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Breaking news for everyone's consumption

Australia Lifts Ban on Beef Imports

On Monday, Australia lifted its nine-year ban on imported meat from countries where cows had tested positive for bovine spongiform encephalopathy (BSE), or “Mad Cow” disease.  While it will be several months before imported beef products will reach grocery store shelves in Australia, shoppers could have access to such products within six months.

Food Standards Australia New Zealand (FSANZ) is prepared to accept applications from countries seeking to export their beef to the region.  Once the application is received, it will take a minimum of 20 weeks for each application to be assessed.  

FSANZ has not yet received any applications for export.  

Under the new protocol Australia will be accepting imports of muscle meat–no brains or spinal cords of animals will be allowed into the country.  Humans can become infected with BSE if they eat pieces of the brains or spinal cords of infected animals.

Companies that apply for export privileges may be subjected to in-country inspection of their processing facility.  They will also be subjected to stringent traceability standards that are equivalent to or better than Australia’s, and all meat products will have to be cleared by Biosecurity Australia.

Beef from the U.S. and United Kingdom reportedly do not meet Australia’s requirements; Japan is rumored to be considering an application.

About BSE

BSE is a chronic degenerative nervous system disease affecting cattle. The disease was first diagnosed in 1986 in Great Britain.  BSE is so named because of the spongy appearance of the brain tissue of infected cattle when sections are examined under a microscope.

Affected animals may display changes in temperament, such as nervousness or aggression, abnormal posture and difficulty in rising, decreased milk production, or loss of body weight despite continued appetite. Affected cattle die or are killed.

The incubation period (the time from when an animal becomes infected until it first shows signs of disease) is from 2 to 8 years. Following the onset of clinical signs, the animal’s condition deteriorates until it dies. This process usually takes from 2 weeks to 6 months.  

Currently, there is no test to detect the disease in a live animal; veterinary pathologists confirm BSE by postmortem microscopic examination of brain tissue or by the detection of the abnormal form of the prion protein.

© Food Safety News
    Scrapie Flock Certification Program
    As of January 31, 2010, there were 1,701 flocks participating in the Scrapie Flock Certification Program (SFCP). Of these flocks, 1,094 were complete monitored flocks, 551 were certified, 51 were export monitored, and 5 were selective monitored flocks (Figures 1 and la). Six flocks were enrolled or certified during January (Figure 2). SFCP open statuses by fiscal year from FY 1997 to FY 2010 are depicted in Chart 1.
    Infected and Source Flocks
    As of January 31, 2010, there were 11 scrapie infected and source flocks with open statuses (Figure 3). There were no flocks designated as infected or source in January. In FY 2010, two new infected flocks and two new source flocks were reported (Figure 4); eight flocks completed a clean-up plan and were released (Figure 5). The ratio of infected and source flocks released to newly identified infected and source flocks for FY 2010 = 2 : 1. New infected and source statuses from FY 1997 to FY 2010 are depicted in Chart 2.
    Positive Scrapie Cases
    As of January 31, 2010, 24 positive cases in sheep or goats were reported by the National Veterinary Services Laboratories (NVSL); 14 were field cases and 10 were Regulatory Scrapie Slaughter Surveillance (RSSS) cases collected between October 1,2009 and January 31,2010 and confirmed by February 19,2010 (Figure 6). Three RSSS cases and one field case were diagnosed as Nor98-like scrapie. Field cases are positive animals tested as part of a disease investigation including potentially exposed, exposed, and suspect animals. Twenty one cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002 (Figure 7). The most recent positive goat case was confirmed rectal biopsy positive in November 2009 and originated in the same herd in Michigan as the positive goat cases that were found in FY 2008. The positive goat has been held in quarantine for research by USDA’s Agricultural Research Service since 2008.
    Regulatory Scrapie Slaughter Surveillance (RSSS)
    RSSS started April 1, 2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks. Samples have been collected from 246,453 animals since April 1, 2003. There have been 431 NVSL confirmed positive animals since the beginning ofRSSS. As of January 31, 2010, 15,184 samples have been collected in FY 2010. Seven samples collected in FY 2010 have tested positive for classical scrapie”; the face colors of the positive sheep were 5 black-face and 2 mottled-face. Three samples (2 mottled-face and 1 white-face sheep) tested positive for Nor98-like scrapie. The percent of samples that have tested positive for each face color from FY 2003 through 2010 is depicted in Chart 3. Cumulative regional sample collection numbers are shown in Chart 4 and are based upon the state in which the animal was tagged. The number ofRSSS animals collected for FY 2010 by month and by region where collected is shown in Chart 5. A monthly comparison ofRSSS collections by fiscal year is displayed in Chart 6. A retrospective 6 month rolling average of the percent positive, black-faced sheep sampled at RSSS collections sites is shown in Chart 7.
    *RSSS positives are reported based on collection date and may have been confirmed after January 31,2010.
    Animals Sampled for Scrapie Testing
    As of January 31, 2010,15,693 animals have been sampled for scrapie testing: 15,184 RSSS samples, 428 regulatory field cases, and 81 live-animal biopsies (Chart 8).
    This report is based on information and test results available at the time of report generation. Numbers are subject to change due to later reporting of test results and updates in the database.
    Unusual event if you consider the officials hypothisis that Nor-98 atypical scrapie is a spontaneous event. seems there was a great deal of spontaneous mutations for the this time period ;-)…TSS
    Atypical Nor-98 states in this report for January 2010 include ; Maine, Pennsylvania, Ohio, and Oregon
    kind regards, terry
    Monday, December 14, 2009
    Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
    hmmm, this is getting interesting now…
    Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits,
    see also ;
    All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.
    see full text ;
    Monday, December 14, 2009
    Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
    Epidemiology of Scrapie in the United States 1977
    Tuesday, April 28, 2009
    Nor98-like Scrapie in the United States of America
    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.
    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.
    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
    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.
    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.
    NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 2007
    Tuesday, June 3, 2008 SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
    Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single “virus”. The U.S. Department of Agriculture concluded that it could “no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants” (ARC 84/77)” The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias”
    Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the “scorched meat” policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
    Nature. 1972 Mar 10;236(5341):73-4.
    Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). Gibbs CJ Jr, Gajdusek DC.
    Nature 236, 73 – 74 (10 March 1972); doi:10.1038/236073a0
    Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
    C. J. GIBBS jun. & D. C. GAJDUSEK
    National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
    SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
    Thursday, January 07, 2010
    Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008
    This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ……..
    Rangen Inc 2/11/10
    Department of Health and Human Services Public Health Service Food and Drug Administration Seattle District Pacific Region 22201 23rd Drive SE Bothell, WA 98021-4421 Telephone: 425-486-8788 FAX: 425-483-4996
    February 11, 2010
    In reply refer to Warning Letter SEA 10-11
    Christopher T. Rangen, President Rangen, Inc. 115-13th Avenue South PO Box 706 Buhl, Idaho 83316
    Dear Mr. Rangen: On June 9-11, 2009, U.S. Food and Drug Administration (FDA) investigators inspected your animal feed manufacturing facilities located at 115-13th Avenue South, Buhl, Idaho. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Section 589.2000 (21 C.F.R. 589.2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation, resulting in products being manufactured and distributed by your facility that were adulterated within the meaning of section 402(a)(4) of the Federal Food, Drug, and Cosmetic Act (the Act), 21 U.S.C. § 342(a)(4), and misbranded within the meaning of section 403(a)(1) of the Act, 21 U.S.C. § 343(a)(1). Our investigation determined that adulteration resulted from the failure of your firm to provide for measures to avoid commingling or cross-contamination. The adulterated feed was subsequently misbranded because it was not properly labeled. Specifically, we found:
    1. Your firm failed to provide for and use cleanout procedures or other means adequate to prevent carry-over of products that contain or may contain proteins derived from mammalian tissues into animal feed that may be used for ruminants, as required by 21 CFR 589.2000(e)(1)(iii)(B). Since your feed is prepared, packed, or held under these conditions it is, therefore, adulterated under section 402(a)(4) of the Act, 21 U.S.C. § 342(a)(4).
    . Mink feed that was not labeled “Do not feed to cattle or other ruminants,” in accordance with 21 CFR 589.2000(e)(1)(i) and that, therefore, might be fed to ruminants, was produced using the same equipment as aquaculture feed that contains proteins derived from mammalian tissues, such as meat and bone meal. You conducted no clean-outs or flushes of equipment to remove proteins derived from mammalian tissues that may have been present before manufacturing the mink feed that might be fed to ruminants.
    . The auger trucks you used to deliver bulk mink feed which contained or may have contained proteins derived from mammalian tissues were not subject to an effective clean-out prior to their use to deliver bulk animal feed, including ruminant feed, that did not contain such materials. There were no procedures to clean the trucks to remove proteins derived from mammalian tissues before shipment of animal feeds that did not contain such materials.
    2. You failed to label all products which contained or may have contained proteins derived from mammalian tissues with the statement, “Do not feed to cattle or other ruminants,” as required by 21 C.F.R. 589.2000(e)(1)(i). Such products are misbranded under Section 403(a)(1) of the Act, 21 U.S.C. § 343(a)(1). The misbranded product includes bulk mink feed.
    . On June 9, 2009, the investigators observed approximately (b)(4) pallets of (b)(4) 50 pound bags of (b)(4) MINK FEED, lot 06/05/09. All bagged mink feed, as well as approximately (b)(4)% of bulk mink feed, manufactured at your facility, was produced using the aquaculture feed production equipment used to produce feed containing proteins derived from mammalian tissues. Because mink feed produced using this equipment may have contained mammalian tissues, it was not properly labeled, as required by 21 C.F.R. 589.2000(e)(1)(i).
    This letter is not intended to serve as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct the above violations and you should establish a system whereby violations do not occur. Failure to promptly correct these violations may result in regulatory action, such seizure and/or injunction, without further notice.
    We acknowledge your July 31, 2009 letter detailing procedures you had implemented or planned to implement to prevent future violations of FDA regulations relating to mammalian proteins in animal feed. In particular the letter stated that Rangen would no longer purchase meat and bone meal for use in any of its animal feeds and that existing inventories of mammalian protein ingredients would be exhausted by December 31, 2009. Division Manager, Joy Kinyon made similar assertions in the course of FDA’s June 2009 inspection. The July 31, 2009 letter further set out procedures Rangen would use to remedy observed violations of FDA regulations while mammalian proteins were still being used at Rangen. Finally you explained steps taken to recover or relabel feed that may have been contaminated due to commingling resulting from your manufacturing and distribution procedures. Within fifteen (15) working days of receiving this letter you should, in writing, confirm the steps you took prior to receiving this letter and notify FDA of steps you have taken since receiving this letter to bring your firm into compliance with the law. Your response should include each step that has been taken or will be taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within fifteen (15) working days, state the reason for the delay and the time frame within which the corrections will be completed. Please include copies of any available documentation demonstrating that corrections have been made.
    Your written reply should be directed to Scott A. Nabe, Compliance Officer, U.S. Food and Drug Administration, 22201 23rd Drive SE, Bothell, Washington 98021-4421. If you have any questions about this letter, please contact Mr. Nabe at (425) 483-4753.
    Charles M. Breen District Director Seattle District
    cc: Joy A. Kinyon, Division Manager, Aquaculture Feeds-General Feeds Rangen, Inc. PO Box 706 115-13th Avenue South Buhl, Idaho 83316
    Monday, March 1, 2010
    Tuesday, March 2, 2010
    Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
    . Mink feed that was not labeled “Do not feed to cattle or other ruminants,” in accordance with 21 CFR 589.2000(e)(1)(i) and that, therefore, might be fed to ruminants, was produced using the same equipment as aquaculture feed that contains proteins derived from mammalian tissues, such as meat and bone meal. You conducted no clean-outs or flushes of equipment to remove proteins derived from mammalian tissues that may have been present before manufacturing the mink feed that might be fed to ruminants.95%) downer or dead dairy cattle…
    An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie’s, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
    SEE PAGE 114 ;
    LIKE i said before, the OIE not only sold their soul to the devil over the BSE MRR, they sold yours too ;
    Wednesday, February 10, 2010
    The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
    Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the USA Question number: EFSA-Q-2003-083
    Adopted: 1 July 2004 Summary (0.1Mb)
    Report (0.2Mb)
    The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
    The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
    A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
    EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
    Monday, November 23, 2009
    HAVE we come to a point to where sub-clinical disease is an acceptable factor ???
    LEGALLY, is it o.k. to be sub-clinically infected from a contaminated product ???
    IF SO, what is the legality from the second passage infection from that sub-clinical host to clinical infection via the pass it forward and or friendly fire mode of transmission for any iatrogenic Transmissible Spongiform encephalopathy to second, third, fourth passage ???
    5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
    Monday, May 19, 2008
    Sunday, August 10, 2008
    A New Prionopathy OR more of the same old BSe and sporadic CJD
    full text ;
    Saturday, February 27, 2010
    SEAC Agenda 104th meeting on Friday 5th March 2010
    Saturday, February 27, 2010
    Prions: Protein Aggregation and Infectious Diseases
    Institute of Neuropathology, University Hospital of Zurich, Zurich, Switzerland
    3. Sporadic Creutzfeldt-Jakob disease Approximately 85% of all human prion diseases are sporadic forms of CJD. For sCJD, there is no association with a mutant PRNP allele, nor is there any epidemiological evidence for exposure to a TSE agent through contact with people or animals infected with TSEs. sCJD cases are currently subclassified according to the methionine/valine polymorphism at codon 129 of the PRNP gene and the size and glycoform ratio of proteaseresistant prion protein identified on western blot (type 1 or type 2) (174). Heterozygosity (Met/Val) at PrP codon 129 appears to be associated with a lower risk (378) and/or prolonged incubation time (119, 387). The lack of routine laboratory testing for preclinical diagnosis makes the search for agent sources and other risk factors extremely difficult. At present, the means of acquisition of a TSE agent in these patients remains a mystery. So far, there is no evidence for spontaneous PrPSc formation in any animal or human TSE. In humans, the peak age incidence of sporadic CJD is 55–60 years. However, if spontaneous misfolding were the primary event, one might expect a continuously increasing incidence with age because more time would allow more opportunity for rare misfolding events.
    Physiol Rev • VOL 89 • OCTOBER 2009 • http://www.prv.org
    Science 24 September 2004: Vol. 305. no. 5692, pp. 1918 – 1921 DOI: 10.1126/science.1103581
    Perspectives BIOMEDICINE:
    A Fresh Look at BSE
    Bruce Chesebro*
    BSE caused by spontaneous misfolding of the prion protein has not been proven.
    What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? “Sporadic” pertains to the rarity of disease occurrence. “Spontaneous” pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, “idiopathic” BSE–that is, BSE of unknown etiology–might be a better term to describe the origin of this malady.
    S. B. Prusiner, Proc. Natl. Acad. Sci. U.S.A 95, 13363 (1998) [Medline]. P. G. Smith, R. Bradley, Br. Med. Bull. 66, 185 (2003) [Medline]. C. Weissmann, A. Aguzzi, Curr. Opin. Neurobiol. 7, 695 (1997) [Medline]. A. F. Hill et al., J. Gen. Virol. 80, 11 (1999) [Medline]. R. Chiesa et al., J. Virol. 77, 7611 (2003) [Medline]. G. Legname et al., Science 305, 673 (2004). D. Westaway et al., Cell 76, 117 (1994) [Medline]. B. Chesebro, Science 279, 42 (1998). A. G. Biacabe et al., EMBO Rep. 5, 110 (2004) [Medline]. Y. Yamakawa et al., Jpn. J. Infect. Dis. 56, 221 (2003) [Medline]. C. Casalone et al., Proc. Natl. Acad. Sci. U.S.A. 101, 3065 (2004) [Medline]. E. F. Houston et al., J. Gen. Virol. 83, 1247 (2002) [Medline].
    Laboratory of Persistent Viral Diseases Bruce W. Chesebro, M.D., Chief The Laboratory of Persistent Viral Diseases (LPVD) is concerned with studies of persistent active or latent viral or prion disease infections. Investigators place particular emphasis on persistent infections of the nervous system and of the hemopoietic and lymphoid systems. The laboratory is also studying the roles of persistent infection in the development of retrovirus-induced immunosuppression. Models being examined include prion diseases of various species, murine and human retroviruses, and tick-borne encephalitis viruses.
    Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
    Wednesday, March 3, 2010

    Proof Committee Hansard
    This is an uncorrected proof of evidence taken before the committee. It is made available under the condition that it is recognised as such. BY AUTHORITY OF THE SENATE [PROOF COPY] TO EXPEDITE DELIVERY, THIS TRANSCRIPT HAS NOT BEEN SUBEDITED
    Friday, 5 February 2010 Senate RRA&T 1
    Committee met at 9.01 am
    CHAIR (Senator Nash)—I declare open this public hearing of the Rural and Regional Affairs and Transport References Committee. The committee is hearing evidence on the committee’s inquiry into the impact and consequences of the government’s decision to relax import restrictions on beef. Before the committee starts taking evidence I remind all witnesses that, in giving evidence to the committee, they are protected by parliamentary privilege. It is unlawful for anyone to threaten or disadvantage a witness on account of evidence given to a committee and such action may be treated by the Senate as a contempt. It is also a contempt to give false or misleading evidence to a committee. The committee prefers all evidence to be given in public but, under the Senate’s resolutions, witnesses have the right to request to be heard in private session. It is important that witnesses give the committee notice if they intend to ask to give evidence in camera. If a witness objects to answering a question, the witness should state the ground upon which the objection is taken and the committee will determine whether it will insist on an answer, having regard to the ground which is claimed. If the committee determines to insist on an answer, a witness may request that the answer be given in camera. Such a request may, of course, also been made at any other time. On behalf of the committee, I thank all those who have made submissions and sent representatives here today for their cooperation in this inquiry.
    RRA&T 2 Senate Friday, 5 February 2010
    [9.03 am]
    BELLINGER, Mr Brad, Chairman, Australian Beef Association
    CARTER, Mr John Edward, Director, Australian Beef Association
    CHAIR—Welcome. Would you like to make an opening statement?
    Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:
    You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heinemann variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:
    The OIE— the International Organisation of Epizootics, the arm of the WTO— is a failed global agent that in my opinion is bought off via bogus regulations for global trade and industry reps. I have done this all these years for nothing but the truth. I am a consumer, I eat meat, but I do not have to sit idly by and see the ignorance and greed of it all while countless numbers of humans and animals are being exposed to the TSE agents. All the USA is interested in is trade, nothing else matters.
    Even Dr Stanley Prusiner, who incidentally won the Nobel Health Prize in 1997 for his work on the prion—he invented the word ‘prion’, or it came from him—states:
    The BSC policy was set up for one purpose only, trade—the illegal trading of all strains of TSE globally throughout North America, which is home to CBSC, IBSC and HBSC, many scrapie strains and two strains of CJD to date. (please note typo error, those should have read cBSE, lBSE, and hBSE…tss)
    I would also like, while I have the opportunity, to explain the beef-off-the-shelves myth. At the first Senate hearing on 14 December, it was explained that the reason why they allowed BSC beef into Australia was the beef-off-the-shelves policy, whereby if we found a case of BSC in Australia they would have to recall all—
    Friday, 5 February 2010 Senate RRA&T 3
    Senator HEFFERNAN—Which of course is total BS.
    Mr Bellinger—Correct. This is written in the FSANZ document—Food Standards Australia New Zealand. Why isn’t this same policy in New Zealand? It is not—it is only in Australia. We are the only country in the world to have this idiotic policy. So we again call for the tabling of the WTO obligations paperwork. We do not believe that exists.
    Mr Carter—We have an additional concern about human health. We are not scientists, but on 18 December, four days after the last hearing here, the BBC reported a new wave of deaths due to variant CJD linked to eating BSE infected beef could be underway. This is based on the work of Professor John Collinge of the National Prion Clinic, who reported that a 2009 death in Scotland was from a different genetic pool to that of the 166 deaths already reported in the UK. Those are all thought to share one gene, but Professor Collinge and his colleagues estimate that up to 350 people in this new group, represented by the person who died in Scotland, could get CJD. He thinks that CJD has moved into a new phase, and the incubation period is a long one. We tender the Australian Red Cross donor policy sheet, which bears out what Senator Back brought up last time, questioning the Chief Medical Officer, and we say that blood from people who were in the UK between 1980 and 1996 is not acceptable. That is the current ruling. We believe this now should be extended to anyone who has visited the UK, and this new evidence should ensure that Australia revisits the science of CJD.
    CHAIR—Thank you, Mr Carter. Before we kick off, can I just remind colleagues that we are short of time today, so I ask that we do not traverse ground the we have previously covered and make sure that we stick to new information that is required. Mr Bellinger, when you started you referred to your view that this decision to allow the importation was politically based. I know you are going to go into this in the course of the next 20 minutes or so, but could you just give us a quick outline of what your definition of politically based is and why you think the decision was politically based?
    Mr Bellinger—On the lowering of BSE standards: if you go back to 2006, for example, there were five categories for describing countries that had BSE and Australia was in the category for BSE free. Suddenly, by the time the United States got their third instance of BSE, through the influence of Robert Zoellick—who was the trade minister that signed the BSE corresponding side letter in 2004 and was George Bush’s appointment to the WTO—they suddenly changed the five categories to three categories and, instead of being BSE free, Australia became BSE negligible risk. At the time I put out a press release alerting the media to the dangers of this happening, and we are coming to the stage here when suddenly our government is saying, ‘Now let’s allow the importation of beef from BSE affected countries.’ I believe that the WTO has been influenced by large multinational meat processors and retailers to change and allow the trading of BSE beef throughout the world.
    CHAIR—Thanks, Mr Bellinger.
    Mr Carter—Of course, the side letter that Minister Vaile signed was at the request of Mr Zoellick, who is now in the position that Mr Bellinger has explained.
    Senator HEFFERNAN—I just want to put the committee on notice that, if we do not get through what we have got to get through today, I suggest we have another hearing, because this
    RRA&T 4 Senate Friday, 5 February 2010
    is the greatest ambush of Australia’s farmers of all time by a government. The evidence given at the last meeting was deadset lies. The proposition that this whole change of government policy was led by the industry is a deadset lie. While Simon Crean might want to change his mind because of the WTO and his lack of knowledge, the Australian beef industry, as you know, is under great challenge, not only from the currency but also from the undermining of our markets. This is a disgrace.
    Tuesday, March 16, 2010
    COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 AUSTRALIA
    Proof Committee Hansard
    snip…see full text 110 pages ;
    for those interested, please see much more here ;
    Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518