Monday, February 18, 2013

EU Reauthorisation of non-ruminant processed animal proteins for fish feed and welcomes the likely potential for more TSE prion disease

Greetings,




IF not so serious, it would almost be humorous, i.e. the EU is now saying they can regulate PAPs, and keep them separated, ruminant from non-ruminant, when they can’t even keep the horse meat and the donkey meat from mixing with hamburger meat, i.e. I dubbed the EU horse and donkey gate burger meat scandal, when in the past, the EU could not even distinguish between a cow brain and a sheep brain. once again, big corporate ag and it’s junk science has won out over sound science, and human and animal consumer will be the ones that suffer from this, while the feed manufacturers are laughing all the way to the bank. ...TSS






EU Reauthorisation of non-ruminant processed animal proteins for fish feed



“EU feed industry acknowledges EU Commission decision as a significant step to increase sustainability and competitiveness of EU aquaculture production”



(13) CP 5




Brussels, 24 January 2013




FEFAC President Patrick Vanden Avenne welcomed the European Commission decision to adopt and publish the new regulation on the reauthorisation of non-ruminant processed animal proteins exclusively for use for fish feeding. He stated that “this measure paves the way for our EU aquaculture producers to step up their efforts to encourage the sustainable development of EU aquaculture by creating a level playing field with seafood imports from third countries”. “EFSA has provided clear scientific evidence that non-ruminant PAPs produced in accordance with the high EU processing standards are safe. They can help in reducing the EU dependency on fishmeal imports thus contributing to the Common Fisheries Policy reform goals of pairing sustainable wild fisheries with the sustainable development of aquaculture”.




He highlighted that "the European feed industry is fully committed to support the competitiveness and sustainability of aquaculture production in the EU, as set out in the Commission proposal on the Common Fisheries Policy and supported by the EP Committee on Fisheries in their December 2012 vote on the CFP report of MEP Mrs Ulrike RODUST”. The new measure contributes to global food security, by reducing the EU dependency on seafood imports which account for more than 70% of the current EU consumption". He noted that PAPs are widely used by aquaculture producers in Asia and North- and South-America, who are exporting farmed fish to the EU.




Notes to the editor:




1. FEFAC, the European Compound Feed Manufacturers’ Federation, represents 22 national Associations in 21 EU Member States as well as Associations in Switzerland, Turkey, Croatia, Serbia, Russia and Norway with observer/associate member status. The European compound feed industry employs over 110,000 persons on app. 4,000 production sites often in rural areas, which offer few employment opportunities.




2. Farmed fish in the EU-27 consumes app.1.3 mio. t of fish feed a year. Norway and Turkey produce another 1.6 mio. t of fish feed.




3. For more information see our web site (www.fefac.eu) or please contact Alexander Döring, Secretary General Tel. +32-2-285.00.50, Fax +32-2-230.57.22, e-mail: fefac@fefac.eu.











EU Allows Non-Ruminant Processed Animal Proteins for Fish Feed




February 13, 2013




In this week’s news, the European Commission has announced the reauthorisation of non-ruminant processed animal proteins to be used for fish feeding, helping to reduce the reliance on fishmeal imports and helping to boost the sustainability of aquaculture, writes Lucy Towers, TheFishSite Editor.




European Feed Manufacturers’ Federation (FEFAC) President, Patrick Vanden Avenne stated: “This measure paves the way for our EU aquaculture producers to step up their efforts to encourage the sustainable development of EU aquaculture by creating a level playing field with seafood imports from third countries.”




Global feed company Nutreco has reported a strong year for 2012, with revenue increasing by 10.8 percent to €5,229.1 (US$7,036.229) million. Some of the company’s success was due to its 75 percent acquisition of the leading shrimp and tilapia feed producer in Ecuador. The move took Nutreco into a global top three position for shrimp feed.




Marine Harvest has also reported a major positive market shift in quarter four of 2012, despite a huge decrease in profits compared to the year before, caused partly by low salmon prices.




Salmon prices are now starting to look up, however. Alf-Helge Aarskog, CEO of Marine Harvest commented: “I am very encouraged by the strong market outlook in Europe, with future prices above NOK 30 (US$5.472) per kg for both 2013 and 2014. Marine Harvest is well positioned to take advantage of this as 80 percent of our volume will be originating in Europe combined with high exposure to spot prices.”




Chilean aquaculture experienced record harvests in 2012 of over one million tons, according to preliminary figures released last week by the National Fisheries and Aquaculture service, Sernapesca. Last week was also a good week for fisheries in the EU as the European Parliament voted for an end to discards and a move towards sustainable fishing.




The European Parliament voted 502 to 137 in favour of the draft report by Ulrike Rodust, which sets out the basic regulations of the Common Fisheries Policy reform package. The basic aim of the reform package is to create sustainable fisheries, help fishing fleets to be economically viable and to promote aquaculture in the EU.




Xavier Pastor, Executive Director of Oceana in Europe, said: “The EU took a major step towards the proper management of our fishery resources. On behalf of Oceana, I thank all the representatives of European citizens for backing worldwide calls to act urgently for the health and future of our oceans.”




The Council of Fisheries ministers and the European Parliament will soon start negotiations, along with the Commission, to reconcile their respective positions and reach a final agreement on the reform by June 2013




In disease news, Infectious salmon anaemia (ISA) has been reported on a salmon farm in Nordland, Norway and Viral Haemorrhagic Septicaemia was confirmed on wrasse farms in Scotland, UK.













EU reauthorises non-ruminant PAP for fish feed




Process Managementpap




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The use of non-ruminant processing animal proteins (PAP) for use exclusively for fish feed has been re-authorised by the European Commission last week.




PAP has been prohibited since 2001 in response to the Bovine Spongiform Encephalopath (BSE) epidemic.




Tracking and tracing systems will be implemented to ensure that at no stage of the feed chain will cross-contamination occur with feeding-stuffs intended for species other than fish. In addition, very sensitive analytical tests based on DNA detection will be used to control the correct implementation of the channelling system.




This re-authorisation will apply from 1 June 2013 and will improve the overall sustainability of the aquaculture sector, since these PAPs could be a valuable substitute for fishmeal.




FEFAC President Patrick Vanden Avenne welcomed the European Commission decision to adopt and publish the new regulation on the reauthorisation of non-ruminant processed animal proteins (PAP) exclusively for use for fish feeding.




He stated that “this measure paves the way for our EU aquaculture producers to step up their efforts to encourage the sustainable development of EU aquaculture by creating a level playing field with seafood imports from third countries”.




“EFSA has provided clear scientific evidence that non-ruminant PAPs produced in accordance with the high EU processing standards are safe. They can help in reducing the EU dependency on fishmeal imports thus contributing to the Common Fisheries Policy reform goals of pairing sustainable wild fisheries with the sustainable development of aquaculture”.




He highlighted that "the European feed industry is fully committed to support the competitiveness and sustainability of aquaculture production in the EU, as set out in the Commission proposal on the Common Fisheries Policy and supported by the EP Committee on Fisheries in their December 2012 vote on the CFP report of MEP Mrs Ulrike RODUST”. The new measure contributes to global food security, by reducing the EU dependency on seafood imports which account for more than 70% of the current EU consumption". He noted that PAPs are widely used by aquaculture producers in Asia and North- and South-America, who are exporting farmed fish to the EU.




by AllAboutFeed 18 Feb 2013












18 July 2012 – Member States voted by a qualified majority to accept a proposal by the European Commission to allow pig and poultry processed animal protein (PAP) to be incorporated into farmed fish feed. This measure is currently expected to come into force in June 2013.




A total ban on Processed Animal Protein (PAP) in farmed livestock feed was introduced in 2001 to reinforce earlier bans amid the BSE crisis. This was to prevent cattle, sheep and goats from eating their own meat and bone meal via contaminated feed – the way BSE spreads. However, BSE has declined dramatically, with only 7 cases in the UK in 2011 (1 case to date in 2012), so the EU is looking at ways to reduce unnecessary burdens on the industry.




The European Commission proposes to amend the current restrictions – specifically, to allow pig and poultry processed animal protein (PAP) to be incorporated into farmed fish feed. This follows the European Commission’s TSE Roadmap 2 published in 2010 which considers various future policy options for a managed relaxation in the TSE controls, whilst assuring a high level of food safety and the protection of animal health. As a first step, the Commission presented this specific proposal to Member States on 18 July, where it received a qualified majority. This requires implementation of the new feed testing regime which has just been developed across the EU.




The Government carefully considered the Commission’s proposal for the inclusion of non-ruminant PAPs in fish feed and it recognises the importance of risk based, proportionate policies, underpinned by good science and supports the principles outlined in TSE Roadmap 2. However, it abstained from voting for the Commission proposal, given that effective controls to prevent infective material entering the food chain must be guaranteed, tests which can differentiate the species of origin of PAP have only just been developed and consumer acceptance of any change is expected to be low.




The proposal will now be subject to the Regulatory Procedure with Scrutiny, which is expected to take three months from September, and will come into force six months after it becomes law. At present, therefore, it is expected that this measure will come into force in June 2013.











>>>Therefore it remains impossible to assess the risk of transmitting a TSE by the mean of PAP that would derive from an Atypical BSE case.<<<






SCIENTIFIC OPINION




Scientific Opinion on the revision of the quantitative risk assessment (QRA) of the BSE risk posed by processed animal proteins (PAPs)1 EFSA Panel on Biological Hazards (BIOHAZ)2, 3 European Food Safety Authority (EFSA), Parma, Italy




snip...




4.4.3. Discussion of results




The results in Table 6 show that the estimated exposure for the assumed contamination levels is very low indeed. The worst case, with atmospheric processing of the ruminant Category 3 waste material and Intensive feeding of cattle, gives a mean annual exposure of only 1.3 x 10-8 bovine oral ID50 units per animal per year. This is assuming that the non-ruminant PAP could be contaminated with up to 5% of ruminant PAP that had only been processed using atmospheric methods that do not reduce BSE infectivity. This level of contamination with ruminant material is extremely unlikely to occur. The ruminant feed is then assumed to be contaminated with non-ruminant PAP at the limit of detection (0.1%). Feed is routinely tested for the presence of mammalian proteins and batches with positive results are rejected and not allowed to be used for feed.




An exposure of 1.3 x 10-8 bovine oral ID50 units over a whole year is very unlikely to result in any BSE infection. Even allowing for an uneven distribution of infectivity in the feed these are very low levels indeed. However, the occurrence of a very small number of cases cannot be excluded.




5.1. Conclusions on Atypical BSE




• Data are lacking concerning the pathogenesis, the origin (spontaneous disorder/ contagious origin), the detection performances of the TSE epidemiosurveillance system, the true prevalence and the ability of Atypical BSE agents to be transmitted in cattle and other species after oral exposure.




• Some preliminary results seem to indicate that Atypical BSE infected individual could be a potential source of Classical BSE agent.




• There are no data on the effect of the rendering process on the H- and L- BSE infectivity level.




• In this context, the risk of Atypical BSE transmission through PAPs cannot be assessed but should not be disregarded.




snip...




H- and L- BSE have been transmitted to inbred mice and Tg mice expressing bovine and ovine PrP by intra-cerebral challenge. L-BSE has also been transmitted to various models of transgenic mice expressing alleles of the human prion protein (Beringue et al., 2007; Buschmann et al., 2006; Capobianco et al., 2007). More recently the propagation of L-BSE (Fukuda et al., 2009; Lombardi et al., 2008) in cattle through the intracerebral route was reported.




These results indicate that both Atypical BSE agents identified have the potential capacity to propagate in different host species (including cattle).




At this point there is no published information on:




• the transmissibility of Atypical BSE agents in cattle and other species through the oral route;




• the distribution of the infectivity in peripheral tissues and body fluids of cattle with H- and LBSE;




• the effect of the currently applied TSE agent inactivation process on the H- and L-BSE agents. Therefore it remains impossible to assess the risk of transmitting a TSE by the mean of PAP that would derive from an Atypical BSE case.




Transmission and serial passage in inbred mice and Tg VRQ mice have been interpreted to indicate that, after interspecies passage, L-BSE could generate C-BSE (Beringue et al., 2007; Capobianco et al., 2007). However, it should be noted that L-BSE : C-BSE phenotypic convergence has not observed in other Tg mice, including mice expressing the ARQ allele of sheep PrP (Beringue et al., 2007; Buschmann et al., 2006).




More recently transmission of H-BSE isolates originating from France and Poland in Tg Bov was reported (Espinosa et al., 2010). While in the majority of the cases the propagated TSE was different from Classical BSE, Classical BSE have emerged in a proportion of the inoculated mice inoculated with two distinct isolates (one from France and one from Poland). Together these data indicate that the possibility that Atypical BSE might be a source of Classical BSE should be considered with appropriate attention. 5.1. Conclusions on Atypical BSE




• Data are lacking concerning the pathogenesis, the origin (spontaneous disorder/ contagious origin), the detection performances of the TSE epidemiosurveillance system, the true prevalence and the ability of Atypical BSE agents to be

transmitted in cattle and other species after oral exposure.




• Some preliminary results seem to indicate that Atypical BSE infected individual could be a potential source of Classical BSE agent.




• There are no data on the effect of the rendering process on the H- and L- BSE infectivity level.




• In this context, the risk of Atypical BSE transmission through PAPs cannot be assessed but should not be disregarded.





CONCLUSIONS AND RECOMMENDATIONS




CONCLUSIONS




• The current global limit of detection for PAPs in feed is still considered to be 0.1%.




• The EFSA 2004 QRA model was reviewed and compared with other published similar risk assessments. The structure of the model is considered to be still suitable for purpose of assessing the residual exposure from Classical BSE for cattle posed by bovine derived processed animal proteins at European Union level.




• For more specific questions and questions concerning particular countries, a more specific or different model should be considered.




• An updated version of the EFSA 2004 QRA model was developed (called EFSA QRA PAP model) to answer the specific terms of reference of this mandate.




• Scientific input data were reviewed and updated. Certain parameters were considered to be conservative and uncertainties were identified.




• The EFSA QRA PAP model relies on the continuation of the current SRM policy and TSE monitoring system. It also assumes that only Category 3 Animal By-Product material is allowed to enter in PAP produced from ruminant material.




• The EFSA QRA PAP model relies on the specific scenario described and on specific assumptions like homogenous mixing. While conservative values are used, uncertainties of certain parameters (i.e. the ratio of detected vs undetected infected animals, the probability of incomplete SRM removal and the amount of infectious tissue remaining after incomplete SRM removal) were identified. Changes in scientific knowledge would require an adjustment of the model.




• The EFSA QRA PAP model calculations are based on the present available data, including unofficial data about PAP production communicated directly by industry. Changes in PAP and feed production would require adjustment of the model input data.




• Based on 2009 BSE surveillance data and according to the EFSA QRA PAP model, assuming a 0.1% contamination (which is the limit of detection for PAPs in feed) with non-ruminant PAPs, the total BSE infectivity load that could enter in cattle feed in the EU would be equivalent to 0.2 Co ID50 (9 x 10-5 – 1.3 CI95%) (that would mean that less than one additional BSE infected cattle could be expected in the EU cattle population per year with an upper 95% confidence).




• Considering the many uncertainties related to Atypical BSE L and H (prevalence, tissue distribution of the infectious agent, efficacy of rendering process for agent inactivation) the risk of Atypical BSE transmission through PAPs cannot be assessed. It should however not be disregarded. RECOMMENDATIONS




• In order to improve the limit of detection of animal proteins in feed the development of analytical methods should be continued.




• Considering the limitations of the model (including the scenario and the uncertainties), if the use of some mammalian PAPs for feeding animals should be reintroduced the risk of (re-)emergence of TSEs in cattle should be taken into account.












Fish models in prion biology: Underwater issues ☆




Edward Málaga-Trilloa, , 1, , Evgenia Saltab, 1, Antonio Figuerasc, Cynthia Panagiotidisd, Theodoros Sklaviadisb, ,




a Department of Biology, University of Konstanz, 78457 Konstanz, Germany b Department of Pharmacology, Aristotle University of Thessaloniki, 54124, Thessaloniki, Greece c Instituto de Investigaciones Marinas, CSIC, 36208, Vigo, Spain d Centre for Research and Technology-Hellas, Institute of Agrobiotechnology, 57001, Thessaloniki, Greece




Abstract Transmissible spongiform encephalopathies (TSEs), otherwise known as prion disorders, are fatal diseases causing neurodegeneration in a wide range of mammalian hosts, including humans. The causative agents – prions – are thought to be composed of a rogue isoform of the endogenous prion protein (PrP). Beyond these and other basic concepts, fundamental questions in prion biology remain unanswered, such as the physiological function of PrP, the molecular mechanisms underlying prion pathogenesis, and the origin of prions. To date, the occurrence of TSEs in lower vertebrates like fish and birds has received only limited attention, despite the fact that these animals possess bona fide PrPs. Recent findings, however, have brought fish before the footlights of prion research. Fish models are beginning to provide useful insights into the roles of PrP in health and disease, as well as the potential risk of prion transmission between fish and mammals. Although still in its infancy, the use of fish models in TSE research could significantly improve our basic understanding of prion diseases, and also help anticipate risks to public health. This article is part of a Special Issue entitled Zebrafish Models of Neurological Diseases.




Research Highlights





►Prion diseases may possibly be transmitted to fish species through the food chain.



►Fish and mammalian PrPs share important cellular roles in cell–cell communication.



►The use of zebrafish in prion research may help elucidating the role of PrP in health and disease and also addressing TSE-related issues concerning public health.






Fig. 3. Experimental transmission of prions between mammals and fish. Inoculation of fish with ovine (A), bovine (B) and mouse (C) prions and their various outcomes. The photographs on the upper right corner illustrate the development of abnormal amyloid deposition in the optic tectum of BSE-challenged sea bream, using the periodic acid Schiff (PAS) staining reaction. The right image (scale bar = 10 μm) is a zoom-in of the lesion indicated in the left image (scale bar = 100 μm). i.c., intracerebrally.




Abbreviations TSEs, transmissible spongiform encephalopathies; PrP, prion protein; BSE, bovine spongiform encephalopathy; CJD, Creutzfeldt–Jakob disease; GPI, glycosylphospatidylinositol; MBM, meat and bone meal; p.i., post inoculation; i.c., intracerebrally; PK, proteinase K; GI, gastrointestinal Keywords Prion protein; Transmissible spongiform encephalopathy; Neurodegeneration; Fish; Zebrafish













Open AccessPeer-Reviewed Research Article




Evaluation of the Possible Transmission of BSE and Scrapie to Gilthead Sea Bream (Sparus aurata)




Evgenia Salta equal contributor, equal contributor Contributed equally to this work with: Evgenia Salta, Cynthia Panagiotidis




Affiliation: Department of Pharmacology, Aristotle University of Thessaloniki, Thessaloniki, Greece



X Cynthia Panagiotidis equal contributor, equal contributor Contributed equally to this work with: Evgenia Salta, Cynthia Panagiotidis


Affiliation: Centre for Research and Technology-Hellas, Institute of Agrobiotechnology, Thessaloniki, Greece


X Konstantinos Teliousis, Affiliation: Laboratory of Pathology, School of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece


X Spyros Petrakis, Affiliations: Department of Pharmacology, Aristotle University of Thessaloniki, Thessaloniki, Greece, Max Delbruck Center for Molecular Medicine, Department of Neuroproteomics, Berlin-Buch, Germany


X Eleftherios Eleftheriadis, Affiliation: National Agricultural Research Foundation, Fisheries Research Institute, Nea Peramos, Greece


X Fotis Arapoglou, Affiliation: National Agricultural Research Foundation, Fisheries Research Institute, Nea Peramos, Greece


X Nikolaos Grigoriadis, Affiliation: B' Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece


X Anna Nicolaou, Affiliation: Department of Business Administration, University of Macedonia, Thessaloniki, Greece


X Eleni Kaldrymidou, Affiliation: Laboratory of Pathology, School of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece


X Grigorios Krey, Affiliation: National Agricultural Research Foundation, Fisheries Research Institute, Nea Peramos, Greece


X Theodoros Sklaviadi





Abstract




In transmissible spongiform encephalopathies (TSEs), a group of fatal neurodegenerative disorders affecting many species, the key event in disease pathogenesis is the accumulation of an abnormal conformational isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). While the precise mechanism of the PrPC to PrPSc conversion is not understood, it is clear that host PrPC expression is a prerequisite for effective infectious prion propagation. Although there have been many studies on TSEs in mammalian species, little is known about TSE pathogenesis in fish. Here we show that while gilthead sea bream (Sparus aurata) orally challenged with brain homogenates prepared either from a BSE infected cow or from scrapie infected sheep developed no clinical prion disease, the brains of TSE-fed fish sampled two years after challenge did show signs of neurodegeneration and accumulation of deposits that reacted positively with antibodies raised against sea bream PrP. The control groups, fed with brains from uninfected animals, showed no such signs. Remarkably, the deposits developed much more rapidly and extensively in fish inoculated with BSE-infected material than in the ones challenged with the scrapie-infected brain homogenate, with numerous deposits being proteinase K-resistant. These plaque-like aggregates exhibited congophilia and birefringence in polarized light, consistent with an amyloid-like component. The neurodegeneration and abnormal deposition in the brains of fish challenged with prion, especially BSE, raises concerns about the potential risk to public health. As fish aquaculture is an economically important industry providing high protein nutrition for humans and other mammalian species, the prospect of farmed fish being contaminated with infectious mammalian PrPSc, or of a prion disease developing in farmed fish is alarming and requires further evaluation.




Citation: Salta E, Panagiotidis C, Teliousis K, Petrakis S, Eleftheriadis E, et al. (2009) Evaluation of the Possible Transmission of BSE and Scrapie to Gilthead Sea Bream (Sparus aurata). PLoS ONE 4(7): e6175. doi:10.1371/journal.pone.0006175




Editor: Etienne Joly, Université de Toulouse, France




Received: March 27, 2009; Accepted: May 19, 2009; Published: July 28, 2009




Copyright: © 2009 Salta et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




Funding: This work was funded by the European Commission's Food Quality and Safety: Prevention, Control, Treatment, Management and Risk analysis of Prion Diseases, Neuroprion (NOE), Grant ID: FOOD-CT-2004-506579, URL: http://www.neuroprion.org/en/np-neuropri​on.html and TSE & Fish: Evaluation of the possible transmission of prions (Scrapie and BSE) to different fish species, Grant ID: QLK5-2002-00866, URL: http://ec.europa.eu/research/agriculture​/projects/qlrt_2001_00866_en.htm. Evgenia Salta is a scholar of the Greek States Scholarships Foundation, URL: http://www.iky.gr/. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.




Competing interests: The authors have declared that no competing interests exist.





snip...





The results of this TSE transmission study with gilthead sea bream indicate the development of a CNS histopathology in the brains of the fish challenged with the TSE-inocula. This neuropathology displays characteristics resembling a novel fish amyloidosis more than a classical TSE. Specifically, while the fish in our study showed no brain spongiosis and no clinical abnormalities, we did find numerous plaque-like deposits in the brains of a significant proportion of the BSE-challenged fish, especially. Although much of the PrP associated with these deposits is PK-sensitive, this should not be taken as an indicator of low potential infectivity, as instances of clinical prion disease, and even infectivity, associated with extremely low levels of detectable PK-resistant PrP have been reported [43]–[45].




In light of the serious ramifications that would follow an unequivocal demonstration of prion disease transmission to fish, it must be emphasized here that the abnormal deposition we observed in the brains of the TSE-challenged fish could possibly have resulted from pathogenic factors other than the prions they were fed. Despite the fact that no such naturally occurring, cross-species infections from mammals to fish have ever been reported [46], we cannot completely rule out this possibility. Thus, however unlikely, one must consider the possibility that the brains used to prepare the inocula for the TSE challenge were infected with an undetected virus or bacteria in addition to the scrapie or BSE present. Together, the time course of brain lesion appearance, i.e. months not days, the ability of the agent to survive the oral challenge route, the absence of brain histopathology in any of the control groups and the production of novel histological lesions in both the BSE- and the scrapie-challenged fish, in the absence of inflammation, however, make this possibility a remote one. A more plausible alternate explanation would be that the amyloidogenic nature of the TSE-inocula might have contributed to the development of a novel fish brain amyloidosis.




Infectivity and transmissibility are crucial issues that still need to be addressed. From a public health standpoint, the transmissibility of each prion strain and the relative ease with which it crosses species barriers, are its most significant characteristics. The spectrum of prionopathies, which has broadened in recent years, includes prion diseases that are not readily transmissible (e.g. some GSS cases), prion strains often associated with negligible clinical symptoms (e.g. the Nor98 scrapie strain), and even some without detectable PrPSc (e.g. PSPr) [44], [47], [48]. It is clear, then, that the evaluation and identification of both unusual prion diseases and prion diseases affecting unusual hosts is a complex task, requiring lengthy studies of pathogenesis, infectivity and transmissibility [49]. Until ongoing transmission studies using “bovinized” transgenic mice are completed, the possibility that the affected sea bream brain tissue might be infectious, must be taken seriously in any consideration to lift EU feed bans, especially those related to farmed fish.












TSE AND FISH




Evalution of the possible transmission of prions (scrapie and BSE) to different fish species The pathogen common to all transmissible spongiform encephalopathies (TSEs) is the 'prion', the major or sole component of which is an abnormal glycoprotein (PrPSc). The 'benign' isomer of this protein is normally expressed as cellular prion protein (PrPC), which is converted to its pathological isoform. It is thought that, following oral ingestion, the pathological form of the prion protein (PrPSc) can change the cellular form (PrPC) to a pathological one. TSEs have been studied in higher organisms including primates, rodents, etc, but little is known about TSE pathogenesis in fish and lower vertebrates. However, fish farming is becoming a very important industry, providing high protein nutrition. All farmed fish receive commercial food containing 40-55% protein. Animal proteins may also be present and the occurrence of the pathological protein cannot be excluded.





Objectives





The objectives of this proposal include the study of the effects produced by oral administration of scrapie and BSE infectious material to trout, sea bream and sea bass. It will include the evaluation of tissue lesions in these fish species resulting from the primary transmission. As well, several tissue homogenate samples from fish challenged with experimental mouse scrapie will be used to evaluate any disease symptoms in recipient mice.





Molecular studies will allow the identification and characterisation of DNA sequences encoding fish PrP and PrP-like proteins as potential targets necessary for the transmission of TSEs in these lower vertebrates. Expression of recombinant mature PrPs from fish species may allow antibody production and the identification of markers for neuropathological disorders.





Progress to Date





Partner 1: Pilot studies indicate that the protocols developed for the TSE pathogenesis studies in sea bream and sea bass are feasible.




Partner 2: Identification and cloning of two zebrafish cDNA sequences encoding two distinct proteins exhibiting similarities to the prion protein (PrP).Protein 1, called PrP-like protein and protein 2, called Shadoo, has been accomplished.




Partner 3: Preliminary studies indicate that some residual infectivity is observed in trout intestine taken one day after oral infectious. Some recipient mice inoculated with brain and spleen of turbot resulted positive for scrapie.




Partner 4: Sequence information on PrP-like genes of Atlantic salmon have been obtained.





lassified in ANIMALS, FISHERIES AND AQUACULTURE, HUMAN HEALTH AND WELLBEING




Scientist responsible for the project Assoc. Prof. THEODOROS SKLAVIADIS 6th Km CHARILAOU - THERMI ROAD Box 361 57001 THERMI - THESSALONIKI Greece - GR




Phone: +30 2310 997615 Fax: +30 2310 997645 E-mail: sklaviad@pharm.auth.gr




References Project ID QLRT-2001-00866 Organisation CENTRE FOR RESEARCH AND TECHNOLOGY - HELLAS / INSTITUTE FOR AGROBIOTECHNOLOGY Area 5.1.1 Start date 29 November 2002 Duration (months) 48 Total cost 2 058 876 € Total EC contribution 1 304 432 € Status Ongoing




The partners NORWEGIAN SCHOOL OF VETERINARY SCIENCES, Norway - NO mohasina.syed@veths.no CENTRE FOR RESEARCH AND TECHNOLOGY - HELLAS / INSTITUTE FOR AGROBIOTECHNOLOGY, Greece - GR sklaviad@pharm.auth.gr UNIVERSITA' DEGLI STUDI DI MILANO, Italy - IT bolis@mailserver.unimi.it CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS, Spain - ES pato1@iim.csic.es












I ask Professor Kong ;




Thursday, December 04, 2008 3:37 PM


Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment


''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''


Professor Kong reply ;





.....snip





''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''




Best regards,


Qingzhong Kong,


PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA


END...TSS





Thursday, December 04, 2008 2:37 PM


"we have found that H-BSE can infect humans."


personal communication with Professor Kong. ...TSS


BSE-H is also transmissible in our humanized Tg mice.


The possibility of more than two atypical BSE strains will be discussed.


Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.























P.4.23




Transmission of atypical BSE in humanized mouse models




Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA





Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.





Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.





Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.



*** The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.





Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.





Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.












P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS





Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA





Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.



*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.





III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)


















P.9.21




Molecular characterization of BSE in Canada




Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada




Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.




Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.




Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.




Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.




*** It also suggests a similar cause or source for atypical BSE in these countries.










what about that ALABAMA MAD COW, AND MAD COW FEED THERE FROM IN THAT STATE ???




Saturday, August 14, 2010




BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY




*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)




BANNED MAD COW FEED IN COMMERCE IN ALABAMA


Date: September 6, 2006 at 7:58 am PST PRODUCT


a) EVSRC Custom dairy feed, Recall # V-130-6;


b) Performance Chick Starter, Recall # V-131-6;


c) Performance Quail Grower, Recall # V-132-6;


d) Performance Pheasant Finisher, Recall # V-133-6.


CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.


REASON


Dairy and poultry feeds were possibly contaminated with ruminant based protein.


VOLUME OF PRODUCT IN COMMERCE 477.72 tons


DISTRIBUTION AL



______________________________










PRODUCT Bulk custom dairy pre-mixes,


Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.


VOLUME OF PRODUCT IN COMMERCE 350 tons


DISTRIBUTION AL and MS



______________________________




PRODUCT


a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;


b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;


c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;


d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;


e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;


f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;


g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6


CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.


REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".


VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags


DISTRIBUTION AL, GA, MS, and TN


END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006



###













Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006



Date: August 6, 2006 at 6:16 pm PST PRODUCT




a) CO-OP 32% Sinking Catfish, Recall # V-100-6;


b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;


c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;


d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;


e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;


f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;


g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;


h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;


i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;


j) CO-OP LAYING CRUMBLES, Recall # V-109-6;


k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;


l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;


m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE


Product manufactured from 02/01/2005 until 06/06/2006


RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.


REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".


VOLUME OF PRODUCT IN COMMERCE 125 tons


DISTRIBUTION AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006


###








MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II



______________________________




PRODUCT


a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;


b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;


c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;


d) Feather Meal, Recall # V-082-6 CODE


a) Bulk


b) None


c) Bulk


d) Bulk


RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.


REASON


Possible contamination of animal feeds with ruminent derived meat and bone meal.


VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons


DISTRIBUTION Nationwide


END OF ENFORCEMENT REPORT FOR July 12, 2006


###











Saturday, July 23, 2011


CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE









Saturday, November 6, 2010


TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS


INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation









10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007 10 years (one decade) post August 4, 1997, partial and voluntary mad cow BSE feed ban in the USA, nothing but ink on paper ;




Date: March 21, 2007 at 2:27 pm PST


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II


PRODUCT


Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007


CODE


Cattle feed delivered between 01/12/2007 and 01/26/2007


RECALLING FIRM/MANUFACTURER


Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.


Firm initiated recall is ongoing.


REASON


Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI



___________________________________



PRODUCT


Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007


CODE


The firm does not utilize a code - only shipping documentation with commodity and weights identified.


RECALLING FIRM/MANUFACTURER


Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.


REASON


Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.


VOLUME OF PRODUCT IN COMMERCE


9,997,976 lbs.


DISTRIBUTION


ID and NV


END OF ENFORCEMENT REPORT FOR MARCH 21, 2007










Saturday, August 4, 2012



*** Final Feed Investigation Summary - California BSE Case - July 2012








Thursday, February 14, 2013



Unique Properties of the Classical Bovine Spongiform Encephalopathy Strain and Its Emergence From H-Type Bovine Spongiform Encephalopathy Substantiated by VM Transmission Studies







Thursday, February 14, 2013



The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease










why do we not want to do TSE transmission studies on chimpanzees $





5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.


snip...


R. BRADLEY










Wednesday, February 16, 2011


IN CONFIDENCE


SCRAPIE TRANSMISSION TO CHIMPANZEES


IN CONFIDENCE










Sunday, December 12, 2010


EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010










Sunday, April 18, 2010


SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010










Thursday, December 23, 2010


Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009


Volume 17, Number 1 January 2011










Thursday, November 18, 2010


Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep










Monday, April 25, 2011


Experimental Oral Transmission of Atypical Scrapie to Sheep


Volume 17, Number 5-May 2011










Friday, February 11, 2011


Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues










Thursday, March 29, 2012


atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012


NIAA Annual Conference April 11-14, 2011San Antonio, Texas











Monday, February 11, 2013





TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos













TSS

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