects on carbon footprint
H.C. de Boer1, M.M. van Krimpen1, H. Blonk2, M. Tyszler2 1 Wageningen UR
Livestock Research 2 Blonk Consultants Wageningen UR Livestock Research
Lelystad, November 2014
SNIP...
SNIP...
2.5 Scenario 4: replacement of SBM-SA by poultry meat and bone meal
Introduction
Animal meal (e.g. blood meal, bone meal, meat meal, meat and bone meal)
used to be a valued protein-rich ingredient in animal feed, but was banned from
use in the year 2000 because of increased incidences of 'mad cow disease'
(Bovine spongiform encephalopathy). However, voices are heard in politics that,
under limitations, the use of animal meal should be permitted again. Animal meal
has a low CFP because no upstream CFP is allocated, due to its relatively low
economic value. Therefore, the inclusion level of animal meal in compound feed
could contribute to the replacement of SBM-SA by proteins from European origin,
and potentially lower its CFP.
Input for compound feed formulation
In this scenario, the inclusion level of SBM-SA was not allowed and meat
and bone meal could be included in the diet to a maximum of 3%. Because of the
species to species ban, indicating that animals should be prevented to consume
the remains of their own species, meat meal and meat and bone meal of poultry
origin were used in this scenario. Because the inclusion level of poultry meat
and
Livestock Research Report 819 | 17
bone was very low, poultry meat meal was added later to see if this would
increase the inclusion level. Poultry meat and bone meal 50 Sonac (Appendix 1)
and poultry meal 63 Sonac were used as meat and bone meal and meat meal,
respectively. Prices were set at 40 and 61 € 100-1 kg of product, respectively
(based on information from Vionfood, Eindhoven, the Netherlands).
CFP calculation
The CFP of poultry meat and bone meal was calculated with FeedPrint. For
this scenario, CFP of poultry meat and bone meal (Category 3 rendering) with a
crude fat content of maximal 100 g kg-1 of product was used. This meal was
sourced from the Netherlands (default FeedPrint sourcing).
>>>Animal meal (e.g. blood meal, bone meal, meat meal, meat and
bone meal) used to be a valued protein-rich ingredient in animal feed, but was
banned from use in the year 2000 because of increased incidences of 'mad cow
disease' (Bovine spongiform encephalopathy). *** However, voices are heard in
politics that, under limitations, the use of animal meal should be permitted
again.<<<
American Association of Zoo Veterinarians Infectious Disease Committee
Manual 2013
BOVINE SPONGIFORM ENCEPHALOPATHY (BSE)
Little is known about atypical BSE. The origin and natural routes of
transmission, if any, have yet to be determined. Almost all cases have been in
older cattle (usually > 8 years of age) that have shown little resemblance to
the clinic-pathological picture seen in classical disease. It has been suggested
that the disease may be sporadic or be caused by a genetic mutation, but no
convincing evidence has been found to support either of these ideas. The correct
answer will probably only come by study of the future annual incidence curves of
both types of disease. Regardless of the origin of atypical BSE, the possibility
of recycling the disease in cattle and other ruminants, as well as the potential
for transmission to humans, mandate a continuation of feed and specified-risk
materials (SRM) bans, together with diagnostic testing programs for some time to
come.
snip...
Naturally occurring cases of BSE in species other than cattle have been
very limited and have been linked to exposure to contaminated feed or infected
carcasses. The majority of cases originated in the UK and like BSE in cattle,
have declined with the implementation of feed controls. None of the exotic
animals were infected in the wild.
Experts who may be consulted:
Linda A. Detwiler, DVM
Clinical Professor
Department of Pathobiology and Population Medicine
College of Veterinary Medicine
Mississippi State University
732-580-9391
Fax: 732-741-7751
Saturday, November 6, 2010
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a
non-profit Swiss Foundation
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the
EU
© TAFS, Berne, 2010
Epidemiological evidence implicated contaminated rendered meat and bone
meal as the source of the BSE epidemic in the United Kingdom, continental Europe
as well as a few other countries around the world. With the overall global
decline of BSE cases, national governments are beginning to explore the
possibility of relaxing some of the measures taken to bring the disease under
control. This paper will examine the current scientific knowledge and other
facets that may impact decisions regarding the feed bans.
snip...
Countries outside of Europe
After confirming BSE in September 2001, the government of Japan enacted
many of the same regulations adopted by the European Union. In regard to feed
controls, all meat and bone meal (MBM) is prohibited from being fed to bovines.
Porcine and marine mammal derived MBM is banned from the rations of pigs and
chickens as well. MBM from poultry produced separately may be fed to pigs and
chickens. (Ref. 13)
These feed control measures appear to have been effective in Japan. Japan
has detected a total of 36 cases of BSE (2001-2009) that seemingly peaked in
2006. In 2008 and 2009, only one case/year has been found. To date, with the
exception of one case born in January 2002, all other BSE cases have been born
prior to the feed ban.
BSE has also been identified in both Canada and the United States (US). The
first case of BSE in Canada was reported in May 2003 and the first native-born
case in the US was identified in 2004. Both Canada and the US prohibited the
feeding of most rendered mammalian proteins to ruminants in 1997. It is evident
by the Canadian BSE cases born between 2000-04 that this was not 100%
effective.
In Canada as of July 12, 2007 SRMs (same list as removed from food for
humans) are prohibited from being included in any animal feed including pet food
or fertilizer.
As of October 2009, the US expanded the 1997 feed ban to prohibit the
feeding of certain high risk cattle materials in all animal feed. This list
includes: 1) the entire carcass of BSE-positive cattle, 2) the brains and spinal
cords from cattle 30 months of age and older, 3) the entire carcass of cattle
not inspected and passed for human consumption, unless the cattle are less than
30 months of age or the brains and spinal cords have been effectively removed,
4) tallow derived from BSE-positive cattle, 5) tallow derived from cattle
material prohibited in animal feed (CMPAF) that contains more than 0.15%
insoluble impurities and 6) mechanically separated beef derived from
CMPAF.
Many countries not reporting BSE have taken some precautionary feed control
measures to prevent an internal recycling of the BSE agent if it were to be
introduced into the animal feed chain. The measures usually include a ruminant
to ruminant or mammalian to ruminant ban. Some countries have also excluded SRMs
from animal feed and set parameters for rendering. For example, as of 2001
Australia prohibits the feeding of any material taken from a vertebrate animal
other than tallow, gelatin, milk products or oils extracted from poultry and
fish. It includes rendered products such as blood meal, meat meal, meat and bone
meal, fish meal, poultry meal, feather meal, and compounded feeds made from
these products to be fed to ruminants. In 2002 Argentina enacted a mammalian to
ruminant ban.
snip...
Evaluation of these possible future developments
Disease considerations
In Europe there seems to be general support for the opinion that feeding
any animal proteins to ruminants2 should remain forbidden to ensure that the BSE
epidemic will not be revived and to respect the herbivorous nature of cattle and
sheep. That particular feed ban was at the core of the hugely successful control
of the BSE epidemic in Europe.
2 With the exception of fish meal in milk replacers
The inclusion of non-ruminant feed in the BSE feed ban regulations was not
a result of a direct and proven TSE risk to, or arising from, non-ruminants, but
rather the consequence of the complexity of the rendering and feed industry and
the limited diagnostic capabilities.
Prior to the total feed ban, the production processes for ruminant and
non-ruminant feed were not separated completely. During rendering processes,
feed production, storage or transportation there was ample opportunity for
ingredients of non-ruminant feed to contaminate ruminant feed and vice-versa.
Despite previous feed bans, ruminant feed therefore continued to contain
ruminant proteins, and crossfeeding of ruminants with non-ruminant feed
containing ruminant proteins remained a possibility. The number of BSE cases
born after ruminant-to-ruminant feed bans or mammalian-to-ruminant feed bans
clearly demonstrates that in practice such feed bans were not sufficiently
effective in preventing new infections. This was true for Europe and seems to be
the same at least in Canada. Prior to finding the first case of BSE in Japan
there was only a voluntary feed ban. After the initial case, Japan adopted more
stringent and broader measures than the ruminant to ruminant or mammalian to
ruminant ban.
While maintaining the total ban of PAPs in ruminant feed alone would in
theory (e.g., under ideal, controlled conditions) be sufficient to protect
cattle and sheep from exposure to potentially infected material, erroneous
cross-contamination, labeling errors and fraudulent misconduct could lead to
some contamination with PAPs in ruminant feed if they were to be allowed for
non-ruminants. Inspections and testing (see below) can reduce, but not eliminate
such a risk.
Even if PAPs would, unlawfully or unintentionally, end up in ruminant feed,
they would pose no known TSE risk under the assumption of two important, jointly
sufficient conditions:
1) That the PAPs stem exclusively from non-ruminants. With the complete ban
of ruminant material being rendered into feed for farmed animals this assumption
is very likely to be met, although pet feed could be a source of
contamination.
2) That non-ruminant proteins can under no circumstances trigger the
development of TSE diseases in ruminants even if fed to them. According to an
EFSA opinion (Ref. 6) there is no evidence to suggest the contrary and EFSA
considers the risk of transmitting BSE to pigs utilizing poultry PAPs (and vice
versa) as negligible. On the other hand, there is also only weak evidence to
actively support the scientific validity of this assumption. Additionally, pigs
have been shown to be susceptible to infection with TSE-material of ruminant
origin by parenteral challenge, but experimental transmission of BSE to pigs by
the oral route has been unsuccessful (Ref 16). Given the current paucity of the
experimental evidence, the condition cannot be considered completely satisfied,
since the absence of evidence does not constitute evidence of absence.
No spontaneous development of TSE-like disease has been observed in pigs,
but it is plausible to assume that pigs can develop such diseases as a very rare
event and if left alive long enough. Multiplied by the number of live pigs –
close to 1 billion worldwide – that would result in a non-negligible number of
pigs with TSE. On the other hand by far most, if not all, pigs slaughtered for
human consumption do not live to be even 1 year old.
TAFS 6
If pig-meal is allowed as feed to poultry and vice versa then a closed loop
of material could be established provided that undigested pig proteins contained
in the gastrointestinal tract of poultry is fed back to pigs or the other way
round. This loop can be prevented if all gastrointestinal tracts and their
contents are removed and discarded before the rendering of animal by-products.
This requirement would be – like all other risk reduction measures – subject to
error and fraud, but add to the redundancy of risk management.
In the light of the evolving BSE epidemic, the zoonotic potential of BSE
and consumer concerns, the authorities were therefore forced to take drastic
measures and exclude all animal proteins from all feed for farmed animals, with
a few exceptions as outlined above.
By 2010, the BSE epidemic appears to be phasing out. In 2001, 2,167 BSE
positive cases were detected within the framework of the EU surveillance
activities. By 2008, this number had fallen to 125, 17 times less. Also the
number of BSE cases detected per 10,000 animals tested had fallen dramatically:
2.55 BSE cases per 10,000 in 2001 against 0.12 BSE cases per 10,000 in 2008, a
21-fold reduction (Ref. 10). This also implies that the probability has
diminished significantly that infected cattle erroneously enter the feed
production chain.
Emerging Disease Considerations
Atypical BSE and other TSEs
For almost the entire two decades that BSE had been known in the world it
was thought that there was only one ?train?that infected cattle and caused
disease in other species such as humans (Refs. 17, 18).
In 2004, cases of a bovine prion disease molecularly different than those
already documented as classical BSE were described by scientists in both Italy
(Ref. 18) and France (Ref. 19). In both countries the cattle were over 8 years
of age. The Italian cases (11 and 15 years of age) named bovine amyloidotic
spongiform encephalopathy (BASE) were characterized by an unglycosylated protein
band with a lower molecular mass (thus named L cases) and the predominance of
the monoglycosylated band. In addition, immunohistochemical detection of PrPres
in these cases found greater deposits in the cerebral cortex and thalamus versus
the brain stem, as is characteristic of classical BSE. The French cases found a
higher molecular mass associated with the unglycosylated protein band and were
called H cases. The different ?trains?are now called atypical BSE.
Atypical BSE is a study in progress with more unknowns than knowns. One of
the most important of the unknowns is the significance of atypical BSE in regard
to human and animal health.
Since these two publications, additional cases of atypical BSE have been
found in other countries. H cases have been detected in Canada, France, Germany,
Japan, the Netherlands, Poland, Sweden, Switzerland, the United Kingdom and the
United States. L cases have been diagnosed in Belgium, Canada, Denmark, France,
Germany, Italy, Japan and Poland.
It has now been shown that both the L and H types of atypical BSE are
experimentally transmissible via the intracerebral route. Homogenates from L
cases have been transmitted to wild-type mice, bovinized, ovinized and humanized
transgenic mice, Cynomolgus monkeys and cattle (Refs. 20, 21, and 22).
H cases have been transmitted to bovinized transgenic (Tgbov) and ovinized
transgenic mice (Ref. 23) and cattle (personal communication March 2009).
TAFS 7
Early studies provide some evidence that L type (or BASE) BSE may be more
virulent for primates including humans (Refs. 21, 24, and 25).
Studies on the oral route are underway. These would provide data to
evaluate the potential for natural transmission of the disease.
Atypical BSE may arise spontaneously in a small proportion of cattle. The
existence of sporadic CJD in humans has led to postulation that disease could
arise spontaneously in any animal, but this theory like others has not been
proved.
In the US one of the H-type BSE case was found to be associated with the
novel mutation E211K within the prion protein gene (Prnp) suggesting that this
strain may have a genetic origin (Ref. 26).
As per the SEAC: „here are too few data to enable an assessment of the
natural transmissibility of L- and H-type BSE between cattle, or to sheep or
goats. The present feed control measures which prevent feeding of mammalian meat
and bone meal to ruminants would limit the spread of these forms of BSE to
cattle, sheep and goats should they be transmissible to these species by the
oral route.?
Atypical Scrapie
In 1998, scientists in Norway discovered a previously uncharacterized
strain of scrapie that is now called Nor 98 or atypical scrapie (Ref. 27).
Certain epidemiological evidence indicates that atypical scrapie may be a
sporadic disease (Ref. 28), however additional research is underway to examine
the likelihood of natural transmission and the extent of tissue
distribution.
As with atypical BSE, there are few data on the potential for natural
transmission of the disease to sheep and other species. The disease has been
transmitted to sheep however the route was intracerebral (Ref. 29). Studies
investigating the possibility of oral transmission are underway.
There is some evidence from transmission studies utilizing porcinized
transgenic mice that pigs may be susceptible to atypical scrapie and BSE in
sheep (Ref. 30). These studies do not involve the natural host or route of
transmission so caution may be taken in drawing conclusions.
Potential for TSEs in Other Species
Studies conducted at the National Institutes of Health Rocky Mountain
Laboratory caution against assuming that animals which do not become clinically
ill are not infected. There is experimental evidence to indicate that certain
species may become carriers (i.e., become infected, shed agent but do not
progress to clinical disease) (Ref 31, Ref 32, Ref 33). Specifically, mice
inoculated with 263K hamster scrapie demonstrated a phase of inactive
persistence. That is, after exposure the mice had a prolonged period
(approximately one year), where there was no evidence of infectivity or PrPsc.
This was followed by a period of an increasing infectivity and agent adaptation.
Many of the mice continued to be devoid of detectable PrPsc.
It is important to determine if this persistence and adaptation could occur
naturally as it may have significance in feeding programs which continually
expose species other than ruminants
TAFS 8
to TSE infectivity. The results of Race and colleagues, warns that an
inactive persistent phase might not produce detectable PrPsc, yet tissues may
harbor infectivity (Ref 32).
Very recent research provides illustrations of the accumulation of
infectivity in tongue and nasal mucosa from terminally diseased field cases and
experimentally challenged cases of BSE even when no abnormal PrP was detectable
(Ref 34). This same phenomena has also been reported for peripheral tissues
collected from sheep with atypical scrapie. (Ref 35).
snip...
Key issues to deal with before the feed ban for non-ruminants can be
relaxed
In our opinion, several key requirements need to be met before the feed ban
for non-ruminants can be relaxed:
The feed industry needs to ensure the following:
Ruminant materials remain excluded completely from the entire feed chain.
This requires a complete and reliable traceability system for both ruminant and
non-ruminant materials.
Intra-species feeding is prevented entirely. This requires that pig and
poultry by-products are prevented from mutual cross-contamination by dedicated
separate logistical pathways from slaughterhouses through rendering and feed
production processes.
No animal proteins are included in ruminant feed. This requires that the
ingredients for and the production of ruminant feed is completely separate from
the ingredients for and the production of non-ruminant feed.
Scientific knowledge required:
Diagnostic tools must be developed with the capacity to verify compliance
with any revised feed ban. These tools must be able to differentiate between
PAPs from different animal species, and – in case it is decided to implement a
tolerance level for contamination of feed – they must be able to determine if
the level of contamination exceeds the defined tolerance levels.
More research is needed to support the assumption that non-ruminant
proteins cannot induce TSE-like diseases in ruminants, even if these diseases
circulated among different non-ruminant species beforehand.
The authorities need to ensure the following:
Competent authorities have the means and capacity to monitor the feed
industry closely and assess their capacity to comply with the remaining feed ban
regulations BEFORE any changes are allowed to proceed.
Legislation is in place to hold the industry liable in case of breaches of
the remaining feed ban.
Appropriate diagnostic tools are registered and validated to verify
compliance with the feed regulations.
In the view of TAFS, taking into consideration all of the scientific and
epidemiological knowns and unknowns, the fact that the requirements as listed
above are currently not met and acknowledging the potential for fraudulent
behavior, a relaxation of the feed ban at the present time would not eliminate
all risks. We feel strongly that maintenance of the ban is the only means to
drive the level of risk toward zero.
snip...
see full text and references here ;
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the
EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a
non-profit Swiss Foundation
============================
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
***This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
***It also suggests a similar cause or source for atypical BSE in these
countries.
============================
P.9.21 Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim
McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre,
Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of
Calgary, Canada
Background: Three BSE types (classical and two atypical) have been
identified on the basis of molecular characteristics of the misfolded protein
associated with the disease. To date, each of these three types have been
detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16
Canadian BSE cases based on the biochemical properties of there associated
PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and
relative proteinase K sensitivity of the PrPres from each of the 16 confirmed
Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type
and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and
changes in glycosylation similar to other atypical BSE cases. PK digestion under
mild and stringent conditions revealed a reduced protease resistance of the
atypical cases compared to the C-type cases. N terminal- specific antibodies
bound to PrPres from H type but not from C or L type. The C-terminal-specific
antibodies resulted in a shift in the glycoform profile and detected a fourth
band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a
similar cause or source for atypical BSE in these countries.
Is it more contagious?
“There is some evidence in primates and transgenic mice that it seems to
spread faster – meaning it maybe more virulent – but we don’t know how
representative these models are of the disease in humans,” says Linda Detwiler,
a clinical professor at Mississippi State University’s College of Veterinary
Medicine. Whether or not L-type could jump species without direct injection into
the brain remains unclear, but so far it can transmit to transgenic humanized,
ovinized (modified to genetically mimic sheep), bovinized, and normal mice, as
well as macaques in the lab.
How could this animal have contracted it?
“We do know that L-type can transmit from one cow to another through
injection in the brain,” says Detwiler. “Long term studies are beginning to look
at whether or not it’s capable of transmission orally through feed, but we don’t
have the data yet.”
*** What irks many scientists is the USDA's April 25 statement that the
rare disease is "not generally associated with an animal consuming infected
feed." The USDA's conclusion is a "gross oversimplification," said Dr. Paul
Brown, one of the world's experts on this type of disease who retired recently
from the National Institutes of Health. "(The agency) has no foundation on which
to base that statement."
EFSA Journal 2014;12(7):3798 Suggested citation: European Food Safety
Authority, 2014.
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE.
EFSA Journal 2014;12(7):3798, 55 pp. doi:10.2903/j.efsa.2014.3798 Available
online: www.efsa.europa.eu/efsajournal
© European Food Safety Authority, 2014 SCIENTIFIC REPORT OF EFSA
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE1 European Food Safety Authority2,3 European Food
Safety Authority (EFSA), Parma, Italy
snip...
CONCLUSIONS AND RECOMMENDATIONS
CONCLUSIONS
Data relating to the prevalence and geographical distribution of Atypical
BSE are incomplete.
The recent cessation of the testing of healthy slaughtered cattle in some
EU Member States will lead to a loss of capacity of the monitoring system to
detect Atypical BSE cases.
For transmission studies, i.c. challenge would be an appropriate proxy for
studying the distribution of the agent if the origin of the disease was
spontaneous, and originating in the brain, while oral challenge would be more
appropriate if the origin of the disease was through ingestion of infected
material.
The current lack of information on the distribution of infectivity in
tissues of Atypical BSE-infected cattle does not allow judgement of whether the
current list of bovine SRM, set by EU legislation based on data relating to the
pathogenesis and tissue distribution of C-BSE, is fit for the purpose of
removing most of the Atypical BSE infectivity from bovine carcasses.
Where data exist from both field cases and experimental animals (i.e. for
L-BSE only), there is good agreement of the data with regard to abnormal PrP
distribution. There are no data for field case H-BSE.
Disease-related PrP has been reported consistently in CNS tissues,
peripheral ganglia and nerves, muscles (predominantly muscle spindles), adrenal
glands and retina for both H-BSE and L-BSE. All of these tissues are also
positive in C-BSE.
By contrast with C-BSE, at this stage no lymphoid tissues or
gastrointestinal tissues from H-BSE- and L-BSE-affected animals have tested
positive for PrPSc presence (IHC, WB) or infectivity (bioassay).
The reference method for the estimation of prion infectious titre in
tissues is endpoint dilution titration in animals. To achieve maximum
sensitivity regarding Atypical H-BSE and L-BSE, this bioassay should ideally be
done in mouse lines over-expressing bovine PrPC. Several mouse lines
over-expressing bovine PrPC are available worldwide.
In vitro amplification techniques can be used to determine whether a tissue
contains any prion seeding activity. A correlation must be made between the
sensitivity achieved by the cell-free assays and bioassays using reference
material such as brain tissue from animals at the terminal stage of disease.
The application of the proposed protocol would provide elements allowing
the assessment of the relative infectious titre, PrPSc accumulation and prion
seeding activity in the tissues of cattle that developed H-BSE or L-BSE (using
posterior brainstem as a reference).
Tissues to be covered by further studies are categorised in three
priorities, based on their inclusion in the cattle SRM list, on the presence of
infectivity, or PrPSc presence, demonstrated in Atypical BSEs or other TSEs in
ruminants, and on the importance in terms of input into the food chain in the
EU.
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 32
Applying the protocol only to the tissues obtained through the EURL study
would provide information on some but not all the tissues from the cattle SRM
list. It would also provide information on some additional tissues not included
in the cattle SRM list, but relevant for the food chain.
Material from other studies could be used to augment the range of SRM and
non-SRM tissues available.
There is no identified source able to provide all the samples necessary to
assess infectivity in tissues belonging to the full cattle SRM list in H- and
L-BSE-infected animals. Therefore, to complete this objective, new inoculations
of cattle would have to be considered.
RECOMMENDATIONS
In accordance with former EFSA recommendations, through the implementation
of the protocol information should also be obtained on the performance of
currently validated rapid tests for TSE active surveillance in cattle/bioassay
for detecting H-BSE and L-BSE agents.
If new inoculation experiments are carried out in cattle with H-BSE and
L-BSE, the following should be considered:
- inoculation through both the i.c. and oral route (despite the potential
length of the oral route experiment);
- inclusion of C-BSE controls in the i.c. route experiment;
- sequential time killing of animals;
- collection of all tissues listed in Table 7.
DOCUMENTATION PROVIDED TO EFSA
1. Summary of the samples available and the tests already carried out by
the EURL-TSE. Submitted by the European Commission as Annex 1 to the
mandate.
2. Information on protocols and tests results provided by the EURL-TSE.
Submitted by the European Commission as Annex 2 to the mandate.
REFERENCES
Thursday, July 24, 2014
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical
BSE investigations
2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation
on February 5, 2007.
Firm initiated recall is ongoing.
REASON Blood meal used to make cattle feed was recalled because it was
cross- contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
___________________________________
PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL
Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal,
TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY
Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST
POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY
Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC
MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR,
V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML
W/SMARTA, Recall # V-025-2007 CODE The firm does not utilize a code - only
shipping documentation with commodity and weights identified. RECALLING
FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete. REASON Products manufactured from bulk
feed containing blood meal that was cross contaminated with prohibited meat and
bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Friday, April 19, 2013
FDA BSE TSE PRION NEWS FEED AND ANNUAL INSPECTION OF FEED MILLS REPORTS HAS
CEASED TO EXIST
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical
BSE investigations
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
Atypical BSE: Transmissibility
BASE (L) transmitted to: cattle (IC) - inc < 20 mos and oral?)
Cynomolgus macaques (IC)
Mouse lemurs (IC and oral)
wild-type mice (IC)
bovinized transgenic mice (IC and IP)
humanized transgenic mice (IC)
H cases transmitted to:
cattle – IC incubations < 20 months
bovinized transgenic mice (IC)
ovinized transgenic mice (IC)
C57BL mice (IC)
One study did not transmit to humanized PrP Met 129 mice
Evaluation of Possibility of Atypical
BSE Transmitting to Humans
Possble interpretation:
L type seems to transmit to nonhuman primates with greater ease than
classical BSE
L type also transmitted to humanized transgenic mice with higher attack
rate and shorter incubation period than classical?
H type did not transmit to Tg Hu transgenic mice
Linda Detwiller, 5/10/2011
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform
Encephalopathies (BSE): Public Health Risk Assessment
IS the h-BSE more virulent than typical BSE as well, or the same as cBSE,
or less virulent than cBSE? just curious.....
Professor Kong reply ;
.....snip
As to the H-BSE, we do not have sufficient data to say one way or another,
but we have found that H-BSE can infect humans. I hope we could publish these
data once the study is complete. Thanks for your interest.
Best regards, Qingzhong Kong, PhD Associate Professor Department of
Pathology Case Western Reserve University Cleveland, OH 44106 USA
BSE-H is also transmissible in our humanized Tg mice. The possibility of
more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
P.4.23 Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw
Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1
1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale,
Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research
Institute, Poland; 5Kansas State University (Previously at USDA National Animal
Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the
classical BSE strain (BSE-C) has led to over 200 cases of clinical human
infection (variant CJD). Atypical BSE cases have been discovered in three
continents since 2004; they include the L-type (also named BASE), the H-type,
and the first reported case of naturally occurring BSE with mutated bovine PRNP
(termed BSE-M). The public health risks posed by atypical BSE were argely
undefined.
Objectives: To investigate these atypical BSE types in terms of their
transmissibility and phenotypes in humanized mice.
Methods: Transgenic mice expressing human PrP were inoculated with several
classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the
transmission rate, incubation time, characteristics and distribution of PrPSc,
symptoms, and histopathology were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected
with minimal spongiosis and an average incubation time of 20-22 months, whereas
only one of the C-type BSE-inoculated mice developed prion disease after more
than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse
brains was biochemically different from bovine BASE or sCJD. PrPSc was also
detected in the spleen of 22% of BASE-infected humanized mice, but not in those
infected with sCJD. Secondary transmission of BASE in the humanized mice led to
a small reduction in incubation time. The atypical BSE-H strain is also
transmissible with distinct phenotypes in the humanized mice, but no BSE-M
transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than
classical BSE, has a lymphotropic phenotype, and displays a modest transmission
barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg
mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
14th International Congress on Infectious Diseases H-type and L-type
Atypical BSE January 2010 (special pre-congress edition)
18.173 page 189
Experimental Challenge of Cattle with H-type and L-type Atypical BSE
A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H.
Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany,
2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch,
Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy
Secretariat, Ottawa, Canada
Background: After the detection of two novel BSE forms designated H-type
and L-type atypical BSE the question of the pathogenesis and the agent
distribution of these two types in cattle was fully open. From initial studies
of the brain pathology, it was already known that the anatomical distribution of
L-type BSE differs from that of the classical type where the obex region in the
brainstem always displays the highest PrPSc concentrations. In contrast in
L-type BSE cases, the thalamus and frontal cortex regions showed the highest
levels of the pathological prion protein, while the obex region was only weakly
involved.
Methods:We performed intracranial inoculations of cattle (five and six per
group) using 10%brainstemhomogenates of the two German H- and L-type atypical
BSE isolates. The animals were inoculated under narcosis and then kept in a
free-ranging stable under appropriate biosafety conditions. At least one animal
per group was killed and sectioned in the preclinical stage and the remaining
animals were kept until they developed clinical symptoms. The animals were
examined for behavioural changes every four weeks throughout the experiment
following a protocol that had been established during earlier BSE pathogenesis
studies with classical BSE.
Results and Discussion: All animals of both groups developed clinical
symptoms and had to be euthanized within 16 months. The clinical picture
differed from that of classical BSE, as the earliest signs of illness were loss
of body weight and depression. However, the animals later developed hind limb
ataxia and hyperesthesia predominantly and the head. Analysis of brain samples
from these animals confirmed the BSE infection and the atypical Western blot
profile was maintained in all animals. Samples from these animals are now being
examined in order to be able to describe the pathoge esis and agent distribution
for these novel BSE types.
Conclusions: A pilot study using a commercially avaialble BSE rapid test
ELISA revealed an essential restriction of PrPSc to the central nervous system
for both atypical BSE forms. A much more detailed analysis for PrPSc and
infectivity is still ongoing.
14th ICID International Scientific Exchange Brochure - Final Abstract
Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America.
Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE
have all been documented in North America, along with the typical scrapie's, and
atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME.
All these TSE in different species have been rendered and fed to food producing
animals for humans and animals in North America (TSE in cats and dogs ?), and
that the trading of these TSEs via animals and products via the USA and Canada
has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only
enhances and helps the spreading of human TSE from the continued belief of the
UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to
continue to validate this old myth, will only spread this TSE agent through a
multitude of potential routes and sources i.e. consumption, medical i.e.,
surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics
etc.
Conclusion: I would like to submit a review of past CJD surveillance in the
USA, and the urgent need to make all human TSE in the USA a reportable disease,
in every state, of every age group, and to make this mandatory immediately
without further delay. The ramifications of not doing so will only allow this
agent to spread further in the medical, dental, surgical arena's. Restricting
the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD
knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante,
Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis,
Marsh, et al and many more, that the world of TSE Transmissible Spongiform
Encephalopathy is far from an exact science, but there is enough proven science
to date that this myth should be put to rest once and for all, and that we move
forward with a new classification for human and animal TSE that would properly
identify the infected species, the source species, and then the route.
Tuesday, November 04, 2014
The pathological and molecular but not clinical phenotypes are maintained
after second passage of experimental atypical bovine spongiform encephalopathy
in cattle
Saturday, June 12, 2010
***PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05
Study of Atypical Bse
PRODUCT O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged
in 11-oz. bottles, For Animal Use Only.
Recall # V-043-2007 CODE A06 RECALLING FIRM/MANUFACTURER Springer Magrath
Co., Mc Cook, NE, by telephone on January 2, 2007, fax dated January 9, 2007, by
letters on February 22, 2007, March 12, March 14 and March 21, 2007.
Firm initiated recall is ongoing.
REASON The finished product was manufactured with prohibited bovine blood
meal and did not bear the cautionary BSE statement that the product should not
be fed to ruminants.
VOLUME OF PRODUCT IN COMMERCE
Approximately 13,255 bottles DISTRIBUTION
Nationwide
END OF ENFORCEMENT REPORT FOR JUNE 13, 2007 ###
PRODUCT
Dairy cattle feed blends containing ProLak and/or ProAmino II protein
concentrate, Recall # V-020-2007
CODE
All finished product manufactured from April, 3, 2006 to April 30, 2006
RECALLING FIRM/MANUFACTURER
Eatonton Co-Op Feed Company, Eatonton, GA, by letter on/about December 12,
2006. Firm initiated recall is complete.
REASON
Finished feed product was manufactured from raw feed material that may have
been contaminated with ruminant derived protein.
VOLUME OF PRODUCT IN COMMERCE
25 tons
DISTRIBUTION
GA
___________________________________
END OF ENFORCEMENT REPORT FOR FEBRUARY 28, 2007
###
PRODUCT
O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 9-oz.
bottles, For Animal Use Only, Recall # V-011-2007
CODE
A07
RECALLING FIRM/MANUFACTURER
Springer Magrath Co., McCook, NE, by telephone on January 11, 2007 and fax
on January 12, 2007. Firm initiated recall is complete.
REASON
The bovine blood meal which was used to manufacture the finished product
was cross-contaminated with prohibited bovine meat and bone meal, and the
finished product is not labeled with the cautionary statement that it should not
be fed to ruminants.
VOLUME OF PRODUCT IN COMMERCE
300/9-oz. bottles
DISTRIBUTION
NE
END OF ENFORCEMENT REPORT FOR JANUARY 31, 2007
###
PRODUCT
Bulk Darling's 85% Blood Meal, Flash Dried, distributed in totes and in
1-ton bags (for one customer only), Recall # V-012-2007
CODE
Blood meal distributed between 9/7/2006-2/3/2007.
RECALLING FIRM/MANUFACTURER
Darling National LLC, Omaha, NB, by telephone on January 12, 2007. Firm
initiated recall is ongoing.
REASON
Some of the exempt bovine blood meal was cross-contaminated with prohibited
bovine meat and bone meal that had been manufactured on common equipment and the
labeling did not bear the cautionary BSE statement that it should not be fed to
ruminants.
VOLUME OF PRODUCT IN COMMERCE
1,366,128 lbs.
DISTRIBUTION
WI, TX, NE, TN, CO, and MN
END OF ENFORCEMENT REPORT FOR FEBRUARY 7, 2007
###
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
______________________________
PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE
None
RECALLING FIRM/MANUFACTURER
Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by
telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated
recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based
protein.
VOLUME OF PRODUCT IN COMMERCE
477.72 tons
DISTRIBUTION
AL
______________________________
PRODUCT
a) Dairy feed, custom, Recall # V-134-6;
b) Custom Dairy Feed with Monensin, Recall # V-135-6.
CODE
None. Bulk product
RECALLING FIRM/MANUFACTURER
Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on
June 28, 2006.
Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated
recall is complete.
REASON
Possible contamination of dairy feeds with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
1,484 tons
DISTRIBUTION
TN and WV
END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006
###
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-115-6
CODE
None
RECALLING FIRM/MANUFACTURER
Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or
about July 14, 2006. FDA initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
Approximately 2,223 tons
DISTRIBUTION
KY
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-116-6
CODE
None
RECALLING FIRM/MANUFACTURER
Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006.
FDA initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
1,220 tons
DISTRIBUTION
KY
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-117-6
CODE
None
RECALLING FIRM/MANUFACTURER
Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated
recall is completed.
REASON
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
40 tons
DISTRIBUTION
LA and MS
______________________________
PRODUCT
Bulk Dairy Feed, Recall V-118-6
CODE
None
RECALLING FIRM/MANUFACTURER
Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA
initiated recall is complete.
REASON
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
7,150 tons
DISTRIBUTION
MS
______________________________
PRODUCT
Bulk custom dairy pre-mixes, Recall # V-119-6
CODE
None
RECALLING FIRM/MANUFACTURER
Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm
initiated recall is complete.
REASON
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
VOLUME OF PRODUCT IN COMMERCE
87 tons
DISTRIBUTION
MS
______________________________
PRODUCT
Bulk custom dairy pre-mixes, Recall # V-120-6
CODE
None
RECALLING FIRM/MANUFACTURER
Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm
initiated recall is complete.
REASON
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
VOLUME OF PRODUCT IN COMMERCE
350 tons
DISTRIBUTION
AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,
50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,
50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower,
50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50
lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall #
V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall #
V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall #
V-127-6
CODE
All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER
Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and
visit on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated
recall is ongoing.
REASON
Poultry and fish feeds which were possibly contaminated with ruminant based
protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
7,541-50 lb bags
DISTRIBUTION
AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall #
V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
*** e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50
lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%,
Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to
20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall #
V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall #
V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL,
by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is
complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant
based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006
09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),
Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED,
Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL,
by telephone on June 15, 2006 and by press release on June 16, 2006. Firm
initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
what about that ALABAMA MAD COW, AND MAD COW FEED THERE FROM IN THAT STATE
???
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R
Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter
dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based
protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Monday, March 8, 2010
UPDATE 429,128 lbs. feed for ruminant animals may have been contaminated
with prohibited material Recall # V-258-2009
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
Thursday, September 3, 2009
429,128 lbs. feed for ruminant animals may have been contaminated with
prohibited material Recall # V-258-2009
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals
may have been contaminated with prohibited material Recall # V-258-2009
Tuesday, November 3, 2009
re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited
material Recall # V-258-2009 and Recall # V-256-2009
>>> The generally older age of the identified H-BSE and L-BSE
cases, and their apparently low prevalence in the population, suggest that these
Atypical BSE forms could be arising spontaneously. <<<
if that is the case, then FRANCE has an exceedingly high rate of
spontaneous atypical BSE cases. maybe that’s why France stopped mad cow testing
;
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
LET'S take a closer look at this new prionpathy or prionopathy, and then
let's look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the
genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_
mad cow in the world to date like this, ......wait, it get's better. this new
prionpathy is killing young and old humans, with LONG DURATION from onset of
symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and
the plaques are very similar in some cases too, bbbut, it's not related to the
g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that
they claim is a genetic TSE, has no relation to any gene mutation in that
family. daaa, ya think it could be related to that mad cow with the same genetic
make-up ??? there were literally tons and tons of banned mad cow protein in
Alabama in commerce, and none of it transmitted to cows, and the cows to humans
there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we
identified a novel mutation in the bovine prion protein gene (Prnp), called
E211K, of a confirmed BSE positive cow from Alabama, United States of America.
This mutation is identical to the E200K pathogenic mutation found in humans with
a genetic form of CJD. This finding represents the first report of a confirmed
case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We
hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in
"the approximately 10-year-old cow" carrying the E221K mutation.
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)
her healthy calf also carried the mutation
(J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic
in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the
UK epidemic had most likely originated from such a mutation and argued against
the scrapierelated assumption. Such rare potential pathogenic PRNP mutations
could occur in countries at present considered to be free of BSE, such as
Australia and New Zealand. So it is important to maintain strict surveillance
for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many
countries still feed ruminant proteins to pigs). Removal of specified risk
material, such as brain and spinal cord, from cattle at slaughter prevents
infected material from entering the human food chain. Routine genetic screening
of cattle for PRNP mutations, which is now available, could provide additional
data on the risk to the public. Because the point mutation identified in the
Alabama animals is identical to that responsible for the commonest type of
familial (genetic) CJD in humans, it is possible that the resulting infective
prion protein might cross the bovine-human species barrier more easily. Patients
with vCJD continue to be identified. The fact that this is happening less often
should not lead to relaxation of the controls necessary to prevent future
outbreaks.
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary
Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen
A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier
Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
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
> Response to Public Comments on the Harvard Risk Assessment of Bovine
> Spongiform Encephalopathy Update, October 31, 2005
> RESPONSE TO COMMENTS FROM TERRY S. SINGELTARY SR.
> Comment #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 Scientists, 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?
> Response: The original (October 2003) and the revised (October 2005)
> Harvard BSE risk assessments underwent external peer review. Subsequently,
> revisions were made to the analysis. In the most recent review, the most
> significant revisions have been: *** 1) the addition of explicit modeling
of > the poultry litter pathway for the potential recycling of bovine protein
> into cattle feed; and 2) a decrease in the assumed effectiveness of ante
> mortem inspection in the identification of animals with BSE.
> Comment #2: WITH A RECENT NATION WIDE MAD COW FEED BAN RECALL in the
past > few months 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?
> Response: This question about feed bans is a matter for policy. As
such, > it is not addressed in this response.
FSIS, USDA, REPLY TO SINGELTARY
What Do We Feed to Food-Production Animals? A Review of Animal Feed
Ingredients and Their Potential Impacts on Human Health
Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker1
1Johns Hopkins Center for a Livable Future, Bloomberg School of Public Health,
Baltimore, Maryland, USA; 2Maryland Institute for Applied Environmental Health,
College of Health and Human Performance, University of Maryland, College Park,
Maryland, USA; 3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA
snip...
Table 1. Animal feed ingredients that are legally used in U.S. animal feeds
Animal
Rendered animal protein from Meat meal, meat meal tankage, meat and bone
meal, poultry meal, animal the slaughter of food by-product meal, dried animal
blood, blood meal, feather meal, egg-shell production animals and other meal,
hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals
digest from dead, dying, diseased, or disabled animals including deer and elk
Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and
undried processed animal waste products
snip...
Sapkota et al. 668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health
Perspectives
FDA to add new BSE-related feed rules soon Robert Roos News Editor
Sep 22, 2005 (CIDRAP News) – The head of the Food and Drug Administration
(FDA) said this week the agency will soon align its rules on animal feed more
closely with those in Canada and Europe, signaling a likelihood of new
restrictions to prevent the spread of bovine spongiform encephalopathy (BSE), or
mad cow disease.
The United States and Canada both ban the use of cattle parts in feed for
cattle and other ruminant animals but allow cattle parts in feed for other
animals such as pigs and poultry. However, Canada plans to ban the use of
high-risk cattle parts, such as the brain and spinal cord of cattle older than
30 months, in all animal feeds in the near future. Europe already bans high-risk
parts, called specified-risk materials (SRMs), from all animal feeds.
In July 2004 the FDA said it had reached a "preliminary" decision to ban
SRMs from all animal feed, as recommended by an international panel of experts
after the first US BSE case surfaced in December 2003. The agency promised to
develop a proposal to that effect. SRMs are the tissues most likely to contain
the abnormal proteins associated with BSE in infected animals.
FDA Commissioner Lester Crawford's comments in a Sep 19 speech now suggest
the agency is about to go ahead with the plan, though he gave no date.
Crawford said the new rules will be "quite a bit stronger" than initially
planned, according to a Sep 19 Bloomberg News report on his speech to the
Consumer Federation of America. He said the rules will be similar to those in
Europe and Canada.
"Our regulation will mimic theirs and it will supersede earlier
considerations," Crawford was quoted as saying.
Will D. Hueston, DVM, a University of Minnesota professor who served on the
expert panel that advised the US government about responses to the first BSE
case, said Crawford's comments probably mean the FDA will ban SRMs from all
animal feeds.
"I think it means they'll take additional action to remove SRMs from animal
feeds—I think they' really targeting the high-risk materials, the brain and
spinal cord," Hueston told CIDRAP News. "They're actively collaborating with
Canada to try to get a uniform program, because we have a lot of trade with
Canada in feed and animals and everything else."
"It's the international standard to remove SRMs from animal feed . . . in
countries where BSE has been identified," said Hueston, who directs the
university's Center for Animal Health and Food Safety.
SRMs are banned from human food; they are removed from cattle carcasses at
slaughterhouses and taken to rendering plants, where they can currently be used
in poultry feed and other nonruminant feeds. Hueston said the main concern is
that cattle can be exposed to SRMs if they are accidentally given poultry feed.
"So this [proposed ban] reduces the potential for leakage in the system."
Another pathway that exposes cattle to poultry feed is the practice of
putting poultry litter—spilled bedding, feed, and waste collected underneath
poultry cages—in cattle feed. Hueston said Canada has banned that, while the
United States still permits it.
The FDA said last year it was considering banning the use of poultry litter
in cattle feed. Reports on Crawford's speech didn't mention any comments on that
issue.
"They [the FDA] haven't given a clear indication which way they're going to
move on that," Hueston said. He commented that keeping SRMs out of poultry feed
would address that concern.
According to accounts of his speech, Crawford did not suggest whether the
FDA will ban the use of cattle blood and restaurant leftovers in cattle
feed—practices that some regard as other risk factors for spreading BSE.
The United States has been trying to persuade Japan to reopen its market to
US beef ever since BSE turned up here in 2003. According to the Bloomberg story,
a draft report issued last week by Japan's Food Safety Commission said US cattle
are more exposed to BSE than Japanese cattle because of insufficient feed
regulations.
Hueston said the FDA is undoubtedly weighing the possible effects of its
feed rules on the effort to reopen beef trade with Japan and other countries.
"Aso, you don't want to create a brand-new disparity with Canada, when our beef
industries are essentially joined at the hip," he added.
The Canadian Food Inspection Agency (CFIA) said this week it hopes to ban
SRMs from all animal feeds by the end of this year, according to a Sep 20
Reuters report. The story quoted Billy Hewett, the CFIA's policy director, as
saying, "I know it seems slow, but it is enormously complex."
See also:
Jul 9, 2004, CIDRAP News story "FDA sets BSE-related rules but delays
action on feed"
Overview of Canadian BSE safeguards
*** DO NOT forget what was originally promised years ago !!!
Press Release FOR IMMEDIATE RELEASE Monday, Jan. 26, 2004 FDA Press Office
301-827-6242
Expanded "Mad Cow" Safeguards Announced to Strengthen Existing Firewalls
Against BSE Transmission HHS Secretary Tommy G. Thompson today announced several
new public health measures, to be implemented by the Food and Drug
Administration (FDA), to strengthen significantly the multiple existing
firewalls that protect Americans from exposure to the agent thought to cause
bovine spongiform encephalopathy (BSE, also known as mad cow disease) and that
help prevent the spread of BSE in U.S. cattle.
The existing multiple firewalls, developed by both the U.S. Department of
Agriculture (USDA) and HHS, have been extremely effective in protecting the
American consumer from exposure to BSE. The first firewall is based on import
controls started in 1989. A second firewall is surveillance of the U.S. cattle
population for the presence of BSE, a USDA firewall that led to the finding of
the BSE cow in December. The third firewall is FDA's 1997 animal feed ban, which
is the critical safeguard to help prevent the spread of BSE through cattle herds
by prohibiting the feeding of most mammalian protein to ruminant animals,
including cattle. The fourth firewall, recently announced by USDA, makes sure
that no bovine tissues known to be at high risk for carrying the agent of BSE
enter the human food supply regulated by USDA. The fifth firewall is effective
response planning to contain the potential for any damage from a BSE positive
animal, if one is discovered. This contingency response plan, which had been
developed over the past several years, was initiated immediately upon the
discovery of a BSE positive cow in Washington State December 23.
The new safeguards being announced today are science-based and further
bolster these already effective safeguards.
Specifically, HHS intends to ban from human food (including dietary
supplements), and cosmetics a wide range of bovine-derived material so that the
same safeguards that protect Americans from exposure to the agent of BSE through
meat products regulated by USDA also apply to food products that FDA
regulates.
FDA will also prohibit certain currently allowed feeding and manufacturing
practices involving feed for cattle and other ruminant animals. These additional
measures will further strengthen FDA's 1997 "animal feed" rule.
"Today's actions will make strong public health protections against BSE
even stronger," Secretary Thompson said. "Although the current animal feed rule
provides a strong barrier against the further spread of BSE, we must never be
satisfied with the status quo where the health and safety of our animals and our
population is at stake. The science and our own experience and knowledge in this
area are constantly evolving. Small as the risk may already be, this is the time
to make sure the public is protected to the greatest extent possible."
"Today we are bolstering our BSE firewalls to protect the public," said FDA
Commissioner Mark B. McClellan, M.D., Ph.D. "We are further strengthening our
animal feed rule, and we are taking additional steps to further protect the
public from being exposed to any potentially risky materials from cattle. FDA's
vigorous inspection and enforcement program has helped us achieve a compliance
rate of more than 99 percent with the feed ban rule, and we intend to increase
our enforcement efforts to assure compliance with our enhanced regulations.
Finally, we are continuing to assist in the development of new technologies that
will help us in the future improve even further these BSE protections. With
today's actions, FDA will be doing more than ever before to protect the public
against BSE by eliminating additional potential sources of BSE exposure."
To implement these new protections, FDA will publish two interim final
rules that will take effect immediately upon publication, although there will be
an opportunity for public comment after publication.
The first interim final rule will ban the following materials from
FDA-regulated human food, (including dietary supplements) and cosmetics:
Any material from "downer" cattle. ("Downer" cattle are animals that cannot
walk.) Any material from "dead" cattle. ("Dead" cattle are cattle that die on
the farm (i.e. before reaching the slaughter plant); Specified Risk Materials
(SRMs) that are known to harbor the highest concentrations of the infectious
agent for BSE, such as the brain, skull, eyes, and spinal cord of cattle 30
months or older, and a portion of the small intestine and tonsils from all
cattle, regardless of their age or health; and The product known as mechanically
separated beef, a product which may contain SRMs. Meat obtained by Advanced Meat
Recovery (an automated system for cutting meat from bones), may be used since
USDA regulations do not allow the presence of SRMs in this product. The second
interim final rule is designed to lower even further the risk that cattle will
be purposefully or inadvertently fed prohibited protein. It was the feeding of
such protein to cattle that was the route of disease transmission that led to
the BSE epidemic in United Kingdom cattle in the 1980's and 1990's.
This interim final rule will implement four specific changes in FDA's
present animal feed rule. First, the rule will eliminate the present exemption
in the feed rule that allows mammalian blood and blood products to be fed to
other ruminants as a protein source. Recent scientific evidence suggests that
blood can carry some infectivity for BSE.
Second, the rule will also ban the use of "poultry litter" as a feed
ingredient for ruminant animals. Poultry litter consists of bedding, spilled
feed, feathers, and fecal matter that are collected from living quarters where
poultry is raised. This material is then used in cattle feed in some areas of
the country where cattle and large poultry raising operations are located near
each other. Poultry feed may legally contain protein that is prohibited in
ruminant feed, such as bovine meat and bone meal. The concern is that spillage
of poultry feed in the chicken house occurs and that poultry feed (which may
contain protein prohibited in ruminant feed) is then collected as part of the
"poultry litter" and added to ruminant feed.
Third, the rule will ban the use of "plate waste" as a feed ingredient for
ruminants. Plate waste consists of uneaten meat and other meat scraps that are
currently collected from some large restaurant operations and rendered into meat
and bone meal for animal feed. The use of "plate waste" confounds FDA's ability
to analyze ruminant feeds for the presence of prohibited proteins, compromising
the Agency's ability to fully enforce the animal feed rule.
Fourth, the rule will further minimize the possibility of
cross-contamination of ruminant and non-ruminant animal feed by requiring
equipment, facilities or production lines to be dedicated to non-ruminant animal
feeds if they use protein that is prohibited in ruminant feed. Currently, some
equipment, facilities and production lines process or handle prohibited and
non-prohibited materials and make both ruminant and non-ruminant feed -- a
practice which could lead to cross-contamination.
To accompany these new measures designed to provide a further layer of
protection against BSE, FDA will in 2004 step up its inspections of feed mills
and renderers. FDA will itself conduct 2,800 inspections and will make its
resources go even further by continuing to work with state agencies to fund
3,100 contract inspections of feed mill and renderers and other firms that
handle animal feed and feed ingredients. Through partnerships with states, FDA
will also receive data on 700 additional inspections, for a total of 3,800 state
contract and partnership inspections in 2004 alone, including annual inspections
of 100 percent of all known renderers and feed mills that process products
containing materials prohibited in ruminant feed.
"We have worked hard with the rendering and animal feed production
industries to try and achieve full compliance with the animal feed rule," said
Dr. McClellan, "and through strong education and a vigorous enforcement
campaign, backed by additional inspections and resources, we intend to maintain
a high level of compliance."
Dr. McClellan also noted that, in response to finding a BSE positive cow in
Washington state December 23, FDA inspected and traced products at 22 facilities
related to that positive cow or products from the cow, including feed mills,
farms, dairy farms, calf feeder lots, slaughter houses, meat processors,
transfer stations, and shipping terminals. Moreover, FDA has conducted
inspections at the rendering facilities that handled materials from the positive
cow, and they were found to be fully in compliance with FDA's feed rule.
To further strengthen protections for Americans, FDA/HHS intends to work
with Congress to consider proposals to assure that these important protective
measures will be implemented as effectively as possible.
FDA is also continuing its efforts to assist in the development of better
BSE science, to achieve the same or greater confidence in BSE protection at a
lower cost. For example, to enhance the ability of our public health system to
detect prohibited materials in animal feed, FDA will continue to support the
development and evaluation of diagnostic tests to identify prohibited materials.
These tests would offer a quick and reliable method of testing animal feeds for
prohibited materials and for testing other products for contamination with the
agent thought to cause BSE.
FDA has publicly discussed many of the measures being announced today with
stakeholders in workshops, videoconferences, and public meetings. In addition,
FDA published an Advance Notice of Proposed Rulemaking in November 2002
(available online at http://www.fda.gov/OHRMS/DOCKETS/98fr/110602c.htm
concerning possible changes to the animal feed rule.
Comprehensive information about FDA's work on BSE and links to other
related websites are available at http://www.fda.gov.
###
For Immediate Release July 9, 2004 FSIS Press Office APHIS Press Office FDA
Media Relations
(202) 720-9113 (202) 734-7799 (301) 827-6242
USDA and HHS Strengthen Safeguards Against Bovine Spongiform Encephalopathy
WASHINGTON, July 9, 2004--HHS Secretary Tommy G. Thompson and Agriculture
Secretary Ann M. Veneman today announced three actions being taken to further
strengthen existing safeguards that protect consumers against the agent that
causes bovine spongiform encephalopathy (BSE, also known as "mad cow
disease").
The three documents on display today include:
A joint USDA Food Safety & Inspection Service (FSIS), USDA Animal and
Plant Health Inspection Service (APHIS) and Food and Drug Administration (FDA)
notice that asks for public comment on additional preventive actions that are
being considered concerning BSE; An interim final FDA rule that prohibits the
use of certain cattle-derived materials in human food (including dietary
supplements) and cosmetics; and A proposed FDA rule on recordkeeping
requirements for the interim final rule relating to this ban. "Today's actions
continue our strong commitment to public health protections against BSE,"
Secretary Thompson said. "Although our current rules are strong, when it comes
to public health and safety we cannot be content with the status quo. We must
continue to make sure the public is protected to the greatest extent
possible."
"This Administration is committed to science-based measures to enhance and
protect public health," Veneman said. "The advance notice of proposed rulemaking
will allow the public the opportunity to provide their input."
"The series of firewalls already in place offer excellent protection
against BSE," said Acting Commissioner of the Food and Drug Administration, Dr.
Lester M. Crawford. "With these additional measures, we will make a strong
system even stronger by putting into effect the most comprehensive,
science-based improvements possible."
The steps already taken have been effective in protecting the American
consumer from exposure to BSE. Import controls on live cattle and certain
ruminant products were put in place more than 15 years ago. In 1997, FDA
finalized its animal feed ban, which has been the critical safeguard to stop the
spread of BSE through the U.S. cattle population by prohibiting the feeding of
most mammalian protein to cattle and other ruminant animals. USDA implemented
additional measures in January to ensure that no cattle tissues known to be high
risk for carrying the BSE agent are included in USDA-regulated products.
Finally, as became evident last December, there is a contingency response plan,
developed over the past several years, that is launched immediately to contain
any potential damage after a BSE positive animal is found.
To allow interested parties and stakeholders the opportunity to comment on
the additional regulatory and policy measures under consideration, USDA's APHIS
and FSIS, along with the FDA, developed an advance notice of proposed rulemaking
that includes several additional actions the federal government is considering
regarding BSE.
The ANPR also provides the public a succinct report on the work of the
international review team (IRT) convened by Secretary Veneman to review the U.S.
response to the single case of BSE in the United States (in a cow imported from
Canada), along with a summary of the many actions already taken by each agency
on BSE.
USDA's FSIS continues to seek and address comments on actions taken in
relation to the BSE mitigation measures and put in place in January 2004. FSIS
is also specifically seeking comments on whether a country's BSE status should
be taken into account when determining whether a country's meat inspection
system is equivalent to the U.S. regulations including the provisions in the
FSIS interim final rules.
USDA's APHIS is specifically seeking comments on the implementation of a
national animal identification system. In April, USDA announced the availability
of $18 million in Commodity Credit Corporation funding to expedite development
of a national animal identification system, which is currently underway. APHIS
is inviting comments on when and under what circumstances the program should
move from voluntary to mandatory, and which species should be covered now and
over the long term.
The ANPRM also requests comment on the following measures related to animal
feed, which is regulated by FDA:
removing specified risk materials (SRM's) from all animal feed, including
pet food, to control the risks of cross contamination throughout feed
manufacture and distribution and on the farm due to misfeeding; requiring
dedicated equipment or facilities for handling and storing feed and ingredients
during manufacturing and transportation, to prevent cross contamination;
prohibiting the use of all mammalian and poultry protein in ruminant feed, to
prevent cross contamination; and prohibiting materials from non-ambulatory
disabled cattle and dead stock from use in all animal feed. FDA has reached a
preliminary conclusion that it should propose to remove SRM's from all animal
feed and is currently working on a proposal to accomplish this goal. Comments on
these issues raised in the ANPRM are due to FDA next month.
FDA today also issued an interim final rule that prohibits the use of
cattle-derived materials that can carry the BSE-infectious agent in human foods,
including certain meat-based products and dietary supplements, and in cosmetics.
These highÇrisk cattle-derived materials include SRM's that are known to harbor
concentrations of the infectious agent for BSE, such as the brain, skull, eyes,
and spinal cord of cattle 30 months of age or older, and a portion of the small
intestine and tonsils from all cattle, regardless of their age. Prohibited
high-risk bovine materials also include material from non-ambulatory disabled
cattle, the small intestine of all cattle, material from cattle not inspected
and passed for human consumption, and mechanically separated beef.
This action is consistent with the recent interim final rule issued by USDA
declaring these materials to be inedible (unfit for human food) and prohibiting
their use as human food.
FDA's interim final rule, in conjunction with interim final rules issued by
FSIS in January 2004, will minimize human exposure to materials that scientific
studies have demonstrated are likely to contain the BSE agent when derived from
cattle that are infected with the disease. Consumption of products contaminated
with the agent that causes BSE is the likely cause of a similar disease in
people called variant Creutzfeldt-Jakob disease.
Although FDA's interim final rule has the full force and effect of law and
takes effect immediately upon publication in the Federal Register, FDA is also
asking for public comment on it.
In conjunction with the publication of the interim final rule, FDA is also
proposing to require that manufacturers and processors of FDA-regulated human
food and cosmetics containing cattle-derived material maintain records showing
that prohibited materials are not used in their products. FDA is taking this
action because records documenting the absence of such materials are important
to ensure compliance with requirements of the interim final rule.
Publication of this USDA-FDA notice, as well as the two FDA documents, is
scheduled for mid-July in the Federal Register. Comments should be submitted as
directed in the addresses section of each document. Each document also provides
information about how and where comments received may be viewed.
####
Note to Reporters: USDA news releases, program announcements and media
advisories are available on the Internet. Go to the APHIS home page at
www.aphis.usda.gov and click on the "News" button.
HHS news releases are available online at www.hhs.gov; FDA news releases
can be found at www.fda.gov, which will also provide links to the documents
discussed in this release.
####
STATEMENT BY LESTER M. CRAWFORD, D.V.M., PH.D. DEPUTY COMMISSIONER OF FOOD
AND DRUGS DEPARTMENT OF HEALTH AND HUMAN SERVICES BEFORE THE COMMITTEE ON
AGRICULTURE, NUTRITION, AND FORESTRY UNITED STATES SENATE JANUARY 27, 2004
Introduction
Mr. Chairman, Members of the Committee, thank you for the opportunity to
participate in today’s hearing on measures taken by the Federal government to
safeguard human and animal health in the United States from Bovine Spongiform
Encephalopathy (BSE) and the response to the finding of a BSE-positive cow in
the State of Washington. I am Dr. Lester M. Crawford, Deputy Commissioner, Food
and Drug Administration (FDA or the Agency).
The mission of FDA is to protect the public health by assuring the safety
and efficacy of our nation’s human and veterinary drugs, human biological
products, medical devices, human and animal food supply, cosmetics, and
radiation emitting products. In fulfilling this mission, FDA is the Agency
responsible for assuring that all FDA-regulated products remain safe and
uncompromised from BSE and related diseases. Many FDA-regulated products contain
bovine ingredients, for example, heart valves, ophthalmic devices, dental
products, wound dressings, injectable drugs, vaccines, soups, gravies, sausage
casings, and animal feeds.
FDA has long been actively involved nationally and internationally in
efforts to understand and prevent the spread of BSE. FDA collaborates
extensively with the Centers for Disease Control and Prevention (CDC), the
National Institutes of Health (NIH), the Animal and Plant Health Inspection
Service (APHIS) and the Food Safety and Inspection Service (FSIS) within the
U.S. Department of Agriculture (USDA), Customs and Border Protection (CBP), the
Environmental Protection Agency (EPA), other Federal agencies, state and local
jurisdictions, and with affected industries and consumer groups. Many of these
activities fit within the framework of the Department of Health and Human
Service’s (HHS or the Department) Bovine Spongiform Encephalopathy/Transmissible
Spongiform Encephalopathy (BSE/TSE) Action Plan, which was released in August
2001. This collaboration over many years has enabled FDA to strengthen
safeguards for FDA-regulated products and to respond quickly and effectively to
the first case of BSE within the U.S.
Executive Summary
The mission of the Agency is to protect the public health by assuring the
safety and efficacy of our nation’s human and veterinary drugs, human biological
products, medical devices, human and animal food supply, cosmetics, and
radiation emitting products. In fulfilling this mission, FDA is the Agency
responsible for assuring that all FDA-regulated products remain safe and
uncompromised from BSE and related diseases.
BSE is a progressive neurological disorder of cattle that results from
infection by an unconventional transmissible agent, and was first diagnosed in
the United Kingdom (U.K.) in 1986. Many FDA-regulated products contain bovine
ingredients, for example, heart valves, ophthalmic devices, dental products,
wound dressings, injectable drugs, vaccines, soups, gravies, sausage casings,
and animal feeds and thus must be taken into consideration as part the effort to
prevent infectivity by BSE.
FDA has a longstanding commitment to protecting consumers from BSE by
following multiple measures designed to safeguard FDA-regulated products from
possible contamination by the BSE agent. Under the Federal Food, Drug, and
Cosmetic (FD&C) Act, FDA has the authority to prevent the adulteration and
misbranding of FDA-regulated products. Further, for medical products that
require pre-market approval (e.g., drugs under Section 505 and medical devices
under Section 513 of the FD&C Act), FDA has addressed safety concerns
related to BSE through requirements of the application and approval
process.
The U.S. employs a robust multi-layered approach to preventing the
introduction and amplification of BSE. While the goal of this approach is to
achieve an extremely high level of compliance with each preventative measure,
this multi-layered approach is designed to protect the U.S. consumer from
exposure to the BSE infective material, and to date this approach has been
working. Since 1989, USDA has prohibited the importation of live animals and
animal products from BSE-positive countries. Since 1997, FDA has prohibited the
use of certain mammalian proteins in the manufacture of ruminant feed. FDA
continues to implement policies to keep safe all FDA-regulated products,
including food, food ingredients, dietary supplements, drugs, vaccines, and
cosmetics from risk of any BSE-contaminated bovine material. As a result of
these multiple regulatory safeguards, the risk of exposure to BSE through
products, FDA regulates remains extremely low in the U.S.
FDA’s 1997 animal feed regulation forms the basis of the Agency’s efforts
to prevent the spread of BSE through animal feed. This rule prohibits the use of
most mammalian protein in the manufacture of animal feeds for ruminants. FDA
implemented this rule to establish in our country feeding practices consistent
with the best science and epidemiological knowledge known at the time to prevent
the spread of BSE throughout herds of U.S. cattle. A risk assessment sponsored
by USDA and conducted by the Harvard Center for Risk Analysis, released in
November 2001, identified FDA’s feed ban as one of the primary safeguards
against the spread of BSE in U.S. cattle.
To maximize protection afforded by the feed regulation, FDA has developed
and implemented a BSE/Ruminant Feed Ban Inspection compliance program and
established the goal of 100 percent compliance. FDA’s strategy for achieving
uniform compliance with the feed rule focuses on three areas: education,
inspection, and enforcement. FDA and its state counterparts conduct, at least
annually, targeted BSE inspections of 100 percent of known renderers, protein
blenders, and feed mills processing products containing material prohibited from
use in ruminant feed. Compliance by these establishments with FDA’s feed rule is
estimated to be at better than 99 percent. As of December 20, 2003, FDA had
received over 26,000 inspection reports (6,404 for Fiscal Year 2003). The
majority of these inspections (around 70 percent) were conducted by state
officials for FDA, with the remainder conducted by FDA officials. The total
number of inspection reports represents 13,672 firms, 1,949 of which are active
and handle materials prohibited from use in ruminant feed. The 1,949 active
firms that handle prohibited material have been inspected by FDA and, as of
December 31, 2003, only five were found to have significant violations,
resulting in official action indicated (OAI). FDA is working with these firms to
bring them into compliance.
On December 23, 2003, FDA was notified by USDA of a presumptive-positive
finding of BSE in a cow in Washington State. FDA immediately initiated its BSE
Emergency Response Plan. As part of the plan, FDA has been coordinately closely
with USDA so that we can effectively investigate this BSE case, trace the
various products involved, and take the appropriate steps to protect the public.
FDA investigators and inspectors located the high risk material rendered from
the infected cow, and the rendering plants placed a hold on the rendered
material, which is being disposed of appropriately. I am happy to report that
all of the establishments inspected by FDA during the course of the
investigation were in compliance with the feed ban. In addition, to help address
the concerns of foreign governments and restore confidence in American products,
FDA has participated, along with USDA, in numerous meetings and consultations
with foreign governments since USDA surveillance found the BSE-positive
cow.
In addition to new policies and regulations, new knowledge and tools gained
through applied research can greatly help us to be more effective in our
regulatory mission, such as protecting the country from BSE. Several of FDA’s
Centers, as well as many private laboratories, academic institutions, and other
Federal agencies (most notably NIH) are also involved in significant research
activities relating to TSEs. Basic areas requiring research include: increasing
our understanding of prions, learning how prions are transmitted within a
species and potentially between species, developing diagnostic tests for humans
and animals, developing detection methods for use on regulated products,
developing methods to increase or eliminate infectivity, and designing new
treatments. We are optimistic about the promise of new technologies, such as
better methods to quickly distinguish the species of proteins and sensors to
detect abnormal prions in food. Development of these technologies can contribute
significantly to the effort to prevent the spread of BSE and must be considered
carefully when evaluating potential regulatory changes to address BSE.
At the time that FDA implemented the feed rule in 1997, the Agency also
recognized that evolving, complex scientific and public health issues,
particularly regarding BSE required the Agency to continue to assess and
scrutinize the rule to ensure its integrity as a firewall against the potential
for spread of BSE. To further explore ways the animal feed regulation could be
improved in November 2002, FDA published an advance notice of proposed
rulemaking (ANPR) soliciting information and views from the affected industries
and the public on some potential changes to its current feed regulation,
including ways that the animal feed regulation could be strengthened. Although
the risk of exposure to BSE in the U.S. remains extremely low and the measures
in place are working, as a result of the recently discovered infected cow in the
state of Washington, the Agency is evaluating the appropriateness of additional
science-based measures to further strengthen our current protections.
Yesterday, Department Secretary Tommy Thompson and FDA Commissioner Mark
McClellan announced several additional public health measures to further
strengthen the current robust safeguards that help protect Americans from
exposure to the agent that causes BSE and help prevent the spread of BSE in U.S.
cattle. These measures relate to both protections for foods intended for human
consumption as well as additional measures to strengthen FDA’s 1997 final rule
regulating animal feed. With respect to human foods, FDA announced that it will
extend to FDA-regulated foods, dietary supplements and cosmetics, restrictions
on using specified risk materials that would complement the recent USDA
announcements. Concerning animal feed, the Agency announced a series of measures
designed to lower even further the risk that cattle will be purposefully or
inadvertently fed “ruminant” proteins, including, eliminating an exemption in
the feed rule that allows mammalian blood and blood products at slaughter to be
fed to ruminants as a protein source; banning the use of “poultry litter” as a
feed ingredient for cattle and other ruminants; prohibiting the use of “plate
waste” as a feed ingredient for ruminants, including cattle; and taking steps to
further minimize the possibility of cross-contamination of animal feed via
equipment, facilities or production lines.
Finally, FDA is increasing its inspections of feed mills and renderers in
2004. Our 2001 base funding for BSE-related activities was $3.8 million. We
shifted resources internally in 2001 and received a substantial increase from
Congress in 2002. Our funded level for 2004 is currently approximately $21.5
million, almost a five-fold increase over the 2001 base. FDA will itself conduct
2,800 inspections and will make its resources go even further by working with
state agencies to fund 3,100 contract inspections of feed mills and renderers
and other firms that handle animal feed and feed ingredients. Through
partnerships with states, FDA will also receive data on 700 additional
inspections, for a total of 3,800 state contract and partnership inspections in
2004. These inspections would include 100 percent of all known renderers and
feed mills that process products containing prohibited materials.
The Agency looks forward to continuing to assist Congress as it evaluates
the risks associated with BSE, identifies opportunities to promote technologies
that will detect and prevent the spread of BSE, and considers science-based
approaches to further strengthen regulatory protections and bolster the
resources available to assist Federal, state, local and private efforts to
assure that BSE does not present a threat to human or animal health in the
U.S.
see full text ;
OH, that's right, old lester sold out to the highest bidder $$$
Ex-FDA Chief Faces Fines in Stock Case By ANDREW BRIDGES, Associated Press
Writer 1:55 PM PST, January 19, 2007
WASHINGTON -- Former FDA Commissioner Lester Crawford would face a $50,000
fine and probation but no jail time as punishment for lying about ownership of
illegally held stocks, according to a deal worked out between his attorney and
federal prosecutors.
Crawford and the government both have agreed to the fine and some form of
probation, though his ultimate sentence will be at the discretion of Magistrate
Judge Deborah A. Robinson, according to sentencing memoranda filed with the U.S.
District Court in Washington.
His sentencing is set for Tuesday.
Crawford pleaded guilty in October to charges of having a conflict of
interest and false reporting of information about stocks he and his wife owned
in food, beverage and medical device companies he regulated while head of the
Food and Drug Administration.
The U.S. Attorney's office recommended the $50,000 fine, saying it would
exceed the roughly $39,000 Crawford and his wife, Cathy, made from exercising
options and in dividends from the forbidden stocks they held in the
FDA-regulated companies.
The government also recommended Crawford be sentenced to probation and
community service but skip any jail time, according to its sentencing memo filed
with the court. Crawford could face up to six months in jail under sentencing
guidelines.
"Given his early acceptance of responsibility, the defendant's actions
merit the stigma of criminal convictions, a fine, and probation, but not
incarceration," according to the government memo, signed by assistant U.S.
attorneys Howard R. Sklamberg and Timothy G. Lynch. Sklamberg declined to
comment Friday.
Crawford's attorney, Barbara Van Gelder, said her client agreed to pay the
fine, according to her memo to the court. However, Van Gelder specifically
requested unsupervised probation, which would allow Crawford to travel overseas
for work. Van Gelder did not mention community service in her memo. She did not
immediately return a message seeking comment.
In October, Crawford admitted to falsely reporting that he had sold or did
not own stock when he continued holding shares in the firms governed by rules of
the FDA, which is illegal. Beginning in 2002, Crawford filed seven incorrect
financial reports with a government ethics office and Congress, leading to the
misdemeanor charges.
Although Crawford lied about ownership of the stocks -- including under
oath before the Senate -- government attorneys acknowledged there is no evidence
he was "engaged in a concerted scheme to use his high office for personal
gain."
Van Gelder, meanwhile, suggested Crawford's wife, secretary and financial
adviser prepared and handled the inaccurate financial statements Crawford filed
with the government. She acknowledged, however, that Crawford remained
ultimately responsible for their accuracy.
Crawford, a veterinarian and food-safety expert, abruptly resigned from the
FDA in September 2005 but gave no reason for leaving. He had held the job for
two months, following his confirmation by the Senate.
On the Net:
Food and Drug Administration: http://www.fda.gov
Date: October 18, 2006 at 7:44 am PST
Former FDA Commissioner Pleads Guilty to Conflict of Interest and Making
False Financial Disclosures
WASHINGTON, Oct. 17, 2006 - Lester M. Crawford, a former Commissioner of
the Food and Drug Administration (FDA), has pled guilty to a Conflict of
Interest charge and Making False Financial Disclosures to the U.S. Senate and
the Executive Branch, announced U.S. Attorney Jeffrey A. Taylor and Inspector
General Daniel Levinson, U.S. Department of Health and Human Services.
Crawford entered his guilty plea to the two misdemeanor charges this
afternoon in the U.S. District Court for the District of Columbia before U.S.
Magistrate Judge Deborah Robinson. Crawford is scheduled to be sentenced on
January 22, 2007. He faces a sentence of up to one year in prison on each
charge.
"One of the most important principles of our ethics laws is that public
officials cannot have a financial interest in any decision that they make,”
stated U.S. Attorney Taylor. “Lester Crawford, who held one of the most
important jobs in government, blatantly violated these principles. Today, he is
being held accountable for his actions."
Inspector General Levinson stated, "Any Government official's disregard of
the conflict of interest laws undermines the integrity of the rules of conduct
established for all those in Government. Taxpayers must have confidence that
administrators of Government programs will be objective and free from improper
influences in carrying out their official duties."
Crawford, 68, of Chevy Chase, Maryland, held some of the most senior
positions in the FDA. He served as Deputy Commissioner between February 25, 2002
and March 26, 2004, when he became Acting Commissioner. On February 15, 2005,
Crawford was nominated to become Commissioner. On July 18, 2005, the U.S. Senate
confirmed Crawford, who remained Commissioner until September 30, 2005.
As a senior FDA employee, Crawford was required to file regular Public
Financial Disclosure Reports, known as Standard Form SF 278s. Schedule A of the
SF 278 required the filer to list all investment assets having a value exceeding
$1,000 that were held by the filer or the filer's spouse, as well as sources of
income exceeding $200 earned by the filer during the applicable reporting
period.
Each year, ethics officials at the Department of Health and Human Services
reviewed Crawford's SF 278s to ensure that he and his wife were not holding
stocks or stock options of companies that were "significantly regulated
organizations," which federal regulations defined as organizations for which the
sales of products regulated by the FDA constitute ten percent or more of annual
gross sales in the organization's previous fiscal year. Any FDA employee who was
required to file an SF 278 could not hold a "financial interest," such as stock
or stock options, in a significantly regulated organization.
Crawford's nomination as Commissioner required confirmation by the U.S.
Senate and was considered by the Senate Committee on Health, Education, Labor,
and Pensions. As a nominee, Crawford was required to submit two financial
disclosure documents to the Committee: an SF 278 and a Statement for Completion
by Presidential Nominees. Crawford filed both forms in February 2005.
Crawford’s plea to Making False Writings is based on his failure to
disclose his and his wife’s ownership of stock in “significantly regulated
organizations” to the Senate Committee and to the Executive Branch.
During the relevant time periods, Crawford and/or his wife owned forbidden
stocks in the following “significantly regulated organizations”: Pepsico, Sysco,
Kimberly-Clark, and Embrex.
Crawford filed a number of disclosure forms and other false writings in
which he did not declare his and his wife’s ownership of forbidden stocks and
stock options. Specifically,
•July 1, 2004. In this SF 278, Crawford disclosed ownership of Sysco and
Kimberly-Clark stock. When an HHS ethics official inquired about Crawford’s
ownership of this stock, Crawford responded in a December 28, 2004 email that
the stocks in "Sysco and Kimberly-Clark have in fact been sold." That statement
was false.
• February 23, 2005. Crawford did not disclose on this SF 278 his income
from a November 17, 2004 exercise of Embrex stock options or the Crawfords'
ownership of Kimberly-Clark or Sysco stock.
• February 25, 2005. Crawford failed to disclose in his nominee Statement
to the Senate Committee his income from the exercise of Embrex stock options in
October 2003 and November 2004. Crawford also did not disclose his remaining
Embrex stock options.
Crawford’s ownership of Sysco and Pepsico stock and his role as Chairman of
the FDA’s Obesity Working Group (“OWG”) gave rise to the Conflict of Interest
charge, to which he has also pled guilty. On February 11, 2004, Crawford and the
OWG's Vice Chairman submitted the OWG's final report and recommendations,
entitled "Calories Count: Report of the Working Group on Obesity," to then-FDA
Commissioner Mark McClellan. The report contained many recommendations,
including encouraging manufacturers to re-label serving sizes, noting as an
example that "a 20 oz bottle of soda that currently states 110 calories per
serving and 2.5 servings per bottle could be labeled as 275 calories per
bottle." The FDA publicly released "Calories Count" on March 12, 2004.
On June 3, 2004, Crawford testified before the House of Representatives
Committee on Government Reform about the government's role in combating obesity.
In his testimony, Crawford outlined the OWG's recommendations and again stressed
the importance of re-labeling serving sizes for sodas.
During the entire period from the formation of the OWG to the date of
Crawford's congressional testimony, Crawford and his wife owned 1,400 shares of
Pepsico stock, worth a minimum of about $62,000, and 2,500 shares of Sysco
stock, worth a minimum of about $78,000. Pepsico, a leading manufacturer of soft
drinks and snack foods, and its shareholders had a financial interest in the
OWG's conclusions and recommendations. Sysco, a leading manufacturer of food
products, and its shareholders had a financial interest in the OWG's conclusions
and recommendations.
There is no evidence that the OWG's conclusions were altered because of the
Crawfords' ownership of Pepsico or Sysco stock.
Following the announcement of Crawford’s departure from office, Senators
Mike Enzi and Edward Kennedy and Representatives Maurice Hinchey, Marcy Kaptur,
Lynn Woolsey, Raúl Grijalva, and Sam Farr asked that the Inspector General
investigate this matter.
In announcing today’s guilty plea, U.S. Attorney Taylor and Inspector
General Levinson commended Inspector Thomas Sowinski of the Inspector General’s
office for his outstanding investigation of this case. They also thanked the
Senate Legal Counsel’s Office for the help that it provided in the
investigation. Finally, they commended Assistant U.S. Attorneys Howard Sklamberg
and Timothy Lynch, who prosecuted the case, and intern Vi Do, who assisted in
the investigation.
For Information, Contact Public Affairs Channing Phillips (202) 514-6
SO, in essence, the fda simply hung a carrot out in front of the public,
and the public bit. i ain't biting. it's all about money, to hell with human
health ;
reminds me of ;
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
snip...END full text ;
FOR IMMEDIATE RELEASE P07-08 January 19, 2007 Media Inquiries: Kathleen
Quinn, 301-827-6242 Consumer Inquiries: 888-INFO-FDA
FDA Commissioner Announces Important Personnel Changes
U.S. Food and Drug Administration (FDA) Commissioner Dr. Andrew C. von
Eschenbach is pleased to announce two new personnel changes at the Agency; the
creation of the Office of the Chief Medical Officer which will be overseen by
Deputy Commissioner Dr. Janet Woodcock and the appointment of John R. Dyer, MPH,
as the agency's Deputy Commissioner for Operations and the Chief Operating
Officer (COO).
snip...
"FDA is a science-based agency and science-led Agency; science provides the
foundation for our regulatory decisions and the work we do on a daily basis to
promote and protect the nations' health," said Dr. von Eschenbach. "Creation of
this office, and position, will better ensure we achieve this mission with the
highest scientific quality and effectiveness needed."
snip...
Mr. Dyer most recently served as the Chief Operating Officer for the
Centers for Medicare & Medicaid Services (CMS), a federal agency within the
Department of Health and Human Services that is responsible for providing health
insurance benefits to the elderly, disabled, and indigent through the Medicare
and Medicaid programs. In that capacity, he led the implementation of the
Medicare Modernization Act (MMA) and was responsible for the overall day to day
operations of the agency. Specifically as COO, he helped develop the program
policies and regulations, and stood up the business and systems operations of
the prescription drug program in time for the congressionally mandated start of
open enrollment on Oct 15, 2005 and start of the drug prescription benefits on
January 1, 2006.
Prior to CMS, from 2001-2003, Mr. Dyer worked in the private sector for
information technology and executive leadership companies. He was involved in
entrepreneurial ventures in agriculture, real estate, and industrial enterprises
in Latin America from 2003-2004.
In his federal career from 1972 to 2000, Mr. Dyer held increasingly
responsible executive positions with the Social Security Administration (SSA),
including the Chief Information Officer and Principal Deputy Commissioner where
he assisted the agency by leading the effort to automate and modernize systems
and improve the level of customer service. Other federal positions include the
Director for Budget and Management at CMS (then the Health Care Financing
Administration) from 1984-1998 and Commerce Branch Chief at the Office of
Management and Budget in the Executive Office of the President. While at OMB,
Mr. Dyer had budget and policy review of wide-ranging research and development
programs ranging from mental health to ocean and atmospheric related.
Mr. Dyer has been the recipient of many awards during his federal career
including the Presidential Award for Distinguished Executive. He holds a Masters
Degree in Public Health from the University of Michigan and obtained his
undergraduate Bachelor of Arts in Sociology from Notre Dame.
####
*** UPDATE ON TSE roadmap 2, a road to no where Sunday July 18, 2010 ***
IN reply to ;
Saturday, July 17, 2010
TSE Road map 2 A Strategy paper on TSE, a road to no where
Brussels, 16.7.2010 COM(2010)384 final COMMUNICATION FROM THE COMMISSION TO
THE EUROPEAN PARLIAMENT AND THE COUNCIL
Confucius is confused again. IF BSE was spontaneous, just happens from
nothing occasionally, from a funked out twisted protein, that just happens to
spontaneously change shapes on it's own, as most officials have had us believe
over the years, decades. THEN how is BSE almost eradicated ??? hmm?
WHAT about atypical BSE's ?
WHAT about IBNC BSE ?
SRM's there from all of the above ?
WHAT about SRM from pigs, poultry, fish, AND the potential for passing the
TSE agent surviving the digestinal track to expose further in feed ?
The potential for transmissible spongiform encephalopathies in non-ruminant
livestock and fish
D. Matthews (1) & B.C. Cooke (2) (1) Transmissible Spongiform
Encephalopathy [TSE) Programme Manager, Veterinary Laboratories Agency, Woodham
Lane, New Haw, Addlestone. Surrey KT15 3NB. United Kingdom (2) 1 Jenkins
Orchard, Wick St Lawrence. Weston Super Mare. North Somerset, BS22 7YP. United
Kingdom
Summary
Pigs and poultry in the United Kingdom have undeniably been exposed to the
bovine spongiform encephalopathy (BSE) agent. They consumed the same ruminant
protein that gave rise to the BSE epidemic in cattle, but there has been no
evidence of an epidemic in these species. Experimental investigations have shown
pigs to be susceptible to infection by multiple parenteral challenge, but
resistant to oral exposure with BSE-infected cattle brain. Current but
incomplete evidence suggests that they are also resistant to oral challenge with
sheep scrapie. Studies in domestic chickens indicate that they are resistant to
both parenteral and oral challenge. Unfortunately, no published data exists on
the susceptibility of fish to infection. Incidental findings in the brains of
unexposed pigs are described that could otherwise give rise to concerns about
the presence of a transmissible spongiform encephalopathy in pig populations
around the world.
Keywords
Chicken - Fish - Meat-and-bone meal - Pig - Poultry - Prion - Prion protein
Transmissible spongiform encephalopathy.
Introduction
The recognition of bovine spongiform encephalopathy (BSE) in domestic
cattle in the United Kingdom (UK) in 1986 inevitably led to concerns about the
potential risk to non-ruminant livestock (49). Although the initial focus was on
the identification of the causal agent of BSE and confirmation that the disease
was transmissible (20), research rapidly investigated the likelihood that pigs
and poultry might also be susceptible to infection. lnitial epidemiological
investigations into the source of BSE identified the likely vehicle to be the
consumption by cattle of rendered animal protein of ruminant origin (51). With
time, the decline of the epidemic following the implementation of measures to
remove ruminant protein from cattle feed has confirmed that hypothesis. This is
distinct from the debate about whether the actual origin of the agent was ovine
or bovine. While there has been speculation about whether BSE arose
spontaneously in bovines, rather than from transmission of sheep scrapie to
cattle, the ban dealt with the vehicle of transmission, irrespective of
origin.
Wednesday, April 02, 2008 In vivo prion protein intestinal uptake in
fish
1: APMIS. 2008 Mar;116(3):173-80.
In vivo prion protein intestinal uptake in fish.
Dalla Valle AZ, Iriti M, Faoro F, Berti C, Ciappellano S. Department of
Food Science and Microbiology (DISTAM), Section of Human Nutrition, University
of Milan, Milan, Italy.
Intestinal uptake of abnormal prion protein (PrP(Sc)), the pathological
agent involved in transmissible spongiform encephalopathies (TSEs), has been
investigated in rainbow trout (Oncorhynchus mykiss). Experimental procedures
were conducted in vivo by immunohistological PrP(Sc) localization in intestine
and pyloric caeca after forced feeding of infected material. Results indicate
that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted in the
fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7
days in the distal intestine. It did not remain longer than 15 days in the fish
intestine; furthermore, it did not cross the intestinal barrier.
PMID: 18377582 [PubMed - in process]
Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and
that it persisted
in the fish gastrointestinal tract for up to 3 days in pyloric caeca and
for up to 7 days in the
distal intestine.
It did not remain longer than 15 days in the fish intestine;
WOULD this not be a potential risk factor for transmission of the PrPSc
agent to cattle and other species via fish by-products and or fish feed ???
vCJD in the USA * BSE in U.S.
15 November 1999
snip...
Our feeding and rendering practices have mirrored that of the U.K. for
years, some say it was worse. Everything from the downer cattle, to those
scrapie infected sheep, to any roadkill, including the city police horse and the
circus elephant went to the renders for feed and other products for consumption.
Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs,
chickens, dogs, and cats, and humans were exempt from that ban. So they can
still feed pigs and chickens those potentially TSE tainted by-products, and then
they can still feed those by-products back to the cows.
***I believe it was Dr. Joe Gibbs, that said, the prion protein, can
survive the digestinal track. So you have stopped nothing.
It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent
neurologically ill cattle, some with encephalopathy stamped on the dead slips,
were picked up and sent to the renders, along with sheep carcasses. Speaking of
autopsies, I have a stack of them, from CJD victims. You would be surprised of
the number of them, who ate cow brains, elk brains, deer brains, or hog
brains.
snip...
full text ;
Research article
Scrapie infectivity is quickly cleared in tissues of orally-infected farmed
fish
Loredana Ingrosso1 , Beatriz Novoa2 , Andrea Z Dalla Valle3 , Franco
Cardone1 , Raquel Aranguren2 , Marco Sbriccoli1 , Simona Bevivino1 , Marcello
Iriti4 , Quanguo Liu1 , Vito Vetrugno1 , Mei Lu1 , Franco Faoro4 , Salvatore
Ciappellano3 , Antonio Figueras2 and Maurizio Pocchiari1
1 Istituto Superiore di Sanità , Department of Cellular Biology and
Neuroscience, viale Regina Elena,299,00161 Rome, Italy
2 Instituto Investigaciones Marinas, CSIC, Eduardo Cabello 6, 36208 Vigo,
Spain
3 Section of Human Nutrition, Department of Food Science and Microbiology,
DiSTAM, University of Milan, via Celoria 2, 20133 Milano, Italy
4 Institute of Plant Pathology, University of Milan and Institute of Plant
Virology, CNR, Milano, Italy
author email corresponding author email
BMC Veterinary Research 2006, 2:21doi:10.1186/1746-6148-2-21
Published: 15 June 2006
Abstract Background Scrapie and bovine spongiform encephalopathy (BSE)
belongs to the group of animal transmissible spongiform encephalopathy (TSE).
BSE epidemic in the UK and elsewhere in Europe has been linked to the use of
bovine meat and bone meals (MBM) in the feeding of cattle. There is concern that
pigs, poultry and fish bred for human consumption and fed with infected MBM
would eventually develop BSE or carry residual infectivity without disease.
Although there has been no evidence of infection in these species, experimental
data on the susceptibility to the BSE agent of farm animals other than sheep and
cow are limited only to pigs and domestic chicken. In the framework of a
EU-granted project we have challenged two species of fish largely used in human
food consumption, rainbow trout (Oncorhynchus mykiss) and turbot (Scophthalmus
maximus), with a mouse-adapted TSE strain (scrapie 139A), to assess the risk
related to oral consumption of TSE contaminated food. In trout, we also checked
the "in vitro" ability of the pathological isoform of the mouse prion protein
(PrPSc) to cross the intestinal epithelium when added to the mucosal side of
everted intestine.
Results Fish challenged with a large amount of scrapie mouse brain
homogenate by either oral or parenteral routes, showed the ability to clear the
majority of infectivity load. None of the fish tissues taken at different time
points after oral or parenteral inoculation was able to provoke scrapie disease
after intracerebral inoculation in recipient mice. However, a few recipient mice
were positive for PrPSc and spongiform lesions in the brain. We also showed a
specific binding of PrPSc to the mucosal side of fish intestine in the absence
of an active uptake of the prion protein through the intestinal wall.
Conclusion These results indicate that scrapie 139A, and possibly BSE, is
quickly removed from fish tissues despite evidence of a prion like protein in
fish and of a specific binding of PrPSc to the mucosal side of fish
intestine.
>>>However, a few recipient mice were positive for PrPSc and
spongiform lesions in the brain. We also showed a specific binding of PrPSc to
the mucosal side of fish intestine in the absence of an active uptake of the
prion protein through the intestinal wall. <<<
WOULD this not be further evidence to show that the rendering of such
product after ingesting TSE tainted product, would further expose species that
consume such product, i.e. even if the fish do not contract a TSE, could not the
intestines and the feed that may still be there further expose species eating
those by-products ???
Competing interests
none
An evolutionary basis for scrapie disease: identification of a fish prion
mRNA
References and further reading may be available for this article. To view
references and further reading you must purchase this article.
Eric Rivera-Milla, Claudia A. O. Stuermer and Edward Málaga-Trillo
Department of Biology, University of Konstanz, 78457, Konstanz,
Germany
Available online 11 December 2002.
Abstract Infectious prion proteins cause neurodegenerative disease in
mammals owing to the acquisition of an aberrant conformation. We cloned a Fugu
rubripes gene that encodes a structurally conserved prion protein, and found
rapid rates of molecular divergence among prions from different vertebrate
classes, along with molecular stasis within each class. We propose that a
directional trend in the evolution of prion sequence motifs associated with
pathogenesis and infectivity could account for the origin of scrapie in
mammals.
AS the crow flies, so do TSE...feces
Could Crows Play a Role in Spreading CWD was presented by Dr. Kurt
VerCauteren, NWRC, WS-APHIS- USDA. From the first observations (40 years ago) of
CWD in mule deer (Odocoileus hemionus) and Rocky Mountain elk (Cervus elaphus
nelsoni) in Northern Colorado, the disease has been identified in an increasing
geographic area. Mechanisms for the spread of CWD are incompletely understood.
Birds have been identified as potential vectors for a number of diseases, where
infected material is ingested and the disease agent is later shed in new areas
after flying substantial distances. We hypothesized that avian scavengers have
the potential to disseminate prions associated with transmissible spongiform
encephalopathies (TSEs), like CWD, by a similar process. As prions are resistant
to destruction, it is reasonable that infectious material could pass through the
digestive tract of scavenging birds. Our objective was to determine if
TSE-positive brain material from mice (i.e., mouse-adapted scrapie) could pass
through the digestive tract of American crows (Corvus brachyrhynchos) and still
be infectious to mice. Our experimental design included treatment groups of mice
inoculated intraperitoneally with: 1) normal mouse brain, 2) infected mouse
brain, 3) gamma-irradiated feces from crows gavaged with normal mouse brain, and
4) gamma-irradiated feces from crows gavaged with infected mouse brain. Our
preliminary results indicate feces from each of 20 crows gavaged with infected
mouse brain were infectious for mice (proportion of crows=1.00, 95% CI:
0.83-1.00) and average longevity for mice was 213 days (95% CI: 210-216).
Longevity of mice inoculated with infected mouse brain was slightly less (198
days, 95% CI: 188-207). Most mice inoculated with normal brain, or feces from
crows gavaged with normal brain, were still alive 1 year post inoculation with
no evident clinical signs of TSE disease in any control mice. Our results
demonstrate that a common, migratory North American scavenger, the American
crow, can pass infective prions in feces and, therefore, could play a role in
the spatial dissemination of prion disease.
Sunday, November 01, 2009
American crows (Corvus brachyrhynchos) and potential spreading of CWD
through feces of digested infectious carcases
snip...
PLUS, this goes back to what the late Dr. Gibbs told me, and what the late
Harash Narang book showed, Dr. Gibbs stating that the TSE agent could spread
through the digestinal track, and survive, and could still have the potential to
spread, and Harash Narang's book 'The Link', page 135, where a farmers around
Kent have chickens with BSE. MAFF was aware of this and was suppose to do some
studies? BUT, regardless whether or not these birds become clinical and die, the
fact that the above studies showed that the TSE agent survived the digestinal
tract, and went on to further infect mice via feces, is very disturbing, and
further enhances transmission studies must be done asap. PLUS, this should be
the final straw for chicken litter being fed back to cattle and other food
producing animals for humans and animals. AND not to forget the Red Necked
Ostrich and BSE? ...TSS
snip...
SEI805 Transmissibility of BSE to domestic fowl by injection with brain
homogenate.
1 challenged bird died overnight (42 months p.i.) following a period of
ataxia - histopathological examination pending. 2 further challenged birds are
also showing neurological signs of ataxia and tremor (43 months p.i.). All
affected birds are cock birds. The remaining 4 challenged hens are clinically
normal (43 months p.i.).
2 control birds were culled due to intercurrent disease (40 and 43 months
p.i.) . No significant lesions were observed in one and histopathological
examination is pending on the other.
The remaining 6 control birds are clinically normal.
SE1806 Transmissibility of BSE to domestic fowl by oral exposure to brain
homogenate.
1 challenged cock bird was necropsied (41 months p.i.) following a period
of ataxia, tremor, limb abduction and other neurological signs.
Histopathological examination failed to reveal any significant lesions of the
central or peripheral nervous systems.
94/01.19/7.1
1 other challenged cock bird is also showing ataxia (43 months p.i.). The
remaining 2 challenged cocks and 5 hens are clinically normal (43 months
p.i.).
Ruther examinations are in progress to determine the cause of morbidity in
these studies (SE1805 and SE1806).
For controls see SE1805.
snip...
94/01.19/7.1
also,
TRANSLATION
F437/91
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO
CAMELUS) - SPONGIFORM ENCEPHALOPATHY -
* The Red-Neck Ostrich 'THE AUTOPSY' & TSEs
THE AUTOPSY
Date: Mon, 11 Jun 2001 16:24:51 -0700 Reply-To: Bovine Spongiform
Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S.
Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY'
snip...
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO
CAMELUS) - SPONGIFORM ENCEPHALOPATHY
OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE
ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER
2002
OPINION
1. Necrophagous birds as possible transmitters of BSE. The SSC considers
that the evaluation of necrophagous birds as possible transmitters of BSE,
should theoretically be approached from a broader perspective of mammals and
birds which prey on, or are carrion eaters (scavengers) of mammalian species.
Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons,
eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could
be considered possible vectors of transmission and/or spread of TSE infectivity
in the environment. In view also of the occurrence of Chronic Wasting Disease
(CWD) in various deer species it should not be accepted that domestic cattle and
sheep are necessarily the only source of TSE agent exposure for carnivorous
species. While some information is available on the susceptibility of
wild/exotic/zoo animals to natural or experimental infection with certain TSE
agents, nothing is known of the possibility of occurrence of TSE in wild animal
populations, other than among the species of deer affected by CWD in the
USA.
1 The carrion birds are animals whose diet regularly or occasionally
includes the consumption of carcasses, including possibly TSE infected ruminant
carcasses.
C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc
snip... see full text ;
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE; 1: J Comp Pathol. 2000
Feb-Apr; 122(2-3): 131-43. Related Articles,
Links
Click here to read
The neuropathology of experimental bovine spongiform encephalopathy in the
pig.
Ryder SJ, Hawkins SA, Dawson M, Wells GA.
Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw,
Addlestone, Surrey, KT15 3NB, UK.
In an experimental study of the transmissibility of BSE to the pig, seven
of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral
inoculation with a homogenate of bovine brain from natural BSE cases developed
lesions typical of spongiform encephalopathy. The lesions consisted principally
of severe neuropil vacuolation affecting most areas of the brain, but mainly the
forebrain. In addition, some vacuolar change was identified in the rostral
colliculi and hypothalamic areas of normal control pigs. PrP accumulations were
detected immunocytochemically in the brains of BSE-infected animals. PrP
accumulation was sparse in many areas and its density was not obviously related
to the degree of vacuolation. The patterns of PrP immunolabelling in control
pigs differed strikingly from those in the infected animals.
PMID: 10684682 [PubMed - indexed for MEDLINE]
Title: Experimental Intracerebral and Oral Inoculation of Scrapie to
Swine: Preliminary Report
Authors
Greenlee, Justin Kunkle, Robert Hamir, Amirali
Submitted to: American Association of Veterinary Laboratory Diagnosticians
Publication Type: Abstract Publication Acceptance Date: November 5, 2005
Publication Date: November 5, 2005 Citation: Greenlee, J.J., Kunkle, R.A.,
Hamir, A.N. 2005. Experimental Intracerebral and Oral Inoculation of Scrapie to
Swine: Preliminary Report [abstract]. Proceedings of the American Association of
Veterinary Laboratory Diagnosticians 48th Annual Conference. P. 38.
Technical Abstract: Transmissible spongiform encephalopathies (TSEs, prion
diseases) are chronic neurodegenerative diseases that occur in humans, cattle,
sheep, goats, cervids, and a number of laboratory animal models. In a laboratory
setting, the host range of a given TSE can be tested by inoculating animals with
brain tissue from affected animals through various routes including oral and
intracranial. There is no evidence of the natural occurrence of any form of TSE
in the pig, but pigs have been shown to be susceptible to bovine spongiform
encephalopathy (BSE) infection by multiple-route parenteral challenge. However,
pigs orally exposed at eight weeks of age to large amounts of brain from cattle
clinically affected with BSE did not support infection after seven years of
observation. In the United States, feeding of ruminant by-products to ruminants
is prohibited, but feeding of ruminant materials to swine and poultry still
occurs. The potential for swine to have access to scrapie-contaminated
feedstuffs exists, but the potential for swine to serve as a host for
replication/accumulation of the agent of scrapie is unknown. The purpose of this
study was to perform oral and intracerebral inoculation of the U.S. scrapie
agent to determine the potential of swine as a host for the scrapie agent and
their clinical susceptibility. This study utilized 26 swine randomly divided
into three groups: controls (n=6), oral inoculates (n=8), and intracranial
inoculates (n=12). Brain homogenate (10%) derived from scrapie-affected sheep
was given by a single intracranial injection of 0.75 ml or by oral inoculation
of 15 ml on four consecutive days. Scrapie inoculum was derived from clinically
ill sheep inoculated with material derived from 13 sheep in seven source flocks.
A sample of this material was also inoculated back into sheep to assure
infectivity. Necropsies were planned for six months post inoculation, at
approximately the time the pigs were expected to reach market weight. Samples
collected were examined microscopically after routine staining (hematoxylin and
eosin) and staining by standard immunohistochemical methods for prion protein
(PrP**Sc). After approximately six months incubation time, no histologic lesions
suggestive of spongiform encephalopathy or immunohistochemical evidence of prion
infection were obtained. No evidence of scrapie infection was demonstrated in
this short-term study, but positive results after an incubation period of only
six months would be uncharacteristic. The only TSE with an incubation of six
months or less known at this time is transmissible mink encephalopathy in mink,
skunk, or raccoon hosts. However, scrapie in the raccoon model has a two-year
incubation period. A replicate of littermate pigs has been inoculated and will
be studied after long-term (3-7 years) incubation, and a similar study is
underway with pigs inoculated with material derived from elk, mule deer, and
whitetail deer affected by chronic wasting disease (CWD).
Last Modified: 03/19/2006
EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE
2. It was agreed that there was evidence of scrapie in sheep as a result of
food borne exposure. This is provided by the statistically significant increase
in the incidence of sheep scrape from 1985, as determined from analyses of the
submissions made to VI Centres, and from individual case and flock incident
studies. As the working hypothesis is that there has been recycling of infected
cattle tissues which has augmented the epidemic in cattle the continued
infection of sheep with the BSE agent, via the food born source, cannot be
excluded. There is therfore also a possibility that the BSE agent may have
become endemic in the sheep population, but is is impossible to design any
short-term research programme to elucidate this. ...
http://web.archive.org/web/20030517224223/http://www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE
to other species will invariably present pathology typical of a scrapie-like
disease.
snip...
FELINE SPONGIFORM ENCEPHALOPATHY FSE
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
snip...
To minimise the risk of farmers' claims for compensation from feed
compounders.
To minimise the potential damage to compound feed markets through adverse
publicity.
To maximise freedom of action for feed compounders, notably by maintaining
the availability of meat and bone meal as a raw material in animal feeds, and
ensuring time is available to make any changes which may be required.
snip...
THE FUTURE
4..........
MAFF remains under pressure in Brussels and is not skilled at handling
potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain
illegal traces of ruminant protein. More likely, a few positive test results
will turn up but proof that a particular feed mill knowingly supplied it to a
particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed
compounders are free of it. The longer we can avoid any direct linkage between
feed milling _practices_ and actual BSE cases, the more likely it is that
serious damage can be avoided. ...
SEE full text ;
THIS is what happens when you have the industry run the government, and if
you think anything has changed in the last 2 decades, well you better think
again, junk science and trade policy still rule the day $$$ TSS
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92
BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
Dustin Douglass was indicted and charged with making a fraudulent
application to the VA, in an effort to obtain benefits from injuries Douglas
represented he suffered while deployed in Iraq. Based on his application, the VA
provided benefits totaling $22,148.53. Douglass claimed he suffered various
injuries and illnesses as a result of his service in combat. The investigation
revealed Douglass had, in fact, been deployed to Iraq, but had served as a
computer specialist, had never been in combat, and did not suffer the
service-related injuries and illnesses he claimed to have suffered. Douglass was
placed on supervised release for 3 years, and required to pay $22,148.53 in
restitution. Galen Niehues, an inspector for the Nebraska Department of
Agriculture, (NDA), was convicted of mail fraud for submitting falsified reports
to his employer concerning inspections he was supposed to perform at Nebraska
cattle operations. Niehues was tasked with performing inspections of Nebraska
ranches, cattle and feed for the presence of neurological diseases in cattle
including Bovine Spongiform Encephalopathy (BSE), also known as “Mad Cow
Disease”. Niehues was to identify cattle producers, perform on-site inspections
of the farm sites and cattle operations, ask producers specific questions about
feed, and take samples of the feed. Niehues was to then submit feed samples for
laboratory analysis, and complete reports of his inspections and submit them to
the NDA and to the Federal Food and Drug Administration (FDA). An investigation
by the FDA and NDA revealed Niehues had fabricated approximately 100 BSE
inspections and inspection reports. When confronted, Niehues admitted his
reports were fraudulent, and that had fabricated the reports and feed samples he
submitted to the NDA. Niehues received a sentence of 5 years probation, a 3-year
term of supervised release, and was required to pay $42,812.10 in
restitution.
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February
2007 to charges of theft of Government funds, mail fraud, and wire fraud. The
owner and his company defrauded the BSE Surveillance Program when they falsified
BSE Surveillance Data Collection Forms and then submitted payment requests to
USDA for the services. In addition to the targeted sample population (those
cattle that were more than 30 months old or had other risk factors for BSE), the
owner submitted to USDA, or caused to be submitted, BSE obex (brain stem)
samples from healthy USDA-inspected cattle. As a result, the owner fraudulently
received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1
include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for
specified risk material (SRM) violations and improved inspection controls over
SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in
future semiannual reports as the relevant audits and investigations are
completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
-MORE Office of the United States Attorney District of Arizona
FOR IMMEDIATE RELEASE For Information Contact Public Affairs
February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602)
525-2681
CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD
COW DISEASE SURVEILLANCE PROGRAM
PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of
Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail
fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel
Knauss stated, “The integrity of the system that tests for mad cow disease
relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without
that honest cooperation, consumers both in the U.S. and internationally are at
risk. We want to thank the USDA’s Office of Inspector General for their
continuing efforts to safeguard the public health and enforce the law.” Farm
Fresh Meats and Farabee were charged by Information with theft of government
funds, mail fraud and wire fraud. According to the Information, on June 7, 2004,
Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S.
Department of Agriculture (the “USDA Agreement”) to collect obex samples from
cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The
Targeted Cattle Population consisted of the following cattle: cattle over thirty
months of age; nonambulatory cattle; cattle exhibiting signs of central nervous
system disorders; cattle exhibiting signs of mad cow disease; and dead cattle.
Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per
obex sample for collecting obex samples from cattle within the Targeted Cattle
Population, and submitting the obex samples to a USDA laboratory for mad cow
disease testing. Farm Fresh Meats further agreed to maintain in cold storage the
sampled cattle carcasses and heads until the test results were received by Farm
Fresh Meats.
Evidence uncovered during the government’s investigation established that
Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted
Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or
caused to be submitted, obex samples from healthy, USDA inspected cattle, in
order to steal government moneys.
Evidence collected also demonstrated that Farm Fresh Meats and Farabee
failed to maintain cattle carcasses and heads pending test results and falsified
corporate books and records to conceal their malfeasance. Such actions, to the
extent an obex sample tested positive (fortunately, none did), could have
jeopardized the USDA’s ability to identify the diseased animal and pinpoint its
place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee
pleaded guilty to stealing government funds and using the mails and wires to
effect the scheme. According to their guilty pleas:
(a) Farm Fresh Meats collected, and Farabee directed others to collect,
obex samples from cattle outside the Targeted Cattle Population, which were not
subject to payment by the USDA;
(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests
to the USDA knowing that the requests were based on obex samples that were not
subject to payment under the USDA Agreement;
(c) Farm Fresh Meats completed and submitted, and Farabee directed others
to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s
testing laboratory that were false and misleading;
(d) Farm Fresh Meats completed and submitted, and Farabee directed others
to complete and submit, BSE Surveillance Submission Forms filed with the USDA
that were false and misleading;
(e) Farm Fresh Meats falsified, and Farabee directed others to falsify,
internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats
was seeking and obtaining payment from the USDA for obex samples obtained from
cattle outside the Targeted Cattle Population; and
(f) Farm Fresh Meats failed to comply with, and Farabee directed others to
fail to comply with, the USDA Agreement by discarding cattle carcasses and heads
prior to receiving BSE test results. A conviction for theft of government funds
carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud
convictions carry a maximum penalty of 20 years imprisonment. Convictions for
the above referenced violations also carry a maximum fine of $250,000 for
individuals and $500,000 for organizations. In determining an actual sentence,
Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide
appropriate sentencing ranges. The judge, however, is not bound by those
guidelines in determining a sentence.
Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The
investigation in this case was conducted by Assistant Special Agent in Charge
Alejandro Quintero, United States Department of Agriculture, Office of Inspector
General. The prosecution is being handled by Robert Long, Assistant U.S.
Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE
NUMBER: 2007-051(Farabee) # # #
WE can only hope that this is a single incident. BUT i have my doubts. I
remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5
grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and
the FDA was bragging at the time that the amount of potentially BANNED product
was so little and the cattle were so big ;
"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."
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'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.
WE now know all that was a lie. WE know that literally Thousands of TONS of
BANNED and most likely tainted product is still going out to commerce. WE know
now and we knew then that .005 to a gram was lethal. WE know that CWD infected
deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been
rendered and fed back to livestock (including cattle) for human and animal
consumption.
Paul Brown, known and respected TSE scientist, former TSE expert for the
CDC said he had ''absolutely no confidence in USDA tests before one year ago'',
and this was on March 15, 2006 ;
"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the National
Institutes of Health's Laboratory for Central Nervous System Studies and an
expert on mad cow-like diseases, told United Press International. "The question
was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before one
year ago" because of the agency's reluctance to retest the Texas cow that
initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul
Brown is Senior Research Scientist in the Laboratory of Central Nervous System
... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy detailed
critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ;
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
Table 1. Animal feed ingredients that are legally used in U.S. animal feeds
Animal
Rendered animal protein from Meat meal, meat meal tankage, meat and bone
meal, poultry meal, animal the slaughter of food by-product meal, dried animal
blood, blood meal, feather meal, egg-shell production animals and other meal,
hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals
digest from dead, dying, diseased, or disabled animals including deer and elk
Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and
undried processed animal waste products
snip...
Conclusions
Food-animal production in the United States has changed markedly in the
past century, and these changes have paralleled major changes in animal feed
formulations. While this industrialized system of food-animal production may
result in increased production efficiencies, some of the changes in animal
feeding practices may result in unintended adverse health consequences for
consumers of animal-based food products. Currently, the use of animal feed
ingredients, including rendered animal products, animal waste, antibiotics,
metals, and fats, could result in higher levels of bacteria, antibioticresistant
bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting
animal-based food products intended for human consumption. Subsequent human
health effects among consumers could include increases in bacterial infections
(antibioticresistant and nonresistant) and increases in the risk of developing
chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide
range of potential human health impacts that could result from animal feeding
practices, there are little data collected at the federal or state level
concerning the amounts of specific ingredients that are intentionally included
in U.S. animal feed. In addition, almost no biological or chemical testing is
conducted on complete U.S. animal feeds; insufficient testing is performed on
retail meat products; and human health effects data are not appropriately linked
to this information. These surveillance inadequacies make it difficult to
conduct rigorous epidemiologic studies and risk assessments that could identify
the extent to which specific human health risks are ultimately associated with
animal feeding practices. For example, as noted above, there are insufficient
data to determine whether other human foodborne bacterial illnesses besides
those caused by S. enterica serotype Agona are associated with animal feeding
practices. Likewise, there are insufficient data to determine the percentage of
antibiotic-resistant human bacterial infections that are attributed to the
nontherapeutic use of antibiotics in animal feed. Moreover, little research has
been conducted to determine whether the use of organoarsenicals in animal feed,
which can lead to elevated levels of arsenic in meat products (Lasky et al.
2004), contributes to increases in cancer risk. In order to address these
research gaps, the following principal actions are necessary within the United
States: a) implementation of a nationwide reporting system of the specific
amounts and types of feed ingredients of concern to public health that are
incorporated into animal feed, including antibiotics, arsenicals, rendered
animal products, fats, and animal waste; b) funding and development of robust
surveillance systems that monitor biological, chemical, and other etiologic
agents throughout the animal-based food-production chain “from farm to fork” to
human health outcomes; and c) increased communication and collaboration among
feed professionals, food-animal producers, and veterinary and public health
officials.
REFERENCES...snip...end
Sapkota et al. 668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health
Perspectives
SUMMARY REPORT CALIFORNIA ATYPICAL L-TYPE BOVINE SPONGIFORM ENCEPHALOPATHY
CASE INVESTIGATION JULY 2012 CALIFORNIA
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Final Feed Investigation Summary - California atypical L-type BSE Case -
July 2012
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
Monday, March 19, 2012
*** Infectivity in Skeletal Muscle of Cattle with Atypical Bovine
Spongiform Encephalopathy PLoS One. 2012; 7(2): e31449.
Sunday, January 11, 2015
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
Sunday, December 28, 2014
*** Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE
PRION aka BSE MAD COW TYPE DISEASE December 2014
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been
discovered in a wide verity of species across North America. typical C-BSE,
atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine,
typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98
Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD
in cervid is slowly spreading without any stopping it in Canada and the USA and
now has mutated into many different strains. Transmissible Mink Encephalopathy
TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease
have been silently mutating and spreading in different species in North America
for decades. The USDA, FDA, et al have assured us of a robust Triple BSE TSE
prion Firewall, of which we now know without a doubt, that it was nothing but
ink on paper. Since the 1997 mad cow feed ban in the USA, literally tons and
tons of banned mad cow feed has been put out into commerce, never to return, as
late as December of 2013, serious, serious breaches in the FDA mad cow feed ban
have been documented. The 2004 enhanced BSE surveillance program was so flawed,
that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ;
Brown, who is preparing a scientific paper based on the latest two mad cow cases
to estimate the maximum number of infected cows that occurred in the United
States, said he has "absolutely no confidence in USDA tests before one year ago"
because of the agency's reluctance to retest the Texas cow that initially tested
positive.
see ; http://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/UPI-12841142465253/
The BSE surveillance and testing have also been proven to be flawed, and
the GAO and OIG have both raised serious question as to just how flawed it has
been (see GAO and OIG reports). North America has more documented TSE prion
disease, in different documented species (excluding the Zoo BSE animals in the
EU), then any other place on the Globe. This does not include the very
likelihood that TSE prion disease in the domestic feline and canine have been
exposed to high doses of the TSE prion disease vid pet food. To date, it’s still
legal to include deer from cwd zone into pet food or deer food. Specified Risk
Material i.e. SRM bans still being breach, as recently as just last month. nvCJD
or what they now call vCJD, another case documented in Texas last month, with
very little information being released to the public on about this case? with
still the same line of thought from federal officials, ‘it can’t happen here’,
so another vCJD blamed on travel of a foreign animal disease from another
country, while ignoring all the BSE TSE Prion risk factors we have here in the
USA and Canada, and the time that this victim and others, do spend in the USA,
and exposed to these risk factors, apparently do not count in any way with
regard to risk factor. a flawed process of risk assessment. sporadic CJD, along
with new TSE prion disease in humans, of which the young are dying, of which
long duration of illness from onset of symptoms to death have been documented,
only to have a new name added to the pot of prion disease i.e. sporadic GSS,
sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be
sporadic with no genetic link to any family member? when the USA is the only
documented Country in the world to have documented two different cases of
atypical H-type BSE, with one case being called atypical H-G BSE with the G
meaning Genetic, with new science now showing that indeed atypical H-type BSE is
very possible transmitted to cattle via oral transmission (Prion2014). sporadic
CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old
excuse, better surveillance. You can only use that excuse for so many years, for
so many decades, until one must conclude that CJD TSE prion cases are rising. a
48% incease in CJD in Canada is not just a blip or a reason of better
surveillance, it is a mathematical rise in numbers. More and more we are seeing
more humans exposed in various circumstance in the Hospital, Medical, Surgical
arenas to the TSE Prion disease, and at the same time in North America, more and
more humans are becoming exposed to the TSE prion disease via consumption of the
TSE prion via deer and elk, cattle, sheep and goats, and for those that are
exposed via or consumption, go on to further expose many others via the
iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I
pondered this mode of transmission via the victims of sporadic FFI, sporadic
GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or
sGSS ? what if?
Two decades have passed since Dr. Ironside first confirmed his first ten
nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first
ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is
transmissible. yet all these TSE prion disease and victims in the USA and Canada
are being pawned off as a spontaneous event, yet science has shown, the
spontaneous theory has never been proven in any natural case of TSE prion
disease, and scientist have warned, that they have now linked some sporadic CJD
cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about
this in the public domain. We must make all human and animal TSE prion disease
reportable in every age group, in ever state and internationally, we must have a
serious re-evaluation and testing of the USA cattle herds, and we must ban
interstate movement of all cervids. Any voluntary effort to do any of this will
fail. Folks, we have let the industry run science far too long with regards to
the TSE prion disease. While the industry and their lobbyist continues to funnel
junk science to our decision policy makers, Rome burns. ...end
REFERENCES
Sunday, June 29, 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Tuesday, December 2, 2014
UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion
aka Mad Cow Disease
USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE
WORLD (?) [protected by the BSE MRR policy] $$$
Friday, December 5, 2014
SPECIAL ALERT The OIE recommends strengthening animal disease surveillance
worldwide
OIE BSE TSE PRION AKA MAD COW DISEASE ?
‘’the silence was deafening’’ ...tss
who’s kidding whom $$$ i.e. USDA INC AND THE OIE
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent. Lending support to this hypothesis,
pathological and biochemical similarities have been observed between L-BSE and
an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE
infected non-human primate and another sCJD subtype (MM genotype) [15].
snip...
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion
strains in transgenic mice expressing human prion protein
*** Surprisingly, however, BSE transmission to these transgenic mice, in
addition to producing a vCJD-like phenotype, can also result in a distinct
molecular phenotype that is indistinguishable from that of sporadic CJD with
PrPSc type 2.
These data suggest that more than one BSEderived prion strain might infect
humans;
***it is therefore possible that some patients with a phenotype consistent
with sporadic CJD may have a disease arising from BSE exposure.
snip...
These studies further strengthen the evidence that vCJD is caused by a
BSE-like prion strain.
Also, remarkably, the key neuropathological hallmark of vCJD, the presence
of abundant florid PrP plaques, can be recapitulated on BSE or vCJD transmission
to these mice.
***However, the most surprising aspect of the studies was the finding that
an alternate pattern of disease can be induced in 129MM Tg35 mice from primary
transmission of BSE, with a molecular phenotype indistinguishable from that of a
subtype of sporadic CJD. This finding has important potential implications as it
raises the possibility that some humans infected with BSE prions may develop a
clinical disease indistinguishable from classical CJD associated with type 2
PrPSc. This is, in our experience, the commonest molecular sub-type of sporadic
CJD. In this regard, it is of interest that the reported incidence of sporadic
CJD has risen in the UK since the 1970s (Cousens et al., 1997)...
To date the OIE/WAHO assumes that the human and animal health standards set
out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE
which include the H-type and L-type atypical forms. This assumption is
scientifically not completely justified and accumulating evidence suggests that
this may in fact not be the case. Molecular characterization and the spatial
distribution pattern of histopathologic lesions and immunohistochemistry (IHC)
signals are used to identify and characterize atypical BSE. Both the L-type and
H-type atypical cases display significant differences in the conformation and
spatial accumulation of the disease associated prion protein (PrPSc) in brains
of afflicted cattle. Transmission studies in bovine transgenic and wild type
mouse models support that the atypical BSE types might be unique strains because
they have different incubation times and lesion profiles when compared to C-type
BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE.
***In addition, non-human primates are specifically susceptible for
atypical BSE as demonstrated by an approximately 50% shortened incubation time
for L-type BSE as compared to C-type. Considering the current scientific
information available, it cannot be assumed that these different BSE types pose
the same human health risks as C-type BSE or that these risks are mitigated by
the same protective measures.
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a
Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have
attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you
will find in the paper, we have managed to associate the alternate phenotype to
type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim
any further sub-classification in respect of Heidenhain variant CJD or Vicky
Rimmer's version. It will take further studies, which are on-going, to establish
if there are sub-types to our initial finding which we are now reporting. The
main point of the paper is that, as well as leading to the expected new variant
CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an
alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can
be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
<>
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial
College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44
(0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until
9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
____________________________________
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
Moreover, transmission experiments to non-human primates suggest that some TSE
agents in addition to Classical BSE prions in cattle (namely L-type Atypical
BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
*** HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL
CDC ***
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
in June 2014 confirmed as USA case NOT European
the patient had resided in Kuwait, Russia and Lebanon. The completed
investigation did not support the patient's having had extended travel to
European countries, including the United Kingdom, or travel to Saudi Arabia. The
specific overseas country where this patient’s infection occurred is less clear
largely because the investigation did not definitely link him to a country where
other known vCJD cases likely had been infected.
Sunday, December 14, 2014
ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report
Thursday, January 15, 2015
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE
Prion: Case Report
Saturday, January 17, 2015
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed
with the extremely rare Creutzfeldt-Jakob disease
Wednesday, January 21, 2015
Norway detects "probable" case of mad cow disease
Friday, November 28, 2014
BOVINE SPONGIFORM ENCEPHALOPATHY BSE AKA MAD COW DISEASE PORTUGAL CONFIRMED
Monday, December 1, 2014
***Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A
Review December 1, 2014
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Monday, May 5, 2014
Brazil BSE Mad Cow disease confirmed OIE 02/05/2014
Brazil covered up it’s first mad cow case for two years before it was
finally confirmed
Friday, December 07, 2012
ATYPICAL BSE BRAZIL 2010 FINALLY CONFIRMED OIE 2012
“The two year delay in Brazil’s disease notification is a symptom of the
failure of the OIE’s global system that erroneously assumes foreign countries,
particularly developing countries, have the same means, commitment and
capabilities as the United States to control and eradicate diseases, says Max
Thornsberry, who chairs R-CALF USA’s Animal Health Committee.
Thornsberry said USDA’s reliance on foreign countries and OIE to protect
U.S. citizens from unsafe imports is “absolutely foolish” and again points up
the need for country-of-origin labeling.
Friday, December 5, 2014
SPECIAL ALERT The OIE recommends strengthening animal disease surveillance
worldwide
BSE TSE PRION AKA MAD COW TYPE DISEASE, THE SILENCE WAS DEAFENING $$$
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
‘’LOL LAUGH OUT LOUD’’...TSS
IT is of my opinion, that the OIE and the USDA et al, are the soul reason,
and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion
diseases, including typical and atypical BSE, typical and atypical Scrapie, and
all strains of CWD, and human TSE there from, spreading around the globe.
I have lost all confidence of this organization as a regulatory authority
on animal disease, and consider it nothing more than a National Trading
Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i
said before, OIE should hang up there jock strap now, since it appears they will
buckle every time a country makes some political hay about trade protocol,
commodities and futures. IF they are not going to be science based, they should
do everyone a favor and dissolve there organization.
JUST because of low documented human body count with nvCJD and the long
incubation periods, the lack of sound science being replaced by political and
corporate science in relations with the fact that science has now linked some
sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of
CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call
for this organization to be dissolved. ...
Monday, May 05, 2014
Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing
Monday, May 05, 2014
Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing
UPDATE May 13, 2014
Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing
Greetings everyone,
Finally, got a confirmation from top official inside OIE.
YES!
Indeed, CHRONIC WASTING DISEASE CWD has been brought to the OIE table, by
more than one country, and WILL BE BROUGHT TO THE TABLE AGAIN, WHEN THE NEXT AD
HOC EXPERT GROUP IS CONVENED...tss
‘’On more than one occasion our Commission has received a request from a
Member Country to list CWD as a disease notifiable to the OIE. However, it is
not our practice to specify which Member Countries make specific requests to us.
All countries which submit national comments to us at our February and September
meetings are listed in the reports of our meetings. However, the country names
are not linked to specific comments or requests.’’
’’they may also evaluate CWD against the OIE’s CRITERIA.’’
‘’That is where the situation stands at present. Next time an ad hoc group
is convened to consider issues of listing and delisting, CWD will be evaluated.
I have no idea of time frames.’’
personal communication with OIE top official...tss
Rome was not built overnight I suppose...tss
> In response to a _Member Country’s_ detailed justification for listing
of chronic wasting disease of cervids (CWD) against the criteria of Article
1.2.2., the Code Commission _recommended_ this disease be reconsidered for
listing.
Annual report of the Scientific Network on BSE-TSE EFSA, Question No
EFSA-Q-2013-01004, approved on 11 December 2013
*** Further, it was addressed that recently discussions have being held at
OIE level on Chronic Wasting Disease of cervids.
page 6;
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS
COMMISSION Paris, 19–28 February 2013
In response to a Member Country’s detailed justification for listing of
chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2.,
the Code Commission recommended this disease be reconsidered for listing.
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS
COMMISSION Paris, 17–26 September 2013
Item 5 Criteria for listing diseases (Chapter 1.2.)
Comments were received from Australia, EU, Japan, New Zealand, Switzerland,
Thailand and AU-IBAR The Code Commission noted a Member Country’s comment
suggesting that greater clarity was needed for the term ‘significant morbidity
and mortality’. As noted in the February 2013 report, the Code Commission
considered that the structured process of listing diseases, first by an expert
group whose conclusions are documented and circulated for Member Countries’
review and comment, then consideration by the World Assembly of Delegates before
final adoption, is sufficiently rigorous and transparent.
greetings,
what is criteria of Article 1.2.2. ???
curious as to what country detailed justification for listing ???
kind regards, terry
*******UPDATE ON OIE ARTICLE 1.2.2********
OIE Article 1.2.2.
The criteria for the inclusion of a disease, infection or infestation in
the OIE list are as follows:
1) International spread of the agent (via live animals or their products,
vectors or fomites) has been proven.
AND
2) At least one country has demonstrated freedom or impending freedom from
the disease, infection or infestation in populations of susceptible animals,
based on the animal health surveillance provisions of the Terrestrial Code, in
particular those contained in Chapter 1.4.
AND
3)
a) Natural transmission to humans has been proven, and human infection is
associated with severe consequences.
OR
b) The disease has been shown to cause significant morbidity or mortality
in domestic animals at the level of a
country or a zone.
OR
c) The disease has been shown to, or scientific evidence indicates that it
would, cause significant morbidity or
mortality in wild animal populations.
AND
4) A reliable means of detection and diagnosis exists and a precise case
definition is available to clearly identify cases
and allow them to be distinguished from other diseases, infections and
infestations.
OR
5) The disease or infection is an emerging disease with evidence of
zoonotic properties, rapid spread, or significant morbidity or mortality and a
case definition is available to clearly identify cases and allow them to be
distinguished from other diseases or infections.
2 2013 © OIE - Terrestrial Animal Health Code Chapter 1.2.- Criteria for
the inclusion of diseases, infections and infestations on the OIE list
*** URGENT CWD UPDATE Friday, January 17, 2014
FINALLY, 12 years later, the OIE becomes concerned with CWD to humans, not
that I did not try and warn them 12 years ago. ...kind regards, terry
Friday, January 17, 2014
Annual report of the Scientific Network on BSE-TSE EFSA, Question No
EFSA-Q-2013-01004, approved on 11 December 2013
*** Further, it was addressed that recently discussions have being held at
OIE level on Chronic Wasting Disease of cervids.
*** 2002 Singeltary vs O.I.E. on CWD to human risk factor ;
Subject: Re: CWD AMERICA ???
Date: Fri, 12 Jul 2002 19:10:18 +0200
From: "INFORMATION DEPT"
Organization: O.I.E
To: "Terry S. Singeltary Sr."
References: <3d2f0169 .3="" wt.net=""> < 012901c229b2 ad43bb90=""
f00000a=""> 3D2F2358.5010700@wt.net
I agree with you Dr Terry. The OIE, namely the International Animal Health
Code Commission is working on making proposals to Member Countries to change the
OIE lists so to avoid some the problems mentioned in you e-mail. This will take
at least two years before adoption by the International Committee. For BSE,
countries asked the OIE to post information on BSE on the OIE web site.
Personally, I am interested in Chronic Wasting Disease and I follow what is
distributed through ProMed. Delegates of OIE Member Countries can propose
diseases to be added to the list.
Kind regards.
Karim Ben Jebara
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: "INFORMATION DEPT"
Sent: Friday, July 12, 2002 8:43 PM
Subject: Re: CWD AMERICA ???
>>> *** Further, it was addressed that recently discussions have
being held at OIE level on Chronic Wasting Disease of cervids. <<<
> hello Dr. Jebara,
>
> many thanks for your swift and kind reply.
>
> if i am not mistaken, it was the same email address.
> it was 3 or 4 weeks ago i wrote, as it is, i don't
> save 'sent' emails anymore, unless very important.
>
> my main concern (besides the fact that a potential TSE
> has been in the USA cattle for some time, but the APHIS
> do not test to find), is that the CWD could very well be
> transmitting to humans, and i just did not see to much
> posted about it on OIE site.
>
> > Coming back to your question, Chronic Wasting Disease is not an
OIE
>
> > listed disease. Please see OIE disease lists at
>
>
> why is this TSE (CWD) not listed and followed as with BSE ?
>
> Article 1.1.3.2.
> 1. Countries shall make available to other countries, through
the
> OIE, whatever information is necessary to minimise the spread of
> important animal diseases and to assist in achieving better
worldwide
> control of these diseases.
>
>
> The USA CWD is an important animal disease.
>
> why is it not followed?
>
> > The decision to add or delete a disease from the OIE lists,
come
>
> > through proposals made by Member Countries and it has to be
adopted by
>
> > the International Committee.
>
> i _urgently_ suggest a proposal to the OIE to follow this disease
very
> closely, and to propose _more_ testing in the USA for TSEs in the
USA
> cattle...
>
> kindest regards,
> terry
>
> INFORMATION DEPT wrote:
>
> > Dear Sir,
> >
> > This is the first time that I receive your e-mail. To whom have
you written
> > in the OIE or to which address?
> >
> > Coming back to your question, Chronic Wasting Disease is not an
OIE listed
> > disease. Please see OIE disease lists at
> >
> > Countries should report to the OIE any disease even is not listed
in the
> > OIE's lists in some conditions (example: an exceptional
epidemiological
> > event). Please read Chapter 1.1.3 of the International animal
health code to
> > have more information on disease notification and
epidemiological
> > information agreed by OIE Member Countries at :
> >
> > The decision to add or delete a disease from the OIE lists, come
through
> > proposals made by Member Countries and it has to be adopted by
the
> > International Committee.
> >
> > Hope that I answered to your question.
> >
> > Best regards.
> >
> > Dr Karim Ben Jebara
> > Head
> > Animal Health Information Department
> > OIE
> >
> >
> >
> > ----- Original Message -----
> > From: "Terry S. Singeltary Sr."
> > To:
> > Sent: Friday, July 12, 2002 6:18 PM
> > Subject: CWD AMERICA ???
> >
> >
> >
> >>I WROTE TO OIE RECENTLY ASKING 'WHY OIE DOES NOT FOLLOW CWD
IN
> >>AMERICA' ? with no reply ? i am still seeking an answer
?
> >>
> >>many thanks,
> >>and kind regards,
> >>terry
=====================
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing ***
STILL WAITING...TSS
Sunday, December 28, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE AKA MAD DEER DISIEASE
USDA USAHA INC DECEMBER 28, 2014
SEE FEED ;
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
Wednesday, December 4, 2013
Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine
Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December
4, 2013
TO ALL IMPORTING COUNTRIES THAT IMPORTS FROM THE USA, BE WARNED, NEW MAD
COW BSE REGULATIONS USDA, AND OIE, not worth the paper the regulations were
wrote on, kind of like the mad cow feed ban of August 1997, nothing but ink on
paper $$$
full text ;
Comment from Terry Singeltary Sr.
This is a Comment on the
Animal and Plant Health Inspection Service (APHIS) Notice: Agency Information Collection Activities; Proposals,
Submissions, and Approvals: Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products
For related information,
Open Docket Folder
 Comment
Docket No. APHIS-2014-0107 Bovine Spongiform
Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
;
I believe that there is more risk to the world from Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from the United States and all of North America, than there is risk coming to the USA and North America, from other Countries. I am NOT saying I dont think there is any risk for the BSE type TSE prion coming from other Countries, I am just saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present mad cow risk factors in North America like they are not here? North America has more strains of TSE prion disease, in more species (excluding zoo animals in the early BSE days, and excluding the Feline TSE and or Canine TSE, because they dont look, and yes, there has been documented evidence and scientific studies, and DEFRA Hound study, that shows the canine spongiform encephalopathy is very possible, if it has not already happened, just not documented), then any other Country in the world. Mink TME, Deer Elk cervid CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type BSE cattle, atyical HG type BSE cow (the only cow documented in the world to date with this strain), typical sheep goat Scrapie (multiple strains), and the atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical Scrapie has spread from coast to coast. sporadic CJD on the rise, with different strains mounting, victims becoming younger, with the latest nvCJD human mad cow case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL CDC. typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al), and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. its all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$ the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing but ink on paper. for this very reason I believe the BSE MRR policy is a total failure, and that this policy should be immediately withdrawn, and set back in place the BSE GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all TSE PRION disease in all species of animals, and that the BSE GBR risk assessments be made stronger than before. lets start with the recent notice that beef from Ireland will be coming to America. Ireland confirmed around 1655 cases of mad cow disease. with the highest year confirming about 333 cases in 2002, with numbers of BSE confirmed cases dropping from that point on, to a documentation of 1 confirmed case in 2013, to date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad cow feed ban, and the enforcement of that ban, has drastically reduced the number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in 2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow disease in the USA, we still have no clue as to the true number of cases of BSE mad cow disease in the USA or North America as a whole. ...just saying. Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide* (excluding the United Kingdom) Country/Year snip...please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS Attachments(1)Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
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Sunday, January 11, 2015
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
Terry S. Singeltary Sr.
Bacliff, Texas 77518
