Wednesday, April 25, 2012

ACTUALITY – USDA Chief Veterinary Officer On Surveillance And Milk Safety and BSE aka MAD COW DISEASE

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: B-roll of cows follows Dr. Clifford’s actuality on the file available on the FTP site.

FTP Download instructions:




User name: usdanews


Password: Newscontent1


Filename for TV Actuality: Clifford safeguards


The new file is in QuickTime Movie (H.264)




Please email bob.ellison@usda.gov if you have problems or suggestions.


Also, use this free ftp client if you have problems.





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.











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...










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






Rick Perry, Texas, BSE aka mad cow disease, CJD, and 12 years of lies there from

http://sciencebushwhacked.blogspot.com/2011/08/rick-perry-texas-bse-aka-mad-cow.html
BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!





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








layperson
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net

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