RAPID ADVICE 17-2014 : Evaluation of the risk for public health of casings in countries with a “negligible risk status for BSE” and on the risk of modification of the list of specified risk materials (SRM) with regard to BSE
Subject: RAPID ADVICE 17-2014 : Evaluation of the risk for public health of
casings in countries with a “negligible risk status for BSE” and on the risk of
modification of the list of specified risk materials (SRM) with regard to BSE
SCIENTIFIC COMMITTEE OF THE BELGIAN FEDERAL AGENCY FOR THE SAFETY OF THE
FOOD CHAIN
RAPID ADVICE 17-2014
Subject: Evaluation of the risk for public health of casings in countries
with a “negligible risk status for BSE” and on the risk of modification of the
list of specified risk materials (SRM) with regard to BSE (Dossier SciCom
2014/22) Rapid advice approved by the Scientific Committee on 22nd October
2014.
Summary
The Scientific Committee was asked to answer two questions in regard to a
proposal from the European Commission to no longer obligate Member States with a
negligible BSE risk status to remove and dispose the specified risk materials as
specified in Annex V to Regulation (EC) No 999/2001 of the European Parliament
and of the Council of 22 May 2001 laying down rules for the prevention, control
and eradication of certain transmissible spongiform encephalopathies. The aim of
this modification of the Regulation is to ensure that conditions for imports of
commodities from third countries are not more favorable than the conditions
applying to Member States with the same OIE BSE negligible risk status. More
specifically it was asked to the Scientific Committee:
- If there is a difference in public health risk between the casings
imported from third countries with a “negligible risk status for BSE” and
casings that come from the 18 EU Member States with a “negligible risk status
for BSE”?
- If there is a significantly increased public health risk if, in the EU
Member States with a “negligible risk status for BSE”, the intestines are no
longer removed as SRM and if the other risk materials for BSE (the skull
including the brains and eyes, the spinal cord, the tonsils and the spine) are
indeed considered as SRM?
Due to lack of availability of data on true prevalence and tissue
infectivity of BSE (classical as well as atypical BSE) the Scientific Committee
was not able to thoroughly investigate the questions.
Removal of specified risk materials from cattle at slaughter prevents BSE
infected materials from entering the human food chain.
The Scientific Committee is of the opinion that, taking into consideration
the uncertainties in regard to the true prevalence of BSE (classical as well as
atypical BSE) in countries with a “negligible risk status for BSE” and given the
problems related with the early detection of asymptomatic BSE and given the
zoonotic significance of atypical BSE, that stopping with the routine removal of
specified risk materials during bovine slaughter will increase the risk for
public health.
2/14
The Scientific Committee is not able to compare the public health risk of
casings from third countries and from the 18 EU Member States, both with a
negligible risk status for BSE, because of lack of data on true BSE prevalence
and BSE tissue infectivity (classical BSE and atypical BSE) in the considered
countries.
The Scientific Committee is also not able to properly answer the second
question if there is a significantly increased public health risk if, in the EU
Member States with a “negligible risk status for BSE”, the intestines are no
longer removed as SRM due to lack of quantitative data on tissue infectivity of
different specified risk materials in slaughtered bovines in these countries.
There is also no information on tissue infectivity of atypical BSE cases. It is
known however that intestines are the portal of entry of prions and that they
are already infective before the prions reach the central nervous system.
The final decision pertaining the need of removal of all or part of the
specified risk materials is a risk management decision and goes beyond the
competencies of the Scientific Committee.
Samenvatting Sneladvies over de risico’s voor de volksgezondheid van
worstenvellen in landen met een “verwaarloosbaar risicostatuut voor BSE” en over
de risico’s van wijziging van een lijst van gespecifieerde risicomaterialen
(GRM) voor BSE
snip...
In conclusion the Scientific Committee is not able to answer this question
with an acceptable degree of uncertainty because of lack of data on true
prevalence of BSE (classical as well as atypical forms of BSE) in the considered
countries. It reiterates its concern regarding the import of certain animal
products from third countries with a ‘negligible BSE risk status’ as stated in
rapid advice SciCom 16-2013.
snip...
2. Is there a significantly increased public health risk if, in the EU
Member States with a “negligible risk status for BSE”, the intestines are no
longer removed as SRM while the other risk materials for BSE (the skull
including the brains and eyes, the spinal cord, the tonsils and the spine) are
indeed considered as SRM?
Once again the Scientific Committee is not able to properly answer this
question because of lack of quantitative data on tissue infectivity of different
specified risk materials in slaughtered bovines in EU Member States with a
“negligible risk status for BSE”.
BSE infected animals may enter undetected the food chain due to the low
sensitivity of the diagnostic tests. Further on the classical BSE agent
accumulates from the first months post exposure in particular segments of the
bovine intestines and persists till clinical onset. In addition no information
is available about the infectivity of tissues by the atypical BSE agent,
especially in the intestines.
If intestines from cattle in EU Member States with a “negligible risk
status for BSE” are no longer removed as SRM and are allowed to enter the food
chain the public health risk will be increased. The degree of rise in risk level
cannot be determined. According to EFSA Journal 2014;12(2):3554, the TSEi model
indicated that the removal of the last four meters of the small intestine and of
the caecum from the food and feed chain would result in a major reduction of the
Classical BSE exposure risk associated with intestine and mesentery in
cattle.
Referring to its previous advice 16-2013 the Scientific Committee repeats
that stopping with the routine removal of all specified risk materials during
bovine slaughter will increase the risks of exposure of the population to BSE
because of the uncertainty related to the detection of BSE. This uncertainty is
the consequence of the long incubation period (especially in cases of atypical
BSE), the low sensitivity of the available diagnostic methods, the apparent
spontaneous nature of atypical BSE, the lack of a clear clinical picture of
atypical BSE cases and the reduction in number of tests in healthy slaughtered
animals.
The final decision pertaining the need of removal of all or part of the
specified risk materials is a decision to be taken by the risk manager and goes
beyond the competencies of the Scientific Committee.
5. Conclusion
Removal of specified risk materials from cattle at slaughter prevents BSE
infected materials from entering the human food chain.
The Scientific Committee is of the opinion that, taking into consideration
the uncertainties in regard to the true prevalence of BSE (including classical
as well asaAtypical BSE) in countries with a “negligible risk status for BSE”
and given the problems related with the early detection of asymptomatic BSE and
given the zoonotic character of atypical BSE, stopping with the routine removal
of all specified risk materials during bovine slaughter will increase the risk
for public health.
12/14
The Scientific Committee is not able to compare the public health risk of
casings from third countries and from the 18 EU Member States both with a
negligible risk status for BSE because of lack of data on true BSE prevalence
(classical BSE and atypical BSE) in the considered countries.
The Scientific Committee is not able to properly answer the question if
there is a significantly increased public health risk if, in the EU Member
States with a “negligible risk status for BSE”, the intestines are no longer
removed as SRM due to lack of quantitative data on tissue infectivity of
different specified risk materials in slaughtered bovines in these countries.
There is also no information on tissue infectivity by the agent of atypical
BSE.
On behalf of the Scientific Committee, The President Prof. Dr. E. Thiry
(Sgd.) Brussels, 06/11/2014
References
snip...end
Thursday, July 24, 2014
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA
P7.09
Biochemical screening for identification of atypical bse in belgium,
1999-present
Authors
Alexandre DobIy: Caroline Rodeghiero, Riet Geeroms; Stephanie Durand,
Jessica De Sloovere, Emanuel Yanopdenbosch, Stefan Roels,
Content
Background: Recently atypical forms of BSE have been described. Western
blot analyses showed that, in comparison to the classic BSE (C-type), they are
demonstrable by a higher or lower molecular weight of the unglycosylated PrPres.
They Viere thus named H-type and L-type BSE (L-type is also called BASE). In
addition they show a lower proportion of diglycosylated PrPres than C-type.
These emerging types represent different strains of BSE. They show unique
incubation periods and histological lesions. Such types have been described on
different continents. Indeed they might correspond to "sporadic" forms of BSE.
In 2004 we already described one L-type in Belgium.
Objective: We retrospectively analysed the bovines at least 7-year-old in
the Belgian archive of BSE diagnosed cattle in order to determine the
prevalence of the two types of atypical BSE in Belgium.
Methods: We analysed homogenates from 39 bovines of 93 months old in median
(min: 84, max: 181 months). The most recent one was diagnosed in 2006. We used
Western blot with a panel of anti-PrP antibodies (Ab). They detect different
regions of the PrP protein, from N-terminal to C-terminal: 12B2, 9A2, Sha31.
SAFB4, 94B4. Their combination is aimed at an efficient typing diagnostic. We
detected bound Ab with SuperSignal West Dura (Pierce) and analysed PrPres,
signals with an image-analysis software (Quantity One, Bio-Rad).
Results: The results are still under analysis. We will detail the most
crucial characteristics for typing PrPres. These include 1) the apparent
molecular mass of the an-, mono- and diglycosylated bands, 2) the binding
affinity to the five Ab (e.g.12B2 for H-type), 3) the presence of a fourth
(unglycosylated) band and 4) the glycoprofile based on the relative proportions
of the visible bands.
Discussion: The emergence of atypical types of BSE is partially due to a
better knowledge of prion strains and more efficient diagnostic techniques. As
the area in the brain where the PrPres is deposited can differ drastically
between the types, it is essential to ascertain that the sampling techniques and
analyses are adapted to these new types. As these new strains seem more virulent
than classic types, they represent one of the next challenges in the field of
prions.
Atypical Case of Bovine Spongiform Encephalopathy in an East-Flemish Cow in
Belgium
H. De Bosschere, DVM, PhD
S. Roels, DVM, PhD
E. Vanopdenbosch, DVM, Lic
Veterinary and Agrochemical Research Centre (CODA/CERVA)
National Reference Laboratorium for Veterinary TSEs
Groeselenberg 99, B-1180
Ukkel (Brussels), Belgium
KEY WORDS: Bovine spongiform encephalopathy, BSE, Western blot, atypical
BSE.
ABSTRACT
For many years, researchers believed that only one bovine spongiform
encephalopathy (BSE) strain existed, in contrast to the many different scrapie
strains found. However, only very recently reports emerged about unconventional
BSE strains seen in Italy, France, and Japan. The present case describes an
atypical strain of BSE in Belgium in a 64-month-old East-Flemish cow with an
electrophoretic profile and other features similar to those described in Japan.
INTRODUCTION
Transmissible spongiform encephalopathies (TSEs), or prion diseases, are a
group of fatal neurodegenerative diseases including sheep and goat scrapie,
bovine spongiform encephalopathy (BSE), and Creutzfeldt-Jakob disease (CJD) in
humans. They are characterized by the accumulation of an abnormal protein,
called PrPsc, which is formed post-translationally from the normal isoform
(PrPc).1,2 At present, the agent causing TSEs is still incompletely
characterized, although PrPsc is believed to be its major if not unique
constituent.3
Research in mice showed the existence of different scrapie strains.4,5
Scrapie strain discrimination is currently based on biologic typing in a panel
of inbred mice, using incubation time and brain pathology scoring as criteria.6
However, no large-scale studies of the molecular features of PrPsc have been
reported for bovine BSE to date. Till now, the BSE strain seemed to maintain
constant biologic and molecular properties even after experimental or accidental
passages into different species, such as mice, humans, primates, and sheep.7-10
However, very recently, variant forms of BSE have been reported in Japan, Italy,
and France.11-13 These forms were characterized by atypical histopathologic,
immunohistochemical, or biochemical phenotypes. The present case is the
description of the first atypical BSE case in Belgium.
snip...
In conclusion, this Belgian case should be added to the list of atypical
BSE strains only very recently detected worldwide and may contribute to further
research studies about epidemiologic significance. Current continued research on
BSE would appear to reveal different BSE strains in analogy with the different
scrapie strains.
-------- Original Message --------
Subject: Atypical Case of Bovine Spongiform Encephalopathy in an
East-Flemish Cow in Belgium
Date: Fri, 04 Feb 2005 10:59:33 –0600
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy
CC: cjdvoice@yahoogroups.com
Atypical Case of Bovine Spongiform Encephalopathy in an East-Flemish Cow
in Belgium
H. De Bosschere, DVM, PhD
S. Roels, DVM, PhD
E. Vanopdenbosch, DVM, Lic
Veterinary and Agrochemical Research Centre (CODA/CERVA)
National Reference Laboratorium for Veterinary TSEs
Groeselenberg 99, B-1180
Ukkel (Brussels), Belgium
KEY WORDS: Bovine spongiform encephalopathy, BSE, Western blot, atypical
BSE.
ABSTRACT
For many years, researchers believed that only one bovine spongiform
encephalopathy (BSE) strain existed, in contrast to the many different scrapie
strains found. However, only very recently reports emerged about unconventional
BSE strains seen in Italy, France, and Japan. The present case describes an
atypical strain of BSE in Belgium in a 64-month-old East-Flemish cow with an
electrophoretic profile and other features similar to those described in Japan.
INTRODUCTION
Transmissible spongiform encephalopathies (TSEs), or prion diseases, are a
group of fatal neurodegenerative diseases including sheep and goat scrapie,
bovine spongiform encephalopathy (BSE), and Creutzfeldt-Jakob disease (CJD) in
humans. They are characterized by the accumulation of an abnormal protein,
called PrPsc, which is formed post-translationally from the normal isoform
(PrPc).1,2 At present, the agent causing TSEs is still incompletely
characterized, although PrPsc is believed to be its major if not unique
constituent.3
Research in mice showed the existence of different scrapie strains.4,5
Scrapie strain discrimination is currently based on biologic typing in a panel
of inbred mice, using incubation time and brain pathology scoring as criteria.6
However, no large-scale studies of the molecular features of PrPsc have been
reported for bovine BSE to date. Till now, the BSE strain seemed to maintain
constant biologic and molecular properties even after experimental or accidental
passages into different species, such as mice, humans, primates, and sheep.7 10
However, very recently, variant forms of BSE have been reported in Japan, Italy,
and France.11-13 These forms were characterized by atypical histopathologic,
immunohistochemical, or biochemical phenotypes. The present case is the
description of the first atypical BSE case in Belgium.
MATERIALS AND METHODS
Since January 2001, all cattle older than 30 months are tested for TSE via
a rapid test (TeSeE-kit, Bio-Rad, Nazareth, Belgium) after EC regulation
999/2001.14,15 Samples positive according to the enzyme-linked immunosorbent
assay (ELISA) screening are further subjected to scrapie-associated fibrils
(SAF), histopathology, immunohistochemistry, and Western blot (WB) testing16,17
at the National Reference Laboratory (NRL).
RESULTS
A positive ELISA sample from a 64-month-old East-Flemish cow or Belgian
white and red (Figure 1) was presented at the NRL for confirmation. The animal
was reported healthy before slaughter. The optical density (OD) titers at the
local laboratory were 2.324 and 2.116.16 The OD titers at the NRL were 0.953 and
0.708 (sample taken at the contralateral side of the first sampling side of the
obex region). The histopathology of the obex, pons, and midbrain showed no
spongiform changes; immunohistochemistry of the brainstem revealed no signal of
PrPsc accumulation typical for BSE; and SAF was negative. However, WB analysis
(Bovine WB, Bio-Rad, France; antibodies 12F10 and SAF60) of the same homogenate
that was prepared from the obex region for ELISA revealed a small amount of
PrPsc with an electrophoretic profile different from that of typical
BSE-associated PrPsc.18,19 The band on the gel of the non-glycosylated form of
PrPsc of the present case clearly showed a lower migration pattern compared with
that of a typical BSE case (Figure 2).
DISCUSSION
For many years, researchers assumed that only one BSE strain existed.7 10
Only in the past months, reports of atypical BSE cases were announced.11 13 The
Japanese case11 describes a very young bull (23 months) characterized by the
absence of spongiform changes and PrPsc deposits immunohistochemically. The WB
analysis revealed an electrophoretic profile different from that of typical BSE,
characterized by low content of the di-glycosylated molecular form of PrPsc and
a faster migration of the nonglycosylated form of PrPsc. In Italy,12 two BSE
affected cattle with a previously unrecognized neuropathologic profile and PrPsc
type were seen. These cases were determined using a different staining pattern
on immunohistochemistry, a difference in size and glycoform ratio of PrPsc on
immunoblot and a difference in regional distribution of lesions. The two cases
in France13 showed variant molecular features with a different PrPsc
electrophoretic profile from other BSE cases, mainly characterized by a higher
molecular mass of the nonglycosylated PrPsc. The present case shows the most
similarities (ie, identical electrophoretic profile, only ELISA and WB positive
and histopathology and immunohistochemistry negative) with the Japanese case,11
although the cow in the Japanese case was only 23 months old, and the cow in
this case was 64 months old.
The fact that these strains were detected worldwide and in several breeds
suggest that there is no local or breed-dependent feature involved. It could be
that the WB techniques have become more specific within the past year in the
detection of minor differences in di-, mono-, and nonglycosylated molecular
forms of PrPsc. Infection of cattle by scrapie could also be considered since
scrapie can be transmitted by direct contact between animals or through
environmental contamination.13
In conclusion, this Belgian case should be added to the list of atypical
BSE strains only very recently detected worldwide and may contribute to further
research studies about epidemiologic significance. Current continued research on
BSE would appear to reveal different BSE strains in analogy with the different
scrapie strains.
ACKNOWLEDGMENTS
The authors wish to thank Rita Geeroms, Patrick Van Muylem, Stephanie
Durand, Raphaël Foubert and Amina Chama for their technical assistance. Mario
Vanpoucke is acknowledged for providing references.
REFERENCES
1. Oesch B, Westaway D, Walchii M, et al: A cellular gene encodes PrP 27 30
protein. Cell 40:735 746, 1985.
2. Prusiner SB, De Armond SJ: Prion diseases and neurodegeneration. Annu
Rev Neurosci 17:311 339, 1994.
3. Prusiner SB: Scrapie prions. Annu Rev Microbiol 43:345 374, 1989.
4. Bruce M, Dickinson AG: Biological evidence that scrapie agent has an
independent genome. J Gen Virol 68:79 89, 1987.
5. Fraser H, Dickinson AG: Scrapie in mice: Agent strain differences in the
distribution and intensity of grey matter vacuolation. J Comp Pathol 83:29 40,
1973.
6. Bruce M, McConnell I, Fraser H, Dickinson AG: The disease
characteristics of different strains of scrapie in Sinc Congenic mice lines:
Impications for the nature of the agent and host control of pathogenesis. J
Virol 72:595 603, 1991.
7. Bruce M, Chree A, McDonnell I, et al: Transmission of bovine spongiform
encephalopathy and scrapie to mice: Strain variation and the species barrier.
Philos Trans R Soc Lon Ser B 343:405 411, 1994.
8. Bruce M, Will RG, Ironside JW, et al: Transmissions to mice indicate
that new variant CJD is caused by the BSE agent. Nature 389:498 501, 1997.
9. Foster JD, Bruce M, McDonnell I, et al: Detection of BSE infectivity in
brain and spleen of experimentally infected sheep. Vet Rec 138:546 548, 1996.
10. Lasmezas CI, Fournier J-G, Nouvel V, et al: Adaptation of the bovine
spongiform encephalopathy agent to primates and comparison with
Creutzfeldt-Jakob disease: Implications for human health. Proc Natl Acd Sci U S
A 98:4142 4147, 2001.
11. Yamakawa Y, Hagiwara K, Nohtomi K, et al, for the Expert Commitee for
BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan: Atypical
proteinase K-resistant prion protein (PrPres) observed in an apparently healthy
23-month-old Holstein steer. Jpn J Infect Dis 56:221 222, 2003.
12. Casalone C, Zanusso G, Acutis PL, et al: Identification of a novel
molecular and neuropathological BSE phenotype in Italy: International Conference
on Prion Disease: from basic research to intervention concepts. Gasreig,
München, 8 10 October, 2003.
13. Biacabe AG, Laplanche JL, Ryder S, Baron T: A molecular variant of
bovine spongiform encephalopathy. International Conference on Prion Disease:
From basic research to intervention concepts. Gasreig, München, 8 10 October,
2003.
14. De Becker D, Roels S, Vanopdenbosch E: BSE onderzoek: opsporen van
PrPres door middel van de BIO-RAD Platelia BSE-kit. Vlaams Diergeneeskundig
Tijdschrift 69:382 384, 2000.
15. Roels S, Demeyer G, Tedik K, et al: Variance of mass (volume) taken
with the calibrated syringe and of the results provided by the Bio-Rad Platelia
BSE test upon storage of brainstem samples at 20°C. Anim Res 51:493 499, 2002.
16. Roels S, De Bosschere H, Saegerman C, et al: BSE and scrapie testing in
Belgium: general overview. New Food: accepted, 2004.
17. Vanopdenbosch E, Dechamps P, Dufey J, et al: Le premier cas
d encephalopathie spongioforme bovine diagnostique en Belgique. Annales de
Médicine Vétérinaire 142:111 118, 1998.
18. Collinge J, Sidle KCL, Meads J, et al: Molecular analysis of prion
strain variation and the aetiology of new variant CJD. Nature 383:685 690, 1996.
19. Hill AF, Desbruslais M, Joiner S, et al: The same prion strain causes
vCJD and BSE. Nature 389:448 450, 1997.
Figure 1. Photograph of the East-Flemish cattle breed or the Belgian white
and red.
Figure 2. Bovine Western blot (Bio-Rad, France) using antibodies 12F10 and
SAF60. MM, Magic mark; Atyp. BSE, Atypical BSE case (present case); Ref1,
Reference 1 of a classical BSE case; Ref2, Reference 2 of a classical BSE case.
The third band of the non-glycosylated PrPsc of the Atyp. BSE case (left
rectangle) shows a markedly faster migration compared to the Ref1 and Ref2 cases
(right rectangle).
P.6.- Atypical case of bovine spongiform encephalopathy in an East-Flemish
cow in Belgium.
H. De Bosschere1, S. Roels2, E. Vanopdenbosch3
1 Veterinary and Agrochemical Research Centre (CODA / CERVA), National
Reference Laboratory for Veterinary TSE (Belgium & Luxemburg) , Unit
Pathology, Department of Biocontrol, Groeselenberg 99, B-1180 Brussels (Ukkel),
Belgium, (hedeb@var.fgov.be)
2 idem, (stroe@var.fgov.be)
3 idem, (emvan@var.fgov.be)
Bovine spongiform encephalopathy (BSE) is a prion disease with a fatal
neurodegenerative pathogenesis. It is characterized by the accumulation of an
abnormal protein (PrPres), formed posttranslationally from the normal isoform
(PrPc). Research in mice showed the existence of different sheep scrapie
strains. Scrapie strain discrimination is currently based upon biological typing
in a panel of inbred mice. However, no large scale studies of the molecular
features of PrPres have been reported for bovine BSE to date. Till now, the BSE
strain seemed to maintain constant biological and molecular properties even
after experimental or accidental passages into different species. Very recently,
variant forms of BSE have been reported in Japan, Italy and France. These forms
were characterized by atypical histopathological, immunohistochemical and/or
biochemical phenotype compared to the classical BSE strain. The present case
describes the first Belgian atypical BSE case. Since January 1st 2001, all
cattle older than 30 months is tested for TSE via a rapid test following EC
regulation 999/2001. Samples positive according to the ELISA screening are
further subjected to scrapie associated fibrils (SAF), histopathology,
immunohistochemistry and Western blot (WB) at the NRL. A positive ELISA sample
from a 64 month-old East-Flemish or Belgian white and red cow was presented at
the NRL for confirmation. The histopathology of the obex, pons and midbrain was
negative, immunohistochemistry and SAF were also negative. However, WB analysis
was positive with an electrophoretic profile different from that of a typical
BSE case. The band on the gel of the non-glycosylated form of PrPres of the
present case clearly showed a lower migratrion pattern compared to that of a
typical BSE case. For many years it was assumed that there was only one BSE
strain. Only very recently, reports of atypical BSE cases were announced in
Japan, Italy and France. The Japanese case describes a very young bull (23
months) negative on histopathology and immunohistochemistry and a WB
electrophoretic profile different from that of classical BSE. The Italians
observed two BSE affected cattle with a a different staining pattern on
immunohistochemistry, a difference in size and glycoform ratio of PrPres on WB
and a difference in regional distribution of lesions. The French two cases
showed variant molecular features with a different electrophoretic profile from
other BSE cases. The present case shows the most similarities with the Japanese
case (except for the age). The fact that these strains were detected worldwide
and in several breeds suggest that there is no local or breed dependent feature
involved. It could be that the WB techniques have become more specifique within
the last year or infection of cattle by scrapie could also be considered. In
conclusion, continued research on BSE reveals nowadays different BSE strains in
analogy with the different sheep scrapie strains. Atypical BSE cases may
question the significance and efficiency of the BSE epidemio-surveillance
protocol and the validation of the confirmatory tests.
Keywords
Bovine spongiform encephalopathy, BSE, Western Blot, atypical BSE
Report on the assessment of the Geographical BSE-risk of BELGIUM July
2000
- 42 -
5. CONCLUSION ON THE GEOGRAPHICAL BSE RISK
5.1 The current GBR
The current geographical BSE-risk (GBR) level is III, i.e. BSE is confirmed
in domestic cattle (last and only case in 1997) at a lower level. However, the
observed incidence of clinical cases over the last 12 months (1 March 1999 to 29
February 2000) was 2.7 per 1 Million adult cattle. This figure is generated by a
passive surveillance system that is not able to identify all clinical
cases.
5.2 The expected development of the GBR
Assuming that measures in place continue to be appropriately implemented
and no new external challenge occurs, the GBR is expected to decrease over time.
However, this does not exclude that cattle infected by the BSE-agent in the
past (before 1998/99) may be identified as clinical cases in the foreseeable
future.
5.3 Recommendations for influencing the future GBR
Good implementation of the bans should be ensured.
In addition, expanding the surveillance system to target asymptomatic
cattle in risk sub-populations such as adult fallen stock and adult cattle
presented for emergency slaughter will allow verification of the current
GBR-assessment and monitoring its future trend.
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 ldetwiler@belle-terre.com
Published in : European Journal of Epidemiology (2006), vol. 21, pp.
443-447
Status : Postprint (Author’s version)
Increased incidence of sporadic Creutzfeldt-Jakob disease in the age groups
between 70 and 90 years in Belgium
B. Van Everbroeck1, A. Michotte2, R. Sciot3, C. Godfraind4, M. Deprez5, S.
Quoilin6, J.-J. Martin1 & P. Cras1 1Born-Bunge Institute (BBI), University
of Antwerp (UA), Campus Drie Eiken (CDE), Antwerp, Belgium; 2Department of
Neuropathology, Academic hospital, Free University of Brussels, Brussels,
Belgium; 3Department of Pathology, Catholic University of Leuven, Leuven,
Belgium; 4Pathology Laboratory, Catholic University of Louvain, Brussels,
Belgium; 5Laboratory of Neuropathology, University of Liège, Sart Tilman, Liège,
Belgium; 6Institute of Public Health-Louis Pasteur, Brussels, Belgium
Abstract
From 1998 a prospective surveillance study of Creutzfeldt-Jakob disease
(CJD) has been initiated in Belgium. In addition to epidemiological data,
information on cerebrospinal fluid biomarkers, prion protein gene and brain
neuropathology was collected. From 1-1-1998 to 31-12-2004, 188 patients were
referred to the surveillance system. In 85 patients a 'definite' diagnosis of
sporadic CJD (sCJD) could be made, whereas 26 patients remained 'probable'. We
further identified two unrelated patients with an E200K mutation, and two
patients with a seven octapeptide repeat insertion in one family. In one patient
a familial history was noted but genetic analysis was not performed. In 72
patients different final diagnoses were made, Alzheimer's disease being the most
frequent (N = 20). The demographic parameters of the Belgian population were
similar to those observed in the rest of Europe. We did notice a significantly
increased age-specific incidence (>6/106/ year) of sCJD patients between 70
and 90 years old in the period 2002-2004 compared to 1998-2001 and
retrospectively obtained data (1990-1997, p < 0.01). We undertook a detailed
clinical and biochemical analysis to investigate this increase but could not
identify any reason other than an increased vigilance for the diagnosis. In
conclusion, our study identified that in the past sCJD may have been
underestimated in patients over age 70 although these patients are both
clinically and neurobiochemically similar to the general sCJD phenotype.
Keywords : Diagnosis ; Epidemiology ; Prion disease ; Transmissible
spongiform encephalopathy
To date, 27 cases of L-BSE and 24 cases of H-BSE have been reported
worldwide (16), thus meaning that the prevalence of atypical BSE is considerably
lower than that of C-BSE. However, recent studies showed that L-BSE is easily
transmissible to transgenic mice expressing human (17,18) or bovine (19,20)
prion protein, as well as to non-human primates (21), with shorter incubation
periods than for the transmission of C-BSE to these animals.
***The virulent nature of L-BSE has stimulated new concern for human public
health since the transmission of C-BSE to humans resulted in variant
Creutzfeldt-Jakob disease (vCJD) (4-7), a new emergent prion disease.
***Infectivity in skeletal muscle of BASE-infected cattle
***The present data offer novel information on the tropism of the BASE
agent and highlight relevant public health issues. While the transmission
barrier for classical BSE is high in most species, BASE prions are readily
transmissible to a variety of mammals including non-human primates [11–13,35].
Accordingly, the possibility of spreading of BASE prions through skeletal muscle
to other species should be taken into account and evaluated in risk analysis
studies.
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 largely
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.
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...
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...
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...
Atypical BSE: Transmissibility
Linda Detwiller, 5/10/2011
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.
snip... see more breaches in the BSE aka mad cow Triple Firewall, that
never was here ;
Friday, January 23, 2015
*** Replacement of soybean meal in compound feed by European protein
sources and relaxing the mad cow ban $
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 Docket folder icon
--------------------------------------------------------------------------------
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Comment View document: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 No documents available. AttachmentsView All (1) Empty Docket No.
APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and
Animal Products Singeltary Submission View Attachment:
Sunday, January 11, 2015
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
Friday, January 23, 2015
*** Replacement of soybean meal in compound feed by European protein
sources and relaxing the mad cow ban $
Saturday, January 24, 2015
*** Bovine Spongiform Encephalopathy: Atypical Pros and Cons
Monday, December 1, 2014
Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review
December 1, 2014
Thursday, January 29, 2015
Identification of H-type BSE in Portugal
Thursday, January 29, 2015
OIE REPORT Bovine spongiform encephalopathy Prion (atypical BSE type H),
Norway Information received on 29/01/2015
Thursday, July 24, 2014
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05
Study of Atypical Bse
Sunday, December 28, 2014
Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION
aka BSE MAD COW TYPE DISEASE December 2014
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
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
Saturday, August 30, 2014
Maine Firm Recalls Ribeye and Carcass Products That May Contain Specified
Risk Materials SRM TSE PRION aka mad cow type disease
Friday, December 19, 2014
Rancho Alleged Cancerous Eyeball Case Going To Trial
Thursday, November 28, 2013
Department of Justice Former Suppliers of Beef to National School Lunch
Program Settle Allegations of Improper Practices and Mistreating Cows
seems USDA NSLP et al thought that it would be alright, to feed our
children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high
risk cattle for mad cow type disease, and other dangerous pathogens, and they
did this for 4 years, that was documented, then hid what they did by having a
recall, one of the largest recalls ever, and they made this recall and masked
the reason for the recall due to animal abuse (I do not condone animal abuse),
not for the reason of the potential for these animals to have mad cow BSE type
disease (or other dangerous and deadly pathogens). these TSE prion disease can
lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE
NEXT 5 DECADES FOR CJD ???
Saturday, September 21, 2013
Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry
Center January 2010 THE FLIM-FLAM REPORT
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH
RISK FOR MAD COW DISEASE ??? this recall was not for the welfare of the animals.
...tss you can check and see here ; (link now dead, does not work...tss)
try this link ;
Sunday, November 13, 2011
*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer
livestock
Thursday, February 13, 2014
HSUS VS USDA ET AL BAN DOWNER CALVES FOR HUMAN CONSUMPTION (*veal) and
potential BSE risk factor there from
Saturday, November 10, 2012
Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk
Materials Nov 9, 2012 WI Firm Recalls Beef Tongues
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials
SRMs
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS
KANSAS
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the
tongue and nasal mucosa of terminally diseased cattle
SPECIFIED RISK MATERIALS SRMs
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
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 ;
Friday, January 23, 2015
Replacement of soybean meal in compound feed by European protein sources
and relaxing the mad cow ban $
spontaneous atypical BSE ???
if that's the case, then France is having one hell of an epidemic of
atypical BSE, probably why they stopped testing for BSE, problem solved
$$$
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
so 20 cases of atypical BSE in France, compared to the remaining 40 cases
in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+
cases per country, besides Frances 20 cases. you cannot explain this away with
any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
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
|
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
View Attachment:
 |
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
posted by Terry S. Singeltary Sr. at
10:54 AM
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