Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
Subject: Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE
JULY 2016
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: A comparison of classical and H-type bovine spongiform
encephalopathy associated with E211K prion protein polymorphism in wild type and
EK211 cattle following intracranial inoculation
Authors
item Moore, S - item West Greenlee, M - item Smith, Jodi item Vrentas,
Catherine item Nicholson, Eric item Greenlee, Justin
Submitted to: Frontiers in Veterinary Science Publication Type: Peer
Reviewed Journal Publication Acceptance Date: April 15, 2016 Publication Date:
N/A
Interpretive Summary: Cases of bovine spongiform encephalopathy (BSE) or
mad cow disease can be subclassified into at least 3 distinct disease forms with
the predominate form known as classical BSE and the others collectively referred
to as atypical BSE. Atypical BSE can be further subdivided into H-type and
L-type cases that are distinct from classical BSE and from each other. Both of
the atypical BSE subtypes are believed to occur spontaneously, whereas classical
BSE is spread through feeding contaminated meat and bone meal to cattle. Work by
other research groups suggests that the stability of the distinguishing features
of atypical BSE cases (phenotypical stability) can change to closely resemble
classical BSE after experimental passage implicating atypical BSE as a possible
origin of classical BSE. Interestingly, one case of H-type BSE in the US was
associated with an inherited mutation in the prion protein gene referred to as
E211K. The purpose of this work was to compare wild type and cattle with the
E211K mutation after experimental inoculation with either classical BSE or H-BSE
from the original E211K case. This study demonstrates that the disease features
of E211K BSE-H remain stable when transmitted to cattle without the K211
polymorphism. In addition, passage of classical BSE to cattle with the K211
polymorphism results in disease with features consistent with classical BSE and
not a switch to atypical BSE-H as a result of the K211 polymorphism. As the
origin of classical, feedborne BSE remains unknown and low numbers of atypical
BSE are diagnosed each year, parties with interest in the cattle and beef
industries and regulatory officials responsible for safe feeding practices of
cattle will be interested in this work.
Technical Abstract: In 2006, a case of H-type bovine spongiform
encephalopathy (BSE-H) was diagnosed in a cow that was associated with a
heritable polymorphism in the bovine prion protein gene (PRNP) resulting in a
lysine for glutamine amino acid substitution at codon 211 (called E211K) of the
prion protein. Although the prevalence of this polymorphism is low, cattle
carrying the K211 allele may be predisposed to rapid onset of BSE-H when exposed
or to the potential development of a genetic BSE. This study was conducted to
better understand the relationship between the K211 polymorphism and its effect
on BSE phenotype. BSE-H from the US 2006 case was inoculated intracranially (IC)
in one PRNP wild type (EE211) calf and one EK211 calf. In addition, one wild
type calf and one EK211 calf were inoculated IC with brain homogenate from a US
2003 classical BSE case. All cattle developed clinical disease. The survival
times of the E211K BSE-H inoculated EK211 calf (10 months) was shorter than the
wild type calf (18 months). This genotype effect was not observed in classical
BSE inoculated cattle (both 26 months). Significant changes in retinal function
were observed in H-type BSE challenged cattle only. Cattle challenged with the
same inoculum showed similar severity and neuroanatomical distribution of
vacuolation and disease-associated prion protein deposition in the brain, though
differences in neuropathology were observed between E211K BSE-H and classical
BSE inoculated animals. Western blot results for brain tissue from challenged
animals were consistent with the inoculum strains. This study demonstrates that
the phenotype of E211K BSE-H remains stable when transmitted to cattle without
the K211 polymorphism, and exhibits a number of features that differ from
classical BSE in both wild type and heterozygous EK211 animals.
Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies
2015 Annual Report
1a.Objectives (from AD-416): 1. Investigate the pathobiology of atypical
transmissible spongiform encephalopathies (TSEs) in natural hosts. A.
Investigate the pathobiology of atypical scrapie. B. Investigate the
pathobiology of atypical bovine spongiform encephalopathy (BSE). 2. Investigate
the horizontal transmission of TSEs. A. Assess the horizontal transmission of
sheep scrapie in the absence of lambing. B. Determine routes of transmission in
chronic wasting disease (CWD) infected premises. C. Assess oral transmission of
CWD in reindeer. 3. Investigate determinants of CWD persistence. A. Determine
CWD host range using natural routes of transmission. B. Investigate the
pathobiology of CWD.
1b.Approach (from AD-416): The studies will focus on three animal
transmissible spongiform encephalopathy (TSE) agents found in the United States:
bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic
wasting disease (CWD) of deer, elk, and moose. The research will address sites
of accumulation, routes of infection, environmental persistence, and ante mortem
diagnostics with an emphasis on controlled conditions and natural routes of
infection. Techniques used will include clinical exams, histopathology,
immunohistochemistry and biochemical analysis of proteins. The enhanced
knowledge gained from this work will help mitigate the potential for
unrecognized epidemic expansions of these diseases in populations of animals
that could either directly or indirectly affect food animals.
3.Progress Report: Research efforts directed toward meeting objective 1 of
our project plan include work in previous years starting with the inoculation of
animals for studies designed to address the pathobiology of atypical scrapie,
atypical bovine spongiform encephalopathy (BSE), as well as a genetic version of
BSE. Post-mortem examination of the animals inoculated with atypical scrapie has
been initiated and laboratory analysis of the tissues is ongoing. Atypical BSE
animals have developed disease and evaluation of the samples is currently
underway. Animals inoculated with a genetic version of BSE have developed
disease with a manuscript reporting these results was published (2012), and
additional laboratory comparisons of genetic BSE to atypical and classical BSE
are ongoing. In addition, we have investigated the possibility that atypical
scrapie was present earlier than previously detected in the national flock by
analyzing archived field isolates using methods that were unavailable at the
time of original diagnosis. Sample quality was sufficiently degraded that modern
methods, beyond those applied to the tissues at the time the tissues were
archived, were not suitable for evaluation. In research pertaining to objective
2, "Investigate the horizontal transmission of TSEs", we have initiated a study
to determine if cohousing non-lambing scrapie inoculated sheep is sufficient to
transmit scrapie to neonatal lambs. At this time, scrapie free ewes have lambed
in the presence of scrapie inoculated animals and the lambs are cohoused with
these inoculated animals.
4.Accomplishments 1. Changes in retinal function in cattle can be used to
identify different types of bovine spongiform encephalopathy (BSE). BSE belongs
to a group of fatal, transmissible protein misfolding diseases known as
transmissible spongiform encephalopathies (TSEs). Like other protein misfolding
diseases including Parkinson's disease and Alzheimer's disease, TSEs are
generally not diagnosed until the onset of disease after the appearance of
unequivocal clinical signs. As such, identification of the earliest clinical
signs of disease may facilitate diagnosis. The retina is the most accessible
part of the central nervous system. ARS scientist in Ames IA described
antemortem changes in retinal function and thickness that are detectable in BSE
inoculated animals up to 11 months prior to the appearance of any other signs of
clinical disease. Differences in the severity of these clinical signs reflect
the amount of PrPSc accumulation in the retina and the resulting inflammatory
response of the tissue. These results are the earliest reported clinical signs
associated with TSE infection and provide a basis for understanding the
pathology and evaluating therapeutic interventions. Further, this work shows
that High-type BSE and classical BSE can be differentiated by eye examination
alone, the first time BSE strains have been differentiable in a live animal.
2. Sheep genetics influences the susceptibility of sheep to scrapie. Sheep
scrapie is a transmissible spongiform encephalopathy that can be transmitted
between affected animals resulting in significant economic losses in affected
flocks. The prion protein gene (PRNP) profoundly influences the susceptibility
of sheep to the scrapie agent and the tissue levels and distribution of PrPSc in
affected sheep. In this study, sheep of 3 different prion genetic types (denoted
VRQ/VRQ, VRQ/ARR and ARQ/ARR) were inoculated and subsequently euthanized upon
onset of disease. Disease aspects were uniform across genotypes and consistent
with manifestations of classical scrapie. Mean survival time differences were
associated with the genetic type such that VRQ/VRQ sheep survived 18 months,
whereas VRQ/ARR and ARQ/ARR sheep survived 60 and 56 months, respectively.
Microscopic evaluation revealed similar accumulations in central nervous system
tissues regardless of host genetic type. PrPSc in lymphoid tissue was
consistently abundant in VRQ/VRQ, present but confined to tonsil or
retropharyngeal lymph node in 4/5 VRQ/ARR, and totally absent in ARQ/ARR sheep.
The results of this study demonstrate the susceptibility of sheep with the
ARQ/ARR genotype to scrapie by the intracranial inoculation route with PrPSc
accumulation in CNS tissues, but prolonged incubation times and lack of PrPSc in
lymphoid tissue. These results are important for science based policy with
regard to testing of sheep for scrapie where some live animal testing is
conducted using lymphoid tissues which would not detect scrapie in some specific
genetic types which could limit the national scrapie eradication program.
Review Publications Greenlee J.J. 2014. The prion diseases of animals. In:
McManus, L.M., Mitchell, R.N., editors. Pathobiology of Human Disease. San
Diego: Elsevier. p. 1124-1133. Greenlee, J.J., Kunkle, R.A., Richt, J.A.,
Nicholson, E.M., Hamir, A.N. 2014. Lack of prion accumulation in lymphoid
tissues of PRNP ARQ/ARR sheep intracranially inoculated with the agent of
scrapie. PLoS One. 9(9):e108029. Greenlee, J.J., West Greenlee, M.,H. 2015. The
transmissible spongiform encephalopathies of livestock. ILAR Journal.
56(1):7-25. Munoz-Gutierrez, J.F., Schneider, D.A., Baszler, T.V., Dinkel, K.D.,
Greenlee, J.J., Nicholson, E.M., Stanton, J.J. 2015. hTERT-immortalized ovine
microglia propagate natural scrapie isolates. Virus Research. 198:35-43.
Nicholson, E.M. 2015. Detection of the disease-associated form of the prion
protein in biological samples. Bioanalysis. 7(2):253-261. West Greenlee, M.H.,
Smith, J.D., Platt, E.M., Juarez, J.R., Timms, L.L, Greenlee, J.J. 2015. Changes
in retinal function and morphology are early clinical signs of disease in cattle
with bovine spongiform encephalopathy. PLoS ONE. 10(3):e0119431. Comoy, E.E.,
Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand,
V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J.,
Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie
prions to primate after an extended silent incubation period. Scientific
Reports. 5:11573.
Emergence of a novel bovine spongiform encephalopathy (BSE) prion from an
atypical H-type BSE
Kentaro Masujin , Hiroyuki Okada , Kohtaro Miyazawa , Yuichi Matsuura ,
Morikazu Imamura , Yoshifumi Iwamaru , Yuichi Murayama & Takashi Yokoyama
Scientific Reports 6, Article number: 22753 (2016) doi:10.1038/srep22753
Download Citation Infectious-disease diagnostics Microbiology
Received:23 November 2015Accepted:19 February 2016Published online:07 March
2016
Abstract
The H-type of atypical bovine spongiform encephalopathy (H-BSE) was
serially passaged in bovinized transgenic (TgBoPrP) mice. At the fourth passage,
most challenged mice showed a typical H-BSE phenotype with incubation periods of
223 ± 7.8 days. However, a different phenotype of BSE prion with shorter
incubation periods of 109 ± 4 days emerged in a minor subset of the inoculated
mice. The latter showed distinct clinical signs, brain pathology, and abnormal
prion protein profiles as compared to H-BSE and other known BSE strains in mice.
This novel prion was transmitted intracerebrally to cattle, with incubation
periods of 14.8 ± 1.5 months, with phenotypes that differed from those of other
bovine prion strains. These data suggest that intraspecies transmission of H-BSE
in cattle allows the emergence of a novel BSE strain. Therefore, the
continuation of feed ban programs may be necessary to exclude the recycling of
H-BSE prions, which appear to arise spontaneously, in livestock. Such measures
should help to reduce the risks from both novel and known strains of BSE.
Introduction
Prions cause transmissible spongiform encephalopathies (TSEs), which are
characterized by a spongiform change in the central nervous system and the
accumulation of an abnormal prion protein (PrPSc). PrPSc is a disease-associated
isoform of the host-encoded prion protein1, and the conversion of the normal
isoform (PrPC) to PrPSc is thought represent a central event in prion
pathogenesis. PrPSc has been recognized as the major component of prions2, and
variations in PrPSc are associated with different prion strains that, in turn,
cause distinct disease phenotypes3.
Bovine spongiform encephalopathy (BSE) is a TSE of cattle. Most BSE cases
show a unique phenotype that is thought to be caused by a single prion strain4.
However, other atypical neuropathological and molecular phenotypes of BSEs
(atypical BSEs) have been identified in aged animals5,6. Atypical BSEs have been
classified into two groups, L-BSE and H-BSE, based on their biological and
biochemical features5,6, which differ from those of classical BSE (C-BSE).
The worldwide occurrence of BSE is declining, primarily because of
effective feed ban programs6. The emergence of atypical BSE cases has raised
questions as to whether additional and/or modified control measures might be
needed. Thus, characterization of atypical BSE prions is necessary for risk
evaluation.
H-BSE was first reported in France7, and has been subsequently detected in
several European countries and North America5,6. In one of two H-BSE cases
detected in the U.S., a prion protein (PrP) amino-acid substitution that is
associated with familial Creutzfeldt–Jakob disease in humans has been reported.
This suggested the possibility that H-BSE might occur spontaneously or
sporadically8. Regardless of its origin, previous studies have shown that H-BSE
is transmissible to cattle9,10,11,12, as well as to wild type13,14, bovinized,
and ovinized PrP transgenic mice that express murine, bovine, or ovine PrPC,
respectively15,16,17. Those studies also revealed different characteristics of
H-BSE relative to C-BSE and L-BSE.
Serial passages of H-BSE in wild type18,19 and bovinized PrP transgenic
mice20 can lead to the emergence of a C-BSE-like phenotype. This suggests that
H-BSE-affected cattle harbor heterogeneous prions and that structural variants
of H-BSE might generate a C-BSE-like phenotype. This, in turn, raises the
possibility that C-BSE originated from H-BSE. To attempt to clarify the origin
of C-BSE, we serially passaged H-BSE in bovinized PrP transgenic (TgBoPrP) mice.
In contrast to previous studies, we did not detect C-BSE-like prions during
serial passages. However, a novel BSE prion—different from C-BSE, L-BSE, and
H-BSE prions—was detected in a subset of inoculated mice. When this novel prion
was inoculated intracerebrally into cattle, a novel BSE phenotype was confirmed.
This study suggests that a novel BSE emerges during intraspecies transmission of
H-BSE in cattle.
Results
Serial transmission of H-BSE in TgBoPrP mice
The results of serial transmission of the H-BSE isolate in TgBoPrP mice are
shown in Table 1. All the H-BSE challenged mice developed progressive
neurological disease with the incubation periods of 320.1 ± 12.2 days at primary
passage. H-BSE-affected animals showed a distinctive clinical sign, namely,
constant chewing of the bedding, as reported previously16. The incubation
periods of the second and third passages were 226.9 ± 4.2 and 215.6 ± 5.0 days,
respectively (Table 1)16. No clear differences were observed in their clinical
signs, the banding pattern of PrPSc, and histopathological features from the
primary to third passage mice. At the fourth passage, mice from a single
experimental group (#3), out of eight experiments, showed shorter incubation
periods (108.8 ± 4.0 days) than the other groups. This group was challenged with
brain homogenates of a mouse with 221-day incubation period. Group #3 animals
showed weight loss, but no constant chewing of the bedding. This short
incubation-type of BSE was designed BSE-SW (short incubation with weight loss)
strain. BSE-SW was transmitted to TgBoPrP mice with 97.3 ± 3.7 day incubation
periods, and their clinical signs were identical to those of mice in the
experimental group #3. The other mice in the fourth passage groups showed the
symptomatic chewing of the bedding, and their incubation periods were 223.3 ±
7.8 days (Table 1).
SNIP...
Molecular features of PrPcore of BSE-SW-affected cattle
Western blot analysis detected PrPSc from the obex tissue of the challenged
cattle. The molecular features of PrPcore of BSE-SW-affected cattle were
distinctly different from C-BSE, L-BSE, and H-BSE (Fig. 5). The molecular mass
of PrPcore #1 of BSE-SW, as determined by mAb 6H4, was lower than H-BSE and
similar to C-BSE (Fig. 5b). MAb P4 did not detect PrPcore of BSE-SW (Fig. 5a).
PrPcore #2 was also observed in BSE-SW (Fig. 5c,d). These results revealed that
the biochemical properties of BSE-SW have indeed been transmitted to cattle.
SNIP...
Discussion
Our previous reports have revealed the usefulness of TgBoPrP mice for
characterizing BSE prions16,21,22. In this study, a novel BSE, BSE-SW, was
detected using this mouse model. The incubation periods of H-BSE, L-BSE, and
C-BSE prions in the TgBoPrP mice were approximately 215 days, 150 days, and 190
days, respectively16,21,22. The BSE-SW prion showed the shortest incubation
period (approximately 90 days) among the known BSE prions. We have previously
performed several transmission experiments of sheep scrapie to TgBoPrP mice, but
their incubation periods were over 170 days23, and we have not observed any
prions with ~90-day incubation periods in these mice. In addition, the
biochemical and biological properties of PrPSc from BSE-SW were clearly
different from C-BSE, L-BSE, H-BSE, and sheep scrapie (data not shown). PrPSc of
BSE-SW has some similarity to H-BSE on the account of the presence of truncated
12-kDa fragments (PrPcore #2). Fig. 6 shows the putative PK digestion site of
PrPSc from BSE-SW, as assessed by immunoreactivity with mAbs P4, 6H4, and SAF84.
These results argue against the possibility that the BSE-SW prion resulted from
a contamination of other laboratory prion strains.
SNIP...
It is known that sheep scrapie comprises different prion strains24,25, and
some affected sheep harbor these mixed scrapie prion strains3. Numerous scrapie
strains had emerged in the course of several passage histories26. We have also
previously isolated distinct scrapie strains from the brain of a
scrapie-affected sheep after primary passage in wild type mice27. The different
scrapie prion strains appeared after primary passage in sheep scrapie cases,
which was considered to be due to prion strain selection. For H-BSE prions,
French and Polish cases were reported, which transformed into a C-BSE-like
phenotype during mouse passages18,19,20, revealing their potential
heterogeneity. However, the BSE-SW prions described herein appear to have
emerged by a different manner than our previous scrapie case27. The average
incubation period of H-BSE in TgBoPrP mice was 320 days at first passage, and
then shortened to 227 days and 216 days at secondary and third passages,
respectively. Based on this observation, H-BSE prions were adapted to TgBoPrP
mice at second passage. By the third passage, no multiple prion strains in the
H-BSE material were evident. BSE-SW prion with a shorter incubation period
emerged after H-BSE has adapted to TgBoPrP mice. The results of this study
suggest that BSE-SW emerged through a conformational rearrangement.
Alternatively, the BSE-SW prion was only present in a very small titer in H-BSE
and required several passages in sensitive animals to emerge after selection
from a mixture of preexisting prion strains. The Canadian H-BSE sample that was
used in this study was also used to inoculate wild type mice, but we did not
observe the emergence of a C-BSE-like phenotype in those circumstances
(unpublished data). The underlying mechanisms of the emergence of new prion
strains are important to elucidate prion heterogeneity. This novel BSE strain
has never been observed in field BSE cases, but our experiments reveal the
potential risk associated with H-BSE.
It has been suggested that different conformations of PrPSc are involved in
the prion strain diversity28, and that rearrangement of PrPSc from a uniform
conformation causes the emergence of new host-adapted PrPSc 3. PrPSc of BSE-SW
exhibited different conformational stability from H-BSE. It is also known that
strain “mutation or transformation” may occur upon intraspecies transmission,
where the PrP amino acid sequences of the host and the donor are identical3.
These finding are consistent with the conclusion that PrPSc of BSE-SW has a
different conformation than H-BSE.
Furthermore, our new strain was successfully transmitted to cattle.
Standard diagnostic testing for BSE confirmed the presence of spongiform changes
associated with PrPSc accumulation in the obex, and the challenged cattle
fulfilled BSE criteria (Figs 4 and 5). The disease phenotype and features of
PrPSc, different from the known types of BSE, indicated that this prion could
cause a novel type of atypical BSE. The shorter incubation periods in cattle
were consistent with the relative incubation periods in TgBoPrP mice, and
indicate high virulence of this novel prion. Further analysis of diseased cattle
is necessary to clarify its characteristics. Such studies could help to
elucidate the mechanisms of conformational change in PrPSc, which lead to the
propagation of new prion strains.
The ban on meat-and-bone meal in livestock feed has contributed to the
decline in C-BSE occurrences6. Recently, easing of the BSE-related regulations
and control measures has been discussed. The origin of atypical BSE remains
unknown, but it has been proposed to be spontaneous or sporadic29. H-BSE has
been reported to transform into a C-BSE-like phenotype during animal
passages18,19,20. Furthermore, we have shown here that the sequential
transmission of H-BSE in TgBoPrP mice, i.e., to a homologous bovine PrP context,
generated a novel type of BSE. Considering these observations, a continuous feed
ban program may be necessary even after C-BSE is eradicated. Prohibiting the
recycling of spontaneously occurring H-BSE prions in cattle should help to
prevent both re-emerging and emerging types of BSEs.
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain
location and PrPsc by PMCA only, how many cases have we missed?
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67
PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in
unusual brain location and PrPsc detection by PMCA only.
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards
Singeltary Comment Submission
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
ABSTRACT
Information on the pathogenesis and tissue distribution of Atypical Bovine
Spongiform Encephalopathy (BSE) in cattle through the study of field cases and
experimental transmission studies is lacking. The latter are limited to
transmission of Atypical BSE through intracerebral (i.c.) inoculation of cattle.
All data currently available relate to the presence or absence of PrPSc, but do
not quantify relative amounts of PrPSc or levels of infectivity. A laboratory
protocol for further studies is recommended, to allow 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 those studies are categorised in three
priorities, based on their inclusion in the list of specific risk material in
cattle, on the presence of infectivity, or PrPSc presence, demonstrated in
Atypical BSEs or other Transmissible Spongiform Encephalopathies (TSEs) in
ruminants, and on the importance in terms of input into the food chain in the
EU. The protocol provides details in terms of the minimum number of animals to
be tested, processing and preparation of tissues, and methods to be used to
identify abnormal PrP and quantify infectivity, also depending on the expected
level of infectivity and amount of tissue available for analysis. It is
recommended that, 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.
© European Food Safety Authority, 2014
KEY WORDS
Atypical BSE, cattle, H-BSE, L-BSE, laboratory protocol, prion
1 On request from the European Commission, Question No EFSA-Q-2013-01015,
approved on 11 July 2014.
2 Correspondence: biohaz@efsa.europa.eu
3 Acknowledgement: EFSA wishes to thank the members of the Working Group on
Atypical BSE study protocol: Olivier Andreoletti, Anne Balkema-Buschmann,
Vincent Béringue, Marion Simmons and Juan-Maria Torres for the preparatory work
on this scientific output, the members of the EFSA Panel on Biological Hazards
(BIOHAZ) for their endorsement of the scientific output, and EFSA staff members:
Winy Messens and Pietro Stella for the support provided to this scientific
output.
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 2
SUMMARY
Following a request from the European Commission, EFSA was asked to provide
scientific and technical assistance on a protocol for further laboratory
investigations into the distribution of infectivity of Atypical Bovine
Spongiform Encephalopathy (BSE).
The European Union Reference Laboratory (EURL) for Transmissible Spongifom
Encephalopathies (TSEs) conducted experiments (referred to as the EURL study)
that resulted in the collection and storage of reference material originating
from cattle experimentally infected with Atypical BSE (H-BSE and L-BSE). With
the intention to generate relevant data that could inform further policy options
regarding BSE, in particular as regards rules on specified risk material (SRM),
DG SANCO wished to explore the possibility to submit these tissue samples to
further investigations. EFSA was therefore asked to propose a laboratory
protocol to perform new studies aimed at investigating the presence,
distribution and relative level of infectivity of Atypical BSE (H-BSE and
L-BSE). EFSA was also expected to reflect on whether the tissues available from
the EURL study are sufficient for the purpose and/or suggest that investigations
on other tissues might be possibly needed.
Data relating to the prevalence and geographical distribution of Atypical
BSE in the European Union (EU) are incomplete and subject to variation owing to
the ongoing retrospective typing of BSE cases. So far, 80 cases of Atypical BSE
have been reported by EU Member States from 2001 to 2014. All Atypical BSE cases
have been detected by active surveillance, typically in animals over eight years
of age, with a similar number of cases detected each year.
This report provides an overview of the biological material collected from
field cases of Atypical BSE and transmission studies, both in the framework of
the EURL study and additional published scientific studies. It was concluded
that information on the pathogenesis and tissue distribution of Atypical BSE in
cattle through the study of field cases and experimental transmission studies is
lacking. The latter are limited to transmission of Atypical BSE through
intracerebral (i.c.) inoculation of cattle. 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. All data currently available relate to the presence or absence of
PrPSc, but do not quantify relative amounts of PrPSc or levels of
infectivity.
Approaches to quantify Atypical BSE prions in cattle tissues are described
and reviewed, including bioassay and in vitro methods.
A laboratory protocol for further studies is recommended. Its application
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 those studies were 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. The protocol
provides details in terms of the minimum number of animals to be tested,
processing and preparation of tissues, and methods to be used to identify
abnormal PrP and quantify infectivity, also depending on the expected level of
infectivity and amount of tissue available for analysis.
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.
It is acknowledged that 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, and therefore, to complete this
objective, new inoculation experiments with H- and L-BSE agents in cattle would
have to be considered. Recommendations on general principles for such new
experiments are provided.
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 3
In accordance with former EFSA recommendations, it is recommended that,
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.
snip...
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
>>> Both of the atypical BSE subtypes are believed to occur
spontaneously,<<<
LOL!
SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Atypical BSE...Spontaneous...LOL
BSE identified in France
Posted May 2, 2016
A cow in northern France has been confirmed to have bovine spongiform
encephalopathy, according to the World Organisation for Animal Health
(OIE).
The cow had developed partial paralysis and was euthanized March 1, a March
25 OIE report states.
BSE is a fatal neurologic prion disease with a typical incubation period of
four to five years. The cow in France was almost 5 years old.
The affected cow had the classic form of BSE, which is most often
associated with feed containing neurologic tissue from infected animals. It is
distinct from atypical BSE, which may develop spontaneously, according to
information from the U.S. Centers for Disease Control and Prevention.
Investigators were trying to identify the source of infection and other
animals at risk for BSE at the time the report was published.
The affected bovine, a Salers female born on April, 8th 2011, showed
paresis and was euthanized on March, 1st 2016. Samples made on March, 4th 2016
during rendering were analyzed at the Department Laboratory of La Somme. The
rapid test proved positive on March, 8th 2016 and the samples were then sent for
further analysis to the National Reference Laboratory, ANSES, which confirmed a
case of classical BSE on March, 21st 2016. The European Union Reference
Laboratory confirmed those results on the basis of documentation on March, 23rd
2016.
>>> It is distinct from atypical BSE, which may develop
spontaneously, according to information from the U.S. Centers for Disease
Control and Prevention.
THIS IS A MYTH $$$
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
***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, March 24, 2016
FRANCE CONFIRMS BOVINE SPONGIFORM ENCEPHALOPATHY BSE MAD COW (ESB) chez une
vache dans les Ardennes
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
If you Compare France to other Countries with atypical BSE, in my opinion,
you cannot explain this with ‘spontaneous’.
Table 1: Number of Atypical BSE cases reported by EU Member States in the
period 2001–2014 by country and by type (L- and H-BSE) (extracted from EU BSE
databases on 1 July 2014). By 2015, these data might be more comprehensive
following a request from the European Commission to Member States for re-testing
and retrospective classification of all positive bovine isolates in the EU in
the years 2003–2009
BSE type
Country 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013(a)
2014(a) Total
H-BSE Austria 1 1
France(b) 1 2 3 1 2 2 2 2 15
Germany 1 1 2
Ireland 1 1 2 1 5
The Netherlands 1 1
Poland 1 1 2
Portugal 1 1
Spain 1 1 2
Sweden 1 1
United Kingdom 1 1 1 1 1 5
Total 2 3 3 1 1 2 2 2 4 4 5 1 4 1 35
L-BSE Austria 1 1 2
Denmark 1 1
France(b) 1 1 1 1 2 1 3 2 1 1 14
Germany 1 1 2
Italy 1 1 1 1 1 5
The Netherlands 1 1 1 3
Poland 1 2 2 1 2 1 2 1 12
Spain 2 2
United Kingdom 1 1 1 1 4
Total 0 5 3 4 3 3 6 3 3 4 3 6 1 1 45
Total Atypical cases (H + L)
2 8 6 5 4 5 8 5 7 8 8 7 5 2 80
(a): Data for 2013-2014 are incomplete and may not include all
cases/countries reported.
(b): France has performed extensive retrospective testing to classify BSE
cases, which is probably the explanation for the higher number of Atypical BSE
cases reported in this country.
The number of Atypical BSE cases detected in countries that have already
identified them seems to be similar from year to year. In France, a
retrospective study of all TSE-positive cattle identified through the compulsory
EU surveillance between 2001 and 2007 indicated that the prevalence of H-BSE and
L-BSE was 0.35 and 0.41 cases per million adult cattle tested, respectively,
which increased to 1.9 and 1.7 cases per million, respectively, in tested
animals over eight years old (Biacabe et al., 2008). No comprehensive study on
the prevalence of Atypical BSE cases has yet been carried out in other EU Member
States. All cases of Atypical BSE reported in the EU BSE databases have been
identified by active surveillance testing (59 % in fallen stock, 38 % in healthy
slaughtered cattle and 4 % in emergency slaughtered cattle). Cases were reported
in animals over eight years of age, with the exception of two cases (one H-BSE
and one L-BSE) detected in Spain in 2011/2012. One additional case of H-BSE was
detected in Switzerland in 2012 in a cow born in Germany in 2005 (Guldimann et
al., 2012).
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 8
Table 1: Number of Atypical BSE cases reported by EU Member States in the
period 2001–2014 by country and by type (L- and H-BSE) (extracted from EU BSE
databases on 1 July 2014). By 2015, these data might be more comprehensive
following a request from the European Commission to Member States for re-testing
and retrospective classification of all positive bovine isolates in the EU in
the years 2003–2009
BSE type Country 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011
2012 2013(a) 2014(a) Total
H-BSE
Austria 1 1
France(b) 1 2 3 1 2 2 2 2 15
Germany 1 1 2 Ireland 1 1 2 1 5
The Netherlands 1 1
Poland 1 1 2
Portugal 1 1
Spain 1 1 2
Sweden 1 1
United Kingdom 1 1 1 1 1 5
Total 2 3 3 1 1 2 2 2 4 4 5 1 4 1 35
L-BSE
Austria 1 1 2
Denmark 1 1
France(b) 1 1 1 1 2 1 3 2 1 1 14
Germany 1 1 2 Italy 1 1 1 1 1 5
The Netherlands 1 1 1 3
Poland 1 2 2 1 2 1 2 1 12
Spain 2 2
United Kingdom 1 1 1 1 4
Total 0 5 3 4 3 3 6 3 3 4 3 6 1 1 45
Total Atypical cases (H + L) 2 8 6 5 4 5 8 5 7 8 8 7 5 2 80
(a): Data for 2013-2014 are incomplete and may not include all
cases/countries reported.
(b): France has performed extensive retrospective testing to classify BSE
cases, which is probably the explanation for the higher number of Atypical BSE
cases reported in this country.
SNIP...
The current lack of information on the distribution of infectivity in
tissues from Atypical BSE-infected cattle does not allow judgement of whether
the current list of bovine SRM, set by EU Atypical BSE study protocol
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. As is the case for C-BSE, Atypical BSE (H-BSE
and/or L-BSE) agents are able to propagate in experimentally challenged foreign
species such as mice, sheep, voles, primates and hamsters, and in transgenic
mice expressing heterologous, i.e. non-bovine, PrP sequences.
EFSA Journal 2014;12(7):3798 13
SNIP...
2.4. Concluding remarks
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.
All data currently available relate to the presence or absence of PrPSc,
but do not quantify relative amounts of PrPSc or levels of infectivity.
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).
There are insufficient data at present to be clear about whether these
apparent differences in the distribution of disease-specific markers reflect
absolute differences between C-BSE and the H-BSE and L-BSE variants, whether
they are a consequence of detection threshold limitations, or whether they are a
consequence of the different routes of challenge.
No studies have been explicitly designed to address the issue of Atypical
BSE with respect to SRM regulations. Without further experimental challenges or
tissue collection from ongoing studies it will not be possible to obtain any
data on duodenum, the jejunum and ileum (without Peyer’s patches), the caecum,
the colon and the mesenteric fat.
SNIP...
4.1. Selection of tissues
4.1.1. BSE infectivity in bovine tissues
The current SRM list in cattle (see Table 5) has been established and
amended in accordance with current knowledge related to C-BSE agent distribution
in the tissues of infected cattle.
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 24
The SRM measure is aimed at preventing the entry into the food chain of
tissues and anatomical structures that might contain significant amounts of
infectivity. In the framework of C-BSE infection in cattle, these measures are
extremely efficient. However, certain tissues that might contain low amounts of
infectivity in certain BSE-infected cattle are not included in the cattle SRM
list (Table 6).
Table 5: Bovine SRM list, as defined in Regulation (EC) No 999/2001
Bovine SRM list
The skull excluding the mandible and including the brain and eyes, and the
spinal cord of animals aged over 12 months
The vertebral column excluding the vertebrae of the tail, the spinous and
transverse processes of the cervical, thoracic and lumbar vertebrae and the
median sacral crest and wings of the sacrum, but including the dorsal root
ganglia, of animals aged over 30 months
The tonsils, the intestines from the duodenum to the rectum and the
mesentery of animals of all ages
Table 6: Cattle tissues with known infectivity or PrPSc presence for C-BSE
according to WHO (2010), and their inclusion or not in the current SRM
list
Higher-infectivity tissues
SRM
Brain
Dura mater
Spinal cord
Optic nerve
Retina
Spinal ganglia
Trigeminal ganglia
Lower-infectivity tissues
Nictitating membrane
Autonomic ganglia
Tonsil
Ileum
Jejunum
Non-SRM
Peripheral nerves
Adrenal glands
Bone marrow
Skeletal muscle
All the TSE agents replicate and accumulate at a high level in the CNS and
can disseminate (centrifugally and centripetally) along the peripheral
(autonomic and motor) nervous system. However, in a given host the agent
distribution and the relative level of infectivity in other tissues can vary
substantially according to the TSE strain.
For instance, in humans, although sCJD infectivity is mostly confined to
the CNS, numerous lymphoid organs have been shown to be infectious in patients
affected with variant CJD (vCJD) (Gill et al., 2013).
Similarly, in sheep infected with Classical scrapie, a significant level of
infectivity can be found in lymphoid organs (about 103 times less than in the
same weight of brain tissue), whereas in animals affected with Atypical scrapie
lymphoid organs contain either very low (about 107 times less than in the same
weight of brain tissue) or no detectable infectivity (Andreoletti et al.,
2011).
There are currently no quantitative data on the distribution of H-BSE and
L-BSE in cattle tissues.
4.1.2. Prioritisation of tissues to be included in further studies
In order to assess the adequacy and the relative effectiveness of the
current SRM measures for mitigating human dietary exposure to H-BSE and L-BSE, a
large number of tissues/anatomical structures need to be tested for the presence
of PrPSc and/or infectivity.
Considering the potential number of samples and the requirement for
bioassay, the choice of tissues to be tested should be prioritised according to
three criteria:
the level of infectivity they contain in C-BSE-infected cattle (SRM list);
the presence of infectivity, or PrPSc presence, demonstrated in Atypical
BSEs or other TSEs in ruminants;
the importance in terms of input into the food chain in the EU.
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
>>>(b): France has performed extensive retrospective testing to
classify BSE cases, which is probably the explanation for the higher number of
Atypical BSE cases reported in this country.<<<
LMAO!!!
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
we have seen the spontaneous BSE epidemic in France, what about the other
HIGH INCIDENCE ATYPICAL BSE COUNTRY OF POLAND, another atypical spontaneous
event of high incidence. how can this be blamed on a happenstance of nothing,
i.e. old age? goes against all junk science to date on the spontaneous atypical
BSE i.e.
> In 2015, the OIE determined that atypical BSE occurred spontaneously
at a low rate in all cattle populations and would be excluded for BSE risk.
...
>Atypical BSE occurs in older cattle, usually 8 years of age or greater,
and does not appear to be associated with contaminated feed. Like classic or
sporadic CJD in humans, it seems to arise rarely and spontaneously.
and if you believe that lie, myth, junk science, then you will believe this
i.e.
> Regulations from the Food and Drug Administration (FDA) have
prohibited the inclusion of mammalian protein in feed for cattle and other
ruminants since 1997 and have also prohibited high risk tissue materials in all
animal feed since 2009.
LAUGH OUT LOUD ! LOL!
POLAND ATYPICAL BSE AND SPORADIC CJD
Issue 2 Journal for Veterinary Medicine, Biotechnology and Biosafety
Volume 1, Issue 2, June 2015, Pages 12–14
ISSN 2411-3174 (print version) ISSN 2411-0388 (online version)
EPIDEmIOLOGY Of BOVINE SPONGIfORm ENCEPHALOPATHY IN CATTLE IN POLAND
Polak M. P., Zmudzinski J. F.
National Veterinary Research Institute, Pulawy, Poland e-mail:
ppolak@piwet.pulawy.pl
Download PDF (print version)
Citation for print version: Polak M. P. and Zmudzinski J. F. (2015)
‘Epidemiology of bovine spongiform encephalopathy in cattle in Poland’, Journal
for Veterinary Medicine, Biotechnology and Biosafety, 1(2), pp. 12–14.
Download PDF (online version)
Citation for online version: Polak M. P. and Zmudzinski J. F. (2015)
‘Epidemiology of bovine spongiform encephalopathy in cattle in Poland’, Journal
for Veterinary Medicine, Biotechnology and Biosafety. [Online] 1(2), pp. 12–14.
Available at:
Summary. The aim of the paper was to present the epidemiological situation
regarding BSE epidemic in Poland with respect to cattle population, active
surveillance and the control measures. Epidemiological data from the archives of
the national reference laboratory for animal TSEs at the National Veterinary
Research Institute and from the archives of the General Veterinary Inspectorate
in Warsaw were used in the study. Between 2001 and the end of April 2015 BSE was
diagnosed in 75 animals. Sixty one cases were classical BSE and 14 were atypical
BSE (12 of L-type and 2 of H-type). Almost 6 million animals were tested using
rapid tests. Dynamics of C-type BSE shows constant rise until 2005 when the
highest number of cases (20) was recorded with sharp drop in the following
years. Prevalence of atypical BSE shows stable trend with slight fluctuations.
Traditional feeding was used in 65 and 90% of classical and atypical BSE cases,
respectively. On the other hand, traditional feed was supplemented with MBM and
milk replacers in 46 and 10% of classical and atypical BSE cases, respectively.
Despite the high infectious load introduced into Poland especially with MBM, the
number of cases was relatively low. In Poland, relatively high number of
atypical BSE cases was recorded, comprising 19% of all BSE-positive animals.
Mean age of classical BSE cases diagnosed annually does not show a decreasing
trend which may reflect the late introduction of feed ban in Poland.
Keywords: bovine spongiform encephalopathy, Poland, prevalence, prion
protein, control measures
References:
Baron, T., Biacabe, A.‑G., Arsac, J.‑N., Benestad, S. and Groschup, M. H.
(2007) ‘Atypical transmissible spongiform encephalopathies (TSEs) in ruminants’,
Vaccine, 25(30), pp. 5625–5630. doi: http://dx.doi.org/10.1016/j.vaccine.2006.10.058
Baron, T. and Biacabe, A.‑G. (2006) ‘Origin of bovine spongiform
encephalopathy’, The Lancet, 367(9507), pp. 297–298. doi: http://dx.doi.org/10.1016/s0140-6736(06)68060-4
Biacabe, A.‑G., Laplanche, J.‑L., Ryder, S. and Baron, T. (2004) ‘Distinct
molecular phenotypes in bovine prion diseases’, EMBO reports, 5(1), pp. 110–115.
doi: http://dx.doi.org/10.1038/sj.embor.7400054
Brown, P., McShane, L., Zanusso, G. and Detwiler, L. (2006) ‘On the
question of sporadic or atypical bovine spongiform encephalopathy and
Creutzfeldt-Jakob disease’, Emerging Infectious Diseases, 12(12), pp. 1816–1821.
doi: http://dx.doi.org/10.3201/eid1212.060965
Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D.,
Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser,
H. and Bostock, C. J. (1997) ‘Transmissions to mice indicate that 'new variant'
CJD is caused by the BSE agent’. Nature, 389(6650), pp. 498–501. doi: http://dx.doi.org/10.1038/39057
Buschmann, A. and Groschup, M. H. (2005) ‘Highly bovine spongiform
encephalopathy–sensitive transgenic mice confirm the essential restriction of
infectivity to the nervous system in clinically diseased cattle’, The Journal of
Infectious Diseases, 192(5), pp. 934–942. doi: http://dx.doi.org/10.1086/431602
Casalone, C., Zanusso, G., Acutis, P., Ferrari, S., Capucci, L.,
Tagliavini, F., Monaco, S. and Caramelli, M. (2004) ‘Identification of a second
bovine amyloidotic spongiform encephalopathy: Molecular similarities with
sporadic Creutzfeldt-Jakob disease’, Proceedings of the National Academy of
Sciences, 101(9), pp. 3065–3070. doi: http://dx.doi.org/10.1073/pnas.0305777101
Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F.
(1996) ‘Molecular analysis of prion strain variation and the aetiology of ‘new
variant’ CJD’, Nature, 383(6602), pp. 685–690. doi: http://dx.doi.org/10.1038/383685a0
Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C., Gowland, I.,
Collinge, J., Doey L. J. and Lantos, P. (1997) ‘The same prion strain causes
vCJD and BSE’. Nature, 389(6650), pp. 448–450. doi: http://dx.doi.org/10.1038/38925
Jacobs, J. G., Langeveld, J. P. M., Biacabe, A.‑G., Acutis, P.‑L., Polak,
M. P., Gavier-Widen, D., Buschmann, A., Caramelli, M., Casalone, C., Mazza, M.,
Groschup, M., Erkens, J. H. F., Davidse, A., van Zijderveld, F. G. and Baron, T.
(2007) ‘Molecular discrimination of atypical bovine spongiform encephalopathy
strains from a geographical region spanning a wide area in Europe’, Journal of
Clinical Microbiology, 45(6), pp. 1821–1829. doi: http://dx.doi.org/10.1128/jcm.00160-07
Polak, M. P., Rożek, W., Rola, J., Żmudziński, J. F. (2004). ‘Prion protein
glycoforms from BSE cases in Poland’. Bulletin of Veterinary Institute in
Pulawy, 48(3), pp. 201–205. Available at: http://bulletin.piwet.pulawy.pl/images/stories/pdf/20043/20043201206.pdf
Simmons, M. M., Harris, P., Jeffrey, M., Meek, S. C., Blamire, I. W. H. and
Wells, G. A. H. (1996) ‘BSE in Great Britain: consistency of the
neurohistopathological findings in two random annual samples of clinically
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2015-2016 © NSC IECVM All rights reserved.
Opinion of the
Scientific Steering Committee
on the
GEOGRAPHICAL RISK OF
BOVINE SPONGIFORM
ENCEPHALOPATHY (GBR) in
POLAND
Adopted on 30/03/2001
Opinion of the Scientific Steering Committee on the
GEOGRAPHICAL RISK OF BOVINE SPONGIFORM
ENCEPHALOPATHY (GBR)
in Poland
THE QUESTION
The Scientific Steering Committee (SSC) was asked by the Commission to
express its scientific opinion on the Geographical BSE-Risk (GBR), i.e. the
likelihood of the presence of one or more cattle being infected with BSE,
pre-clinically as well as clinically, at a given point in time, in a number of
Third Countries.
This opinion addresses the GBR of Poland.
THE BACKGROUND
In December 1997 the SSC expressed its first opinion on Specified Risk
Materials where it stated, inter alia, that the list of SRM could probably be
modulated in the light of the species, the age and the geographical origin of
the animals in question.
In June 2000 the European Commission adopted a Decision on SRM
(2000/418/EC), prohibiting the import of SRM from all Third Countries that have
not been "satisfactorily" assessed with regard to their BSE-Risk.
In July 2000 the SSC adopted its final opinion on "the Geographical Risk of
Bovine Spongiform Encephalopathy (GBR)". This opinion described a method and a
process for the assessment of the GBR and summarised the outcome of its
application to 23 countries. Detailed reports on the GBR-assessments were
published on the Internet for each of these countries.
In September 2000 the Commission invited 46 Third Countries, which are
authorised to export products to the EU that are listed in annex II to the above
mentioned SRM-Decision, to provide a dossier for the assessment of their
GBR.
Until today 36 dossiers have been received, 6 are already assessed, and 30
are in different state of assessment.
This opinion concerns only one country, Poland. The Commission requested
this opinion as essential input into its Decision concerning the treatment of
SRM that will be requested from Poland. It is recommended that this opinion on
Poland is read in the light of the GBR of the SSC of July 2000.
The SSC is concerned that the available information was not confirmed by
inspection missions as they are performed by the FVO in the Member States. It
recommends that BSE-related aspects are included in the program of future
inspection missions, as far as feasible.
THE ANALYSIS
Poland was exposed to a very low challenge between 1980-86, a very high
external challenge between 1987-90 and an extremely high external challenge
since 1991, mainly due to massive imports of MBM from BSE affected countries (in
the range of 1,700,000 tonnes in total, mainly from DE: around 1,000,000 tonnes
in total). High imports of cattle are also recorded for the period since
1988.
The BSE/cattle system of Poland was and is very unstable since 1980.
Feeding MBM to cattle was legally possible until March 1997 and is likely to
have occurred, even if it was uncommon practice. The efficiency of the feed-ban
cannot be assessed, as feed controls were apparently not carried out. Rendering
is and was common practice in Poland. Material includes ruminant material,
including SRM, condemned material, and a limited proportion of fallen stock. The
rendering processes used were adequate for reducing BSE-infectivity since a long
time.
There is no SRM ban. Cross contamination is most probable (no specified
feed lines, no controls described). BSE is notifiable since 1997 and
surveillance was nearly non existent until 1997. Since 1977, passive
surveillance does not fulfil OIE requirements. Active surveillance has started
in 2001.
It is concluded that it is likely but not confirmed that one or several
cattle that are (pre-clinically or clinically) infected with the BSE agent are
currently present in the domestic herd of Poland (GBR III).
Given the very unstable system and the fact that the BSE-agent is likely to
be already present in the country, it is assumed that the GBR is
increasing.
A summary of the reasons for the current assessment is given in annex 1 to
this opinion.
Likely present since 1987 and growing.
B. OIE LIST B DISEASES
International
Bovine Spongiform Encephalopathy
BSE in Poland, May 2002 -- A nine year old cow tested positive for BSE in
the village of Mochnaczka near Poland’s southern border with Slovakia. Poland
began routine testing for BSE in October 2001. Over 100,000 cattle have been
tested under this program and this is the first case detected in Poland. Three
other cows which had been kept together with the positive cow were tested and
found negative.
Source: CEI Impact Worksheet, OIE, Agworldwide, AGAM
Bovine Spongiform Encephalopathy, Poland
Impact Worksheet, May 7, 2002
[ Impact Worksheets | CEI Home ]
Summary:
The first case of bovine spongiform encephalopathy (BSE) in Poland was
confirmed on May 2, 2002. The affected nine-year old cow tested BSE positive at
a slaughterhouse located in the village of Mochnaczka Wyzna, province of Little
Poland (Malopolskie) near Poland’s southern border with Slovakia. Poland began
routine testing for BSE of all slaughtered cattle over 24 months of age in
October 2001. In January 2002, testing was changed to all slaughtered cattle
over the age of 30 months.
In December 1997, APHIS prohibited the importation of live ruminants and
most ruminant products from all of Europe including Poland. In December 2000,
import restrictions regarding BSE were expanded to prohibit all imports of
rendered animal protein products, regardless of species, from Europe. Between
1998 and 2001, the US imported non-species specific animal products used in
animal feeds and non-species specific sausage and offal products. Given US
restrictions on ruminant product imports, these US imports should not have
contained ruminant material.
Poland’s stocks of cattle and sheep were less than 1 percent of world
stocks in 2001. Poland is the world’s 5th largest exporter of live cattle
exporting nearly 600,000 animals in 2000. Cattle exports go primarily to
European countries although Israel imported significant numbers of Polish cattle
in 2000 and 2001.
______________________________________________________________________________
How extensive is the outbreak of BSE in Poland?
The first case of bovine spongiform encephalopathy (BSE) in Poland was
confirmed on May 2, 2002. The affected nine-year old cow tested BSE positive at
a slaughterhouse located in the village of Mochnaczka Wyzna, province of Little
Poland (Malopolskie), near Poland’s southern border with Slovakia. Poland began
routine BSE testing of all slaughtered cattle over the age of 24 months in
October 2001. In January 2002, testing was changed to all slaughtered cattle
over the age of 30 months. The affected cow was the first positive test result
in over 100,000 cattle tested. Police and veterinary services are investigating
the source of the disease.
Sources: OIE; Promed (ABC news); USDA, Foreign Agricultural Service GAIN
Reports #PL1037 (October 11, 2001) and #PL2004 (February 1, 2002)
What actions has Poland taken to protect its livestock from BSE?
The Polish Veterinary Service banned imports of cattle from BSE countries
in December 2000. A ban on imports of meat and bone meal was enacted in January
2001.
Source: USDA, Foreign Agricultural Service GAIN Report #PL1037, October 11,
2001
What is Poland’s production and trade in affected animals and animal
products?
Poland's stocks of cattle and sheep were less than 1 percent of world
stocks in 2001 (Table 1). Cattle imports totaled nearly 7,000 animals in 2000
while sheep imports were less than 200 head. Cattle imports were from European
countries. Poland is the 5th largest exporter of live cattle in the world,
exporting nearly 600,000 animals in 2000 (6 percent of world trade). Polish
farmers produce young fattening cattle for export as a side enterprise of their
dairy herds. Cattle exports were sent primarily to Italy (over 50 percent of the
total), the Netherlands, Germany, Spain, Greece, Croatia, Bosnia-Herzegovina,
and Slovenia. Israel received over 50,000 cattle from Poland in 2000. In
addition to cattle, Poland exported over 200,000 sheep in 2000. The destination
of these sheep exports was not available.
Table 1. Poland’s live animal stocks and exports and imports of live
animals.
Live Animal 2001 Stocks Trade
2000 Exports 2000 Imports
Head % World Head % World Head % World
Cattle 5,723,000 <1 1.3="" 161="" 212="" 337="" 593="" 6.2="" 6="" div="" sheep1="">
Poland’s production of beef/veal and mutton/lamb in 2001 was small on a
worldwide scale representing less than 1 percent of total world production
(Table 2). Beef production within Poland has been decreasing since 1998. Polish
consumers have been reducing their beef consumption due to BSE fears and
switching to poultry. Poland’s imports and exports of beef/veal and mutton/lamb
were also small representing less than 1 percent of world imports and exports.
Table 2. Production and trade in relevant products by Poland.
Products 2001 Production Trade
2000 Exports 2000 Imports
Metric Ton % World Metric Ton % World Metric Ton % World
Beef and Veal 300,000 <1 162="" 1="" 24="" 96="" 9="" and="" div="" lamb1="" mutton="">
1 Sheep were included in Table 1 and Table 2 as ‘affected’ because
USDA/APHIS includes all ruminants and ruminant products in its restrictions
pertaining to BSE. Goat production and trade information was unavailable.
Source: United Nations FAO; USDA, Foreign Agricultural Service GAIN Reports
#PL1022 (July 30, 2001) and #PL2004 (February 1, 2002)
What are the U.S. imports of affected animals or animal products from
Poland?
The US imported no live ruminant animals or ruminant meat from Poland
during 1998 to 2001. During the past four years (1998 - 2001), US imports from
Poland included non-species specific animal products used in animal feeds and
non-species specific sausage and offal products (Table 3). Given US restrictions
on ruminant product imports, these US imports should not have contained ruminant
material.
Mexico imported non-species specific preparations used in animal feed (HS
code 23099099) from Poland during 1998 to 2001. Canada did not import any items
of risk from Poland during 1998 to 2001.
Table 3. Relevant US imports from Poland in 1998, 1999, 2000, and
2001
HS Code Description Unit 1998 1999 2000 2001
Feed - non species specific Total 6,684 0 0 0
0511993000 Products Used as Food, For Animals KG 6,684 0 0 0
Meat & offal- non species specific Total 92,945 27,274 44,102
78,332
0504000040 Gut/Bladder/Stomach of Animals For Sausage Casing, Not Hog or
Fish KG 0 0 420 280
1601006060 Sausage/Similar Prdct Meat Etc NESOI Food Prep Cnd KG 81,413
25,872 0 0
1602204000 Animal Livers Except Goose, Prepared or Preserved KG 11,532
1,402 43,682 78,052
Source: World Trade Atlas
Did the US have restrictions on ruminant imports from Poland prior to this
case?
In December 1997, APHIS prohibited the importation of live ruminants and
most ruminant products from all of Europe including Poland until a thorough
assessment of the risks of introduction of BSE into the US could be made. Prior
to December 1997, import restrictions were applied only to those countries which
had reported cases of BSE in native animals. Also, importation of ruminant meat
from BSE-affected countries was permitted if the meat was deboned and free of
visually identifiable lymphatic and nervous tissue and if it met other
restrictions. Import regulations enacted December 1997 extended the import
restrictions to countries which had not had a declared BSE case, yet had risk
factors for BSE occurrence.
These regulatory changes also removed provisions that allowed importation
of ruminant meat from the restricted countries, and thereby prohibited
importation of ruminant meat from all Europe. These import restrictions also
applied to bone meal, blood meal, meat meal, offal, fat, glands, and serum from
ruminants. In December 2000, APHIS expanded its import restrictions regarding
BSE to prohibit all imports from Europe of rendered animal protein products,
regardless of species.
Source: USDA, APHIS, VS
What is the level of passenger traffic arriving in the United States from
Poland?
A total of 188,946 passengers arrived at US airports on direct flights from
Poland in fiscal year 2000. An undetermined number of passengers arrived in the
US from Poland via indirect flights.
Under APHIS-PPQ’s agricultural quarantine inspection monitoring, 451 air
passengers from Poland were sampled for items of agricultural interest in fiscal
year 2000. Thirteen (13) of these passengers, or 2.9 percent, carried a total of
26.2 kg of meat items that could potentially harbor the pathogen(s) that cause
BSE. None of these passengers from whom meat items were confiscated reported
plans to visit or work on a ranch or farm during their visit to the US.
Source: US Department of Transportation, and APHIS-PPQ Agricultural
Quarantine Inspection data base
CEI’s plans for follow up:
CEI has no plans to provide additional information on this situation.
If you need more information or wish to comment, you may contact Judy
Akkina at (970) 490-7852 or Carol Tuszynski at (970) 490-7893.
What measures has USDA-APHIS taken to prevent the introduction of BSE? To
prevent BSE from entering the United States, APHIS has restricted the
importation of live ruminants and certain ruminant products from countries where
BSE is known to exist.
In 1989, APHIS banned the importation of all ruminants and restricted the
importation of certain cattle products from the United Kingdom and other
countries where BSE was diagnosed.
On December 6, 1991, APHIS restricted the importation of ruminant meat and
edible products and banned most byproducts of ruminant origin from countries
known to have BSE (56 Federal Register [FR] 63868 and 63869). Prior to this, the
products were prohibited by not issuing permits.
Certain products cannot be imported into the United States, except under
special permit for scientific, educational or research purposes, or under
special conditions to be used in cosmetics. These products include serum,
glands, collagen, etc.
As of December 12, 1997, APHIS has prohibited the importation of live
ruminants and most ruminant products from all of Europe. The restrictions
applied to Albania, Austria, Bosnia-Herzegovina, Bulgaria, Croatia, Czech
Republic, Denmark, Federal Republic of Yugoslavia, Finland, Germany, Greece,
Hungary, Italy, the former Yugoslavian republic of Macedonia, Norway, Poland,
Romania, Slovak Republic, Slovenia, Spain, and Sweden. These actions were in
addition to those already in place regarding countries that had reported BSE in
native cattle.
This action was taken in 1997 because the Netherlands, Belgium, and
Luxembourg have reported their first cases of BSE in native-born cattle. There
is evidence that European countries may have had high BSE risk factors for
several years and less-than-adequate surveillance.
An interim rule was published and the comment period closed on March 9,
1998. Criteria to assess the risk factors were developed in accordance with the
standards adopted by the Office of International Epizootics (OIE).
TECHNICAL REPORT
Annual report of the Scientific Network on BSE-TSE 20131 European Food
Safety Authority2, 3 European Food Safety Authority (EFSA), Parma, Italy
snip...
Case study on the typing of a potential BSE-like isolate from a goat in
Poland
The representative from Poland described the scientific, technical and
procedural aspects for the typing of TSE isolates from small ruminants. Firstly,
the description of the bases for BSE and Scrapie strain-differentiation where
presented with detail. This included not only the laboratory methods used but
also an indication of the criteria that is applied for the characterisation of
TSE isolates in animals. Secondly, available results of the typing of a
potential BSE-like isolate from a goat in Poland were shown with detail. The
EURL-TSE Strain Typing Expert Group (STEG) has preliminary classified the strain
as not BSE, but BSE could not be fully excluded. Inoculation studies employing
bioassay are ongoing in order to gain further information on the characteristics
of this strain.
*** The EURL-TSE Strain Typing Expert Group (STEG) has preliminary
classified the strain as not BSE, but BSE could not be fully excluded.
I am not sure exactly what the hell that means...TSS
Subject: A Surprisingly High Number of the Plaque-Like VV sCJD Subtype
Among the Polish sCJD-is There a Connection with BASE?
PPo4-15: A Surprisingly High Number of the Plaque-Like VV sCJD Subtype
Among the Polish sCJD—is There a Connection with BASE?
Beata Sikorska and Pawel P. Liberski Department of Molecular Pathology and
Neuropathology; Medical University of Lodz; Lodz,
Poland Recently described bovine amyloidotic spongiform encephalopathy
(BASE) or L type BSE—was is overrepresented in Poland (15% of all cases of BSE).
Moreover, the number of BASE cases in Poland per million bovines is the highest
in Europe. A potential human risk from BASE is evident from experimental
transmission to “humanized” transgenic animals and primates. Taking into
consideration that non-human primate inoculated with BASE had a shorter
incubation period than monkeys infected with classical BSE, and that humanized
Tg mice have been found to be highly susceptible to infection with atypical form
of BSE, it seems probable that BASE may be more pathogenic for humans than BSE,
but the transmitted disease may differ from BSE-derived vCJD. Among 47 cases
which have been diagnosed as definite in our laboratory, in 19 cases complete
histopathological examination and codon 129 status were available. On the basis
of the histological pattern and codon 129 status the cases of sCJD were divided
into subtypes according to the Parchi&Gambetti classification. The results
are as follows: type 1 (MMorMV)- 42%, type 2 (VV)-32%, type 3 (MV)-10.5%, type
4c (MM)- 10.5% and type 5 (VV)-5 %. Although the number of cases is too low to
conclude a significantly different distribution of sCJD subtypes in Polish
population those data show surprisingly high number of the plaque-like VV sCJD
subtype. Interestingly, it was shown before that Tg mice inoculated with BASE
showed granular and plaque-like aggregates or PrPSc in brains resembling those
observed in VV2 subtype of sCJD.
PPo2-26: Transmission of Classical and Atypical (L-type) Bovine Spongiform
Encephalopathy (BSE) Prions to Cynomolgus macaques
Fumiko Ono,1 Yoshio Yamakawa,2 Minoru Tobiume,3 Yuko Sato,3 Harutaka
Katano,3 Kenichi Hagiwara,2 Iori Itagaki,1 Akio Hiyaoka,1 Katuhiko Komatuzaki,1
Yasunori Emoto,1 Hiroaki Shibata,4 Yuichi Murayama,5 Keiji Terao,4 Yasuhiro
Yasutomi4 and Tetsutaro Sata3 1The Corporation for Production and Research of
Laboratory Primates; Tsukuba City, Japan; 2Departments of Cell Biology and
Biochemistry; and 3Pathology; National Institute of Infectious Diseases; Tokyo,
Japan; 4Tsukuba Primate Research Center; National Institute of Biomedical
Innovation; Tsukuba City, Japan; 5Prion Disease Research Team; National
Institute of Animal Health; Tsukuba City, Japan
Key words: L-type BSE, cBSE, cynomolgus macaques, transmission
BSE prion derived from classical BSE (cBSE) or L-type BSE was characterized
by inoculation into the brain of cynomolgus macaques. The neurologic
manifestation was developed in all cynomolgus macaques at 27–43 months after
intracerebral inoculation of brain homogenate from cBSE-affected cattle (BSE
JP/6). Second transmission of cBSE from macaque to macaque shortened incubation
period to 13–18 months. cBSE-affected macaques showed the similar clinical signs
including hyperekplexia, tremor and paralysis in both primary and second
transmission. Two macaques were intracerebrally inoculated brain homogenate from
the L-type BSE-affected cattle (BSE JP/24). The incubation periods were 19–20
months in primary transmission. The clinical course of the L-type BSE-affected
macaques differed from that in cBSE-affected macaques in the points of severe
myoclonus without hyperekplexia. The glycoform profile of PrPSc detected in
macaque CNS was consistent with original pattern of either cBSE or L-typeBSE
PrPSc, respectively. Although severe spongiform change in the brain was
remarkable in all BSE-affected macaques, severe spongiform spread widely in
cerebral cortex in L-type BSE-affected macaques. Heavy accumulation of PrPSc
surrounded by vacuola formed florid plaques in cerebral cortex of cBSE-affected
macaques. Deposit of PrPSc in L-type BSE-affected macaque was weak and diffuse
synaptic pattern in cerebrum, but large PrPSc plaques were evident at
cerebellum. MRI analysis, T2, T1, DW and flair sequences, at the time of autopsy
revealed that brain atrophy and dilatation of cerebral ventricles were
significantly severe in L-type BSE-affected macaques. These results suggest that
L-type BSE is more virulent strain to primates comparing to cBSE.
SP1-4: Evidence from Molecular Strain Typing
Gianluigi Zanusso Department of Neurological and Visual Sciences; Section
of Clinical Neurology; University of Verona; Verona, Italy
Key words: molecular analysis, strain typing, atypical BSE, CJD
In 2001, active surveillance for bovine spongiform encephalopathy (BSE) led
to the discovery of atypical BSE phenotypes in aged cattle distinct from
classical BSE (C-type). These atypical BSE cases had been classified as low
L-type (BASE) or high H-type BSE based on the molecular mass and the degree of
glycosylation of of the pathological prion protein (PrPSc). Transmission studies
in TgBov mice showed that H-type BSE, C-type BSE and BASE behave as distinct
prion strains with different incubation periods, PrPSc molecular patterns and
pathological phenotypes. A still unclear issue concerns the potential
transmissibility and phenotypes of atypical BSEs in humans. We previously
indicated that BASE was similar to a distinct subgroup of sporadic form of
Creutzfeldt-Jakob disease (sCJD) MV2, based on molecular similarities and on
neuropathological pattern of PrP deposition. To investigate a possible link
between BASE and sCJD, Kong et al. and Comoy et al. experimentally inoculated
TgHu mice (129MM) and a non-human primate respectively, showing in both models
that BASE was more virulent compare to BSE. Further, non-human primate
reproduced a clinical phenotype resembling to that of sCJD subtype MM2. Here, we
presented a comparative analysis of the biochemical fingerprints of PrPSc
between the different sCJD subtypes and animal TSEs and after experimental
transmission to animals.
Opinion of the Scientific Steering Committee on the GEOGRAPHICAL RISK OF
BOVINE SPONGIFORM ENCEPHALOPATHY (GBR) in POLAND Adopted on 30/03/2001 It is
concluded that it is likely but not confirmed that one or several cattle that
are (pre-clinically or clinically) infected with the BSE agent are currently
present in the domestic herd of Poland (GBR III).
Number of reported cases of bovine spongiform encephalopathy (BSE) in
farmed cattle worldwide*(excluding the United Kingdom) Country/Year
89 90 91 92 93 94 95 96 97 98 99 00 01 02 03 04 05 06 07 08 09 10
Poland
0 0 0 0 0 0 0 0 0 0 0 0 0 4f 5 11 19 10 9 5 4
Annual incidence rate* of bovine spongiform encephalopathy (BSE) in OIE
Member Countries that have reported cases, excluding the United Kingdom
Bovine Spongiform Encephalopathy, Poland Impact Worksheet, May 7, 2002 What
is the level of passenger traffic arriving in the United States from Poland? A
total of 188,946 passengers arrived at US airports on direct flights from Poland
in fiscal year 2000. An undetermined number of passengers arrived in the US from
Poland via indirect flights. Under APHIS-PPQ’s agricultural quarantine
inspection monitoring, 451 air passengers from Poland were sampled for items of
agricultural interest in fiscal year 2000. Thirteen (13) of these passengers, or
2.9 percent, carried a total of 26.2 kg of meat items that could potentially
harbor the pathogen(s) that cause BSE. None of these passengers from whom meat
items were confiscated reported plans to visit or work on a ranch or farm during
their visit to the US. Source: US Department of Transportation, and APHIS-PPQ
Agricultural Quarantine Inspection data base
Diagnosis of the first cases of scrapie in Poland
Miroslaw P. Polaka, , , Magdalena Larskaa, Jan P.M. Langeveldb, Anne
Buschmannc, Martin H. Groschupc, Jan F. Zmudzinskia
.doi:10.1016/j.tvjl.2009.07.032Get rights and content
Abstract
This is the first report of cases of scrapie in Poland. The disease was an
atypical phenotype, diagnosed in two aged sheep which were found dead. Brainstem
samples from both animals were positive on the applied ELISA rapid test, while
the confirmatory immunoblot indicated abnormal banding patterns of protease
resistant prion protein (PrPres). The genotypes of these sheep were ALRQ/ALHQ
and ALRQ/ALRR. The absence of premonitory clinical signs, the advanced age of
the affected sheep, the higher concentration of PrPres in the cerebellum
relative to the obex, the unusual banding profile of the prion protein and its
relatively low resistance to proteolytic degradation confirmed the diagnosis of
atypical scrapie (Nor98-like) in both cases.
Keywords Sheep; Atypical scrapie; Nor98; Western blot; Molecular typing
Corresponding author. Tel.: +48 81889 3316; fax: +48 81886 2595. Copyright
© 2009 Elsevier Ltd. All rights reserved.
Wednesday, November 13, 2013
Atypical Scrapie Prions from Sheep and Lack of Disease in Transgenic Mice
Overexpressing Human Prion Protein
Thursday, July 31, 2014
EFSA Scrapie reduction unlikely without effective breeding programme
http://efsaopinionbseanimalprotein.blogspot.com/2014/07/efsa-scrapie-reduction-unlikely-without.html
Sunday, July 27, 2008
Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection
Act of 2002; Toxin List Docket Type Rulemaking APHIS-2007-0033-0001
Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection
Act of 2002; Biennial Review and Republication of the Select Agent and Toxin
List Docket Type Rulemaking Document APHIS-2007-0033-0001 Document Title
Agricultural Bioterrorism Protection Act of 2002; Biennial Review and
Republication of the Select Agent and Toxin List Public Submission
APHIS-2007-0033-0002.1 Public Submission Title Attachment to Singeltary
comment
Comment DOCKET APHIS-2007-0033 Agricultural Bioterrorism Protection Act of
2002; Biennial Review and Republication of the Select Agent and Toxin List
August, 29, 2007
Greetings APHIS,
I would kindly like to submit the following to ;
DEPARTMENT OF AGRICULTURE Animal and Plant Health Inspection Service
7 CFR Part 331 9 CFR Part 121
Docket No. APHIS-2007-0033 RIN 0579-AC53
This is my second submission to APHIS about Bioterrorism and the
Transmissible Spongiform Encephalopathy TSE agent. My first submission was Mon,
27 Jan 2003 15:54:57 -0600 Docket No: 02-088-1 RE-Agricultural Bioterrorism
Protection Act of 2002 (see my old submission at bottom dated Subject: Docket
No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; Date: Mon, 27
Jan 2003 15:54:57 -0600 From: "Terry S. Singeltary Sr." To:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000328/!x-usc:mailto:regulations@aphis.usda.gov
).
WHAT I am most concerned about is that ONLY BSE is listed as a dangerous
toxin in the family of TSE. With the ever growing list of atypical TSE like
atypical BSE BASE, and the atypical Scrapie Nor-98, and also the typical scrapie
strains, and Chronic Wasting Disease CWD, why is it only BSE is listed ?
I think that all of these TSE's should be listed with the BSE agent as a
potential Biological weapon. With these atypical TSE, even more so, due to the
fact the possibility of vertical and lateral transmission, unlike BSE (not
documented to date to transmit that way). With the atypical BSE BASE being more
virulent to humans than the typical BSE, why is it not listed ?
WHY is the atypical Scrapie Nor-98, with this being a potential threat to
not only animals, but humans as well, why is this not listed ?
WHY is Chronic Wasting Disease CWD of deer and elk not listed, especially
since CWD has transmitted to the bovine by inoculation to date, with oral
studies still ongoing, and the fact the oral route would take much longer, would
CWD wreck havoc on a countries economy too, let alone the very real potential
for CWD to transmit to humans, why is CWD not listed as a Bio-toxin ?
IF these terrorist are willing to walk into a mall and blow themselves up
as a walking bomb, what is to keep them from exposing themselves to one of these
deadly TSEs, and then going to a hospital and exposing many with CJD somehow.
This may seem far fetched, but very possible. Why is CJD not listed ?
IN short, and very simple, all you would have to do is change the BSE, to
human and animal TSE, thus all bases would be covered. but in only including the
BSE strain of TSE agent, I think you are only fooling yourselves, again.
...
SOURCES
snip....
more on non-species coding system and TSEs and potential 'suitcase
bombs';
To: Bovine Spongiform Encephalopathy Subject: Re: POLAND FINDS 4TH MAD COW
CASE/USA IMPORTS FROM POLAND/non-species coding system strikes again References:
<[log in to unmask]> Content-Type: text/plain; charset=ISO-8859-1;
format=flowed Content-Transfer-Encoding: 8bit X-Virus-Scanner: Found to be
clean
Greetings again List Members,
let me kick a madcow around here a bit.
on the imports from Poland and the infamous USA 'non-species' coding
system.
the USDA/APHIS states;
During the past four years (1998 - 2001), US imports from Poland included
non-species specific animal products used in animal feeds and non-species
specific sausage and offal products (Table 3). Given US restrictions on ruminant
product imports, these US imports should not have contained ruminant
material.
NOW, if you read Polands GBR risk assessment and opinion on BSE, especially
_cross-contamination_, it states;
ANNEX 1
Poland - Summary of the GBR-Assessment, February 2001
EXTERNAL CHALLENGE STABILITY INTERACTION OF EXTERNAL CHALLENGE AND
STABILITY
The very high to extremely high external challenge met a very unstable
system and could have led to contamination of domestic cattle in Poland from
1987 onwards.
This internal challenge again met the still very unstable system and
increased over time.
The continuing very high external challenge supported this
development.
Not OK MBM-ban since 1997, but no feed controls. Reasonably OK Heat
treatment equivalent to 133°C / 20min / 3 bar standards, but no evidence
provided on compliance.
Not OK. No SRM-ban, SRM are rendered and included in cattle feed.
BSE surveillance:
Not sufficient before 2001.
Cross-contamination:
Lines for ruminant and non-ruminant feed in feed-mills only separated in
time and no analytical controls carried out. Likely present since 1987 and
growing.
see full text and ANNEX 1 at;
so in my humble opinion, the statement by the USDA/APHIS that ''these US
imports _should_ not have contained ruminant materials, is a joke. a sad joke
indeed.
* POLAND BSE GBR RISK ASSESSMENT
snip...
PLEASE NOTICE THAT SPORADIC CJD IN POLAND TRIPLED FROM THE YEAR 2008 TO
2009, FROM 10 TO 30 CASES. AS with sporadic CJD in the USA drastically
increasing over the years. ...TSS
BSE Cases Identified in the United States
There have been 4 cases of BSE identified in the United States. The
following information provides descriptions of these four cases:
2012 - California collapsed On April 24, 2012, the USDA confirmed a BSE
case in a dairy cow in California. This cow was tested as part of the USDA
targeted BSE surveillance at rendering facilities in the United States. The cow
was 10 years and 7 months old and was classified as having the L-type BSE
strain.
For more information, see the USDA/APHIS notice, the SDA/APHIS Final
Report[PDF – 179 KB] and the FDA Final Feed Investigation Summary.
2006 - Alabama collapsed On March 15, 2006, the USDA announced the
confirmation of BSE in a cow in Alabama. The case was identified in a
non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a
local veterinarian and buried on the farm. The age of the cow was estimated by
examination of the dentition as 10 years old.
It had no ear tags or distinctive marks; the herd of origin could not be
identified despite an intense investigation (see Alabama BSE Investigation,
Final Epidemiology Report, May 2006[PDF - 105KB]).
In August 2008, several ARS investigators reported that a rare, genetic
abnormality that may persist within the cattle population "is considered to have
caused" BSE in this atypical (H-type) BSE animal from Alabama. (See
Identification of a Heritable Polymorphism in Bovine PRNP Associated with
Genetic Transmissible Spongiform Encephalopathy: Evidence of Heritable BSE. Also
see BSE Case Associated with Prion Protein Gene Mutation.)
2005 - Texas collapsed On June 24, 2005, the USDA announced receipt of
final results from The Veterinary Laboratories Agency in Weybridge, England,
confirming BSE in a cow that had conflicting test results in 2004. This cow was
from Texas, died at approximately 12 years of age, and represented the first
endemic case of BSE in the United States. (see Texas BSE Investigation, Final
Epidemiology Report, August 2005[PDF - 82KB]) 2003 - Washington State collapsed
On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a
presumptive diagnosis of the first known case of BSE in the United States. It
was in an adult Holstein cow from Washington State. This diagnosis was confirmed
by an international reference laboratory in Weybridge, England, on December 25.
Trace-back based on an ear-tag identification number and subsequent genetic
testing confirmed that the BSE-infected cow was imported into the United States
from Canada in August 2001.
Because the animal was non-ambulatory (a "downer cow") at slaughter, brain
tissue samples were taken by USDA’s Animal and Plant Health Inspection Service
as part of its targeted surveillance for BSE. However the animal’s condition was
attributed to complications from calving. After the animal was examined by a
USDA Food Safety and Inspection Service (FSIS) veterinary medical officer both
before and after slaughter, the carcass was released for use as food for human
consumption. During slaughter, the tissues considered to be at high risk for the
transmission of the BSE agent were removed.
On December 24, 2003, FSIS recalled beef from cattle slaughtered in the
same plant on the same day as the BSE positive cow. (see Bovine Spongiform
Encephalopathy in a Dairy Cow—Washington State, 2003(http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5253a2.htm).)
Preliminary Investigation Suggests BSE-Infected Cow in Washington State Was
Likely Imported from Canada
On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a
presumptive diagnosis of bovine spongiform encephalopathy (BSE, or "mad cow"
disease) in an adult Holstein cow from Washington State. Samples were taken from
the cow on December 9 as part of USDA's BSE surveillance program. The BSE
diagnosis was made on December 22 and 23 by histopathology and
immunohistochemical testing at the National Veterinary Services Laboratory,
Ames, Iowa. The diagnosis was confirmed by an international reference laboratory
in Weybridge, England, on December 25. Preliminary trace-back based on an
ear-tag identification number suggests that the BSE-infected cow was imported
into the United States from Canada in August 2001.
USDA, in close cooperation with Canadian agricultural authorities, has
launched an epidemiologic investigation to determine the source of the disease.
Beef from the slaughtered cow had been processed for human consumption. On
December 23, 2003, the Food Safety and Inspection Service (FSIS), USDA announced
the recall of all beef from cattle slaughtered on December 9 at the involved
slaughter plant.
Strong evidence indicates that BSE has been transmitted to humans primarily
in the United Kingdom, causing a variant form of Creutzfeldt-Jakob disease
(vCJD)(http://www.cdc.gov/prions/vcjd/about.html).
In the United Kingdom, where over 1 million cattle may have been infected with
BSE, a substantial species barrier appears to protect humans from widespread
illness. As of December 1, 2003, a total of 153 vCJD cases had been reported
worldwide; of these, 143 cases had occurred in the United Kingdom. The risk to
human health from BSE in the United States is extremely low.
CDC monitors the trends and current incidence of CJD in the United States
by analyzing death certificate information from U.S. multiple cause-of-death
data compiled by the National Center for Health Statistics. With the support of
the Council of State and Territorial Epidemiologists, CDC conducts follow-up
review of clinical and neuropathology records of CJD decedents younger than 55
years of age. In addition, during 1996-1997, in collaboration with the American
Association of Neuropathologists (AANP), CDC established the National Prion
Disease Pathology Surveillance Center at Case Western Reserve University in
Cleveland, Ohio. This pathology center provides free, state-of-the-art
diagnostic services to U.S. physicians. It also helps to monitor the possible
occurrence of emerging forms of prion diseases, such as vCJD, in the United
States. For more information about the center visit its website at:
USDA About BSE FDA Bovine Spongiform Encephalopathy CDC Prion Diseases(http://www.cdc.gov/prions/index.html)
NIH NINDS Creutzfeldt-Jakob Disease Information Page For more information about
BSE in the United States, see the Animal and Plant Health Inspection Service,
USDA BSE site.
Related Links Prion Diseases(http://www.cdc.gov/prions/index.html)
Chronic Wasting Disease (CWD)(http://www.cdc.gov/prions/cwd/index.html)
Creutzfeldt-Jakob Disease (CJD)(http://www.cdc.gov/prions/cjd/index.html)
Variant Creutzfeldt-Jakob Disease (vCJD)(http://www.cdc.gov/prions/vcjd/index.html)
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file Zip Archive file SAS file ePub file RIS file Page last reviewed: February
10, 2015 Page last updated: February 10, 2015 Content source: Centers for
Disease Control and Prevention National Center for Emerging and Zoonotic
Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and
Pathology (DHCPP)
Saturday, July 23, 2016
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING,
AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016 ***
SPONTANEOUS TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW
TYPE DISEASE ???
*** We describe the transmission of spongiform encephalopathy in a
non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie.
Because of this extended incubation period in a facility in which other prion
diseases are under study, we are obliged to consider two alternative
possibilities that might explain its occurrence. We first considered the
possibility of a sporadic origin (like CJD in humans). Such an event is
extremely improbable because the inoculated animal was 14 years old when the
clinical signs appeared, i.e. about 40% through the expected natural lifetime of
this species, compared to a peak age incidence of 60–65 years in human sporadic
CJD, or about 80% through their expected lifetimes.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
>>> Moreover, sporadic disease has never been observed in breeding
colonies or primate research laboratories, most notably among hundreds of
animals over several decades of study at the National Institutes of Health25,
and in nearly twenty older animals continuously housed in our own facility.
<<<
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.
Maximizing profits is all that is going on now, thanks to the OIE BSE MRR
policy, the legal trading of all strains of TSE prion disease globally. ...Terry
S. Singeltary Sr.
atypical BSE spontaneous sporadic ???
Saturday, May 26, 2012
Are USDA assurances on mad cow case 'gross oversimplification'?
SNIP...
*** 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.”
*** “We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an
official with the USDA during the Clinton Administration now at Mississippi
State.
*** In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows
the origins of atypical cases of BSE,” she said
*** The argument about feed is critical because if feed is the cause, not a
spontaneous mutation, the California cow could be part of a larger outbreak.
SNIP...
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND
SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
O.08: H-type bovine spongiform encephalopathy associated with E211K prion
protein polymorphism: Clinical and pathologic features in wild-type and E211K
cattle following intracranial inoculation
S Jo Moore, M Heather West Greenlee, Jodi Smith, Eric Nicholson, Cathy
Vrentas, and Justin Greenlee
United States Department of Agriculture; Ames, IA USA
In 2006 an H-type bovine spongiform encephalopathy (BSE) case was reported
in an animal with an unusual polymorphism (E211K) in the prion protein gene.
Although the prevalence of this polymorphism is low, cattle carrying the K211
allele are predisposed to rapid onset of H-type BSE when exposed. The purpose of
this study was to investigate the phenotype of this BSE strain in wild-type
(E211E) and E211K heterozygous cattle.
One calf carrying the wild-type allele and one E211K calf were inoculated
intracranially with H-type BSE brain homogenate from the US 2006 case that also
carried one K211 allelle. In addition, one wild-type calf and one E211K calf
were inoculated intracranially with brain homogenate from a US 2003 classical
BSE case. All animals succumbed to clinical disease. Survival times for E211K
H-type BSE inoculated catttle (10 and 18 months) were shorter than the classical
BSE inoculated cattle (both 26 months). Significant changes in retinal function
were observed in H-type BSE challenged cattle only. Animals challenged with the
same inoculum showed similar severity and neuroanatomical distribution of
vacuolation and disease-associated prion protein deposition in the brain, though
differences in neuropathology were observed between E211K H-type BSE and
classical BSE inoculated animals. Western blot results for brain tissue from
challenged animals were consistent with the inoculum strains.
This study demonstrates that the phenotype of E211K H-type BSE remains
stable when transmitted to cattle without the E211K polymorphism, and exhibits a
number of features that differ from classical BSE in both wild-type and E211K
cattle.
===================
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi
Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, our findings suggest that possible transmission risk of H-type
BSE to sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
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
END...TSS
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
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.
Monday, March 19, 2012
Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform
Encephalopathy PLoS One. 2012; 7(2): e31449.
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform
Encephalopathy Prion Strain
▿ Qingzhong Kong1,*, Mengjie Zheng1, Cristina Casalone2, Liuting Qing1,
Shenghai Huang1,†, Bikram Chakraborty1, Ping Wang1, Fusong Chen1, Ignazio Cali1,
Cristiano Corona2, Francesca Martucci2, Barbara Iulini2, Pierluigi Acutis2, Lan
Wang1, Jingjing Liang1, Meiling Wang1, Xinyi Li1, Salvatore Monaco3, Gianluigi
Zanusso3, Wen-Quan Zou1, Maria Caramelli2 and Pierluigi Gambetti1,* + Author
Affiliations
1Department of Pathology, Case Western Reserve University, Cleveland, Ohio
44106 2CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy
3Department of Neurological and Visual Sciences, University of Verona, 37134
Verona, Italy Next Section ABSTRACT Bovine spongiform encephalopathy (BSE), the
prion disease in cattle, was widely believed to be caused by only one strain,
BSE-C. BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob
disease in humans. Two atypical BSE strains, bovine amyloidotic spongiform
encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in
several countries since 2004; their transmissibility and phenotypes in humans
are unknown. We investigated the infectivity and human phenotype of BASE strains
by inoculating transgenic (Tg) mice expressing the human prion protein with
brain homogenates from two BASE strain-infected cattle. Sixty percent of the
inoculated Tg mice became infected after 20 to 22 months of incubation, a
transmission rate higher than those reported for BSE-C. A quarter of BASE
strain-infected Tg mice, but none of the Tg mice infected with prions causing a
sporadic human prion disease, showed the presence of pathogenic prion protein
isoforms in the spleen, indicating that the BASE prion is intrinsically
lymphotropic. The pathological prion protein isoforms in BASE strain-infected
humanized Tg mouse brains are different from those from the original cattle BASE
or sporadic human prion disease. Minimal brain spongiosis and long incubation
times are observed for the BASE strain-infected Tg mice. These results suggest
that in humans, the BASE strain is a more virulent BSE strain and likely
lymphotropic.
Overwhelming evidence indicates that bovine spongiform encephalopathy
(BSE), a prion disease that has been detected in several hundred thousand cattle
in the United Kingdom and many other countries since the 1980s, has been
transmitted to humans through the consumption of prion-contaminated beef,
causing a prion disease named variant Creutzfeldt-Jakob disease (vCJD) (5, 19,
24). Over 200 cases of vCJD have been reported around the world (19). In 2004,
two types of bovine prion disease that differ from the original BSE, now named
classical BSE (BSE-C), were reported (3, 8). The two atypical BSE types were
associated with prion protein (PrP) scrapie isoforms (PrPSc) that after protease
digestion, displayed distinct electrophoretic mobility or ratios of the PrPSc
glycoforms different from those of BSE-C (3, 8). Currently, a total of at least
36 cases of these two atypical BSE types have been reported for cattle older
than 8 years (5; M. Caramelli, unpublished data). The two atypical BSE types are
identified as BSE-H and bovine amyloidotic spongiform encephalopathy (BASE, also
named BSE-L); the “L” and “H” identify the higher and lower electrophoretic
positions, respectively, of their protease-resistant PrPSc isoforms (7). The
bovine phenotype and the PrPSc molecular features of BASE have previously been
described in detail (8). The histopathology of BASE and the PrP immunostaining
pattern of BASE strains are characterized by the presence of prion amyloid
plaques and a more rostral distribution of the PrPSc, which at variance with
BSE-C is present in the cerebral cortex, including the hippocampus, but is
underrepresented in the brain stem (8). These phenotypic features and PrPSc
characteristics resemble a subtype of sporadic Creutzfeldt-Jakob disease (sCJD)
named sCJDMV2, which affects subjects who are methionine (M)/valine (V)
heterozygous at codon 129 of the PrP gene, and it is associated with PrPSc
identified as type 2 (15). This similarity has raised the question of whether
sCJDMV2 is not sporadic but acquired from the consumption of BASE
strain-contaminated meat (5, 8). To begin to investigate the transmissibility to
humans and the “human” disease phenotype of BASE, including the involvement of
the lymphoreticular system, we have inoculated brain homogenates from
BASE-affected cattle to transgenic (Tg) mice expressing normal human PrP with
Met at codon 129 (HuPrP-129M) in a mouse PrP-ablated background [Tg(HuPrP)]
(13). The inoculated Tg mice were examined for attack rates and the disease
phenotype, including the presence and characteristics of protease-resistant
PrPSc in the brain and spleen and the histopathology, along with the PrPSc
topography and pattern of deposition in the brain.
snip...
Two distinct histopathological and PrP immunohistochemical phenotypes have
been reported following BSE-C inoculation: one reproduced the distinctive
features of vCJD with the “florid” plaques that intensely immunostained for PrP,
and the other was reminiscent of sCJDMM1, with prominent spongiform degeneration
and no plaque PrP immunostaining (1, 23). The brain histopathology, the PrPSc
distribution, and the PrP immunostaining pattern of BASE strain-inoculated Tg40
mice were definitely distinct from such features described above (1, 23),
further supporting the notion that BASE and classical BSE are associated with
two distinct prion strains (8).
The relatively easy transmission of BASE to humanized Tg mice indicates
that effective cattle prion surveillance should be maintained until the extent
and origin of this and other atypical forms of BSE are fully understood.
"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 they did before 2005
suspect," Brown said.
Analysis: What that mad cow means
By STEVE MITCHELL, UPI Senior Medical Correspondent | March 15, 2006 at
6:27 PM
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick
to assure the public earlier this week that the third case of mad cow disease
did not pose a risk to them, but what federal officials have not acknowledged is
that this latest case indicates the deadly disease has been circulating in U.S.
herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is thought
that cows usually contract the disease from contaminated feed they consume as
calves. The concern is that humans can contract a fatal, incurable,
brain-wasting illness from consuming beef products contaminated with the mad cow
pathogen.
"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 they did before 2005
suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as
bovine spongiform encephalopathy, or BSE, did not significantly threaten human
or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk
either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers
should be troubled by the USDA's secrecy and its apparent plan to dramatically
cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the
USDA's surveillance program and the failure of the USDA to reveal really
important details," Halloran told UPI. "Consumers have to be really concerned if
they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it
has proposed, even in light of a third case, scaling back the program to 40,000
tests annually.
"They seem to be, in terms of actions and policies, taking a lot more
seriously the concerns of the cattle industry than the concerns of consumers,"
Halloran said. "It's really hard to know what it takes to get this
administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow
tissue into cattle feed (which is thought to spread the disease) and removal of
the most infectious parts of cows, such as the brain and spinal cord, protect
consumers. But the agency glosses over the fact that both of these systems have
been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has
been criticized by the Government Accountability Office in two reports, the most
recent coming just last year. The GAO said the FDA's enforcement of the ban
continues to have weaknesses that "undermine the nation's firewall against
BSE."
USDA documents released last year showed more than 1,000 violations of the
regulations requiring the removal of brains and spinal cords in at least 35
states, Puerto Rico and the Virgin Islands, with some plants being cited
repeatedly for infractions. In addition, a violation of similar regulations that
apply to beef exported to Japan is the reason why Japan closed its borders to
U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system.
The USDA insists the prevalence of mad cow disease is low, but the agency has
provided few details of its surveillance program, making it difficult for
outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without
having a breakdown of the tested population by age and risk status," Elizabeth
Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern,
Switzerland, a company that provides advice on reducing mad cow risk to industry
and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be
able to go away a little bit for (the USDA) if they would just publish a
breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's
surveillance plan via the Freedom of Information Act in May 2004 but nearly two
years later has not received any corresponding documents from the agency,
despite a federal law requiring agencies to comply within 30 days. This leaves
open the question of whether the USDA is withholding the information, does not
have the information or is so haphazardly organized that it cannot locate
it.
Mumford said the prevalence of the disease in U.S. herds is probably quite
low, but there have probably been other cases that have so far gone undetected.
"They're only finding a very small fraction of that low prevalence," she
said.
Mumford expressed surprise at the lack of concern about the deadly disease
from American consumers. "I would expect the U.S. public to be more concerned,"
she said.
Markus Moser, a molecular biologist and chief executive officer of
Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is
that if people are infected, the mad cow pathogen could become "humanized" or
more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical
procedures" and even through the blood supply, Moser said.
"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 they did before 2005
suspect," Brown said.
Emerg Infect Dis. 2006 Dec; 12(12): 1816–1821. doi: 10.3201/eid1212.060965
PMCID: PMC3291375
On the Question of Sporadic or Atypical Bovine Spongiform Encephalopathy
and Creutzfeldt-Jakob Disease
Paul Brown,corresponding author* Lisa M. McShane,† Gianluigi Zanusso,‡ and
Linda Detwiler§
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."
........TSS
48 hr BSE confirmation turnaround took 7+ months to confirm this case, so
the BSE MRR policy could be put into place. ...TSS
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov,
contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at
OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully
request a full inquiry into the cover-up of TSEs in the United States of America
over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff,
Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to:
Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding
further analysis of BSE Inconclusive Test Results
posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days
later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary
for Marketing and Regulatory Programs resigns. Three days later same mad cow
found in November turns out to be positive. Both resignation are unexpected.
just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004. ...TSS OR, what the Honorable Phyllis Fong
of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform
Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and
Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat
Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
FDA STATEMENT FOR IMMEDIATE RELEASE May 4, 2004 Media Inquiries:
301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30th, the Food and Drug Administration learned that a cow
with central nervous system symptoms had been killed and shipped to a processor
for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the animal
came from, and the processor that initially received the cow from the
slaughterhouse.
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That material is
being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as "mad
cow disease," can exhibit such symptoms. In this case, there is no way now to
test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit
the feeding of its rendered protein to other ruminant animals (e.g., cows,
goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing
the firm that FDA will not object to use of this material in swine feed only. If
it is not used in swine feed, this material will be destroyed. Pigs have been
shown not to be susceptible to BSE. If the firm agrees to use the material for
swine feed only, FDA will track the material all the way through the supply
chain from the processor to the farm to ensure that the feed is properly
monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the U.K.
showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action specifying
that the material go only into swine feed means also that it will not be fed to
poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely
with the U.S. Department of Agriculture on all BSE issues. The animal feed rule
provides crucial protection against the spread of BSE, but it is only one of
several such firewalls. FDA will soon be improving the animal feed rule, to make
this strong system even stronger.
#
SEE FULL TEXT OF ALL THIS HERE ;
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
ALABAMA MAD COW CASE
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
(see COPIOUS AMOUNTS OF mad cow feed in COMMERCE IN ALABAMA...TSS)
Texas BSE Investigation Final Epidemiology Report August 2005
State-Federal Team Responds to Texas BSE Case
JUNE 30, 2005
(please note 7+ month delay in final confirmation so the BSE MRR policy
could be set in stone first. $$$...tss)
SEE ATTEMPTED COVER-UP BEFORE THE END AROUND BY FONG ET AL OF THE O.I.G
The U.S. Department of Agriculture confirmed June 29 that genetic testing
had verified bovine spongiform encephalopathy (mad cow disease) in a 12-year-old
cow that was born and raised in a Texas beef cattle herd.
Subsequent epidemiological investigations resulted in the culling and
testing of 67 adult animals from the index herd. Bio-Rad tests for BSE were
conducted on all 67 animals by the National Veterinary Services Laboratory
(NVSL) in Ames, Iowa. All tests were negative.
On July 12, Texas officials lifted the quarantine on the source herd. At
press time, USDA's Animal and Plant Health Inspection Service was tracing
animals of the same age that had left the ranch.
Timeline
The BSE-positive animal was a Brahman-cross cow born and raised in a single
Texas herd. The location of the ranch was not disclosed.
On Nov. 11, 2004, the 12-year-old cow was taken to a Texas auction market.
Because of its condition, the cow was sent to Champion Pet Foods in Waco, Texas.
The company produces several blends of dog food, primarily for the greyhound
industry.
On Nov. 15, the animal arrived dead at Champion. Under procedures
established by USDA's intensive surveillance program, a sample was sent to the
USDA-approved Texas Veterinary Medical Diagnostic Testing Laboratory (TVMDL) at
Texas A&M University.
Between June 1, 2004, and June 1, 2005, TVMDL tested nearly 34,000 samples
from Texas, New Mexico, Arkansas and Louisiana. They tested the sample from
Champion on Nov. 19 using a Bio-Rad ELISA rapid test for BSE. Initial results
were inconclusive.
Because of the inconclusive results, a representative from USDA took the
entire carcass to TVMDL where it was incinerated. USDA's Animal and Plant Health
Inspection Service (APHIS) began tracing the animal and herd.
The sample was then sent to the National Veterinary Services Laboratory for
further testing. Two Immunohistochemistry (IHC) tests were conducted and both
were negative for BSE. At that point APHIS stopped their trace.
USDA scientists also ran an additional, experimental IHC "rapid" tissue
fixation test for academic purposes. This test has not been approved
internationally.
Some abnormalities were noted in the experimental test, but because the two
approved tests came back negative, the results were not reported beyond the
laboratory.
Monitoring by OIG
USDA's Office of Inspector General (OIG) has been monitoring implementation
of the BSE expanded surveillance program and evaluating the following:
* Effectiveness of the surveillance program;
* Performance of BSE laboratories in complying with policies and procedures
for conducting tests and reporting results;
* Enforcement of the ban on specified risk materials in meat products;
* Controls to prevent central nervous system tissue in advanced meat
recovery products;
* Ante mortem condemnation procedures; and
* Procedures for obtaining brain tissue samples from condemned cattle.
While reviewing voluminous records, OIG auditors noticed conflicting test
results on one sample-rapid inconclusive, IHC negative, experimental reactive.
Sample retested
At the recommendation of the Inspector General, the sample was retested
during the week of June 5 with a second confirmatory test, the Western Blot. The
results were reactive.
USDA scientists then conducted an additional IHC confirmatory test, using
different antibodies from the November 2004 test. On Friday, June 10, Secretary
of Agriculture Mike Johanns publicly announced the results as a "weak positive."
On June 16 an official with USDA's National Veterinary Services Laboratory
hand-carried samples for further testing to the Veterinary Laboratory Agency
(VLA) in Weybridge, England. Since 1991, the VLA has been a BSE reference
laboratory for the World Organization for Animal Health (OIE).
Experts from the Weybridge lab confirmed the accuracy of the results of
USDA's November confirmatory IHC test, concurring that the case could not have
been confirmed on the basis of this sample. They also examined the November
experimental IHC test and interpreted the results to be positive.
Weybridge also conducted additional tests, including IHC, OIE-prescribed
Western Blot, NaTTA Western Blot and Prionics Western Blot tests.
To better understand the conflicting results, USDA also conducted Bio-Rad
and IDEXX rapid screening tests, IHC and OIE-prescribed Western Blot. USDA also
used DNA sequencing to determine the prion protein gene sequence of the animal.
Texas even had a 'secret' test that showed that mad cow positive;
experimental IHC test results, because the test was not a validated procedure,
and because the two approved IHC tests came back negative, the results were not
considered to be of regulatory significance and therefore were not reported
beyond the laboratory. . A Western blot test conducted the week of June 5, 2005,
returned positive for BSE.
48 hr BSE confirmation turnaround took 7+ months to confirm this case, so
the BSE MRR policy could be put into place. ...TSS
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at
OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully
request a full inquiry into the cover-up of TSEs in the United States of America
over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff,
Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to:
Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding
further analysis of BSE Inconclusive Test Results
posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days
later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary
for Marketing and Regulatory Programs resigns. Three days later same mad cow
found in November turns out to be positive. Both resignation are unexpected.
just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004. ...TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 -0600
From: "Terry S. Singeltary Sr."
To: Carla EverettReferences: [log in to unmask]; [log in to unmask] ;
Greetings Carla, still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up for
something, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...
can you confirm??? terry
============================================================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."References;[log in to unmask];
The USDA has made a statement, and we are referring all callers to the USDA
web site. We have no information about the animal being in Texas.
Carla
At 09:44 AM 11/19/2004, you wrote:
Greetings Carla,
i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from
TEXAS. can you comment on this either way please?
thank you,
Terry S. Singeltary Sr
======================================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."References: <[log in to unmask]><[log
in to unmask] us><[log in to unmask]> <[log in to unmask]us>
<[log in to unmask]>
our computer department was working on a place holder we could post USDA's
announcement of any results. There are no results to be announced tonight by
NVSL, so we are back in a waiting mode and will post the USDA announcement when
we hear something.
At 06:05 PM 11/22/2004,
you wrote:
why was the announcement on your TAHC site removed?
Bovine Spongiform Encephalopathy:
November 22: Press Release title here
star image More BSE information
terry
Carla Everett wrote:
no confirmation on the U.S.'inconclusive test...
no confirmation on location of animal. ;
FROM HERE, IT TOOK 7 MONTHS TO CONFIRM THIS MAD COW, while the BSE MRR
policy was being bought and sold...(in my opinion...tss)
Texas has been covering up mad cow disease for decades. on the second
attempt at covering up a second mad cow in Texas, myself and others wrote to the
Honorable Phyllis Fong of the OIG and asked for a second test be done in
Weybridge, this after I wrote ever scientist around the globe. finally, this 2nd
attempt at covering up mad cow disease in Texas failed, the Texas BSE madcow was
finally confirmed, 7 months after a supposedly 48 hour turnaround on testing per
their own BSE RED BOOK. this is why I have absolutely no faith in what’s going
on now in Texas. it’s just another dog pony show imo...
BSE RED BOOK
Saturday, August 16, 2008
Qualitative Analysis of BSE Risk Factors in the United States February 13,
2000 at 3:37 pm PST (BSE red book)
Statement of Gov. Rick Perry on BSE Announcement
Thursday, June 30, 2005 • Press Release
AUSTIN – Gov. Rick Perry issued the following statement today on the
announcement by the U.S. Department of Agriculture that a cow recently tested
for Bovine Spongiform Encephalopathy – commonly known as mad cow disease – is
from a Texas herd.
“I want to urge calm and reassure the public that they can have the highest
confidence in our beef supply, and the safeguards we have in place to protect
the public from the spread of BSE. There is not, nor has there ever been, a
known instance of BSE contaminating the food supply in Texas or anywhere else in
the United States.
The animal in question was not processed into food or any other product.
Texans can be sure that the beef they buy at their local supermarkets or
restaurants is as safe today as it was yesterday, and I encourage Texans to
continue to enjoy Texas beef products.”
Section 2. Testing Protocols and Quality Assurance Controls
In November 2004, USDA announced that its rapid screening test, Bio-Rad
Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test
result as part of its enhanced BSE surveillance program. The ELISA rapid
screening test performed at a BSE contract laboratory produced three high
positive reactive results.40 As required,41 the contract laboratory forwarded
the inconclusive sample to the APHIS National Veterinary Services Laboratories
(NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again
produced three high positive reactive results.42 In accordance with its
established protocol, NVSL ran its confirmatory test, an immunohistochemistry
(IHC) test, which was interpreted as negative for BSE. In addition, NVSL
performed a histological43 examination of the tissue and did not detect
lesions44 consistent with BSE.
Faced with conflicting results, NVSL scientists recommended additional
testing to resolve the discrepancy but APHIS headquarters officials concluded no
further testing was necessary because testing protocols were followed. In our
discussions with APHIS officials, they justified their decision not to do
additional testing because the IHC is internationally recognized as the "gold
standard." Also, they believed that conducting additional tests would undermine
confidence in USDA’s established testing protocols.
USDA orders silence on mad cow in Texas
Susan Combs by no means has public and consumer health at heart while she
is protecting the cattle industry. She is oblivious to mad cow disease. Her soul
purpose is to protect the cattle industry at all cost, including my mothers life
(DOD 12/14/97), or maybe one of your family members from any strain of mad cow
disease in TEXAS. SHE helped cover-up mad cow disease in TEXAS both on that
inconclusive that was positive so many times it will make your head spin. PLUS,
the other mad cow in TEXAS they rendered without testing at all, that came from
the top out of Austin. THEY should be tried for murder. corporate homicide is
what i call it. they knew for years, but kept on keeping on.
Faced with conflicting results between the rapid screening and IHC tests,
NVSL scientists recommended additional testing to resolve the discrepancy but
APHIS headquarters officials concluded that no further testing was necessary
since testing protocols were followed and the confirmatory test was negative. In
our discussions with APHIS officials, they justified their decision to not do
additional testing because the IHC test is internationally recognized as the
“gold standard” of testing. Also, they believed that
USDA/OIG-A/50601-10-KC/ Page iv
conducting additional tests would undermine confidence in USDA’s testing
protocols.
OIG obtained evidence that indicated additional testing was prudent. We
came to this conclusion because the rapid screening tests produced six high
positive reactive results, the IHC tests conflicted, and various standard
operating procedures were not followed. Also, our review of the relevant
scientific literature, other countries’ protocols, and discussions with experts
led us to conclude that additional confirmatory testing should be considered in
the event of conflicting test results.
To maintain objectivity and independence, we requested that USDA’s
Agricultural Research Service (ARS) perform the Office International des
Epizooties (OIE) Scrapie-Associated Fibrils (SAF) immunoblot test. The
additional testing produced positive results. To confirm, the Secretary of
Agriculture requested that an internationally recognized BSE laboratory in
Weybridge, England (Weybridge) perform additional testing. Weybridge conducted
various tests, including their own IHC tests and three Western blot tests. The
tests confirmed that the cow was infected with BSE. The Secretary immediately
directed USDA scientists to work with international experts to develop new
protocols that include performing dual confirmatory tests in the event of an
inconclusive BSE screening test.
We attribute the failure to identify the BSE positive sample to rigid
protocols, as well as the lack of adequate quality assurance controls over its
testing program. Details of our concerns are discussed in Findings 3 and 4.
Texas BSE Investigation Final Epidemiology Report August 2005
Executive Summary
In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample
from November 2004, that had originally been classified as negative on the
immunohistochemistry test, was confirmed positive on SAF immunoblot (Western
blot). The U.S. Department of Agriculture (USDA) identified the herd of origin
for the index cow in Texas; that identification was confirmed by DNA analysis.
USDA, in close cooperation with the Texas Animal Health Commission (TAHC),
established an incident command post (ICP) and began response activities
according to USDA’s BSE Response Plan of September 2004. Response personnel
removed at-risk cattle and cattle of interest (COI) from the index herd,
euthanized them, and tested them for BSE; all were negative. USDA and the State
extensively traced all at-risk cattle and COI that left the index herd. The
majority of these animals entered rendering and/or slaughter channels well
before the investigation began. USDA’s response to the Texas finding was
thorough and effective.
Background of the Investigation
On June 10, 2005, USDA announced that the November 2004 inconclusive BSE
sample tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s
National Animal Disease Center (NADC) upon the recommendation of USDA’s Office
of the Inspector General. Samples were sent to a World Organization for Animal
Health (OIE) reference laboratory for BSE in Weybridge, England, for
confirmatory tests. Farm A, located in Texas, was the suspected farm of origin
for the index cow and was placed under hold order on June 20, 2005 pending
confirmation of the positive results and DNA analysis of the herd. Weybridge
confirmed the BSE positive on June 24, 2005. The carcass of the index cow had
been disposed of by incineration in November 2004.
News Release
Texas Animal Health Commission
Box l2966 * Austin, Texas 78711 * (800) 550-8242 * FAX (512) 719-0719
Bob Hillman, DVM * Executive Director
For info, contact Carla Everett, information officer, at 1-800-550-8242,
ext. 710, or
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:mailto:ceverett@tahc.state.tx.us
For immediate release---
State-Federal Team Responds to Texas BSE Case
The US Department of Agriculture announced June 29 that genetic testing has
verified that an aged cow that tested positive for Bovine Spongiform
Encephalopathy or BSE originated from a Texas beef cattle herd. Tissues for
laboratory testing were initially collected from the animal in November 2004,
and the carcass was incinerated and did not enter the human food, animal feed or
fertilizer supply system. While tests in November indicated the animal did not
have BSE, retesting in England in June confirmed the animal had the disease. The
Texas Animal Health Commission (TAHC), the state’s livestock and poultry health
regulatory agency, and USDA have jointly assigned a state-federal team to
conduct the epidemiological investigation and response.
“The TAHC and US Department of Agriculture’s Veterinary Services are
working with a complement of experts from federal and state animal health, food
safety, public health and feed regulatory agencies to ensure the continued
safety and wholesomeness of our meat supply,” said Dr. Bob Hillman, Texas state
veterinarian and executive director of the TAHC, the state’s livestock and
poultry health regulatory agency. “Epidemiological investigations are thorough
and focus on verifying the herd of origin, and when, where and how the animal
and potentially, any herd mates, were exposed to the abnormal prion, or disease
agent, that causes BSE. Additionally, epidemiology investigations trace the
infected animal’s movement and herd mates. Animals potentially exposed to the
disease will be depopulated, with proper disposal. The animals will not be
introduced into the human or animal food chain.”
The USDA’s BSE testing protocol requires testing of emaciated or injured
cattle, cattle that exhibit central nervous system disorder, cattle unable to
rise or to walk normally, and cattle that die of unknown causes. Since June 1,
2004, brain tissue samples from more than 394,000 cattle have been tested in the
U.S. and were negative for BSE. Of those, 38,320 were tested in Texas, Dr.
Hillman noted. BSE surveillance has been conducted in the U.S. since l990.
The U.S. has taken preventive measures against the introduction of BSE
since l989, when prohibitions were placed on cattle and other ruminants from
BSE-affected countries, noted Dr. Hillman. In 1997, the importation ban was
extended to all of Europe.
Dr. Hillman said the U.S. Food and Drug Administration (FDA) in 1997 banned
the use of ruminant-derived protein (from animals such as cattle and sheep) in
feed for cattle and other ruminants. There is no evidence that BSE spreads from
live animal to animal in the herd, but cattle can be exposed by eating feed that
contains rendered protein from infected animals. “These measures taken by the
USDA and the FDA are safeguards that work to protect livestock, and ultimately,
our meat supply,” he said.
--30--
Second BSE case occurred in Texas, USDA says Jun 30, 2005 (CIDRAP News) –
The United States' second case of bovine spongiform encephalopathy (BSE) was in
a 12-year-old cow that came from a Texas herd and would have been made into pet
food if it hadn't been flagged for BSE testing, federal officials announced
yesterday evening.
US Department of Agriculture (USDA) officials said the cow was to be
processed at a pet food plant in Waco, Tex., when it was diverted for testing
because it couldn't walk. Officials didn't name the plant or say exactly where
the cow came from. But an Associated Press (AP) report today identified the
plant as Champion Pet Food in Waco and said the cow was already dead when
brought there last November.
"The source herd is now under a hold order as we identify animals of
interest within the herd," USDA Chief Veterinarian John Clifford said in a
prepared statement. Investigators will look for cattle born within a year before
or after the BSE-infected cow and any of the cow's offspring born within the
past 2 years, he explained.
"If the age of the animal cannot be pinpointed, then we may expand our
inquiry to include all animals in this herd before the feed ban went into place
in 1997," Clifford said. To prevent BSE, the government banned putting cattle
protein into cattle feed in August 1997.
The infected cow was incinerated, and no parts were used in human food or
animal feed, according to the USDA. "The safety of our food supply is not in
question," Clifford stated.
Because of the cow's age, the USDA suspects it became infected by eating
contaminated feed before the government ban began in 1997. The USDA and the Food
and Drug Administration (FDA) will try to trace the source herd's feed history,
officials said.
The FDA will also check whether firms that may have processed meat-and-bone
meal from animals from that herd have complied with the 1997 feed ban, Dr. Steve
Sundlof, director of the FDA's Center for Veterinary Medicine, said at a news
conference last night.
The Texas case is the first US BSE case in a native-born animal; Clifford
said the cow lived on one farm all its life. The previous US case, found in
December 2003, involved a Canadian-born dairy cow in Washington state.
An initial screening test on the Texas cow last November was inconclusive,
and two confirmatory immunohistochemistry tests were negative. But early this
month the USDA's inspector general ordered a Western blot test, which came back
positive. Further confirmatory tests at an international reference lab in
Britain were also positive, prompting the USDA to announce the findings last
week.
The USDA waited for the results of DNA tests before announcing that the
infected cow came from Texas. The step was necessary because parts of the
infected cow were stored with those of four other cattle, causing some
uncertainty, officials said.
"We felt that we had the correct herd; we wanted to identify that
appropriately with DNA," Clifford said at the news conference. Investigators
analyzed DNA from the infected animal and then looked for relatives in the
presumed source herd by analyzing DNA from members of the herd, he said. The
investigation turned up two cattle that are related to the infected cow, he
added.
The AP report said Champion Pet Food is under contract to take samples from
animals in poor health. The company's owner, Benjy Bauer, told the AP that his
workers took samples from the cow and sent them to the Texas Veterinary
Diagnostic Laboratory at Texas A&M University. The lab is one of several the
USDA uses to screen cattle for BSE, the story said.
See also:
USDA news release
USDA fact sheet on BSE epidemiologic investiation
USDA press conference transcript
TEXAS OFFICIALS DEAD WRONG ON AMOUNT OF INFECTIVITY TO CAUSE A TSE PRION
DISEASE ;
"FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams – approximately a quarter ounce — of prohibited
material. These animals weigh approximately 600 pounds."
5.5 GRAMS OF INFECTIOUS PROHIBITED MAD COW FEED FOR EACH OF THE 1,222
ANIMALS (5.5 GRAMS X 1,222 ANIMALS) IS ENOUGH INFECTIOUS MAD COW FEED TO KILL A
SMALL HERD OF COWS...TSS
U.S. Food and Drug Administration FDA News | Today the Food and Drug
Administ…U.S. Food and Drug Administration FDA News
Today the Food and Drug Administration announced the results of tests taken
on feed used at a Texas feedlot that was suspected of containing meat and bone
meal from other domestic cattle — a violation of FDA’s 1997 prohibition on using
ruminant material in feed for other ruminants. Results indicate that a very low
level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams – approximately a quarter ounce — of prohibited
material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin
(therefore not likely to contain infected material because there is no evidence
of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated.
According to Dr. Bernard Schwetz, FDA’s Acting Principal Deputy
Commissioner, “The challenge to regulators and industry is to keep this disease
out of the United States. One important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined with
other steps, like U.S. Department of Agriculture’s (USDA) ban on the importation
of live ruminant animals from affected countries, these steps represent a series
of protections, to keep American cattle free of BSE.”
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing
that it is voluntarily purchasing all 1,222 of the animals held in Texas and
mistakenly fed the animal feed containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA believes any
cattle that did not consume feed containing the prohibited material are
unaffected by this incident, and should be handled in the beef supply clearance
process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting
the human error that resulted in the misformulation of the animal feed
supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food supply and that continued vigilance
needs to be taken, by all concerned, to ensure these rules are followed
routinely.
FDA will continue working with USDA as well as State and local officials to
ensure that companies and individuals comply with all laws and regulations
designed to protect the U.S. food supply.
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242
Consumer Inquiries: 888-INFO-FDA
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken
on feed used at a Texas feedlot that was suspected of containing meat and bone
meal from other domestic cattle -- a violation of FDA's 1997 prohibition on
using ruminant material in feed for other ruminants. Results indicate that a
very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams - approximately a quarter ounce -- of prohibited
material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin
(therefore not likely to contain infected material because there is no evidence
of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy
Commissioner, "The challenge to regulators and industry is to keep this disease
out of the United States. One important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined with
other steps, like U.S. Department of Agriculture's (USDA) ban on the importation
of live ruminant animals from affected countries, these steps represent a series
of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing
that it is voluntarily purchasing all 1,222 of the animals held in Texas and
mistakenly fed the animal feed containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA believes any
cattle that did not consume feed containing the prohibited material are
unaffected by this incident, and should be handled in the beef supply clearance
process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting
the human error that resulted in the misformulation of the animal feed
supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food supply and that continued vigilance
needs to be taken, by all concerned, to ensure these rules are followed
routinely.
FDA will continue working with USDA as well as State and local officials to
ensure that companies and individuals comply with all laws and regulations
designed to protect the U.S. food supply.
Friday, April 15, 2016
Whole Blood Gene Expression Profiling in Preclinical and Clinical Cattle
Infected with Atypical Bovine Spongiform Encephalopathy
Saturday, April 16, 2016
*** APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on
Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
***
Thursday, January 29, 2015
Atypical H-TYPE BSE Case Confirmed in Norway
Tuesday, April 12, 2016
The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging
reindeer from the Nordfjella population in South-Norway.
Tuesday, June 14, 2016
*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag
Norway ***
Thursday, July 07, 2016
Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd
Norwegian moose
14/06/2016 - Norway reports a third case
Sunday, July 17, 2016
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Sunday, July 24, 2016
Chronic Wasting Disease Prions in Elk Antler Velvet and Marketing of this
Product in Nutritional Supplements for Humans?
Research Project: TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: THE ROLE OF
GENETICS, STRAIN VARIATION, AND ENVIRONMENTAL CONTAMINATION IN DISEASE CONTROL
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Saturday, July 16, 2016
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Tuesday, June 07, 2016
Comparison of two US sheep scrapie isolates supports identification as
separate strains
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations 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.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
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.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
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. ***
see page 176 of 201 pages...tss
SEE THE DRASTIC REDUCTION OF CONFIRMED BSE CASES IN THE UK ONCE THE FEED
BAN TOOK HOLD FROM THE TOP YEAR DOWN TO THE FIRST ZERO YEAR ;
1992 36680 SLAUGHTERED SUSPECTS IN WHICH BSE CONFIRMED
2013 0 0 0 0 0 0 0 0
Saturday, January 31, 2015
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
In the USA, USDA et al sometimes serves SRM’s up as appetizers or
horderves.
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
Wednesday, March 2, 2016
RANCHO He did not know that they were placing healthy cow heads next to
suspect carcasses BSE TSE Prion
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials BSE TSE Prion
Thursday, June 12, 2014
Missouri Firm Recalls Ribeye and Carcass Products That May Contain
Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal
root ganglia may not have been completely removed
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
USDA BSE TSE PRION SURVEILLANCE, FEED, TESTING, SRM FIREWALLS...LMAO!
THE USDA FDA TRIPLE MAD COW DISEASE FIREWALL, WERE NOTHING MORE THAN INK ON
PAPER !
infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et
al TRIPLE MAD COW FIREWALL, 10 YEARS AFTER ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 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
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL,
TN, AND WV
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
______________________________
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
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA,
MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST
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 MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN
COMMERCE 27,694,240 lbs
Date: August 6, 2006 at 6:14 pm PST
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall #
V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J.
Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm
initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated
with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI
END OF ENFORCEMENT REPORT FOR AUGUST 2, 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
###
Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? Date:
August 6, 2006 at 6:19 pm PST
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm 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
?????
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
CJD WATCH MESSAGE BOARD TSS
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
###
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006
Date: June 27, 2006 at 7:42 am PST
Public Health Service
Food and Drug Administration
New Orleans District 297 Plus Park Blvd. Nashville, TN 37217
Telephone: 615-781-5380 Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO. 2006-NOL-06
FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State
Street Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration
(FDA) investigator inspected your rendering plant, located at 509 Fortson
Street, Shreveport, Louisiana. The inspection revealed significant deviations
from the requirements set forth in Title 21, Code of Federal Regulations, Part
589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This
regulation is intended to prevent the establishment and amplification of Bovine
Spongiform Encephalopathy (BSE). You failed to follow the requirements of this
regulation; products being manufactured and distributed by your facility are
misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the
Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found you failed to provide measures, including
sufficient written procedures, to prevent commingling or cross-contamination and
to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent
carryover of protein derived from mammalian tissues into animal protein or feeds
which may be used for ruminants. For example, your facility uses the same
equipment to process mammalian and poultry tissues. However, you use only hot
water to clean the cookers between processing tissues from each species. You do
not clean the auger, hammer mill, grinder, and spouts after processing mammalian
tissues.
You failed to maintain written procedures specifying the clean-out
procedures or other means to prevent carryover of protein derived from mammalian
tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived
from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR
589.2000(e)(1)(i), any products containing or may contain protein derived from
mammalian tissues must be labeled, "Do not feed to cattle or other ruminants."
Since you failed to label a product which may contain protein derived from
mammalian tissues with the required cautionary statement. the poultry meal is
misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your
facility. As a manufacturer of materials intended for animal feed use, you are
responsible for ensuring your overall operation and the products you manufacture
and distribute are in compliance with the law. You should take prompt action to
correct these violations, and you should establish a system whereby violations
do not recur. Failure to promptly correct these violations may result in
regulatory action, such as seizure and/or injunction, without further
notice.
You should notify this office in writing within 15 working days of
receiving this letter, outlining the specific steps you have taken to bring your
firm into compliance with the law. Your response should include an explanation
of each step taken to correct the violations and prevent their recurrence. If
corrective action cannot be completed within 15 working days, state the reason
for the delay and the date by which the corrections will be completed. Include
copies of any available documentation demonstrating corrections have been
made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S.
Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie,
Louisiana 70001. If you have questions regarding any issue in this letter,
please contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez Acting District Director New Orleans District
SINCE THE LAST TIME I REPORTED :
Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through
September 30, 2005
Date: March 20, 2006 at 12:58 pm PST
YOU can see that report at the bottom of this update.
UPDATEs AS FOLLOWS ;
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT July 1, 2006 through September 30, 2006
snip...
Table 5. Administrative Actions: Large HACCP Plants (7/01/06 to
9/30/06)
Administrative Actions Pending or Taken at Large HACCP Plants [includes
actions initiated in prior quarters]
CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS
On 6/15/06, a withholding action concerning labels for Advanced Meat
Recovery System product was taken in accordance with 9 CFR Part 500.8.
snip...
EXCEL CORP 00086R M FORT MORGAN, CO
On 8/11/04, a withholding action concerning labels for Advanced Meat
Recovery System product was taken in accordance with 9 CFR Part 500.8. On
12/22/04, plant appealed the withholding action. Appeal was denied on
1/25/05.
snip...
TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action
concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. 00245L M LEXINGTON, NE X On 3/10/05, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
Table 6. Administrative Actions: Small HACCP Plants (7/01/06 to
9/30/06)
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
SSOP HACCP SPS INH INT Other LOI LOW
BOOKER PACKING COMPANY 07162 M BOOKER, TX 6/2/06 6/5/06 X 9/19/06 The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
SSOP HACCP SPS INH INT Other LOI LOW
GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X
8/31/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
HI COUNTRY BEEF JERKY 01248 M01248 P LINCOLN, MT 3/24/06 4/14/06 X 8/31/06
The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X
8/15/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
GIBSON PACKING COMPANY 05843 M05843 P SEYMOUR, MO 9/21/06 X Plant failed to
meet regulatory requirements for Escherichia coli Biotype 1 (E. coli). The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
SSOP HACCP SPS INH INT Other LOI LOW
HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X
9/26/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06
4/14/06 6/30/06 7/5/06 X 8/11/06 On 3/16/06, an enforcement action concerning
failure to meet regulatory requirements for Escherichia coli Biotype 1 (E.coli)
was issued. The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X
7/25/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT April 1, 2006 through June 30, 2006
Table 5. Administrative Actions: Large HACCP Plants (4/01/06 to
6/30/06)
CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X On 6/15/06, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X On 8/11/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8. On
12/22/04, plant appealed the withholding action. Appeal was denied on
1/25/05.
snip...
TYSON FRESH MEATS INC 00245L M LEXINGTON, NE X On 3/10/05, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
SSOP HACCP SPS INH INT Other LOI LOW
TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action
concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
BOOKER PACKING COMPANY 07162 M BOOKER, TX 4/13/06 4/19/06 X Plant failed to
meet regulatory requirements for Escherichia coli Biotype 1 (E. coli).
6/2/06 6/5/06 X The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
???
3/24/06 4/14/06
X
The enforcement action included, as basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X
The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
C & C MEAT SALES, INC., 18494 M18494 P, DURHAM, NC ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL.
snip...
FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X 4/13/06 The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
FRONTIER FOODS & COLD STORAGE, INC 20741 M20741 P EL PASO, TX 5/31/06 X
On 6/8/06, DM closed case by firm’s requested voluntary withdrawal. The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05
10/24/05 X 5/19/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06
4/14/06 6/30/06 X On 3/16/06, an enforcement action concerning failure to meet
regulatory requirements for Escherichia coli Biotype 1 (E.coli) was issued. The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
SAVORY CONNECTION, INC., 31764 M31764 P, SELINGSGROVE, PA. ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL.
snip...
STEAK MASTER, 21159 M21159 P, ELWOOD, NE. ... FAILURE TO COMPLY CONCERNING
SRM MATERIAL.
snip...
THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X 4/4/06 The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X
The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05
X 5/4/06 The enforcement action included, as basis, failure of the establishment
to comply with Agency requirements concerning specified risk material.
snip...
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT January 1, 2006 through March 31, 2006
Table 5. Administrative Actions: Large HACCP Plants (1/01/06 to
3/31/06)
CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X 3/13/06 On 10/11/05, a
withholding action concerning labels for Advanced Meat Recovery System product
was taken in accordance with 9 CFR Part 500.8.
snip...
EXCEL CORP. 00086R M FORT MORGAN, CO 8/11/04 2/22/05 X On 8/11/04, a
withholding action concerning labels for Advanced Meat Recovery System product
was taken in accordance with 9 CFR Part 500.8.
On 12/22/04, plant appealed the withholding action. Appeal was denied on
1/25/05.
snip...
TYSON FRESH MEATS INC. 00245L M 3/12/04 3/18/04 X
LEXINGTON, NE
X On 3/10/05, a withholding action concerning labels for Advanced Meat
Recovery System product was taken in accordance with 9 CFR Part 500.8.
snip...
TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action
concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
GULF PACKING COMPANY, 00696 M00696 P, SAN BENITO, TX, ... FAILURE TO COMPLY
CONCERNING SRM MATERIAL
snip...
HI COUNTRY BEEF JERKY, 01248 M01248 P, LINCOLN, MT, ... FAILURE TO COMPLY
CONCERNING SRM MATERIAL
snip...
HITCHIN POST STEAK COMPANY, 20773 M20773 P, KANSAS CITY, KS, ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL
snip...
NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The
enforcement action included, as basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
ROCK CREEK SLAUGHTER CO., 09150 M09150 P, FAIRBURY, NE, ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL
snip...
WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 X The enforcement
action included, as basis, failure of the establishment to comply with Agency
requirements concerning specified risk material.
snip...
Table 7. Administrative Actions: Very Small HACCP Plants (1/01/06 to
3/31/06)
A.J. CEKAK'S MEAT MARKET 21562 M ORD. NE, ... FAILURE TO COMPLY CONCERNING
SRM MATERIAL
snip...
ALTA VISTA LOCKER 31931 M ALTA VISTA, KS, ... FAILURE TO COMPLY CONCERNING
SRM MATERIAL
snip...
C&C MEAT SALES, INC. 18494 M18494 P UPPER MARLBORO, MD 2/27/06 3/16/06
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X The enforcement
action included, as a basis, failure of the establishment to comply with Agency
requirements concerning specified risk material.
snip...
H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X
3/6/06 The enforcement action included, as a basis, failure of the establishment
to comply with Agency requirements concerning specified risk material.
snip...
PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X 1/13/06
The enforcement action included, as basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
PARAGON SPRAY DRYING, L.L.C. 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X
2/9/06 The enforcement action included, as basis, failure of the establishment
to comply with Agency requirements concerning specified risk material.
snip...
RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05
10/24/05 X The enforcement action included, as basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
SAVORY CONNECTION, INC. 31764 M31764 P SELINGSGROVE, PA 3/14/06 3/31/06 X
The enforcement action included, as basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
STEAK MASTER, 21159 M21159 P, ELWOOD, NW, ... FAILURE TO COMPLY CONCERNING
SRM MATERIAL
snip...
TEARS MARKET, 04535 M04535 P, PENN YAN, NY, ... FAILURE TO COMPLY
CONCERNING SRM MATERIAL
snip...
THE MEAT SHOP, 31561 M BENSON, VT, ... FAILURE TO COMPLY CONCERNING SRM
MATERIAL
snip...
THEURER'S QUALITY MEATS, INC. 31647 M31647 P, LEWISTON, UT, ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL
snip...
TOOELE VALLEY MEATS 20594 M20594 P, GRANTSVILLE, UT, ... FAILURE TO COMPLY
CONCERNING SRM MATERIAL
snip...
WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
WILLIAM. G. MEST PACKING CO. 04431 M STRYKERSVILLE, NY 2/2/06 2/23/06 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material. On 3/21/06, NOIE
was modified and reissued. On 6/29/06, NOIE was rescinded.
YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X 2/23/06
The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005
SRM REMOVAL USA
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005
snip....
CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X X On 10/11/05, a
withholding action concerning labels for Advanced Meat Recovery System product
was taken in accordance with 9 CFR Part 500.8.
EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X X On 8/11/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8. On 12/22/04, plant appealed the withholding
action. Appeal was denied on 1/25/05.
00245L M LEXINGTON, NE 3/12/04 3/18/04 X 5/4/05 X X On 3/10/05, a
withholding action concerning labels for Advanced Meat Recovery System product
was taken in accordance with 9 CFR Part 500.8.
9/16/05 9/29/05 X X TYSON FRESH MEATS INC. 09268 M PASCO, WA X X On
7/28/04, a withholding action concerning labels for Advanced Meat Recovery
System product was taken in accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. X X 00245D M EMPORIA, KS On 12/23/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
DESERET MEAT 04852 M SPANISH FORK, UT 7/20/05 8/1/05 X X 12/29/05 The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X X X
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
A.J. CEKAK'S MEAT MARKET 9/1/05 9/20/05 X X X On 9/1/05, an enforcement
action 21562 M concerning failure to meet regulatory ORD, NE requirements for
Escherichia coli Biotype 1 (E. coli) was taken. The enforcement action included,
as a basis, failure of the establishment to comply with Agency requirements
concerning specified risk material.
ALTA VISTA LOCKER 10/5/05 10/26/05 X X The enforcement action included, as
a 31931 M basis, failure of the establishment toALTA VISTA, KS comply with
Agency requirements concerning specified risk material.
BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 8/8/05 8/16/05 X X X
11/16/05 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
CHAMPLAIN BEEF INC 2/28/05 3/4/05 3/8/05 X X X 08547 M WHITEHALL, NY
10/17/05 X X X The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
FIVE STAR PACK INC. 9/1/05 9/9/05 X X 12/29/05 On 9/1/05, an enforcement
action 08725 M08725 P concerning failure to meet regulatory GOLDEN CITY, MO
requirements for Escherichia coli Biotype 1 (E. coli) was taken. The enforcement
action included, as a basis, failure of the establishment to comply with Agency
requirements concerning specified risk material. FRESH FARMS BEEF 12/16/05
12/28/05 X X X The enforcement action included, as a 18579 M basis, failure of
the establishment toRUTLAND, VT comply with Agency requirements concerning
specified risk material.
GOETZ AND SONS WESTERN 11/15/05 11/23/05 12/1/05 X X MEATS INC 06245 M06245
P EVERETT, WA 12/17/05 12/28/05 X X X On 12/17/05, firm violated a regulatory
control action by selling U.S.D.A retained product.
H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 7/28/05 8/1/05 X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 7/26/05 7/29/05 X X
11/15/05 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material. PARAGON SPRAY
DRYING, LLC 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X X X The enforcement
action included, as a basis, failure of the establishment to comply with Agency
requirements concerning specified risk material.
RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05
10/24/05 X X X The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
S & S MEAT COMPANY 01046 M01046 P KANSAS CITY, MO 8/4/05 8/19/05 X X
11/16/05 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
STEAK MASTER 21159 M21159 P ELWOOD, NE 11/4/05 11/17/05 X X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X X X X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
THEURER'S QUALITY MEATS, INC 31647 M31647 P LEWISTON, UT 7/27/05 7/29/05 X
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
TOOELE VALLEY MEATS 20594 M20594 P GRANTSVILLE, UT 7/25/05 8/1/05 X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
WALNUT VALLEY PACKING LLC 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X
X X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
full text 54 pages ;
Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through
September 30, 2005 Date: March 20, 2006 at 12:58 pm PST
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT July 1, 2005 through September 30, 2005
snip...
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
snip...
DESERET MEAT 04852 M SPANISH FORK, UT 07/27/05 08/01/05 X On 7/27/05, a
suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk
Material was taken in accordance with 9 CFR Part 500.3.
snip...
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
snip...
MONTEBELLO MEAT PROCESSING, INC 19075 M19075 P MANATI, PR 08/01/05 08/18/05
X 09/26/05 On 8/1/05, an enforcement action concerning Bovine Spongiform
Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR
Part 500.4.
snip...
Table 7. Administrative Actions: Very Small HACCP Plants (7/01/05 to
9/30/05)
snip...
A.J. CEKAK'S MEAT MARKET 09/01/05 09/20/05 On 9/1/05, an enforcement
action
21562 M
concerning failure to meet regulatory ORD, NE requirements for Escherichia
coli X X X Biotype 1 (E. coli) and Bovine Spongiform Encephalopathy/Specified
Risk Material was taken in accordance with 9 CFR Part 500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 08/08/05 08/16/05 X On
8/8/05, an enforcement action concerning Bovine Spongiform Encephalopathy and
Specified Risk Material was taken in accordance with 9 CFR Part 500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
FIVE STAR PACK INC. 08725 M08725 P GOLDEN CITY, MO 09/01/05 09/09/05 X X On
9/1/05, an enforcement action concerning failure to meet regulatory requirements
for Escherichia coli Biotype 1 (E. coli) and Bovine Spongiform
Encephalopathy/Specified Risk Material was taken in accordance with 9 CFR Part
500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
H AND P MEATS 21352 M SOUTH PITTSBURG, TN 07/28/05 08/08/05 08/17/05
08/19/05 X X On 8/17/05, a suspension action concerning Bovine Spongiform
Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR
Part 500.3.
snip...
HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 07/28/05 08/01/05 X On
7/28/05, a suspension action concerning Bovine Spongiform Encephalopathy and
Specified Risk Material was taken in accordance with 9 CFR Part 500.3.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 07/26/05 07/29/05 X X
On 7/26/05, a suspension action concerning Bovine Spongiform Encephalopathy and
Specified Risk Material was taken in accordance with 9 CFR Part 500.3.
snip...
PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 09/21/05 X On 9/21/05, an
enforcement action concerning Bovine Spongiform Encephalopathy and Specified
Risk Material was taken in accordance with 9 CFR Part 500.4.
PARAGON SPRAY DRYING, LLC 31792 M31792 P WAUKON, IA 09/06/05 09/12/05 X On
9/6/05, an enforcement action concerning Bovine Spongiform Encephalopathy and
Specified Risk Material was taken in accordance with 9 CFR Part 500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 07/01/05 07/28/05 X On 7/1/05,
an enforcement action concerning Bovine Spongiform Encephalopathy and Specified
Risk Material was taken in accordance with 9 CFR Part 500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
08/04/05
08/19/05
On 8/4/05,
an enforcement action 01046 M01046 P concerning Bovine SpongiformKANSAS
CITY, MO X X Encephalopathy and Specified Risk Material was taken in accordance
with 9 CFR Part 500.4.
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
THE MEAT SHOP 08/18/05 09/06/05
09/09/05
On 9/6/05, a suspension action 31561 M concerning Bovine SpongiformBENSON,
VT Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR
Part 500.3. XX X X X
THEURER'S QUALITY MEATS, 07/27/05 07/29/05
On 7/27/05, a suspension action INC concerning Bovine Spongiform31647
M31647 P Encephalopathy and Specified Risk X X
LEWISTON, UT Material was taken in accordance with 9 CFR Part 500.3.
TOOELE VALLEY MEATS 07/25/05 08/01/05
On 7/25/05, a suspension action 20594 M20594 Pconcerning Bovine
Spongiform
GRANTSVILLE, UT X X Encephalopathy and Specified Risk Material was taken in
accordance with 9 CFR Part 500.3.
snip...
52 pages
PREVIOUS
Monday, June 23, 2014
PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES
***P.170: Potential detection of oral transmission of H type atypical BSE
in cattle using in vitro conversion
Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food
Inspection Agency; Lethbridge, AB Canada
Keywords: Atypical BSE, oral transmission, RT-QuIC
The detection of bovine spongiform encephalopathy (BSE) has had a
significant negative impact on the cattle industry worldwide. In response,
governments took actions to prevent transmission and additional threats to
animal health and food safety. While these measures seem to be effective for
controlling classical BSE, the more recently discovered atypical BSE has
presented a new challenge. To generate data for risk assessment and control
measures, we have challenged cattle orally with atypical BSE to determine
transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon
presentation of clinical symptoms, animals were euthanized and tested for
characteristic histopathological changes as well as PrPSc deposition.
The H-type challenged animal displayed vacuolation exclusively in rostral
brain areas but the L-type challenged animal showed no evidence thereof. To our
surprise, neither of the animals euthanized, which were displaying clinical
signs indicative of BSE, showed conclusive mis-folded prion accumulation in the
brain or gut using standard molecular or immunohistochemical assays. To confirm
presence or absence of prion infectivity, we employed an optimized real-time
quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain
Laboratory, Hamilton, USA.
Detection of PrPSc was unsuccessful for brain samples tests from the orally
inoculated L type animal using the RT-QuIC. It is possible that these negative
results were related to the tissue sampling locations or that type specific
optimization is needed to detect PrPSc in this animal. We were however able to
consistently detect the presence of mis-folded prions in the brain of the H-type
inoculated animal. Considering the negative and inconclusive results with other
PrPSc detection methods, positive results using the optimized RT-QuIC suggests
the method is extremely sensitive for H-type BSE detection. This may be evidence
of the first successful oral transmission of H type atypical BSE in cattle and
additional investigation of samples from these animals are ongoing.
P.126: Successful transmission of chronic wasting disease (CWD) into mice
over-expressing bovine prion protein (TgSB3985)
Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana
Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1
1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of
California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA
Keywords: chronic wasting disease, transmission, transgenic mouse, bovine
prion protein
Background. CWD is a disease affecting wild and farmraised cervids in North
America. Epidemiological studies provide no evidence of CWD transmission to
humans. Multiple attempts have failed to infect transgenic mice expressing human
PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal
human PrPC in vitro provides additional evidence that transmission of CWD to
humans cannot be easily achieved. However, a concern about the risk of CWD
transmission to humans still exists. This study aimed to establish and
characterize an experimental model of CWD in TgSB3985 mice with the following
attempt of transmission to TgHu mice.
Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were
intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse
(CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly
injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD)
or elk (CWD/Elk). Animals were observed for clinical signs of neurological
disease and were euthanized when moribund. Brains and spleens were removed from
all mice for PrPCWD detection by Western blotting (WB). A histological analysis
of brains from selected animals was performed: brains were scored for the
severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain
regions.
Results. Clinical presentation was consistent with TSE. More than 90% of
TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres
in the brain but only mice in the latter group carried PrPCWD in their spleens.
We found evidence for co-existence or divergence of two CWD/ Tga20 strains based
on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk
or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen
by WB. However, on neuropathological examination we found presence of amyloid
plaques that stained positive for PrPCWD in three CWD/WTD- and two
CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and
CWD/Elkinfected mice were similar but unique as compared to profiles of BSE,
BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM
mice tested positive for PrPCWD by WB or by immunohistochemical detection.
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
P.150: Zoonotic potential of L-type BSE prions: A new prion disease in
humans?
Emilie Jaumain,1 Stéphane Haïk,2 Isabelle Quadrio,3 Laetitia Herzog,1
Fabienne Reine,1 Armand Perret-Liaudet,3 Human Rezaei,1 Hubert Laude,1 Jean-Luc
Vilotte,4 and Vincent Béringue1 1INR A (Institut National de la Recherche
Agronomique); UR892; Virologie Immunologie Moléculaires; Jouy-en-Josas, France;
2IN SERM; Equipe maladie d’Alzheimer et maladies à Prions; CRicm; UMRS 1127; CNR
S; UPMC. R.; ICM, Hôpital de la Salpêtrière; Paris, France; 3Neurobiologie, CMRR
, Gériatrie, Hospices Civils de Lyon, Université Lyon 1-CNR S UMR5292-IN SERM
U1028; Lyon, France; 3INR A; UMR1313; Génétique Animale et Biologie Intégrative;
Jouy-en-Josas, France
In summary, L-type prions can be passaged on the human PrP sequence without
any obvious transmission barrier. The phenotype obtained differs from the
classical CJD prion types known so far. Careful extrapolation would suggest that
the zoonotic transmission of this agent could establish a new prion disease type
in humans.
Wednesday, May 30, 2012
PO-028: Oral transmission of L-type bovine spongiform encephalopathy
(L-BSE) in primate model Microcebus murinus
Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle
Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel
Verdier1
1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux Civils
de Lyon; Lyon, France
Here, we demonstrate that the L-BSE agent can be transmitted by oral route
from cattle to young and adult mouse lemurs. In comparison to IC inoculated
animals, orally challenged lemurs were characterized by longer survival periods
as expected with this route of infection.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral
Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6;
Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique,
France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious
Disease control, Sweden; 5Georg August University, Germany; 6German Primate
Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to
contract BSE through contaminated food. For this purpose, BSE brain was titrated
in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose
(MID50) for oral exposure to BSE in a simian model, and, by in doing this, to
assess the risk for humans. Secondly, we aimed at examining the course of the
disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE
brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals
were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the onset of
the clinical phase. However, there are differences in the clinical course
between orally and intracerebrally infected animals that may influence the
detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate. The difference in the incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years).
However, there are rapid progressors among orally dosed monkeys that develop
simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE
in primates“ supported by the EU (QLK1-2002-01096).
What Do We Feed to Food-Production Animals? A Review of Animal
FeedIngredients and Their Potential Impacts on Human Health
Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly
Walker11Johns Hopkins Center for a Livable Future, Bloomberg School of
PublicHealth, Baltimore, Maryland, USA; 2Maryland Institute forApplied
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
bonemeal, poultry meal, animal the slaughter of food by-product meal, dried
animal blood, blood meal, feather meal, egg-shell production animals andother
meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, andanimal 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, antibiotic
resistant bacteria, prions, arsenic, and dioxin like 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 (antibiotic resistant 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
Calves were challenged by mouth with homogenised brain from confirmed cases
of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were
then left to develop BSE, but were not subjected to the normal stresses that
they might have encountered in a dairy herd. Animals in all four groups
developed BSE. There has been a considerable spread of incubation period in some
of the groups, but it appears as if those in the 1 and 10g challenge groups most
closely fit the picture of incubation periods seen in the epidemic. Experiments
in progress indicate that oral infection can occur in some animals with doses as
low as 0.01g and 0.001g. ......... http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose
look at the table and you'll see that as little as 1 mg (or 0.001 gm)
caused7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in
primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian
Herzog,Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,
NathalieLescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown,
Jean-PhilippeDeslysSummary The uncertain extent of human exposure to bovine
spongiformencephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob
disease(vCJD)--is compounded by incomplete knowledge about the efficiency of
oralinfection and the magnitude of any bovine-to-human biological barrier
totransmission. We therefore investigated oral transmission of BSE tonon-human
primates. We gave two macaques a 5 g oral dose of brain homogenatefrom a
BSE-infected cow. One macaque developed vCJD-like neurologicaldisease 60 months
after exposure, whereas the other remained free of diseaseat 76 months. On the
basis of these findings and data from other studies, wemade a preliminary
estimate of the food exposure risk for man, whichprovides additional assurance
that existing public health measures canprevent transmission of BSE to
man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15
(7%)1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine
inoculumused in our study with primates against a bovine brain inoculum with
asimilar PrPres concentration that was inoculated into mice and cattle.8 *Data
are number of animals positive/number of animals surviving at the time of
clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log.
icip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle
infectedorally with similar BSE brain inocula
Published online January 27, 2005
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
16 years post mad cow feed ban August 1997
2013
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
17 years post mad cow feed ban August 1997
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
*** Monday, October 26, 2015 ***
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
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 ;
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following reasons...
======
In the USA, under the Food and Drug Administrations 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.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Draft Guidance for Industry on Ensuring Safety of Animal Feed Maintained
and Fed On-Farm; Availability
# 203 entitled “Ensuring Safety of Animal Feed Maintained and Fed On-Farm.”
Terry S. Singeltary Sr. submission ;
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
Posted: 12/30/2014ID: APHIS-2014-0107-0001
Notice: Environmental Impact Statements; Availability, etc.: Animal Carcass
Management
Document ID: APHIS-2013-0044-0001 Docket ID: APHIS-2013-0044 Comment ID:
APHIS-2013-0044-0002
(APHIS) Notice: Agency Information Collection Activities; Proposals,
Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program
Agency Information Collection Activities; Proposals, Submissions, and Approvals:
Chronic Wasting Disease Herd Certification Program (Document ID
APHIS-2011-0032-0001)
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
FSIS, USDA, REPLY TO SINGELTARY
From:Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent:Thursday, September 08, 2005 6:17 PM
To:fsis.regulationscomments@fsis.usda.gov
Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified
Risk Materials for Human Food and Requirements for the Disposition of
Non-Ambulatory Disabled Cattle
APHIS-2006-0118-0096 CWD
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 0500 EMC 1
Terry S. Singeltary Sr. Vol #: 1
PLEASE SEE FULL TEXT SUBMISSION ;
2001 Terry S. Singeltary Sr. comment submission
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
PRION 2016 TOKYO CONFERENCE
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans.
Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is
an animal prion disease that also causes variant Creutzfeldt-Jakob disease in
humans. Over the past decades, c-BSE's zoonotic potential has been the driving
force in establishing extensive protective measures for animal and human health.
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND
SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Wednesday, May 2, 2012
ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND
ANIMAL HEALTH
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05
Study of Atypical Bse
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of
Atypical BSE UPDATE July 28, 2010
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** 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.
Sunday, July 17, 2016
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Sunday, July 24, 2016
Chronic Wasting Disease Prions in Elk Antler Velvet and Marketing of this
Product in Nutritional Supplements for Humans?
Research Project: TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: THE ROLE OF
GENETICS, STRAIN VARIATION, AND ENVIRONMENTAL CONTAMINATION IN DISEASE CONTROL
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Thursday, April 14, 2016
Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
Terry S. Singeltary Sr. Bacliff, Texas USA
posted by Terry S. Singeltary Sr. at
12:22 PM
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