BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
***********OCTOBER 2015*************
*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***
THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and
Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and
Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.
P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine
Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge;
Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology
Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and
food-borne fatal neurological disease which can be orally transmitted to cattle
and humans. Due to the presence of contaminated milk replacer, it is generally
assumed that cattle become infected early in life as calves and then succumb to
disease as adults. Here we challenged three 14 months old cattle per-orally with
100 grams of C-type BSE brain to investigate age-related susceptibility or
resistance. During incubation, the animals were sampled monthly for blood and
feces and subjected to standardized testing to identify changes related to
neurological disease. At 53 months post exposure, progressive signs of central
nervous system disease were observed in these 3 animals, and they were
euthanized. Two of the C-BSE animals tested strongly positive using standard BSE
rapid tests, 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. Our study demonstrates susceptibility of adult
cattle to oral transmission of classical BSE. We are further examining
explanations for the unusual disease presentation in the third challenged
animal.
>>>At 53 months post exposure, progressive signs of central
nervous system disease were observed in these 3 animals, and they were
euthanized. Two of the C-BSE animals tested strongly positive using standard BSE
rapid tests, 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.<<<
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?
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, Val erie 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 longe 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...
===============
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
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.
==========================================
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.***
================
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
***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
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
Singeltary et al
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** 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
Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
Nadine Mestre-Francés, Simon Nicot, Sylvie Rouland, Anne-Gaëlle Biacabe,
Isabelle Quadrio, Armand Perret-Liaudet, Thierry Baron, and Jean-Michel
Verdier
We report transmission of atypical L-type bovine spongiform encephalopathy
to mouse lemurs after oral or intracerebral inoculation with infected bovine
brain tissue. After neurologic symptoms appeared, transmissibility of the
disease by both inoculation routes was confi rmed by detection of
disease-associated prion protein in samples of brain tissue.
Transmissible spongiform encephalopathies, also known as prion diseases,
are fatal neurodegenerative disorders that affect humans and animals. An
atypical form of bovine spongiform encephalopathy (BSE) was recently identifi ed
in cattle in Europe (1,2), North America (3), and Japan (4). This atypical BSE
was designated L-type BSE (L-BSE) because Western blot analysis showed that the
disease-associated protease-resistant prion protein (PrPres) was of lower
apparent molecular mass than in the agent of classical BSE, which is involved in
the major foodborne epizooty in cattle and in variant Creutzfeldt-Jakob disease
in humans (5).
Evidence from experimental studies in primate models (6,7) and transgenic
mice expressing human prion protein (PrP) (8,9) suggests that the rare and
putatively sporadic form of L-BSE (10) presents a higher risk than classical BSE
for transmission to humans. However, a major unresolved issue is whether L-BSE
can be transmitted by the oral route. To address this issue, we inoculated gray
mouse lemurs (Microcebus murinus), a nonhuman primate model, by the oral and
intracerebral (IC) routes with the agent of L-BSE.
Conclusions
We demonstrated that the agent of L-BSE can be transmitted by the oral
route from cattle to mouse lemurs. As expected, orally inoculated animals
survived longer than IC-inoculated animals. Orally inoculated lemurs had less
severe clinical signs and symptoms, with no evidence of motor dysfunction. It
was previously suggested that the agent of L-BSE might be involved in the
foodborne transmission of a prion disease in mink (11,12), a species in which
several outbreaks of transmissible mink encephalopathy had been identifi ed,
notably in the United States (13).
Our study clearly confi rms, experimentally, the potential risk for
interspecies oral transmission of the agent of L-BSE. In our model, this risk
appears higher than that for the agent of classical BSE, which could only be
transmitted to mouse lemurs after a fi rst passage in macaques (14). We report
oral transmission of the L-BSE agent in young and adult primates. Transmission
by the IC route has also been
reported in young macaques (6,7). A previous study of L-BSE in transgenic
mice expressing human PrP suggested an absence of any transmission barrier
between cattle and humans for this particular strain of the agent of BSE, in
contrast to fi ndings for the agent of classical BSE (9). Thus, it is imperative
to maintain measures that prevent the entry of tissues from cattle possibly
infected with the agent of L-BSE into the food chain.
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
Two novel prion strains, referred to as BSE-L and BSE-H, have been
recognized in bovines through active prion surveillance programs, both being
distinct from the epizootic, ‘classical’, BSE strain (C-BSE). Both H and L-types
have been detected worldwide as rare cases occurring in aged animals. Like C-BSE
prions, H- and L-types prions can propagate with relative ease in foreign
species or in transgenic mouse lines expressing heterologous PrP sequences. A
prion exhibiting biological properties similar to C-BSE agent sometimes emerged
from these cross-species transmissions. Previously, L-type prions were shown to
transmit to transgenic mice expressing human PrP with methionine at codon 129
with higher efficacy than C-BSE prions. Here, we examined whether L-type prions
propagate without any apparent transmission barrier in these mice and whether
such ‘humanised’ L-type prions share biological properties with CJD prions.
L-type prions and a panel of human CJD cases with various genotypes at codon 129
and electrophoretic PrPres signatures were serially transmitted by intracerebral
route to human PrP mice. The biological phenotypes induced by these agents were
compared by all the standard methods currently used to distinguish between prion
strains. At each passage, L-type prions were also transmitted back to bovine PrP
mice to assess whether the agent has evolved upon passaging on the human PrP
sequence. L-type prions transmitted to human PrP mice at 100% attack rate,
without notable alteration in the mean incubation times over 5 passages. At each
passage, ‘humanized’ L-type prions were able to transmit back to bovine PrP
transgenic mice without apparent transmission barrier, as based on the survival
time and the restoration of a L-type BSE phenotype. Comparison of mean
incubation times on primary and subsequent passages in human PrP mice showed no
overlap between L-type and sporadic CJD agents. While the electrophoretic
signature and regional distribution of PrPres in L-type diseased mouse brains
resembled that seen after transmission of MM2 CJD strain type, both agents
exhibited distinct resistance of the associated PrPres molecules to protease
denaturation.
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.
========Prion2013==========
2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday,
August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation
period in cattle – an update Timm Konold1*, Mark E Arnold1, Anthony R
Austin2, Saira Cawthraw1, Steve AC Hawkins1, Michael J Stack3, Marion M
Simmons1, A Robin Sayers1, Michael Dawson3, John W Wilesmith4 and Gerald AH
Wells5
Abstract
Background: To provide information on dose–response and aid in modelling
the exposure dynamics of the BSE epidemic in the United Kingdom groups of cattle
were exposed orally to a range of different doses of brainstem homogenate of
known infectious titre from clinical cases of classical bovine spongiform
encephalopathy (BSE). Interim data from this study was published in 2007. This
communication documents additional BSE cases, which occurred subsequently,
examines possible influence of the bovine prion protein gene on disease
incidence and revises estimates of effective oral exposure.
Findings: Following interim published results, two further cattle, one
dosed with 100 mg and culled at 127 months post exposure and the other dosed
with 10 mg and culled at 110 months post exposure, developed BSE. Both had a
similar pathological phenotype to previous cases. Based on attack rate and
incubation period distribution according to dose, the dose estimate at which 50%
of confirmed cases would be clinically affected was revised to 0.15 g of the
brain homogenate used in the experiment, with a 95% confidence interval of
0.03–0.79 g. Neither the full open reading frame nor the promoter region of the
prion protein gene of dosed cattle appeared to influence susceptibility to BSE,
but this may be due to the sample size.
Conclusions: Oral exposure of cattle to a large range of doses of a BSE
brainstem homogenate produced disease in all dose groups. The pathological
presentation resembled natural disease. The attack rate and incubation period
were dependent on the dose.
SNIP...
Results and discussion
Previously published results of the first phase of the study established
BSE in all ten cattle dosed with 3×100 g (IP range: 33–45 mpe) and 100 g (IP
range: 31– 60 mpe), in seven of nine cattle dosed with 10 g (IP range 41–72 mpe,
the tenth died of an intercurrent disease at 14 mpe), and in seven of ten cattle
dosed with 1 g (IP range: 45–72 mpe) [1]. In the second phase interim published
results reported BSE in three of four cattle dosed with 1 g (IP range: 58–73
mpe), in seven of fifteen dosed with 100 mg (IP range: 53–98 mpe) and in single
cattle from groups of fifteen dosed with 10 mg (IP: 56 mpe) or 1 mg (IP: 68
mpe).
After publication of the interim findings, two further cases of BSE were
diagnosed in cattle in the second phase, one dosed with 100 mg and the other
with 10 mg. For completeness of the data from the second phase the times from
exposure to onset of the different clinical stages and cull for all BSE-positive
cases are given in Table 1 and for all other cattle where BSE was excluded by
postmortem tests in Table 2. Neuropathological examination confirmed a vacuolar
profile in the brain of the case dosed with 10 mg consistent with that reported
previously in the study and with that of naturally affected cattle [1]. The
animal dosed with 100 mg and culled with spastic syndrome did not present with
vacuolar changes in the brain but in both cases the diagnosis of BSE was
confirmed by detection of PrPd immunohistochemically and PrPres on WB.
The clinical duration in confirmed BSE cases (time from onset of possible
signs to cull, excluding those animals that were culled prior to displaying
definite signs) ranged from 4 months (CM917 dosed with 1 g) to 48 months (CM923
dosed with 1 mg). Although there was a tendency of cattle exposed to extremely
high doses (3× or single dose of 100 g) to have a shorter clinical duration
compared to lower doses [median (range; standard deviation) for 3×100 g: 9
(5–18, 4.5), for 100 g: 13 (6–33; 8.7), for 10 g: 18 (11–43; 13.0), for 1 g:
18.5 (4–32; 8.9) and for 100 mg: 15 (5–37; 12.8) months; see [1] and Table 1],
the difference was not statistically significant (P = 0.08, Kruskal-Wallis test,
GraphPad Prism version 5, GraphPad Software, La Jolla, USA). Determination of
the exact clinical onset to estimate clinical duration is invariably subjective
because it is often based on the display of behavioural changes that may also
occur to some extent in “normal” cattle, as observed in undosed controls in this
study, even in the absence of another underlying condition. It is for this
reason that throughout the study IP has been defined on the basis of onset of
definite signs.
No novel polymorphisms were detected in the ORF regions of the 86 tested
cattle. Variations in the number of N-terminal octapeptide repeats among PrP
gene sequences were reported previously [1]. The other ORF DNA polymorphisms
detected were silent in that they do not result in an amino acid change. A
summary of the results is given in Table 3. The findings were consistent with
those reported previously [5]. Five common promoter genotypes were identified in
this study, with the sixth (23 bp −/−, 12 bp +/+) being relatively rare (only
found in one animal, see Table 3), which is consistent with previous findings
[7]. Proportional hazard regression analysis using the data from 76 orally dosed
cattle revealed that the dose was the most important predictor of hazard (P <
0.0001), which was expected, whereas none of the genotype parameters were
significant predictors (P > 0.3). In other words, the main factor that
determined how rapidly orally dosed cattle succumbed to BSE was the dose of
inoculum, and the genotype did not appear to have a significant influence.
Whilst it has been reported that homozygous carriers of the 12 bp insertion
allele (12 bp +/+) have a lower risk of developing natural BSE [7], this
promoter genotype did not appear to reduce susceptibility to oral exposure to
BSE. This may be due to sample size in the current study: to have a reasonable
power (80%) to detect the differences (20.5%) as observed by Juling et al. [7],
for UK Holstein cattle sample sizes of 60 (12 bp +/+) and 210 (12 bp +/− or −/−)
would have been required.
Using the individual IP data for each confirmed BSE case (Table 1 and [1]
for phase 1 of the study), the probability of infection given the dose S (d)
could be expressed as: S(d) = exp(α+β*d)/(1+exp(α+β*d)) with parameters (and 95%
confidence intervals) given by α = −3.01 (−3.59, −2.44) and β = 1.12 (0.93,
1.33) (see Figure 1), which is a slight modification to the parameters reported
previously (α = −3.50; β = 1.26 [1]), and the additional data resulted in a
revised estimate of one cattle oral ID50 being equivalent to 102.7 mouse i.c./
i.p. ID50/g (with 95% confidence interval of 102.0, 103.4) compared to the
previous estimate of 102.8 mouse i.c./i.p. ID50/g (with 95% confidence interval
of 102.1, 103.5). This ID50 estimate is equivalent to 0.15 g of the brain
homogenate used in the experiment (previous estimate:
0.20 g), with a 95% confidence interval of 0.03–0.79 g. As it has been
shown that one mouse i.c./i.p. ID50 equals 102.7 cattle i.c. ID50 [8], it can be
extrapolated that one cattle oral ID50 equals 105.4 cattle i.c. ID50,
(previously estimated at 105.5 cattle i.c. ID50).
The IP followed a lognormal distribution with parameters of μ =
a−b×log10(dose), with a = 4.66 (4.54, 4.71) and b = 0.14 (0.13, 0.17), and σ =
0.23 (previously: μ = 4.54−0.14×log10(dose), σ = 0.21), where dose is the titre
of brain homogenate in terms of mouse i.c./i.p. ID50/g [see Figure 2, which
shows the association between mean IP (given by exp(μ+0.5σ2) and the
dose].
Preliminary findings from the original study contributed to quantitative
risk assessment of the exposure of humans to consumption of infected bovine
products [9]. An estimate of human ID50 assumed the worst case of a cattle to
human species barrier of a factor of one, giving the range of human oral ID50s
in 1 g of brain from a clinically affected cow as approximately 0.52 to 5. Data
from the previously published interim results revised this estimate to 1.0 to 20
and additional results in the present study indicate that this range should now
be revised to 1.3 to 33.3, although, as previously, it could be greater with
higher titres of BSE affected brain than used in the present study. These
estimates have been used to assess the impact of BSE control measures on
potential consumption of BSE infectivity (BSE control model [10]). Although the
reduced ID50 based on the present results would increase estimates of the
exposure of humans in terms of bovine oral ID50s, the effect would be
comparatively small relative to the uncertainty in such risk assessments.
Nevertheless, with decline of the BSE epidemic and the potential for relaxation
of certain controls, the revised estimate of human oral ID50 is available to
revisit risk assessments.
The present data do not affect the previous approximation that single doses
in the range from 100 mg to 1 g of the brainstem homogenate used correspond to
the range of mean IPs of cattle through the BSE epidemic [1]. The observation
that a relatively small, single exposure (less than 1 g of high titre brain) can
result in infection reinforces the importance of preventing crosscontamination
during feed ingredient storage and feed production. This proved to be
problematical in feed mills producing ruminant and non-ruminant feedstuffs as is
evident from the incomplete effect of the initial statutory control on the
feeding of meat and bone meal to ruminants introduced in the UK in 1988. The low
dose phenomenon, together with the persistent viability of the BSE agent, has
required the removal of specific high risk tissues from cattle at slaughter and
the total ban on the use of mammalian meat and bone meal for use in farmed
livestock [11].
Conclusions
The present results concur with the interim findings of this study, that
the oral exposure of cattle to BSE brain homogenate produced dose dependent
effects on IP and attack rate such that in general the higher the dose the
shorter the IPs and the greater the attack rate. In all cases the induced
disease closely resembled the pathology of the natural disease. This is in
keeping with the analysis of the pathology in orally dosed cattle from another
study [12] and reinforces the validity of the oral exposure model for the study
of classical BSE in the natural host. The estimate of a cattle oral ID50 is
revised to 0.15 g brain material used for the studies. Decline of the BSE
epidemic indicates that the use of a revised estimate of human oral ID50 in risk
assessments is, in future, likely to contribute mainly to reassessments in
relation to possible relaxation of controls.
Keywords: Bovine spongiform encephalopathy, BSE, Cattle, Oral dose,
Dose–response, Attack rate, Incubation period, Model, Risk of infection, Prion
protein gene
Experimental Classical Bovine Spongiform Encephalopathy: Definition and
Progression of Neural PrP Immunolabeling in Relation to Diagnosis and Disease
Controls
Veterinary Pathology OnlineFirst, published on November 15, 2010 as
doi:10.1177/0300985810387072
M. M. Simmons1,2, J. Spiropoulos1,2, P. R. Webb1, Y. I. Spencer1, S.
Czub3,4, R. Mueller5, A. Davis1,6, M. E. Arnold7, S. Marsh1, S. A. C. Hawkins1,
J. A. Cooper1, T. Konold1, and G. A. H. Wells1
Abstract
Tissues from sequential-kill time course studies of bovine spongiform
encephalopathy (BSE) were examined to define PrP immunohistochemical labeling
forms and map disease-specific labeling over the disease course after oral
exposure to the BSE agent at two dose levels. Study was confined to brainstem,
spinal cord, and certain peripheral nervous system ganglia—tissues implicated in
pathogenesis and diagnosis or disease control strategies. Disease-specific
labeling in the brainstem in 39 of 220 test animals showed the forms and
patterns observed in natural disease and invariably preceded spongiform changes.
A precise temporal pattern of increase in labeling was not apparent, but
labeling was generally most widespread in clinical cases, and it always involved
neuroanatomic locations in the medulla oblongata. In two cases, sparse labeling
was confined to one or more neuroanatomic nuclei of the medulla oblongata. When
involved, the spinal cord was affected at all levels, providing no indication of
temporal spread within the cord axis or relative to the brainstem. Where minimal
PrP labeling occurred in the thoracic spinal cord, it was consistent with
initial involvement of general visceral efferent neurons. Labeling of ganglia
involved only sensory ganglia and only when PrP was present in the brainstem and
spinal cord. These experimental transmissions mimicked the neuropathology in
BSE-C field cases, independent of dose of agent or stage of disease. The model
supports current diagnostic sampling approaches and control measures for the
removal and destruction of nervous system tissues in slaughtered cattle.
Keywords
transmissible spongiform encephalopathy, prion, bovine, central nervous
system, immunohistochemistry, pathogenesis, diagnosis, peripheral nervous
system
PRION 2009 CONGRESS BOOK OF ABSTRACTS
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral
transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard
Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera
and Vaccines, Germany; 2Department of Neuropathology, Georg-August University,
Göttingen, Germany, 3Department of Virology and Immunology, German Primate
Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal
model to study the pathogenesis of variant Creutzfeldt-Jacob disease
(vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase
of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time
points during the incubation period and 7 orally BSE-dosed macaques were
sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues
were tested for the presence of proteinase-K-resistant prion protein (PrPres) by
western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres
deposits were widely spread in neuronal tissues (including the peripheral
sympathetic and parasympathetic nervous system) and in lymphoid tissues
including tonsils. In asymptomatic disease carriers, PrPres deposits could be
detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were
negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and
medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas
sympathetic trunk and all thoracic/cervical segments of the spinal cord were
still negative for PrPres. However, tonsil samples were negative in all
asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via
autonomic fibres of the splanchnic and vagus nerves indicating that
trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils
were predominantly negative during the main part of the incubation period
indicating that epidemiological vCJD screening results based on the detection of
PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of
vCJD among humans.
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate.
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in
TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm)
caused 7% (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, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to non-human
primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months
after exposure, whereas the other remained free of disease at 76 months. On the
basis of these findings and data from other studies, we made a preliminary
estimate of the food exposure risk for man, which provides additional assurance
that existing public health measures can prevent transmission of BSE to
man.
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 inoculum
used in our study with primates against a bovine brain inoculum with a similar
PrPres concentration that was inoculated into mice and cattle.8 *Data are number
of animals positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of bioassays is generally
judged to be about plus or minus 1 log. ic ip=intracerebral and
intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula
Published online January 27, 2005
Oral infection by the bovine spongiform encephalopathy prion
R. G. Will and J. W. Ironside Author Affiliations
National Creutzfeldt-Jakob Disease Surveillance Unit, Western General
Hospital, Edinburgh, EH4 2XU, United Kingdom Extract Full Text Authors &
Info Metrics Related Content Related Article PDF The route by which prion
infection spreads from peripheral tissues to the brain has been the subject of
interest and research for decades. The seminal pathogenesis studies by Hadlow
and colleagues (1, 2) demonstrated that in natural scrapie in Suffolk sheep
infectivity initially was detected at 10–14 months of age in tonsil, lymph
nodes, spleen, and intestine, including ileum and upper colon. The tissue
distribution of infectivity was consistent with uptake from the alimentary tract
and, by implication, oral exposure as the likely portal of entry of infection.
By the time clinical disease developed, peripheral tissues continued to exhibit
a similar distribution and titer of infectivity, but there was also evidence of
infectivity in the central nervous system, with higher titers of infectivity,
initially in the medulla and diencephalon. Laboratory studies of oral scrapie
infection in rodents have confirmed these findings and suggest that infection
spreads from the lymphoreticular system to the spinal cord, presumptively via
the autonomic nervous system, and thence rostrally to the brain (3). The
importance of peripheral pathogenesis is underlined by the marked increase in
incubation time in mice after splenectomy (4).
There is, however, variation in pathogenesis that is determined by factors
including the interaction between host genome and agent strain. Some breeds of
sheep affected by natural scrapie, for example, Montadales, have no detectable
infectivity in peripheral tissues, and the distribution of infectivity in the
brain may vary according to the breed of sheep (5). In bovine spongiform
encephalopathy (BSE) infectivity has not been detected in peripheral tissues in
natural disease, except for dorsal root ganglia and possibly bone marrow,
although infectivity has been found in terminal ileum after experimental oral
challenge with BSE brain (6). An important implication of this data is that,
accepting the limits of the sensitivity of bioassay …
It also appears to Mr MacLean that Mr Bradley’s answer (that it would take
less than say 100 grams) was probably given with the benefit of hindsight:
particularly if one considers that later in the same answer Mr Bradley expresses
his surprise that it could take as little of 1 gram of brain to cause BSE by the
oral route within the same species. This information did not become available
until the “attack rate” experiment had been completed in 1995/96. This was a
titration experiment designed to ascertain the infective
2
dose. A range of dosages was used to ensure that the actual result was
within both a lower and an upper limit within the study and the designing
scientists would not have expected all the dose levels to trigger infection. The
dose ranges chosen by the most informed scientists at that time ranged from 1
gram to three times one hundred grams. It is clear that the designing scientists
must also have shared Mr Bradley’s surprise at the results because all the dose
levels right down to 1 gram triggered infection.
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.
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. ...
10 years post mad cow feed ban August 1997
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
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
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials 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
***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
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? ***
Terry S. Singeltary Sr.
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** 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
Monday, November 23, 2015
Dynamics of the natural transmission of bovine spongiform encephalopathy
within an intensively managed sheep flock Vet Res. 2015; 46: 126.
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
SUMMARY: We are reopening the comment period for our proposed rule that
would revise completely the scrapie regulations, which concern the risk groups
and categories established for individual animals and for flocks, the use of
genetic testing as a means of assigning risk levels to animals, movement
restrictions for animals found to be genetically less susceptible or resistant
to scrapie, and recordkeeping requirements. This action will allow interested
persons additional time to prepare and submit comments.
DATES: The comment period for the proposed rule published on September 10,
2015 (80 FR 54660-54692) is reopened. We will consider all comments that we
receive on or before December 9, 2015. ...
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I
kindly submit the following ;
>>>The last major revision of the scrapie regulations occurred on
August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket
No. 97-093-5) a final rule amending part 79 by imposing additional restrictions
on the interstate movement of sheep and goats.<<<
Indeed, much science has changed about the Scrapie TSE prion, including
more science linking Scrapie to humans. sadly, politics, industry, and trade,
have not changed, and those usually trump sound science, as is the case with all
Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing
animals and the OIE. we can look no further at the legal trading of the Scrapie
TSE prion both typical and atypical of all strains, and CWD all stains. With as
much science of old, and now more new science to back this up, Scrapie of all
types i.e. atypical and typical, BSE all strains, and CWD all strains, should be
regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE,
and all trading partners to take heed to the latest science on the TSE prion
disease, all of them, and seriously reconsider the blatant disregards for human
and animal health, all in the name of trade, with the continued relaxing of TSE
Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set
up to fail in the first place. If the world does not go back to the ‘BSE RISK
ASSESSMENTS’, enhance, and or change that assessment process to include all TSE
prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we
continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’
PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they
will continue to mutate and spread among species of human and animal origin, and
they will continue to kill. ...
please see ;
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 longe 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***
===============
***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.
***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.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Evaluation of the zoonotic potential of transmissible mink
encephalopathy Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Ruchoux,
Marie-Madeleine - item Durand, Valerie - item Luccantoni-Freire, Sophie - item
Dehen, Capucine - item Correia, Evelyne - item Casalone, Cristina - item Richt,
Juergen item Greenlee, Justin item Torres, Juan Maria - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Pathogens Publication Type: Peer Reviewed Journal Publication
Acceptance Date: July 30, 2013 Publication Date: July 30, 2013 Citation: Comoy,
E.E., Mikol, J., Ruchoux, M., Durand, V., Luccantoni-Freire, S., Dehen, C.,
Correia, E., Casalone, C., Richt, J.A., Greenlee, J.J., Torres, J.M., Brown, P.,
Deslys, J. 2013. Evaluation of the zoonotic potential of transmissible mink
encephalopathy. Pathogens. 2:(3)520-532.
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.
Transmissible mink encephalopathy (TME) is another prion disease that transmits
to cattle and show similarities to L-type BSE when subjected to laboratory
testing. The purpose of this study was to use non-human primates (cynomologous
macaque) and transgenic mice expressing the human prion protein to determine if
TME could represent a potential risk to human health. TME from two sources
(cattle and raccoons) was able to infect non-human primates and transgenic mice
after exposure by the intracranial route. This result suggest that humans may be
able to replicate TME prions after an exposure that allows infectious material
access to brain tissue. At this time, it is unknown whether non-human primates
or transgenic mice would be susceptible to TME prions after oral exposure. The
results obtained in these animal models were similar to those obtained for
L-type BSE. Although rare, the existence of TME and that it transmits to cattle,
non-human primates, and transgenic mice suggest that feed bans preventing the
feeding of mammalian tissues to cattle should stay in place and that regular
prion surveillance during the slaughter should remain in place. 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: Successful transmission of Transmissible Mink Encephalopathy (TME) to
cattle supports the bovine hypothesis to the still controversial origin of TME
outbreaks. Human and primate susceptibility to classical Bovine Spongiform
Encephalopathy (c-BSE) and the transmissibility of L-type BSE to macaques assume
a low cattle-to-primate species barrier: we therefore evaluated the zoonotic
potential of cattle-adapted TME. In less than two years, this strain induced in
cynomolgus macaques a neurological disease similar to L-BSE and distinct from
c-BSE. TME derived from another donor species (raccoon) induced a similar
disease with shorter incubation periods. L-BSE and cattle-adapted TME were also
transmissible to transgenic mice expressing human PrP. Interestingly, secondary
transmissions to transgenic mice expressing bovine PrP showed the maintenance of
prion strain features for the three tested bovine prion strains (cattle TME,
c-BSE and L-BSE) regardless of intermediate host. Thus, TME is the third animal
prion strain transmissible to both macaques and humanized transgenic mice,
suggesting zoonotic potentials that should be considered in the risk analysis of
animal prion diseases for human health. Moreover, the similarities between TME
and L-BSE are highly suggestive of a link between those strains, and of the
presence of L-BSE decades prior to its identification in USA and Europe.
Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies 2014 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, Investigate the pathobiology of atypical transmissible
spongiform encephalopathies (TSEs) in natural hosts, 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. Animals inoculated with atypical
scrapie have not yet developed disease. 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 and the manuscript has been
published (2012). 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 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. Evaluated enzyme immunoassay for rapid identification
of prion disease in livestock. Scrapie of sheep and bovine spongiform
encephalopathy of cattle are diseases that cause damage to the central nervous
system including the retina in the eye. The infectious agent is an abnormal
protein called a prion that has misfolded from its normal state and is resistant
to breakdown by the host cells. Current diagnostic methods require the testing
of brain material, which can be difficult to collect and may lead to
contamination of the environment and exposure of personnel to the infectious
agent. Eyes can be readily collected without opening the skull. ARS researchers
at Ames, Iowa demonstrated that the enzyme immunoassay results using eyes of
negative controls or samples collected from sheep or cattle with clinical signs
were in agreement with approved confirmatory assays (western blot or
immunohistochemistry). These results indicate the retina is a useful tissue for
rapid diagnosis of prion disease in clinically ill sheep and cattle and could be
considered to greatly increase the number of samples submitted for prion disease
diagnosis with a minimal investment of time and limited exposure of personnel to
prion agents.
2. Evaluated E211K cattle as a model for inherited human prion disease.
Prion diseases cause damage to the central nervous system of animals and humans.
The infectious agent is an abnormal protein called a prion that has misfolded
from its normal state and is resistant to breakdown by the host cells and thus
accumulates and damages those cells. Some forms of prion disease are genetic and
can be inherited. Current models of genetic prion disease in humans rely on
mouse models expressing either the human prion protein (E200K) or a combination
of both mouse and human sequences. In addition to being an entirely artificial
system these mouse models have a short lifespan making them a less than ideal
system to study a naturally occurring genetic disorder with a long incubation
time and late onset of disease. Cattle, however, exhibit a number of
similarities to humans with regard to prion disease and perhaps most notable is
the late onset of genetic prion disease. ARS researchers at Ames, Iowa have
produced cattle containing both 1 and 2 chromosome copies of the cattle prion
gene (E211K) and evaluated many aspects of this prion protein from cattle
including protein stability, protein expression levels and ratios, as well as
evidence of oxidative stress. Taken together, these results highlight the
differences between mouse models of genetic prion disease and a naturally
occurring prion disease system in cattle and suggest that cattle will provide a
more relevant understanding of genetic prion disease in humans than do current
rodent models.
Review Publications Smith, J.D., Greenlee, J.J. 2014. Detection of
misfolded prion protein in retina samples of sheep and cattle by use of a
commercially available enzyme immunoassay. American Journal of Veterinary
Research. 75(3):268-272. Haldar, S., Beveridge, A.J., Wong, J., Singh, A.J.,
Galimberti, D., Borroni, D., Zhu, X., Blevins, J., Greenlee, J., Perry, G.,
Mukhopadhyay, C.K., Schmotzer, C., Singh, N. 2014. A low-molecular-weight
ferroxidase is increased in the CSF of sCJD Cases: CSF ferroxidase and
transferrin as diagnostic biomarkers for sCJD. Antioxidants & Redox
Signaling. 19(14):1662-1675.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=421870&fy=2014
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=421870
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=260467
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Tuesday, August 4, 2015
FDA U.S. Measures to Protect Against BSE
Saturday, December 21, 2013
Complementary studies detecting classical bovine spongiform encephalopathy
infectivity in jejunum, ileum and ileocaecal junction in incubating cattle
Wednesday, May 2, 2012
ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND
ANIMAL HEALTH
2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday,
August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
in the url that follows, I have posted
SRM breaches first, as late as 2011.
then
MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until
2007, when they ceased posting them.
then,
MAD COW SURVEILLANCE BREACHES.
Friday, May 18, 2012
Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy
(BSE) in the United States Friday May 18, 2012
Monday, August 6, 2012
TAFS BSE in USA August 6, 2012
BSE in USA
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...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
Singeltary et al
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** 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
spontaneous atypical BSE ???
don’t let anyone fool you. spontaneous TSE prion disease is a hoax in
natural cases, never proven.
all one has to do is look at France. France is having one hell of an
epidemic of atypical BSE, probably why they stopped testing for BSE, problem
solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow
disease in numbers they could find any with, after those atypical BSE cases
started showing up. shut down the testing to numbers set up by OIE that are so
low, you could only by accident find a case of BSE aka mad cow disease. and this
brilliant idea by the WHO et al, to change the name of mad cow disease, thinking
that might change things is preposterous. it’s all about money now folks, when
the OIE, USDA and everyone else went along and made the TSE prion disease aka
mad cow type disease a legal trading commodity by the BSE MRR policy, I would
say everyone bit off more then they can chew, and they will just have to digest
those TSE Prions coming from North America, and like it, and just prey you don’t
get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE
prion disease in the decades to come, and or pass it to some other poor soul via
the iatrogenic medical surgical tissue friendly fire mode of transmission i.e.
second hand transmission. it’s real folks, just not documented much, due to lack
of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the
iatrogenic event is tracked down and documented, and put into the academic and
public domain, which very seldom happens. ...
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
***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
UNITED STATES OF AMERICA USA
a review of the mad cow debacle by USDA et al under Agriculture Secretary
Ann Veneman ;
US SENATOR AND STAN THE MAN SLAM USDA ''DAMNING TESTIMONY''
Senator Michael Machado from California
''USDA does not know what's going on''.
''USDA is protecting the industry''.
''SHOULD the state of California step in''
Stanley Prusiner
''nobody has ever ask us to comment''
''they don't want us to comment''
''they never ask''
i tried to see Venemon, after Candian cow was discovered with BSE. went to
see lyle. after talking with him... absolute ignorance... then thought I should
see Venemon... it was clear his entire policy was to get cattle bonless beef
prods across the border... nothing else mattered...
his aids confirmed this... 5 times i tried to see Venemon, never worked...
eventually met with carl rove the political... he is the one that arranged
meeting with Venemon... just trying to give you a sense of the distance... healh
public safety...
was never contacted...
yes i believe that prions are bad to eat and you can die from them... END
Dr. Stan bashing Ann Veneman - 3 minutes
Recall Authority and Mad Cow Disease: Is the Current System Good for
Californians?
Tuesday, February 24, 2004
JOINT HEARING
AGRICULTURE AND WATER RESOURCES HEALTH AND HUMAN SERVICES AND SELECT
COMMITTEE ON GOVERNMENT OVERSIGHT - MACHADO, ORTIZ, and SPEIER, Chairs
ALL VIDEOS OF THIS HEARING HAVE BEEN REMOVED FROM THE WWW, LIKE IT NEVER
HAPPENED...but we know different...TSS
-------- Original Message --------
Subject: Re: Congressman Henry Waxmans's Letter to the Honorable Ann
Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW
Date: Wed, 9 Jun 2004 16:48:31 –0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de References: 40A8CD52.1070308@wt.net
######## Bovine Spongiform Encephalopathy #########
USA BSE RED BOOK
October 1998
BSE Red Book 2.1-36
7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer will
advise the READE(3 Director concerning laboratory capabilities and appropriate
laboratory examinations to be conducted to provide needed results as rapidly as
possible. This individual will assist with interpretation of results.
seems that if the 'enhanced BSE/TSE testing program' is to test some
400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.
BSE Red Book 2.1-39
7.6 Depopulation Procedures
Under no circumstances may BSE suspects be sent fo slaughhter or
rendering.
snip...
BSE Red Book 2.1-40
7.7 Disposal Under no circumstances may BSE suspects be sent to slaughter
or rendering. Notify FDA, CVM if you suspect that the carcass of a BSE-confirmed
animal has moved to rendering or animal feed manufacturing. Field personel
should arrange for the carcass to be transported to and examined by a qualified
veterinary pathologist or field veterinary medical officer. After the pathologic
examination has been completed and the necessary diagnostic specimens have been
obtained, field personnel should arrange for disposal of the carcass. Before a
method of disposal is selected, there are many factors that must be considered,
and often other State and Federal agencies must be consulted. The environmental
and legal impacts of the operation must be considered. Upon recommendation of
the State or Federal agencies, VS may consider other disposal methods.
snip...
7.7.3 Rendering Because BSE is spread by rendered animal protein,
BSE-suspect and confirmed carcasses must not be rendered, unless the rendered
material is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or
carcasses have moved to rendering or animal feed manufacturing.
snip...
7.10.11 Prevention--Suspects and animals confirmed to have BSE must not be
rendered. Producers, feed mills, and rendering establishments should adhere to
U.S. State and local rendering policies and FDA regulations concerning the
feeding of rendered animal protein to ruminants.
TSS
Terry S. Singeltary Sr. wrote:
######## Bovine Spongiform Encephalopathy #########
ONE HUNDRED EIGHTH CONGRESS CONGRESS OF THE UNITED STATES HOUSE OF
REPRESENTATIVES COMMITTEE ON GOVERNMENT REFORM 2157 RAYBURN HOUSE OFFICE
BUILDING WASHINGTON, DC 20515-6143
> www.house.gov/reform > > May 13, 2004 > > The Honorable
Ann M. Veneman Secretary of Agriculture Department of Agriculture 1400
Independence Avenue, SW Washington, DC 20250
Dear Madam Secretary:
I am writing to express concern that the recent failure of the U.S.
Department of Agriculture (USDA) to test a Texas cow with neurological symptoms
for bovine spongiform encephalopathy (BSE) may reflect wider problems in the
surveillance program. USDA apparently does not keep track of how many cows
condemned for central nervous system symptoms are tested for BSE nor does it
require that suspect carcasses be held pending testing. Effective surveillance
and control of BSE in the United States require a reliable system for ensuring
that potentially infected cows are tested and that no infected materials enter
the animal or human food supply.
Under USDA regulations, any cow that exhibits signs of central nervous
system (CNS) problems must be condemned by Food Safety Inspection Service (FSIS)
personnel at the plant.1 According to a 1997 Animal and Plant Health Inspection
Service (APHIS) Memorandum, brain samples all of such animals should be sent for
BSE testing.2 The memorandum notes that "[i]t is essential that brain specimens
be collected from adult cattle condemned for CNS signs as part of our national
surveillance of BSE."3
The cow slaughtered at the Lone Star Beef slaughterhouse last week
staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a
request from APHIS personnel at the plant to conduct BSE testing, however, an
APHIS supervisor in Austin reportedly refused the test and instructed the plant
to send the carcass for rendering.5
1 9 CFR 309.4.
2 USDA APHIS, Veterinary Services Memorandum No. 580.16. Procedures/or
Investigation of Adult Cattle With Clinical Signs of Central Nervous System
(CNS) Disease and Procedures for Surveillance of Downer Cows for Bovine
Spongiform Encephalopathy (BSE) (June 11,1997). 3 Id.
4 U.S. Confirms a Failure to Use Mad Cow Test, Wall Street Journal (May 4,
2004).
The Honorable Ann M. Veneman May 13,2004 Page 2
This sequence of events is troubling, and it raises the question of
whether this is an isolated incident. In 1997, USDA noted a major gap between
the number of cattle condemned for CNS symptoms and the number of these cows
actually tested for mad cow disease. The Department found:
Based on information provided by the Food Safety and Inspection Service
(FSIS), the number of adult cattle (2 years of age or greater) condemned at
slaughter due to CNS signs is much greater than the number whose brains have
been collected for testing.6
Despite recognizing the problem more than six years ago, however, USDA
apparently did not adopt procedures to ensure that these samples would be
collected. In March 2004, the Government Reform Committee asked USDA to provide,
for each of the last five years, the number of BSE tests performed on cattle
condemned by FSIS inspectors on the basis of CNS symptoms.7 In response, USDA
provided information on the numbers of cattle condemned for CNS symptoms by
FSIS, but replied that "[i]t is not possible to determine, from the data we
currently collect, how many of these cattle were tested by APHIS for BSE."8 It
thus appears that not only does USDA not routinely track the gap between the
number of condemned and tested cattle, but that USDA could not even calculate
this gap when requested to do so by Congress.
There also appears to be a lack of clarity regarding the disposition of
cattle with CNS symptoms while BSE tests are pending. In the past, companies
could send cattle awaiting BSE testing results for rendering, which would allow
their remains to be used in feed for animals other than ruminants, such as pigs
and chickens. After this incident, both FDA and USDA policy appear to have
changed — in different ways.
USDA policy has apparently shifted to requesting that companies not send
cattle to rendering while awaiting test results. A May 5, 2004 memo from APHIS
states, "it is requested — though not required — that [the cattle] not go to
inedible rendering until the sample comes
USDA's San Angelo Vets and Techs Ordered Not to Test Suspect Cow, Meating
Place (May 5, 2004).
6 USDA APHIS, supra note 2.
7 Letter from Rep. Tom Davis and Rep. Henry A- Waxman to Secretary of
Agriculture Ann M. Veneman (Mar. 8, 2004).
8 Letter from Ronald F. Hicks, Assistant Administrator, Office of Program
Evaluation, Enforcement, and Review- FSIS. to Reo. Henrv A. Waxman- Attachment 1
(Mar. 22- 2004).
The Honorable Ann M. Veneman May 13,2004 Page 3
back negative."9 There is no explanation of why this course of action is
requested, but not required.
FDA policy also appears to have shifted towards prohibiting the use of
carcasses of cattle with CNS symptoms and indeterminate BSE status in certain
types of animal feed. On April 30, FDA requested that the rendering company
holding the remains of the Texas cow either destroy them or use them exclusively
in swine feed. m the case that the remains are included in swine feed, 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."10
Any confusion over what to do with cattle condemned for CNS symptoms
awaiting testing for BSE seems unnecessary. The obvious approach is to require
companies either to destroy the carcasses or hold them until test results become
available. Such a policy would avoid any need for complicated traceback
procedures after the discovery of a positive result. According to the
information provided to the Committee by USDA, the FSIS has condemned only 200
to 250 cows per year because of signs of central nervous system damage."
Mandating the destruction or holding of their carcasses would have minimal
economic impact.
The experience with the BSE-infected cow in Washington State illustrates
the prudence of waiting for the results of BSE tests. Prior to December 2003,
USDA permitted cattle that were sampled as part of the BSE surveillance program
to enter commerce even while BSE tests were pending. As a result, when the
BSE-infected cow was discovered, it had already entered the food supply. This
led to a complicated and partially successful traceback procedure in which
hundreds of thousands of pounds of beef had to be destroyed. Because of this
debacle, USDA quickly developed a new policy to require holding all carcasses
from the human food chain during BSE testing.
I appreciate that you have taken steps to enhance the safety of the U.S.
food supply since the discovery of BSE in the United States. I urge you to
consider the lessons of this latest
9 Memo from John R. Clifford, Acting Deputy Administrator, Veterinary
Services, and William Smith, Assistant Administrator, Office of Field
Operations, Food Safety and Inspection Service, to VSMT, Regional Directors,
Area Veterinarians in Charge, and Veterinary Services, Subject: Policy Statement
Regarding BSE Sampling of Condemned Cattle at Slaughter Plants - for Immediate
Implementation (May 5, 2004) (online at http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf).
10 FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. 20,
2004) (online at http://www.fda.gov/bbs/topics/news/2004/NEW01061.html).
11 The yearly totals of FSIS antemortem CNS condemnation for all adult
cattle were 233 (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003). The
database for 2003 had not yet closed.
The Honorable Ann M. Veneman May 13,2004 Page 4
incident. USDA should develop a process that ensures the tracking of
cattle condemned for CNS signs and should institute a policy requiring all
carcasses with pending BSE tests to be destroyed or held. If there are any
statutory barriers to these steps, please do not hesitate to let me know.
Sincerely,
XXXXX X. XXXXXX
Henry A. Waxman
Ranking Minority Member
Congressman Henry Waxmans's Letter to the Honorable Ann Veneman
TSS
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html
##########
*** Qualitative Analysis of BSE Risk Factors in the United States
February 13, 2000 at 3:37 pm PST (BSE red book)
Tuesday, July 14, 2009 U.S.
*** Emergency Bovine Spongiform Encephalopathy Response Plan Summary and
BSE Red Book
Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
*********-------- 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 --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to
unmask] us>
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: ...sniptss
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.>>>>>>
==========================
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to
unmask] us>
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
forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION
YET...can you confirm???
terry
==============================
2004, highly suspect stumbling and staggering mad cow reported, however,
NO TESTING DONE, ON ORDERS FROM AUSTIN $
May 4, 2004
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)...
USDA regulations, any cow that exhibits signs of central nervous system
(CNS)
According to a 1997 Animal and Plant Health Inspection Service (NHIS)
Memorandum, brain samples all of such animals should be sent for BSE testing.2
The memorandum notes that "it is essential that brain specimens be collected
from adult cattle condemned for CNS signs as part of our national surveillance
of BSE."
The cow slaughtered at the Lone Star Beef slaughterhouse last week
staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a
request from APHIS personnel at the plant to conduct BSE testing, however, an
APHIS supervisor in Austin reportedly refused the test and instructed the plant
to send the carcass for rendering.5
May 13,2004
Page 2
snip...
The cow slaughtered at the Lone Star Beef slaughterhouse last week
staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a
request from APHIS personnel at the plant to conduct BSE testing, however, an
APHIS supervisor in Austin reportedly refused the test and instructed the plant
to send the carcass for rendering.5
This sequence of events is troubling, and it raises the question of whether
this is an isolated incident. In 1997, USDA noted a major gap between the number
of cattle condemned for CNS symptoms and the number of these cows actually
tested for mad cow disease. The Department found:
USDA did not test possible mad cows
By Steve Mitchell
United Press International
Published 6/8/2004 9:30 PM
WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims
ittested 500 cows with signs of a brain disorder for mad cow disease last year,
but agency documents obtained by United Press International show the agency
tested only half that number.
"These 9,200 cases were different because brain tissue samples were
preserved with formalin, which makes them suitable for only one type of
test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in
the bovine, and these were probably from the most high risk cattle pool, the
ones the USDA et al, SHOULD have been testing. ...TSS
TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND CALLS
FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS
CONFIRMED
THE USDA MAD COW FOLLIES POSITIVE TEST COVER UP
JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED
OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7
MONTHS LATER
TEXAS MAD COW
THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE
BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i
confirmed this case 7 months earlier to the TAHC, and then, only after i
contacted the Honorable Phyllis Fong and after an act of Congress, this animal
was finally confirmed ;
During the course of the investigation, USDA removed and tested a total of
67 animals of interest from the farm where the index animal's herd originated.
All of these animals tested negative for BSE. 200 adult animals of interest were
determined to have left the index farm. Of these 200, APHIS officials determined
that 143 had gone to slaughter, two were found alive (one was determined not to
be of interest because of its age and the other tested negative), 34 are
presumed dead, one is known dead and 20 have been classified as untraceable. In
addition to the adult animals, APHIS was looking for two calves born to the
index animal. Due to record keeping and identification issues, APHIS had to
trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter
channels, four are presumed to have entered feeding and slaughter channels and
one calf was untraceable.
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.
snip...
Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having
received an animal of interest. The herd was placed under hold order on 7/27/05.
The herd inventory was conducted on 7/28/05. The animal of interest was not
present within the herd, and the hold order was released on 7/28/05. The person
who thought he sold the animal to the owner of Trace Herd 3 had no records and
could not remember who else he might have sold the cow to. Additionally, a
search of GDB for all cattle sold through the markets by that individual did not
result in a match to the animal of interest. The animal of interest traced to
this herd was classified as untraceable because all leads were exhausted.
Trace Herd 4 The owner of Trace Herd 4 was identified as having received
one of the COI through an order buyer. Trace Herd 4 was placed under hold order
on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05.
There were 233 head of cattle that were examined individually by both State and
Federal personnel for all man-made identification and brands. The animal of
interest was not present within the herd. Several animals were reported to have
died in the herd sometime after they arrived on the premises in April 2005. A
final search of GDB records yielded no further results on the eartag of interest
at either subsequent market sale or slaughter. With all leads having been
exhausted, this animal of interest has been classified as untraceable. The hold
order on Trace Herd 4 was released on 8/23/05.
Trace Herd 5 The owner of Trace Herd 5 was identified as having received
two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67
head of cattle in multiple pastures. During the course of the herd inventory,
the owner located records that indicated that one of the COI, a known birth
cohort, had been sold to Trace Herd 8 where she was subsequently found alive.
Upon completion of the herd inventory, the other animal of interest was not
found within the herd. A GDB search of all recorded herd tests conducted on
Trace Herd 5 and all market sales by the owner failed to locate the
identification tag of the animal of interest and she was subsequently classified
as untraceable due to all leads having been exhausted. The hold order on Trace
Herd 5 was released on 8/8/05.
Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having
received an animal of interest and was placed under hold order on 8/1/05. This
herd is made up of 58 head of cattle on two pastures. A herd inventory was
conducted and the animal of interest was not present within the herd. The owner
of Trace Herd 6 had very limited records and was unable to provide further
information on where the cow might have gone after he purchased her from the
livestock market. A search of GDB for all cattle sold through the markets by
that individual did not result in a match to the animal of interest.
Additionally, many of the animals presented for sale by the owner of the herd
had been re-tagged at the market effectually losing the traceability of the
history of that animal prior to re-tagging. The animal of interest traced to
this herd was classified as untraceable due to all leads having been exhausted.
The hold order on Trace Herd 6 was released on 8/3/05.
Trace Herd 7 The owner of Trace Herd 7 was identified as having received
an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7
contains 487 head of cattle on multiple pastures in multiple parts of the State,
including a unit kept on an island. The island location is a particularly rough
place to keep cattle and the owner claimed to have lost 22 head on the island in
2004 due to liver flukes. Upon completion of the herd inventory, the animal of
interest was not found present within Trace Herd 7. A GDB search of all recorded
herd tests conducted on Trace Herd 7 and all market sales by the owner failed to
locate the identification tag of the animal of interest. The cow was
subsequently classified as untraceable. It is quite possible though that she may
have died within the herd, especially if she belonged to the island unit. The
hold order on Trace Herd 7 was released on 8/8/05.
*** 2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006 ***
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. ...
snip...see full text ;
Thursday, October 22, 2015
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad
cow disease USDA and what really happened
Comments on technical aspects of the risk assessment were then submitted to
FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received on
the 2005 updated Harvard BSE risk assessment. Please bear the following points
in mind:
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
Singeltary to APHIS FDA USDA et al ;
CJDIBSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific
Advisors and Consultants Staff January 2001 Meeting (short version)
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
CANADA BSE TSE PRION
Confirmed Cases of Bovine Spongiform Encephalopathy (BSE) in 2015
BSE is a reportable disease under the Health of Animals Regulations. This
means that all suspected cases must be reported to the CFIA.
Current as of: 2015-11-30
The following table lists individual animals confirmed to be infected with
BSE in Canada in 2015.
Date confirmed
Location
Animal type infected
Age of Animal
February 11 Alberta Beef cow 70 months
Monday, November 30, 2015
*** Report on the Investigation of the Nineteenth Case of Bovine Spongiform
Encephalopathy (BSE) in Canada November 2015 ***
Herds infected with Chronic Wasting Disease in Canada in 2015
The CFIA works with provincial governments and industry to conduct regular
Chronic Wasting Disease (CWD) surveillance. Ongoing provincial surveillance for
CWD varies with each particular province's perceived threat and infection
status. Testing is mandatory in Manitoba, Saskatchewan, Alberta and the Yukon;
it is voluntary, completed by random submission, or organized through policy in
other provinces and territories.
In addition, CWD is a reportable disease under the Health of Animals
Regulations. This means that all suspected cases must be reported to the
CFIA.
Current as of: 2015-11-30
Domestic cervid herds confirmed to be infected with CWD in Canada in 2015
Date confirmed
Location
Animal type infected
November 25 Saskatchewan Deer
July 16 Alberta Elk
June 11 Saskatchewan Elk
April 9 Saskatchewan Deer
March 19 Saskatchewan Elk
January 16 Alberta Elk
Flocks infected with Scrapie in Canada in 2015
The CFIA, in co-operation with provincial governments and industry,
launched a national scrapie surveillance program in 2005. Under the program,
producers are encouraged to report animals that die on the farm or exhibit
symptoms of the disease.
In addition, scrapie is a reportable disease under the Health of Animals
Regulations. This means that all suspected cases must be reported to the
CFIA.
Current as of: 2015-11-30
Sheep flocks and/or goat herds confirmed to be infected with classical
scrapie in Canada in 2015
Date confirmed
Location
Animal type infected
January 5 Ontario Goat
May 22 Quebec Sheep
June 16 Ontario Sheep
Friday, July 10, 2015
CANADA TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION UPDATE
Monday, February 23, 2015
20th BSE Case Raises New Concerns about Canada's Feeding Practices and
Voluntary Testing Program; Highlights Importance of COOL
Friday, February 20, 2015
A BSE CANADIAN COW MAD COW UPDATE Transcript - Briefing (February 18, 2015)
Saturday, February 14, 2015
Canadian Food Inspection Agency Confirms Bovine Spongiform Encephalopathy
(BSE) in Alberta
SNIP...see more TSE prion stats from Canada with CJD update as well...
Friday, July 10, 2015
CANADA TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION UPDATE
EDMONTON - Some of former Alberta premier Ralph Klein's most colourful
quotes — and the reactions they elicited:
SNIP...
"This all came about through the discovery of a single, isolated case of
mad cow disease in one Alberta cow on May 20th. The farmer — I think he was a
Louisiana fish farmer who knew nothing about cattle ranching. I guess any
self-respecting rancher would have shot, shovelled and shut up, but he didn't do
that." — Klein recalls how the mad cow crisis started and rancher Marwyn
Peaster's role. The premier was speaking at the Western Governors Association
meeting in Big Sky, Mont. September 2004.
"The premier meant that in an ironic or almost a sarcastic way." — Klein
spokesman Gordon Turtle.
---
"You would have to eat 10 billion meals of brains, spinal cords, ganglia,
eyeballs and tonsils." — Klein speaking in Montreal in January 2005 on the risk
of humans contracting mad cow disease.
---
"I would offer $5 billion to have a Japanese person to come over here and
eat nothing but Alberta beef for a year. And if he gets mad cow disease, I would
be glad to give him $5 billion — make it $10 billion — Canadian." — Klein
speaking after Japan closed its borders to Canadian beef.
---
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011
and how to hide mad cow disease in Canada Current as of: 2011-01-31
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
Tuesday, May 21, 2013
Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common
origin and why the SSS policy is in full force $$$
2015
***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.
***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.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
*** Title: Transmission of scrapie prions to primate after an extended
silent incubation period
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.
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
please see file attachment for full submission and recent science and my
deep concerns on the TSE Prion disease... No documents available.
AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what
otherwise would have been unreported findings of atypical scrapie in sheep. In
2009, five new cases have been reported in Quebec, Ontario, Alberta, and
Saskatchewan. With the exception of Quebec, all cases have been diagnosed as
being the atypical form found in older animals. Canada encourages producers to
join its voluntary surveillance program in order to gain scrapie-free status.
The World Animal Health will not classify Canada as scrapie-free until no new
cases are reported for seven years. The Canadian Sheep Federation is calling on
the government to fund a wider surveillance program in order to establish the
level of prevalence prior to setting an eradication date. Besides long-term
testing, industry is calling for a compensation program for farmers who report
unusual deaths in their flocks.
Current as of: 2015-01-31
Sheep flocks and/or goat herds confirmed to be infected with classical
scrapie in Canada in 2015 Date confirmed Location Animal type infected January 5
Ontario Goat
Tuesday, February 10, 2015
Alberta Canada First case of chronic wasting disease found in farm elk
since 2002
Atypical Scrapie Canada
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National
Veterinary Insitute, Sweden; 2National Veterinary Institute,
Norway Nor98 is a prion disease of old sheep and goats. This atypical form
of scrapie was first described in Norway in 1998. Several features of Nor98 were
shown to be different from classical scrapie including the distribution of
disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is generally the most affected brain area in Nor98. The study here
presented aimed at adding information on the neuropathology in the cerebellum of
Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A
panel of histochemical and immunohistochemical (IHC) stainings such as IHC for
PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers
for phagocytic cells were conducted. The type of histological lesions and tissue
reactions were evaluated. The types of PrPd deposition were characterized. The
cerebellar cortex was regularly affected, even though there was a variation in
the severity of the lesions from case to case. Neuropil vacuolation was more
marked in the molecular layer, but affected also the granular cell layer. There
was a loss of granule cells. Punctate deposition of PrPd was characteristic. It
was morphologically and in distribution identical with that of synaptophysin,
suggesting that PrPd accumulates in the synaptic structures. PrPd was also
observed in the granule cell layer and in the white matter. The pathology
features of Nor98 in the cerebellum of the affected sheep showed similarities
with those of sporadic Creutzfeldt-Jakob disease in humans.
***The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.
PR-26
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B.
Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto
Superiore di Sanità, Department of Food Safety and Veterinary Public Health,
Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna,
Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo,
Norway
Molecular variants of PrPSc are being increasingly investigated in sheep
scrapie and are generally referred to as "atypical" scrapie, as opposed to
"classical scrapie". Among the atypical group, Nor98 seems to be the best
identified. We studied the molecular properties of Italian and Norwegian Nor98
samples by WB analysis of brain homogenates, either untreated, digested with
different concentrations of proteinase K, or subjected to enzymatic
deglycosylation. The identity of PrP fragments was inferred by means of
antibodies spanning the full PrP sequence. We found that undigested brain
homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11),
truncated at both the C-terminus and the N-terminus, and not N-glycosylated.
After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and
N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11.
Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are
mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at
the highest concentrations, similarly to PrP27-30 associated with classical
scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment
of 17 kDa with the same properties of PrP11, that was tentatively identified as
a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in
2% sodium laurylsorcosine and is mainly produced from detergentsoluble,
full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a
sample with molecular and pathological properties consistent with Nor98 showed
plaque-like deposits of PrPSc in the thalamus when the brain was analysed by
PrPSc immunohistochemistry. Taken together, our results show that the
distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids
~ 90-155. This fragment is produced by successive N-terminal and C-terminal
cleavages from a full-length and largely detergent-soluble PrPSc, is produced in
vivo and is extremely resistant to PK digestion.
*** Intriguingly, these conclusions suggest that some pathological features
of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
119
A newly identified type of scrapie agent can naturally infect sheep with
resistant PrP genotypes
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne
Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?,
Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author
Affiliations
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et
Cytogénétique, Institut National de la Recherche Agronomique, 78350
Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la
Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte
Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire
des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon,
France; **Pathologie Infectieuse et Immunologie, Institut National de la
Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology,
National Veterinary Institute, 0033 Oslo, Norway
***Edited by Stanley B. Prusiner, University of California, San Francisco,
CA (received for review March 21, 2005)
Abstract Scrapie in small ruminants belongs to transmissible spongiform
encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative
disorders that affect humans and animals and can transmit within and between
species by ingestion or inoculation. Conversion of the host-encoded prion
protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP
(PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified
surveillance of scrapie in the European Union, together with the improvement of
PrPSc detection techniques, has led to the discovery of a growing number of
so-called atypical scrapie cases. These include clinical Nor98 cases first
identified in Norwegian sheep on the basis of unusual pathological and PrPSc
molecular features and "cases" that produced discordant responses in the rapid
tests currently applied to the large-scale random screening of slaughtered or
fallen animals. Worryingly, a substantial proportion of such cases involved
sheep with PrP genotypes known until now to confer natural resistance to
conventional scrapie. Here we report that both Nor98 and discordant cases,
including three sheep homozygous for the resistant PrPARR allele (A136R154R171),
efficiently transmitted the disease to transgenic mice expressing ovine PrP, and
that they shared unique biological and biochemical features upon propagation in
mice. *** These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
Authors
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon
S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J.
M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France;
ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex,
France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway,
INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Content
Atypical scrapie is a TSE occurring in small ruminants and harbouring
peculiar clinical, epidemiological and biochemical properties. Currently this
form of disease is identified in a large number of countries. In this study we
report the transmission of an atypical scrapie isolate through different species
barriers as modeled by transgenic mice (Tg) expressing different species PRP
sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock.
inoculation into AHQ/AHQ sheep induced a disease which had all
neuro-pathological and biochemical characteristics of atypical scrapie.
Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate
retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different
v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and
biochemical characteristics similar to those of atypical BSE L in the same mouse
model. Moreover, whereas no other TSE agent than BSE were shown to transmit into
Tg porcine mice, atypical scrapie was able to develop into this model, albeit
with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed
similar biological and biochemical characteristics than BSE adapted to this
porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross
species barriers
(ii) the possible capacity of this agent to acquire new characteristics
when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on
the origin of the diversity of the TSE agents and could have consequences on
field TSE control measures.
Tuesday, April 28, 2009
Nor98-like Scrapie in the United States of America
Saturday, September 12, 2015
The Canadian Management of Bovine Spongiform Encephalopathy in Historical
and Scientific Perspective, 1990-2014
>>>We propose that Canadian policies largely ignored the implicit
medical nature of BSE, treating it as a purely agricultural and veterinary
issue. In this way, policies to protect Canadians were often delayed and
incomplete, in a manner disturbingly reminiscent of Britain’s failed management
of BSE. Despite assurances to the contrary, it is premature to conclude that BSE
(and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of
Canada’s past: BSE remains very much an issue in Canada’s present.
<<<
Sunday, October 18, 2015
*** World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
From: Terry S. Singeltary Sr.
Sent: Friday, October 16, 2015 5:23 PM
To: kebanks@bmj.com
Cc: gill.harris@bmj.com ; lhoney@bmj.com ; gmills@bmj.com ;
joflaherty@bmj.com ; sjarvis@bmj.com Subject: THE World Organisation for Animal
Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis
research
Veterinary Record 2015;177:381 doi:10.1136/vr.h5454 News and Reports One
health THE World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
THE World Organisation for Animal Health (OIE) and the Institut Pasteur
have agreed to strengthen their cooperation in the fields of animal disease and
zoonosis research, education, surveillance and control, in line with the One
Health concept, through a new collaborative agreement.
The Institut Pasteur is
Veterinary Record 2015;177:379 doi:10.1136/vr.h5446
News and Reports
Defra seeks a dialogue on animal import controls Defra is seeking ‘ideas
and discussion’ as part of a review in England of the Trade in Animals and
Related Products Regulations 2011. The Regulations govern veterinary border
controls for live animals and products of animal origin.
>THE World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research<
please forgive me if I don’t believe you $$$
I remember...
>>>PARIS -- The World Organization for Animal Health said on
Wednesday it had lowered to the safest level the official risk of six countries
for mad cow disease, a move expected to open international market access for
their beef exports. These countries are France, Ireland, Switzerland, the Czech
Republic, Cyprus and the Lichtenstein.<<<
THIS move is _not_ based on science, but on corporate profits and big ag.
to say now that France is a "negligible risk", would be like saying North
America is a "negligible risk", which is preposterous. not based on sound
science, but on greed and special interest. the only _move_ this ‘’BSE mad cow
negligible risk’’ assessment makes, is a move to increase global Transmissible
Spongiform Encephalopathy prion mad cow type disease, via the legal trading of
the TSE prion aka mad cow type disease via the BSE MRR i.e. Minimal Risk Region
policy, a policy set up to fail from the start. please, for whatever God you
pray to sake, please be warned.
‘’AS i said before, OIE should hang up there jock strap now, since it
appears they will buckle every time a country makes some political hay about
trade protocol, commodities and futures. IF they are not going to be science
based, they should do everyone a favor and dissolve there organization.’’
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
Wednesday, March 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
Friday, April 4, 2014
China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa
and Saudi Arabia still retain BSE-related closures
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease
The OIE is nothing more than a trading brokerage for the Transmissible
Spongiform Encephalopathy TSE prion disease aka mad cow type disease. Frances is
still in the midst of a mad cow disease outbreak with atypical BSE cases still
growing. mad cow disease is so bad in France, as with the USA, they stopped
testing for mad cow disease (France altogether and the USA to figures so low,
you would only detect a case of mad cow disease, only by chance).
from the inside looking out ;
Quote: Maybe familirise yourself with the OIE. The primary concern is
animal health of the world they are the animal version of the WHO. It is a long
way down from that ivory tower but here we go, until pressured by the USA
representatives a country could not export animals for 6 years after finding a
BSE/BASE positive animal so under the old rules the US would not be able to
export anywhere in the world for another 4 1/2 years. Who got the risk levels
system put in to allow some trade - your US representatives. You guys want to
change rules - OK , but you do not get special rules that only apply to the US.
As i have told you before Sand h I market all my own slaughter animals and you
know that, so don't do the whole holier than thow act.
With all due respect, it is obvious that you know little about the OIE and
how it actually works. Having been to their offices in Paris and talked
personally with the Head of the Animal Test Section, you would choke if you knew
how many lobby groups attend that office daily. There is a steady stream of paid
lobby groups that have one goal in life and that is to sway the Section Heads of
each department within the OIE to suit the needs of different jurisdictions
around the world, which curiously enough, also includes the USA and Canada.
Anyone can go there and chat with them - providing they can provide valid cause
to be let in. To say that the only goal of the OIE is animal health is actually
only part of their function. They are more than that and my discussions with Dr.
Diaz there has showed me that. But to blindly make a statement regarding what
they do when you have no idea what they actually do is like eating the skin of
the orange and not knowing what is actually under.
Interestingly you state that the US Government applied pressure (to the
OIE) I assume and that is a great example of the lobby groups doing their job.
So, at the end of the day, one can safely assume that it is the pressure applied
by certain influential lobby groups that will determine a likely outcome to an
apparent OIE directive. Man alive, isn't it great to live in a democracy wherein
the people get to make the choices and not just some "other" interested party or
group - say like........Cargill or Tyson for example?
So, one last question, question?
Who wags the tail of that dog?? And for what reason other than one that is
purely associated with trade and international agreements and greed?
And you think it is so simply explainable.
end...tss
Subject: UPDATED WHO Guidelines include tissues from Cervidae affected with
Chronic Wasting Disease (CWD)
snip...see full text ;
Sunday, October 18, 2015
*** World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
IRELAND
Saturday, October 3, 2015
Wales Welsh Government Written Statement - Isolated case of Classical
Bovine spongiform encephalopathy detected in deceased bovine
Thursday, June 11, 2015
Ireland Department of Agriculture, Food and the Marine Identifies Suspected
BSE Case
Saturday, September 19, 2015
*** An interview with Professor John Collinge: VIDEO Director of the MRC
Prion Unit Part of the Hayward Gallery's History Is Now ***
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Singeltary et al
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Friday, May 29, 2015
GAO FEDERAL VETERINARIANS US Federal Government Is Unprepared for a
Large-Scale Animal Disease Outbreak
Thursday, September 10, 2015
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory
Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
Sunday, October 25, 2015
USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE
LIVESTOCK CWD SCRAPIE TSE PRION
Thursday, July 30, 2015
Professor Lacey believes sporadic CJD itself originates from a cattle
infection number of cattle farmers falling victim to Creutzfeld-Jakob Disease is
much too high to be mere chance
Thursday, October 1, 2015
H-type bovine spongiform encephalopathy associated with E211K prion protein
polymorphism: clinical and pathologic features in wild-type and E211K cattle
following intracranial inoculation
Master Obi-Wan Kenobi, Kemosabe...THIS IS NOT GOOD
GOOSE!...grasshopper...tonto...tss
BRAZIL
Friday, October 30, 2015
Brazil Agriculture minister to visit Saudi Arabia over BSE mad cow trade
WALES WELSH
Saturday, October 3, 2015
Wales Welsh Government Written Statement - Isolated case of Classical
Bovine spongiform encephalopathy detected in deceased bovine
SLOVENIA
Wednesday, September 16, 2015
Ljubljana Slovenia First Mad Cow Disease Case in Eight Years Confirmed
ITALY BSE
Italye BSE 1994-2b 2001-48 2002-38 2003-29 2004-7 2005-8 2006-7 2007-2
2008-1 2009-2
e Italy: Year 2002 - Includes 2 imported cases.
Monday, September 07, 2015
ITALY REPORTING INCREASE IN CASES OF MAD COW TYPE TSE PRION DISEASE IN
HUMANS CJD
Tuesday, October 20, 2015
FBI: Agroterrorism not likely, but very possible, Dr. Stephen Goldsmith
FBI Laboratory Division, here's your sign
CC-Dr. Steve Goldsmith, FBI Laboratory Division
please note, I tried to forward this to the FBI, spoke with several folks
at FBI headquarters, and they were not interested...just saying...terry
Friday, May 29, 2015
GAO FEDERAL VETERINARIANS US Federal Government Is Unprepared for a
Large-Scale Animal Disease Outbreak
Saturday, December 12, 2015
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
*** CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
RIP MOM December 14, 1997
USDA Announces Preliminary Concurrence with OIE Risk Designations for BSE
in 16 Countries USDA Animal and Plant Health Inspection Service sent this
bulletin at 12/04/2015 11:15 AM EST
Bookmark and Share
USDA Announces Preliminary Concurrence with World Animal Health
Organization Risk Designations for Bovine Spongiform Encephalopathy in 16
Countries
December 4, 2015—The United States Department of Agriculture’s Animal and
Plant Health Inspection Service (APHIS) is preliminarily concurring with the
World Organization for Animal Health’s (OIE) bovine spongiform encephalopathy
(BSE) risk designations for 16 countries. The OIE recognizes these regions as
being of negligible risk for BSE. APHIS reviewed the information supporting the
OIE’s risk designations for these regions and agrees with the OIE designations.
The 16 countries are: Bulgaria, Cyprus, Czech Republic, Estonia, France,
India, Korea (Republic of), Hungary, Latvia, Liechtenstein, Luxembourg, Malta,
Portugal, Romania, Slovakia, and Switzerland.
The OIE recommendations regarding each of the above countries can be viewed
online.
APHIS considers all countries of the world to fall into in one of three
BSE risk categories: negligible risk, controlled risk, or undetermined risk. Any
region that is not classified by APHIS as presenting either negligible risk or
controlled risk for BSE is considered to present an undetermined risk.
Under the regulations, APHIS may classify a region for BSE in one of two
ways. One way is for countries that have not received a risk classification from
the World Organization for Animal Health (OIE) to request classification by
APHIS. The other way is for APHIS to concur with the classification given to a
country by the OIE.
This notice is available for 60 days for review and comment. APHIS will
consider all comments received on or before February 2, 2016. After reviewing
any comments we receive, we will announce our final determination regarding the
BSE classification of these countries in the Federal Register.
LMAO !!! pot calling kettle black...BSE MRR policy equals the legal trading
of all strains of TSE Prion aka mad cow disease...any consumers death there from are
now acceptable $$$...TSS
these blogs are for educational use. I do not advertise or make money from
them.
MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget,
and never let them forget...
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
