USDA Chief Veterinary
Officer On Surveillance And Milk
Safety
A
new actuality is available on the USDA FTP site. The
actuality can also be seen on USDA's YouTube channel.
Note for broadcasters:
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safeguards
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ACTUALITY – USDA Chief Veterinary
Officer On Surveillance And Milk Safety
INFO: USDA Chief Veterinary Officer Dr. John Clifford explains the
system of strong interlocking safeguards designed to protect human and animal
health.
Dr. John Clifford, Chief Veterinary
Officer For the United States of America:
Hello, I’m Dr. John
Clifford, chief veterinary officer for the United States of America. At USDA, we
oversee a system of strong interlocking safeguards that protect human and animal
health, as well as food safety in the United States. Those safeguards include
targeted surveillance activities. Through that surveillance program, on April
24th we confirmed the nation’s 4th case of bovine spongiform
encephalopathy, or BSE, in a dairy cow on the west coast. BSE is a fatal disease
affecting the central nervous system of adult cattle. We proactively test for
BSE in order to detect the disease at the very low level of less than 1 case per
million adult cattle, to assess any change in the BSE status of U.S. cattle,
and to identify any rise in BSE
prevalence in the country. Our
targeted surveillance program has been in place since 1990. We currently test
for BSE at levels 10 times greater than World Animal Health Organization
standards. We test approximately 40,000 animals per year, taking those samples from cattle
where the disease is most likely to be found. This includes animals that have clinical
signs consistent with BSE, have other central nervous system abnormalities, die
for unknown reasons, or cannot walk or move well. We collect samples from a variety of
locations where the targeted groups of animals are found. The samples from the animal in
question were taken at a rendering facility in California. Our surveillance works. We found this
case of BSE. The carcass of the
animal was held at the rendering facility and then will be destroyed. It was
never presented for processing for human consumption. At no time did it present a risk to
the food supply. Our food supply remains safe. With California being a large dairy
state, there have been some concerns raised about milk. Let me assure you, our
milk is safe to drink. Scientific
research demonstrates that BSE cannot be transmitted in cow’s milk, even if that
milk comes from a cow with BSE. The World Health Organization has stated that
tests on milk from BSE-infected animals have not shown any BSE infectivity. Milk
and milk products, are, therefore considered safe to consume. Let me assure consumers and our
trading partners that ongoing BSE surveillance allows the USDA to detect BSE at very low
levels in the U.S. cattle population. The safeguarding system is working. For
updates on our ongoing investigation and more information about BSE in general,
visit our website at www.usda.gov.
these folks should no now to
never say never $$$
BOTTOM LINE, milk and atypical
L-type BASE BSE, they have no clue yet. they must do transmission studies. with
atypical L-type BASE BSE, this type is much more virulent. ...tss
MILK and Transmissible
Spongiform Encephalopathy TSE PRION
Terry S. Singeltary Sr.
11/18/2011
TO date, and i imphasize 'to date', there has been no documented evidence
of transmission of BSE via milk of BSE infected cow to another cow. however,
with the limited testing done to date, on just the c-BSE, you cannot rule this
out, especially with the atypical BSE L-type i.e. BASE, being much more
virulent. Concern has been increasing due to fluids from TSE species i.e. blood,
urine, and milk, and the fact that infectivity has been detected.
Prion infectivity has now been detected in blood, urine and milk.
please see ;
Seven main threats for the future linked to prions
The NeuroPrion network has identified seven main threats for the future
linked to prions.
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
In small ruminants, a new atypical form of scrapie currently represents up
to 50% of detected cases and even involves sheep selected for resistance to
classical scrapie. The consequences for animal and human health are still
unknown and there may be a potential connection with atypical BSE. These
atypical scrapie cases constitute a second threat not envisioned previously
which could deeply modify the European approach to prion diseases.
Third threat
The species barrier between human and cattle might be weaker than
previously expected and the risk of transmission of prion diseases between
different species has been notoriously unpredictable. The emergence of new
atypical strains in cattle and sheep together with the spread of chronic wasting
disease in cervids renders the understanding of the species barrier critical.
This constitutes a third threat not properly envisioned previously that could
deeply modify the European approach to prion diseases.
Fourth threat
Prion infectivity has now been detected in blood, urine and milk and this
has potential consequences on risk assessments for the environment and food as
well as for contamination of surfaces including medical instruments. Furthermore
the procedures recommended for decontamination of MBM (Meat and Bone Meal),
which are based on older methodologies not designed for this purpose, have
turned out to be of very limited efficacy and compromise current policies
concerning the reuse of these high value protein supplements
(cross-contamination of feed circuits are difficult to control). It should be
noted that the destruction or very limited use of MBM is estimated to still cost
1 billion euros per year to the European economy,
whereas other countries, including the US,
Brazil, and Argentine do not have these constraints.
However, many uncertainties remain concerning the guarantees that can be
reasonably provided for food and feed safety and scientific knowledge about the
causative agents (prions) will continue to evolve. This decontamination and
environmental issue is a fourth threat that could modify deeply the European
approach to prion diseases.
Fifth threat The precise nature of prions remains elusive. Very recent data
indicate that abnormal prion protein (PrPTSE) can be generated from the brains
of normal animals, and under some conditions (including contaminated waste
water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost
unchanged, a finding that underlines the possibility of having BSE without any
detectable diagnostic marker. These are just two areas of our incomplete
knowledge of the fundamental biology of prions which constitute a fifth threat
to the European approach to prion diseases.
Sixth threat The absence of common methods and standardisation in the
evaluation of multiple in vivo models with different prion strains and different
transgenic mice expressing PrP from different species (different genotypes of
cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of
all the data generated by the different scientific groups almost impossible.
This deeply impairs risk assessment. Moreover, the possibility of generating
PrPTSE de novo with new powerful techniques has raised serious questions about
their appropriateness for use as blood screening tests. The confusion about an
incorrect interpretation of positive results obtained by these methods
constitutes a sixth threat to European approach to prion diseases.
Seventh Threat The detection of new or re-emerging prion diseases in
animals or humans which could lead to a new crisis in consumer confidence over
the relaxation of precautionary measures and surveillance programmes constitutes
a seventh threat that could modify the European approach to prion
diseases.
Goat BSE: Proposal for Improvement of Goat TSE Discriminative Diagnosis and
Susceptibility based Assessment of BSE Infectivity in Goat Milk and Meat
Funded by EU, DEFRA This project is run by a consortium of ten research
teams in seven EU countries.
In light of the known ability of the BSE agent to cross the animal/human
species barrier, recent evidence establishing the presence of BSE in goat is
especially alarming, as it represents a new potential risk of food-born
contamination to human consumers of goat milk and meat products. The main
objective is to determine the tissue distribution of BSE after oral exposure of
goats and to do this while simultaneously generating data on genetic
susceptibility in the most common used production breeds. This proposal aims at
(i) providing data for the evaluation of human risk associated with goat BSE,
(ii) providing pathogenesis data and biological material from first and second
passage BSE in goats, (iii) evaluating the possibility of BSE self-maintenance
in goat herds through maternal or horizontal transmission, (iv) validating and
improving our ability to detect caprine BSE and discriminate it from scrapie in
goats. Our approach will establish the influence of PrP gene polymorphisms on
scrapie and BSE susceptibility so that genetics could potentially be used for
the control of field TSE outbreaks in goats. We will also document European
field TSE strain variability in goats by recruiting a large number of TSE goat
isolates from affected European countries. Already established or specifically
created animal models (strain typing) and biochemical tools (PrPSc typing), will
be tested for their ability to efficiently discriminate goat BSE/scrapie.
Finally, by measuring infectivity in various tissues collected from goats at
different stages of BSE infection, we will provide essential data for
quantitative risk assessment.
Vet. Res. (2010) 41:48 Original article
Pathogenesis of natural goat scrapie: modulation by host PRNP genotype and
effect of co-existent conditions
Lorenzo González1*, Stuart Martin1, Stephen A.C. Hawkins2, Wilfred
Goldmann3, Martin Jeffrey1 and Sílvia Sisó1
1 Veterinary Laboratories Agency (VLA-Lasswade), Pentlands Science Park,
Penicuik, Midlothian EH26 0PZ, United Kingdom 2 VLA-Weybridge, Addlestone,
Surrey KT15 3NB, United Kingdom 3 The Roslin Institute and R(D)SVS University of
Edinburgh, Roslin, Midlothian EH25 9PS, United Kingdom
* Corresponding author: l.gonzalez@vla.defra.gsi.gov.uk
Received: 13 January 2010 Accepted: 7 April 2010
Abstract
After detection of a high prevalence of scrapie in a large dairy goat herd,
72 infected animals were examined by immunohistochemistry with prion protein
(PrP) antibody Bar224 to study the pathogenesis of the infection. Tissues
examined included the brain and thoracic spinal cord (TSC), a wide selection of
lymphoreticular system (LRS) tissues, the distal ileum and its enteric nervous
system (ENS), and other organs, including the mammary gland. The whole open
reading frame of the PRNP gene was sequenced and antibodies to caprine
arthritis-encephalitis virus (CAEV) infection were determined. Unexpectedly,
accumulation of disease-associated PrP (PrPd) in the brain was more frequent in
methionine carriers at codon 142 (24/32, 75.0%) than amongst isoleucine
homozygotes (14/40, 35.0%). The latter, however, showed significantly greater
amounts of brain PrPd than the former (average scores of 9.3 and 3.0,
respectively). A significant proportion of the 38 goats that were positive in
brain were negative in the ENS (44.7%) or in the TSC (39.5%). These results,
together with the early and consistent involvement of the circumventricular
organs and the hypothalamus, point towards a significant contribution of the
haematogenous route in the process of neuroinvasion. Chronic enteritis was
observed in 98 of the 200 goats examined, with no association with either
scrapie infection or presence of PrPd in the gut. Lymphoproliferative
interstitial mastitis was observed in 13/31 CAEV-positive and scrapie-infected
goats; PrPd in the mammary gland was detected in five of those 13 goats,
suggesting a possible contribution of CAEV infection in scrapie transmission via
milk.
Key words: scrapie / goat / prion neuroinvasion / transmissible spongiform
encephalopathy / CAEV
© The British Crown, published by INRA/EDP Sciences, 2010
6 January 2010 -
The public “TSEs in goats” website Link:
Since December 2006 a new EU funded project has started that has been
essentially developed from NeuroPrion TSEgoat task group members and their
progress: “GoatBSE: Proposal for improvement of goat TSE discriminative
diagnosis and susceptibility based assessment of BSE infectivity in goat milk
and meat.” (European STREP project FOOD-CT-2006-36353, frame work 6, area
Thematic priority: Food quality and safety). In this project the focus of study
is about consequences of an infection with BSE in goats for disease transmission
and product safety.
Sheep with Scrapie and Mastitis Transmit Infectious Prions through the
Milk?
Ciriaco Ligios1,†, Maria Giovanna Cancedda1, Antonello Carta2, Cinzia
Santucciu1, Caterina Maestrale1, Francesca Demontis1, Mariangela Saba1,
Cristiana Patta1, James C. DeMartini3, Adriano Aguzzi4,†,* and Christina J.
Sigurdson4,5,6,†,*
+ Author Affiliations
1Istituto Zooprofilattico Sperimentale della Sardegna, Sassari, Italy
2Research Unit of Genetics and Biotechnology, DIRPA, AGRIS Sardinia,
Olmedo, Italy
3Department of Microbiology, Immunology, and Pathology, Colorado State
University, Fort Collins, Colorado
4Institute of Neuropathology, UniversitätsSpital Zürich, Zürich,
Switzerland
5 Department of Pathology, School of Medicine, University of California,
San Diego, California
6Department of Pathology, Microbiology, and Immunology, University of
California, Davis, California
Next Section ABSTRACT
Prions are misfolded proteins that are infectious and naturally
transmitted, causing a fatal neurological disease in humans and animals. Prion
shedding routes have been shown to be modified by inflammation in excretory
organs, such as the kidney. Here, we show that sheep with scrapie and lentiviral
mastitis secrete prions into the milk and infect nearly 90% of naïve suckling
lambs. Thus, lentiviruses may enhance prion transmission, conceivably sustaining
prion infections in flocks for generations. This study also indicates a risk of
prion spread to sheep and potentially to other animals through dietary exposure
to pooled sheep milk or milk products.
EFSA Journal 2011; 9(1):1945 Suggested citation:
EFSA Panel on Biological Hazards (BIOHAZ);
Joint Scientific Opinion on any possible epidemiological or molecular
association between TSEs in animals and humans.
EFSA Journal 2011;9(1):1945. [111 pp.] doi:10.2903/j.efsa.2011.1945.
Available online: www.efsa.europa.eu/efsajournal © European Food Safety
Authority, 2011 SCIENTIFIC OPINION Joint Scientific Opinion on any possible
epidemiological or molecular association between TSEs in animals and humans1
EFSA Panel on Biological Hazards (BIOHAZ)2, 3 European Food Safety Authority
(EFSA), Parma, Italy European Centre for Disease Prevention and Control (ECDC)4,
5 Stockholm, Sweden
More recent EFSA opinions focused on the human exposure risk to TSEs
through consumption of products deriving from small ruminants (ovine and caprine
carcasses below six months, milk and milk products), but only focused on human
exposure, without discussing the zoonotic potential of small ruminants TSEs
(EFSA, 2008a, 2008c). A recent EFSA opinion (EFSA Panel on Biological Hazards
(BIOHAZ), 2010a) provided updated data on the TSE infectivity distribution in
small ruminant tissues. It also estimated the relative reduction of BSE
infectivity load that can be achieved in the carcass of a small ruminant through
the implementation of the current or alternative policies in terms of removal of
Specified Risk Material (SRM). The zoonotic potential of TSE agents in small
ruminants is, however, not discussed in the opinion.
The TSE agent disseminates to the CNS (brain and spinal cord) apparently
via the Enteric Nervous System and its nerves fibers (Andreoletti et al., 2000;
Jeffrey et al., 2001; van Keulen et al., 2002), which is considered to
accumulate TSE agents until around half of the incubation period. From there the
agent could redistribute (centrifugally) to the peripheral nervous system and
skeletal muscle (Andreoletti et al., 2004). Additionally, infectivity was also
reported to be present in blood (Hunter et al., 2002), and in blood and in milk
and colostrum (from the first lactation) from animals during incubation (Konold
et al., 2008; Lacroux et al., 2008). In blood, the infectious agent can be
detected as early as at 3 months of age and persists throughout the incubation
period (Andreoletti et al., 2007).
Finally, protection measures applied all along the food chain against small
ruminants TSEs in the EU mainly rely at operational level on specified risk
material (SRM) removal, i.e exclusion from food chain of tissues that can
contain a high infectious load. However, for practical reasons, the SRM measures
do not imply discarding from the food chain of all the infectious tissues and
animal products that could contain infectivity (EFSA, 2008c). Moreover,
infectivity was recently identified in tissues like skeletal muscles or in
products like milk from small ruminants incubating scrapie, tissues that were
previously considered to be non infectious.
Commentary
In vitro amplification of prions from milk in the detection of subclinical
infections
Volume 3, Issue 4 October/November/December 2009 Pages 236 - 239 http://dx.doi.org/10.4161/pri.3.4.10425
Kevin C. Gough, Claire A. Baker, Maged Taema and Ben C. Maddison
View affiliations
Prions can be amplified by serial protein misfolding cyclic amplification
(sPMCA) from the milk of a high proportion of apparently healthy, scrapie
exposed sheep with PRNP genotypes not previously associated with high disease
penetrance1. These data strongly suggest the widespread presence of subclinical
scrapie infections within scrapie-exposed flocks containing sheep with a range
of susceptible PRNP genotypes. These data also lead to the hypothesis that
similar subclinical disease states may be common for other animal and human
prion diseases. Furthermore, the application of sPMCA to milk provides a method
to detect such subclinical disease. Here, we describe the high level
amplification of bovine spongiform encephalopathy (BSE) prions from both ovine
and bovine origin, a methodology that will facilitate the detection of any
prions secreted within bovine and ovine milk during subclinical and clinical BSE
disease.
Prion Protein in Milk
Nicola Franscini,1 Ahmed El Gedaily,1 Ulrich Matthey,1 Susanne Franitza,1
Man-Sun Sy,2 Alexander Bürkle,3 Martin Groschup,4 Ueli Braun,5 and Ralph
Zahn1
Conclusions/Significance
In view of a recent study showing evidence of prion replication occurring
in the mammary gland of scrapie infected sheep suffering from mastitis, the
appearance of PrPC in milk implies the possibility that milk of TSE-infected
animals serves as source for PrPSc.
WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform
Encephalopathies Updated 2010
snip...
Since the publication in 2006
of Annex 1 (Major Categories of Infectivity) in the ‘‘WHO Guidelines on Tissue
Infectivity Distribution in Transmissible Spongiform Encephalopathies’’, some
tissues (ovary, uterus, mammary glands/udder, skin, adipose tissue, and
heart/pericardium) and body fluids (saliva, milk, urine, and feces) in which
infectivity had not been detected, have since been found to contain infectivity
or PrPTSE and therefore have there been moved from the category of ‘‘tissues
with no detectable infectivity’’ ’’ to the category of ‘‘lower-infectivity
tissues.’’
When
L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the
resulting molecular fingerprint had changed, either in the first or a subsequent
passage, from L-type into C-type BSE. In addition, non-human primates are
specifically susceptible for atypical BSE as demonstrated by an approximately
50% shortened incubation time for L-type BSE as compared to C-type. Considering
the current scientific information available, it cannot be assumed that these
different BSE types pose the same human health risks as C-type BSE or that these
risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1 http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
PLoS One. 2012; 7(2): e31449.
Published online 2012 February 21. doi: 10.1371/journal.pone.0031449
PMCID: PMC3283643
Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy
The present data offer novel information on the tropism of the BASE agent and highlight relevant public health issues. While the transmission barrier for classical BSE is high in most species, BASE prions are readily transmissible to a variety of mammals including non-human primates [11]–[13], [35]. Accordingly, the possibility of spreading of BASE prions through skeletal muscle to other species should be taken into account and evaluated in risk analysis studies.
PINK SLIME LFTB MSM MRM BSE TSE PRION
Saturday, April 21, 2012
HISD seeks refund on burgers with 'pink slime'
Wednesday, March 14, 2012
PINK SLIME, MRM’s, BSE AKA MAD COW
DISEASE, AND THE USDA NSLP
Sunday, August 28, 2011
Tuesday, April 24, 2012
MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA
Wednesday, April 25, 2012
4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012
http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/4th-mad-cow-disease-usa-california.html
Wednesday, April 25, 2012
USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 – 2012
http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/usa-mad-cow-disease-and-cjd-there-from.html
America's Mad Cow crisis by John Stauber
http://www.commondreams.org/view/2012/04/26-1
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