EFSA
APPROVED: 23 October 2020
doi:10.2903/sp.efsa.2020.EN-1946
Annual report of the Scientific Network on BSE-TSE 2020
Annual Report of the Scientific Network on BSE-TSE 2020 European Food Safety Authority (EFSA) Abstract The EFSA Scientific Network on bovine spongiform encephalopathies and other transmissible spongiform encephalopathies (BSE-TSE) held its 15th meeting on 7-8 October 2020 as a web-meeting. The meeting served as an opportunity to exchange scientific information on BSE-TSE related issues among EU Member States, countries from the European Free Trade Association, EU candidate countries, EFSA, the European Commission and ad hoc participants. In this occasion, ad hoc representation included the World Animal Health Organisation (OIE). The topics discussed included: TSE activities in Albania, Bosnia and Herzegovina and Turkey, new evidence of the detection of scrapie in goats and the presence of multiple strains in goat scrapie isolates, update on the latest case of CWD in Norway and on the ongoing studies of CWD European isolates; the zoonotic potential of atypical strains of BSE and scrapie. Recent and ongoing the TSE EURL EFSA, OIE and EC activities on TSE were presented, as well as the preliminary results of the 2019 EU TSE summary report. EU candidate countries presented their TSE-related activities.
© European Food Safety Authority, 2020
Key words: CWD, surveillance, meeting, network, TSE Requestor: EFSA Question number: EFSA-Q-2020-00701 Correspondence: biocontam@efsa.europa.eu
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Summary
Establishing a system of Networks of organisations operating in the fields within EFSA’s mission is among the tasks of EFSA, according to its Founding Regulation (Regulation (EC) No 178/2002), in order to facilitate a scientific cooperation framework by the coordination of activities, the exchange of information, the development and implementation of joint projects, the exchange of expertise and best practices. Additionally, the EFSA Science Strategy 2012–2016 set the objective of developing, together with Member States’ competent authorities, multi-annual work programmes focused on filling data gaps and setting priorities for data collections. To implement the above provisions various Networks were established. The Scientific Network on bovine spongiform encephalopathies and other transmissible spongiform encephalopathies (BSE-TSE) was established in 2006. The BSE-TSE Network had its first meeting in 2006 and, following this, one meeting per year has been held. The BSE-TSE Network is currently composed as follows: Network Members representing 27 EU MSs, three countries from the European Free Trade Association and six EU candidate countries. The European Commission Directorate-General of Health and Food Safety and of Research and Innovation are also Observers of the Network.
The 15th meeting of the BSE-TSE Network was held on 7-8 October 2020 as a web-meeting. On this occasion, ad hoc representation included the World Animal Health Organisation (OIE). The topics discussed included: TSE activities in Albania, Bosnia and Herzegovina and Turkey, new evidence of the detection of scrapie in goats and the presence of multiple strains in goat scrapie isolates, update on the latest case of CWD in Norway and on the ongoing studies of CWD European isolates; the zoonotic potential of atypical strains of BSE and scrapie. Recent and ongoing activities on TSE of the EURL TSE, EFSA, OIE and EC were presented, as well as the preliminary results of the 2019 EU TSE summary report. EU candidate countries presented their TSE-related activities.
Table of contents
Abstract .........................................................................................................................................1
Summary .......................................................................................................................................3
1. Introduction ........................................................................................................................5
1.1. Background and Terms of Reference as provided by EFSA .....................................................5
2. Annual meeting 2020 ..........................................................................................................6
2.1. New countries .....................................................................................................................6
2.1.1. Albania ...............................................................................................................................6
2.1.2. Bosnia and Herzegovina (BiH) ..............................................................................................6
2.1.3. Turkey ...............................................................................................................................6
2.1.4. Q&A New countries .............................................................................................................7
2.2. Scrapie in goats ..................................................................................................................7
2.2.1. Detection scrapie in goats: rapid test and genotypes .............................................................7
2.2.2. Norwegian goats with no PrPC (update on CWD) ...................................................................7
2.3. TSE strains and their zoonotic potential ................................................................................8
2.3.1. Multiple strains in goat scrapie and cervid CWD European isolates. ........................................8
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains .......8
2.3.3. Q&A ...................................................................................................................................8
2.4. BSE/TSE Network microsite in Microsoft Teams.....................................................................9
2.5. General session ...................................................................................................................9
2.5.1. Update on the activities of the EURL in the TSE field .............................................................9
2.5.2. EFSA activities in TSE ..........................................................................................................9
2.5.3. EU TSE annual report 2019: preliminary results ....................................................................9
2.5.4. Update on the activities of the OIE in the TSE field .............................................................10
2.5.5. Update on the activities of the EC in the TSE field ...............................................................10
2.5.6. Round-the-table discussion on the topics discussed in the EFSA Scientific Network on BSETSE ..................................................................................................................................10
3. Planned work activities for 2020/2021 ................................................................................11
References...................................................................................................................................11
Abbreviations ...............................................................................................................................12
1. Introduction
1.1. Background and Terms of Reference as provided by EFSA
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2. Annual meeting 2020
The Scientific Network on BSE-TSE was launched in 2006. The BSE-TSE Network had its first meeting in 2006, and, following this, one meeting per year has been held. The 15th meeting of the EFSA Scientific Network on BSE-TSE was held on 7-8 October 2020 as a web-meeting (‘annual meeting 2020’). The annual meeting 2019 was attended by representatives of 25 EU Member States (Austria, Belgium, Croatia, Cyprus, Czechia, Estonia, Finland, France, Germany, Greece, Hungary, Ireland, Italy, Latvia, Lithuania, Malta, the Netherlands, Poland, Romania, Slovakia, Slovenia, Spain and Sweden), by the representative of three European Free Trade Association countries (Iceland, Norway and Switzerland) and of six EU candidate countries (Albania, Bosnia and Herzegovina, Montenegro, North Macedonia, Serbia and Turkey). Apologies were sent by the representatives of Bulgaria. A representative from the European Commission (EC) Directorate-General Health and Consumers (DG SANTE), Fabien Schneegans, was also present at the meeting. Further ad hoc attendee to this meeting included: Fernanda Mejia Salazar from the Standard Department of the World Organisation for Animal Health (OIE).
Topics discussed during the meeting are summarised in the following sections.
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2.2. Scrapie in goats
2.2.1. Detection scrapie in goats: rapid test and genotypes
John Spiropoulos, senior veterinary pathologist of the Animal and Plant Health Agency (APHA) (UK), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Transmissible spongiform encephalopathy in goats: is PrP rapid test sensitivity affected by genotype?’ (Simmons et al., 2020), and ‘The Scrapie Prevalence in a Goat Herd Is Underestimated by Using a Rapid Diagnostic Test’ (Konold et al., 2020). The sensitivity of the Rapid test for the detection of TSE in goats (scrapie and BSE) is not 100%, and is influenced by the polymorphisms in certain codons which may alter epitope binding, the rapid test chosen, sampling issues and other still unknown factors. It should not be assumed that the biology of TSE in goats is similar to that in sheep simply because they are both small ruminants. They are different species. More research is required to elucidate TSE in goats as still many aspects are extrapolated from sheep.
2.2.2. Norwegian goats with no PrPC (update on CWD)
The representative of Norway presented the results of on recently published scientific articles of interest, of which he is co-author: “Goats naturally devoid of PrPC are resistant to scrapie”, Salvesen et al. (2020). The nonsense mutation at codon 32 in the prion protein (PRNP) open reading frame (ORF) – discovered during routine PRNP genetic analysis in dairy goats in Norway – has raised the question of the resistance to scrapie. Animals of the three PRNP genotypes were inoculated intracerebrally with caprine scrapie. Homozygous goats do not replicate prions hence they are resistant to prion disease.
Update on the last case of CWD in Norway: So far 28 cases of CWD have been identified in Norway (7 in moose, 20 in reindeer and 1 in red deer). The last confirmed case of CWD was a wild reindeer (8- year old buck) shot during the ordinary hunt on the Hardanger plateau, about 200 km south of Nordfjella. Material from a lymph node tested positive, while brain tissue was negative. The area holds an open population of 8,000 animals, and 3,500 have tested negative since 2016. Some immediate actions were taken from Food Safety Authorities: ban of the transport of meat/animals, increase hunting in the area, disinfection of tools etc. Next steps will include: PRNP genotype of the case, analysis of agent, increase harvest of bucks.
2.3. TSE strains and their zoonotic potential
2.3.1. Multiple strains in goat scrapie and cervid CWD European isolates.
The representative of Italy presented the results of one recently published scientific article of interest, of which he is the first author: ‘Characterization of goat prions demonstrates geographical variation of scrapie strains in Europe and reveals the composite nature of prion strains’ (Nonno et al., 2020). The results of an inoculation study of a number of goat scrapie isolates into a pool of transgenic mice expressing various sheep and bovine genotypes, as well as wild-type mice and bank voles showed the presence of four categories based on the transmission efficiency (TE), as defined by the attack rate and the incubation period. In a second study of 27 classical scrapie isolates inoculated in bank voles, the authors concluded the presence of five vole-adapted small ruminant-derived CS strains and the sharing of the same CS strains in goats and sheep.
The preliminary conclusions of the ongoing studies on European CWD isolates are: CWD strains in Norway are different from North American (NA) CWD; while a single CWD strain was isolated from North American cervids, different CWD strains were detected in Norwegian reindeer, moose and red deer (one in reindeer, one in red deer and at least there are two CWD strains in moose).
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
In the second study, a number of isolates of atypical scrapie in sheep and goats were passaged through TgBov and then back into Tg sheep expressing VRQ and ARQ alleles, showing BSE features and the loss of the atypical phenotype. The possibility of contamination in the original material was ruled out and the conclusions of the authors are that BSE particles are likely to be ‘created’ during Nor98 replication process in the absence of species barrier passage and that atypical/Nor98 isolates contain low amount of BSE infectivity
2.3.3. Q&A
Following a question about the shortages of reference material, there was a short discussion on the possibility to generate reference material for atypical BSE using in vitro techniques like PMCA or in vivo by inoculation in mice, as opposed to the traditional way of conducting experimental studies inoculating cattle with the strains of choice. There were reservations about the amount of material that can be produced using mice and the nature of the PrPSc that would be produced at large scale by amplification in the PMCA, for example.
To the question of the evolutionary state to the CWD in Europe, the presenter replied that current studies of inoculation of European CWD isolates in gene-edited mice in the USA showed adaptation and similarities to NA CWD, leading to the speculation that European CWD could converge towards a more similar phenotype to the NA CWD, i.e. more transmissible and with less variability.
2.4. BSE/TSE Network microsite in Microsoft Teams
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2.5. General session
2.5.1. Update on the activities of the EURL in the TSE field
The Director of the TSE EURL presented the activities of the TSE EURL in the last year. After nearly 2 years of operation of the new TSE EURL with a workplan of 5 main areas of work, four of them were detailed by the director:
1) to ensure availability and use of high quality methods and to ensure high quality performance by the National Reference Laboratories (NRLs) for the revision and development of guidelines, development of tests and the proficiency testing (PT) and external quality assessment (EQA);
2) to provide scientific and technical assistance to NRLs (liaison with seven Member States this year);
3) to provide scientific and technical assistance to the European commission and other organisations like EFSA, EMA and ECDC, redrafting testing schemes, outbreak investigation and strain typing expert group (STEG); 4) reagents and reference collections by the verification of reagents and batch testing and the discussions about shortage of reference materials.
2.5.2. EFSA activities in TSE
EFSA staff (BIOCONTAM Unit) updated the Network on the TSE-related risk assessment activities that took place in EFSA since the 2019 annual Network meeting. In particular, he presented the approach and conclusions of the mandate to estimate the cattle BSE risk (C-, L- and H-BSE) posed by the use of ruminant collagen and gelatine (both food grade and category 3 animal by-products) in feed intended for non-ruminant animals including aquaculture animals. According to the scientific opinion, the probability that no new case of BSE in the cattle population would be generated through any of the three RP is larger than 99% (almost certain), given the estimated amount of BSE infectivity to which cattle would be exposed. EFSA published in April the assessment of one application for an alternative method for the production of biodiesel from processed fats derived from category 1, 2 and 3 animal-by products. The methodology and conclusions were presented. Finally, a new mandate on the request for scientific and technical assistance to examine the data collected by the Member States in the framework of the 2-year compulsory intensified surveillance in case of atypical scrapie. The resulting EFSA scientific reports will be delivered by 30 June 2021.
2.5.3. EU TSE annual report 2019: preliminary results
EFSA staff (BIOCONTAM Unit) presented the main findings that will be included in the EU Summary Report on TSE for the year 2019. The report presents the results of surveillance of TSE in animals and is expected to be published towards the end of 2020 by EFSA. It includes data from 28 Member States (MS), Iceland, North Macedonia, Montenegro, Norway, Serbia and Switzerland. In total, 1,150,388 cattle were tested by Member States, a 2.7% decrease from 2018. Seven atypical BSE cases were reported in 2019: 1 L-type reported by Poland and 6 H-type, reported by Spain (2) and France (4). Over the year, a total of 338,098 sheep and 143,529 goats were tested in the EU, an increase of 3.9% in both species, compared with 2018. In sheep, 997 cases of scrapie were reported: 911 classical by seven MS and 86 atypical by 11 MS. Random genotyping was only reported by eight MS and after excluding Cyprus showed that 15.7% of the genotyped sheep carried genotypes of the susceptible groups. In goats, 390 cases of scrapie were reported: 379 classical by six MS and 11 atypical by six MS. The six MS implementing mandatory surveillance for CWD reported 7,980 tested cervids with three cases of CWD reported by Sweden in moose. In addition, other six MS reported 2,732 tested cervids with negative results. Norway tested 30,147 cervids with 2 moose cases in 2019 and Iceland reported 114 negative cervids.
2.5.4. Update on the activities of the OIE in the TSE field
The representative of the OIE presented the activities since the last Network meeting. The 2019 campaign for the maintenance of the official BSE status is ongoing. Currently, there are 56 countries and five zones with an official BSE risk status. The new additions from May 2019 include Bolivia, as a country with a negligible BSE risk status and Jersey, as a zone of the United Kingdom also with a negligible BSE risk status. There have been no suspensions or recoveries since the last meeting. During 2019 there have been many activities in OIE linked to the revision of the BSE Standard. Since July 2018 five ad hoc groups have convened so far, with the latest one in June 2020 to address Member comments received in December 2019. In September 2020, the Code Commission made further amendments to the BSE Chapters and will circulate the draft of the BSE chapter for comments. The criteria to define the risk and status of the proposed provisions were explained, with emphasis being on the period when the risk of recycling BSE is negligible, the impact on the trade of certain commodities and the new surveillance based on the reporting of animals lying on the continuum of the BSE clinical spectrum.
2.5.5. Update on the activities of the EC in the TSE field
The representative of the EC presented the activities since the last Network meeting. Three horizontal topics were presented: 1) Feed ban: the discussion on the permission to use pig processed animal protein (PAP) in poultry, poultry PAP in pig feed and insect PAP in poultry and pig feed continues; the conclusions of the EFSA’s ruminant collagen and gelatine opinion will trigger the proposal of the amendment of the feed ban on this point; amendment on the light microscopy methods for detection of animal particles in feed; 2) SRM: the possibility to apply an alternative method to identify ovine and caprine animals aged over 12 months of age will be repealed; 3) Trade-related issues: Serbia negligible risk status; ensure that conditions applicable to ruminant products derived from animals originating in an undetermined risk country are the same when imported from a country with controlled risk and from a country with negligible risk status; and the close monitoring of the revision of the OIE BSE chapter by the EC. Two disease-specific topics were presented: 1) scrapie: amendment on recognition of genetic resistance in goats published in June 2020; the compulsory genotyping of scrapie cases in goats will be added; the repeal of the intensified surveillance of holding with atypical scrapie is on the way; and the amendment requesting only index cases to be subject to discriminatory testing to be published soon;
2) CWD: Sweden will continue CWD surveillance in 2021 and the final assessment of the statutory surveillance will be requested to EFSA in 2022.
2.5.6. Round-the-table discussion on the topics discussed in the EFSA Scientific Network on BSE-TSE
The chair reminded the main topics presented and discussed during the Network meeting and requested Sweden to brief the Network on the latest case of CWD. The representative of Sweden informed that the last case of CWD confirmed in last September was an old female moose in very well-known area since it has been under surveillance by the Agriculture University for a long time and they hold a lot of data. The pattern of the case is similar to the previous cases, whereby females can reach old age since younger males are the main target of hunters. They expect to capture and test more moose at the end of the season after the breeding.
The representative of France reminded the importance of surveillance in the light of the results presented in day 1, and the possibility that C-BSE could be present in species other than cattle. The representative of Croatia expressed uncertainty about the future of TSE laboratories in general, and about the production of diagnostic kits and the need to change to new methods in particular, due to the decrease in the throughput of laboratories, if TSE testing declines.
3. Planned work activities for 2020/2021
Network members were invited to provide, also after the meeting, suggestions for improvement of the functioning of the Network and for possible topics for future discussion in the Network. Network members were invited to share information with EFSA and the other Network members anytime during the year. The chair informed the Network that the mandate of the EFSA’s BSE/TSE Scientific Network expires at the end of 2020. The Advisory Forum is discussing a proposal to put forward to EFSA’s Management Board to renew the mandate. The Network will be informed of the final decision in due course.
References
SNIP...SEE FULL REPORT;
Scientific Opinion
Potential BSE risk posed by the use of ruminant collagen and gelatine in feed for non‐ruminant farmed animals
EFSA Panel on Biological Hazards (BIOHAZ) Konstantinos Koutsoumanis Ana Allende Declan Joseph Bolton Sara Bover‐Cid Marianne Chemaly … See all authors
First published: 28 October 2020 https://doi.org/10.2903/j.efsa.2020.6267
Requestor: European Commission
Question number: EFSA‐Q‐2019–00436
Panel members: Ana Allende, Avelino Alvarez‐Ordóñez, Declan Bolton, Sara Bover‐Cid, Marianne Chemaly, Robert Davies, Alessandra De Cesare, Lieve Herman, Friederike Hilbert, Kostas Koutsoumanis, Roland Lindqvist, Maarten Nauta, Luisa Peixe, Giuseppe Ru, Marion Simmons, Panagiotis Skandamis and Elisabetta Suffredini.
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THE USA BSE TSE Prion surveillance, testing, feed ban, SRM all failed terribly...to this day!
*>>> ''Assuming that current risk control measures are continuously implemented as mentioned above.''
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
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In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
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36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
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In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
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Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
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***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are;
BSE TESTING (failed terribly and proven to be a sham)
BSE SURVEILLANCE (failed terribly and proven to be a sham)
BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham)
these are facts folks. trump et al just admitted it with the feed ban.
see;
FDA Reports on VFD Compliance
John Maday
August 30, 2019 09:46 AM VFD-Form 007 (640x427)
Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.
SUNDAY, SEPTEMBER 1, 2019
***> FDA Reports on VFD Compliance
America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion
***> cattle, pigs, sheep, cwd, tse, prion, oh my!
***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006).
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
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The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
ZOONOSIS OF SCRAPIE TSE PRION
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
***> 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
MONDAY, AUGUST 24, 2020
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
WEDNESDAY, APRIL 24, 2019
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019
WEDNESDAY, JULY 31, 2019
The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.
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.
P03.137
Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan
Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
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
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 argely 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.
see full text ;
P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States.
In 2006, a case of H-type bovine spongiform encephalopathy (BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K).
The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease.
Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route.
The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure.
Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with either H-type BSE from the 2004 US Htype BSE case (n=3) or from the 2006 US H-type case associated with the E211K polymorphism (n=4) using 10% w/v brain homogenates.
Cattle were observed daily throughout the course of the experiment for the development of clinical signs.
At approximately 50 months post-inoculation, one steer (EK211 inoculated with E211K associated H-BSE) developed clinical signs including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and was euthanized.
Enzyme immunoassay confirmed that abundant misfolded protein was present in the brainstem, and immunohistochemistry demonstrated PrPSc throughout the brain.
Western blot analysis of brain tissue from the clinically affected steer was consistent with the E211K H-type BSE inoculum.
With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
PRION 2018 CONFERENCE ABSTRACT
WEDNESDAY, AUGUST 15, 2018
***> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
SUNDAY, MAY 24, 2020
Cosmetics, Intestines, FDA, BSE, TSE, Prion, and Improving Biosecurity Procedures to Minimize the Risk of Spreading Pathogenic Infections Agents After Carcass Recycling
TUESDAY, AUGUST 1, 2017
Could Insulin be contaminated with and potentially spread, Transmissible Spongiform Encephalopathy TSE Prion, what if? Could diabetes spread like mad cow disease?
OR
Could Insulin be contaminated with, and potentially spread, Transmissible Spongiform Encephalopathy TSE Prion, what if?
WEDNESDAY, APRIL 24, 2019
***> USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019 <***
***> Wednesday, January 23, 2019
***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***
WEDNESDAY, APRIL 24, 2019
***> USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019 <***
TUESDAY, AUGUST 28, 2018
USDA finds BSE infection in Florida cow 08/28/18 6:43 PM
http://animalhealthreportpriontse..blogspot.com/2018/08/usda-finds-bse-infection-in-florida-cow.html
WEDNESDAY, AUGUST 29, 2018
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT
WEDNESDAY, AUGUST 29, 2018
Transmissible Spongiform Encephalopathy TSE Prion Atypical BSE Confirmed Florida Update USA August 28, 2018
MONDAY, JANUARY 09, 2017
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle
CDC Volume 23, Number 2—February 2017
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
***> P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE.
We are further examining explanations for the unusual disease presentation in the third challenged animal.
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
MONDAY, JANUARY 09, 2017
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle
CDC Volume 23, Number 2—February 2017
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Ivett Ackermann1 , Anne Balkema‑Buschmann1 , Reiner Ulrich2 , Kerstin Tauscher2 , James C. Shawulu1 , Markus Keller1 , Olanrewaju I. Fatola1 , Paul Brown3 and Martin H. Groschup1*
Abstract
In classical bovine spongiform encephalopathy (C-BSE), an orally acquired prion disease of cattle, the ileal Peyer’s patch (IPP) represents the main entry port for the BSE agent. In earlier C-BSE pathogenesis studies, cattle at 4–6 months of age were orally challenged, while there are strong indications that the risk of infection is highest in young animals. In the present study, unweaned calves aged 4–6 weeks were orally challenged to determine the earli‑ est time point at which newly formed PrPBSE and BSE infectivity are detectable in the IPP. For this purpose, calves were culled 1 week as well as 2, 4, 6 and 8 months post-infection (mpi) and IPPs were examined for BSE infectivity using a bovine PrP transgenic mouse bioassay, and for PrPBSE by immunohistochemistry (IHC) and protein misfolding cyclic amplifcation (PMCA) assays. For the frst time, BSE prions were detected in the IPP as early as 2 mpi by transgenic mouse bioassay and PMCA and 4 mpi by IHC in the follicular dendritic cells (FDCs) of the IPP follicles. These data indi‑ cate that BSE prions propagate in the IPP of unweaned calves within 2 months of oral uptake of the agent.
In summary, our study demonstrates for the frst time PrPBSE (by PMCA) and prion infectivity (by mouse bioassay) in the ileal Peyer’s patch (IPP) of young calves as early as 2 months after infection. From 4 mpi nearly all calves showed PrPBSE positive IPP follicles (by IHC), even with PrPBSE accumulation detectable in FDCs in some animals. Finally, our results confrm the IPP as the early port of entry for the BSE agent and a site of initial propagation of PrPBSE and infectivity during the early pathogenesis of the disease. Terefore, our study supports the recommendation to remove the last four metres of the small intestine (distal ileum) at slaughter, as designated by current legal requirements for countries with a controlled BSE risk status, as an essential measure for consumer and public health protection.
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
___________________________________
PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA,
Recall # V-025-2007
CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete.
REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
PRODUCT O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 11-oz. bottles, For Animal Use Only.
Recall # V-043-2007 CODE A06 RECALLING FIRM/MANUFACTURER Springer Magrath Co., Mc Cook, NE, by telephone on January 2, 2007, fax dated January 9, 2007, by letters on February 22, 2007, March 12, March 14 and March 21, 2007.
Firm initiated recall is ongoing.
REASON The finished product was manufactured with prohibited bovine blood meal and did not bear the cautionary BSE statement that the product should not be fed to ruminants.
VOLUME OF PRODUCT IN COMMERCE
Approximately 13,255 bottles DISTRIBUTION
Nationwide
END OF ENFORCEMENT REPORT FOR JUNE 13, 2007 ###
PRODUCT
Dairy cattle feed blends containing ProLak and/or ProAmino II protein concentrate, Recall # V-020-2007
CODE
All finished product manufactured from April, 3, 2006 to April 30, 2006
RECALLING FIRM/MANUFACTURER
Eatonton Co-Op Feed Company, Eatonton, GA, by letter on/about December 12, 2006. Firm initiated recall is complete.
REASON
Finished feed product was manufactured from raw feed material that may have been contaminated with ruminant derived protein.
VOLUME OF PRODUCT IN COMMERCE
25 tons
DISTRIBUTION
GA ___________________________________
END OF ENFORCEMENT REPORT FOR FEBRUARY 28, 2007
###
PRODUCT
O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 9-oz. bottles, For Animal Use Only, Recall # V-011-2007
CODE
A07
RECALLING FIRM/MANUFACTURER
Springer Magrath Co., McCook, NE, by telephone on January 11, 2007 and fax on January 12, 2007. Firm initiated recall is complete.
REASON
The bovine blood meal which was used to manufacture the finished product was cross-contaminated with prohibited bovine meat and bone meal, and the finished product is not labeled with the cautionary statement that it should not be fed to ruminants.
VOLUME OF PRODUCT IN COMMERCE
300/9-oz. bottles
DISTRIBUTION
NE
END OF ENFORCEMENT REPORT FOR JANUARY 31, 2007
###
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
______________________________
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
a) Dairy feed, custom, Recall # V-134-6;
b) Custom Dairy Feed with Monensin, Recall # V-135-6.
CODE
None. Bulk product
RECALLING FIRM/MANUFACTURER
Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006.
Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete.
REASON
Possible contamination of dairy feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
1,484 tons
DISTRIBUTION
TN and WV
END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006
###
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-115-6
CODE
None
RECALLING FIRM/MANUFACTURER
Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
Approximately 2,223 tons
DISTRIBUTION
KY
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-116-6
CODE
None
RECALLING FIRM/MANUFACTURER
Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
1,220 tons
DISTRIBUTION
KY
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-117-6
CODE
None
RECALLING FIRM/MANUFACTURER
Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed.
REASON
Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
40 tons
DISTRIBUTION
LA and MS
______________________________
PRODUCT
Bulk Dairy Feed, Recall V-118-6
CODE
None
RECALLING FIRM/MANUFACTURER
Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete.
REASON
Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
7,150 tons
DISTRIBUTION
MS
______________________________
PRODUCT
Bulk custom dairy pre-mixes, Recall # V-119-6
CODE
None
RECALLING FIRM/MANUFACTURER
Walthall County Co-op, Tylertown, MS, by telephone on June 26, 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
87 tons
DISTRIBUTION
MS
______________________________
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
###
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
______________________________
BIO-RAD BSE TEST POLITICAL REPLY TO TSS
Subject: Re: USDA/APHIS JUNE 2004 'ENHANCED' BSE/TSE COVER UP UPDATE DECEMBER 19, 2004 USA
Date: Thu, 30 Dec 2004 12:27:06 -0600
From: "Terry S. Singeltary Sr.
BSE-L
snip...
OH, i did ask Bio-Rad about this with NO reply to date;
-------- Original Message --------
Subject: USA BIO-RADs INCONCLUSIVEs
Date: Fri, 17 Dec 2004 15:37:28 -0600
From: "Terry S. Singeltary Sr."
Hello Susan and Bio-Rad,
Happy Holidays!
I wish to ask a question about Bio-Rad and USDA BSE/TSE testing and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated, or is there most likely some human error we are seeing here?
HOW can Japan have 2 positive cows with No clinical signs WB+, IHC-, HP- , BUT in the USA, these cows are considered 'negative'?
IS there more politics working here than science in the USA?
What am I missing?
-------- Original Message --------
Subject: Re: USDA: More mad cow testing will demonstrate beef's safety
Date: Fri, 17 Dec 2004 09:26:19 -0600
From: "Terry S. Singeltary Sr."
snip...end
Experts doubt USDA's mad cow results
snip...END
WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;
Bio-Rad, TSS phone conversation 12/28/04
Finally spoke with ;
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX
at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.
my question;
Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???
ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.
again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there.
"very difficult to answer"
"very political"
"very loaded question"
outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing.
said something about Dr. Houston stating;
any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives?
said something about ''just look at the sheep that tested IHC- but were positive''. ...
TSS
-------- Original Message --------
Subject: Your questions
Date: Mon, 27 Dec 2004 15:58:11 -0800
From: To: flounder@wt.net
Hi Terry:
............................................snip
Let me know your phone number so I can talk to you about the Bio-Rad BSE test.
Thank you
Regards
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email:
=================================
snip...end...TSS
TSS REPORT ON 2ND TEJAS MAD COW Mon, 22 Nov 2004 17:12:15 -0600 (the one that did NOT get away, thanks to the Honorable Phyllis Fong)
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett
References: <[log in to unmask]>
<[log in to unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
terry
============================== ==============================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."
References: <[log in to unmask]>
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas.
Carla At 09:44 AM 11/19/2004, you wrote:
>Greetings Carla,
>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from
>TEXAS. can you comment on this either way please?
>>thank you,
>Terry S. Singeltary Sr.
>>
=================== ===================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."
References: <[log in to unmask]>
<[log in to unmask] us>
<[log in to unmask]>
<[log in to unmask] us>
<[log in to unmask]>
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.
At 06:05 PM 11/22/2004, you wrote: >why was the announcement on your TAHC site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
>>>no confirmation on the U.S.' inconclusive test...
>>no confirmation on location of animal.
>>>>>>
========================== ==========================
THEN, 7+ MONTHS OF COVER-UP BY JOHANN ET AL! no doubt about it now $$$
NO, it's not pretty, be nice, im not pretty, but these are the facts, take em or leave em, however, you cannot change them.
with kindest regards,
I am still sincerely disgusted and tired in sunny Bacliff, Texas USA 77518
Terry S. Singeltary Sr.
FULL 130 LASHINGS TO USDA BY OIG again
FOR IMMEDIATE RELEASE
Statement
May 4, 2004
Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
####
-------- Original Message --------
Subject: Re: Congressman Henry Waxmans's Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW
Date: Wed, 9 Jun 2004 16:48:31 –0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de References: 40A8CD52.1070308@wt.net
######## Bovine Spongiform Encephalopathy #########
USA BSE RED BOOK
October 1998
BSE Red Book 2.1-36
7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer will advise the READE(3 Director concerning laboratory capabilities and appropriate laboratory examinations to be conducted to provide needed results as rapidly as possible. This individual will assist with interpretation of results.
seems that if the 'enhanced BSE/TSE testing program' is to test some 400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.
BSE Red Book 2.1-39
7.6 Depopulation Procedures
Under no circumstances may BSE suspects be sent fo slaughhter or rendering.
snip...
BSE Red Book 2.1-40
7.7 Disposal Under no circumstances may BSE suspects be sent to slaughter or rendering. Notify FDA, CVM if you suspect that the carcass of a BSE-confirmed animal has moved to rendering or animal feed manufacturing. Field personel should arrange for the carcass to be transported to and examined by a qualified veterinary pathologist or field veterinary medical officer. After the pathologic examination has been completed and the necessary diagnostic specimens have been obtained, field personnel should arrange for disposal of the carcass. Before a method of disposal is selected, there are many factors that must be considered, and often other State and Federal agencies must be consulted. The environmental and legal impacts of the operation must be considered. Upon recommendation of the State or Federal agencies, VS may consider other disposal methods.
snip...
7.7.3 Rendering Because BSE is spread by rendered animal protein, BSE-suspect and confirmed carcasses must not be rendered, unless the rendered material is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or carcasses have moved to rendering or animal feed manufacturing.
snip...
7.10.11 Prevention--Suspects and animals confirmed to have BSE must not be rendered. Producers, feed mills, and rendering establishments should adhere to U.S. State and local rendering policies and FDA regulations concerning the feeding of rendered animal protein to ruminants.
TSS
Terry S. Singeltary Sr. wrote:
######## Bovine Spongiform Encephalopathy #########
ONE HUNDRED EIGHTH CONGRESS CONGRESS OF THE UNITED STATES HOUSE OF REPRESENTATIVES COMMITTEE ON GOVERNMENT REFORM 2157 RAYBURN HOUSE OFFICE BUILDING WASHINGTON, DC 20515-6143
> > May 13, 2004
> > The Honorable Ann M. Veneman Secretary of Agriculture Department of Agriculture 1400 Independence Avenue, SW Washington, DC 20250
Dear Madam Secretary:
I am writing to express concern that the recent failure of the U.S. Department of Agriculture (USDA) to test a Texas cow with neurological symptoms for bovine spongiform encephalopathy (BSE) may reflect wider problems in the surveillance program. USDA apparently does not keep track of how many cows condemned for central nervous system symptoms are tested for BSE nor does it require that suspect carcasses be held pending testing. Effective surveillance and control of BSE in the United States require a reliable system for ensuring that potentially infected cows are tested and that no infected materials enter the animal or human food supply.
Under USDA regulations, any cow that exhibits signs of central nervous system (CNS) problems must be condemned by Food Safety Inspection Service (FSIS) personnel at the plant.1
According to a 1997 Animal and Plant Health Inspection Service (APHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2
The memorandum notes that "[i]t is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."3
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4
Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
1 9 CFR 309.4.
2 USDA APHIS, Veterinary Services Memorandum No. 580.16. Procedures/or Investigation of Adult Cattle With Clinical Signs of Central Nervous System (CNS) Disease and Procedures for Surveillance of Downer Cows for Bovine Spongiform Encephalopathy (BSE) (June 11,1997).
3 Id.
4 U.S. Confirms a Failure to Use Mad Cow Test, Wall Street Journal (May 4, 2004).
The Honorable Ann M. Veneman May 13, 2004 Page 2
This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:
Based on information provided by the Food Safety and Inspection Service (FSIS), the number of adult cattle (2 years of age or greater) condemned at slaughter due to CNS signs is much greater than the number whose brains have been collected for testing.6
Despite recognizing the problem more than six years ago, however, USDA apparently did not adopt procedures to ensure that these samples would be collected. In March 2004, the Government Reform Committee asked USDA to provide, for each of the last five years, the number of BSE tests performed on cattle condemned by FSIS inspectors on the basis of CNS symptoms.7
In response, USDA provided information on the numbers of cattle condemned for CNS symptoms by FSIS, but replied that "[i]t is not possible to determine, from the data we currently collect, how many of these cattle were tested by APHIS for BSE."8
It thus appears that not only does USDA not routinely track the gap between the number of condemned and tested cattle, but that USDA could not even calculate this gap when requested to do so by Congress.
There also appears to be a lack of clarity regarding the disposition of cattle with CNS symptoms while BSE tests are pending. In the past, companies could send cattle awaiting BSE testing results for rendering, which would allow their remains to be used in feed for animals other than ruminants, such as pigs and chickens. After this incident, both FDA and USDA policy appear to have changed — in different ways.
USDA policy has apparently shifted to requesting that companies not send cattle to rendering while awaiting test results. A May 5, 2004 memo from APHIS states, "it is requested — though not required — that [the cattle] not go to inedible rendering until the sample comes
USDA's San Angelo Vets and Techs Ordered Not to Test Suspect Cow, Meating Place (May 5, 2004).
6 USDA APHIS, supra note 2.
7 Letter from Rep. Tom Davis and Rep. Henry A- Waxman to Secretary of Agriculture Ann M. Veneman (Mar. 8, 2004).
8 Letter from Ronald F. Hicks, Assistant Administrator, Office of Program Evaluation, Enforcement, and Review- FSIS. to Reo. Henrv A. Waxman- Attachment 1 (Mar. 22- 2004).
The Honorable Ann M. Veneman May 13,2004 Page 3
back negative."9
There is no explanation of why this course of action is requested, but not required.
FDA policy also appears to have shifted towards prohibiting the use of carcasses of cattle with CNS symptoms and indeterminate BSE status in certain types of animal feed. On April 30, FDA requested that the rendering company holding the remains of the Texas cow either destroy them or use them exclusively in swine feed. m the case that the remains are included in swine feed, FDA "will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs."10
Any confusion over what to do with cattle condemned for CNS symptoms awaiting testing for BSE seems unnecessary. The obvious approach is to require companies either to destroy the carcasses or hold them until test results become available. Such a policy would avoid any need for complicated traceback procedures after the discovery of a positive result. According to the information provided to the Committee by USDA, the FSIS has condemned only 200 to 250 cows per year because of signs of central nervous system damage." Mandating the destruction or holding of their carcasses would have minimal economic impact.
The experience with the BSE-infected cow in Washington State illustrates the prudence of waiting for the results of BSE tests. Prior to December 2003, USDA permitted cattle that were sampled as part of the BSE surveillance program to enter commerce even while BSE tests were pending. As a result, when the BSE-infected cow was discovered, it had already entered the food supply. This led to a complicated and partially successful traceback procedure in which hundreds of thousands of pounds of beef had to be destroyed. Because of this debacle, USDA quickly developed a new policy to require holding all carcasses from the human food chain during BSE testing.
I appreciate that you have taken steps to enhance the safety of the U.S. food supply since the discovery of BSE in the United States. I urge you to consider the lessons of this latest incident. USDA should develop a process that ensures the tracking of cattle condemned for CNS signs and should institute a policy requiring all carcasses with pending BSE tests to be destroyed or held. If there are any statutory barriers to these steps, please do not hesitate to let me know.
9 Memo from John R. Clifford, Acting Deputy Administrator, Veterinary Services, and William Smith, Assistant Administrator, Office of Field Operations, Food Safety and Inspection Service, to VSMT, Regional Directors, Area Veterinarians in Charge, and Veterinary Services, Subject: Policy Statement Regarding BSE Sampling of Condemned Cattle at Slaughter Plants - for Immediate Implementation (May 5, 2004) (online at http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf).
10 FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. 20, 2004) (online at http://www.fda.gov/bbs/topics/news/2004/NEW01061.html).
11 The yearly totals of FSIS antemortem CNS condemnation for all adult cattle were 233 (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003). The database for 2003 had not yet closed.
The Honorable Ann M. Veneman May 13, 2004 Page 4
Sincerely,
XXXXX X. XXXXXX
Henry A. Waxman
Ranking Minority Member
Congressman Henry Waxmans's Letter to the Honorable Ann Veneman
TSS
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html ##########
H. Rept. 108-815 - ACTIVITIES of the HOUSE COMMITTEE ON GOVERNMENT REFORM ONE HUNDRED EIGHTH CONGRESS FIRST AND SECOND SESSIONS 2003-2004 (Pursuant to House Rule XI, 1(d)(4)) 108th Congress (2003-2004)
snip...
After the December 23, 2003, USDA announcement of the discovery of the first U.S. case of Bovine Spongiform Encephalopathy [BSE], commonly known as ``mad cow disease,'' the committee initiated a 7-month investigation into concerns about the process for identification of BSE-infected cows and USDA's actions upon discovery of the cow. Committee investigators traveled to Washington State to interview the owner of the slaughterhouse where the BSE-infected cow was identified; requested documents from USDA; and held several meetings with USDA representatives and representatives of the cattle industry.
As a result of the committee's investigation, USDA established written protocols to be followed in case of discovery of another BSE-infected cow. USDA also implemented an expanded BSE surveillance plan to better determine whether BSE is actually present in the U.S. cattle population, and if so, at what level. The committee held a joint hearing with the Committee on Agriculture to examine USDA's expanded surveillance plan, including concerns regarding the written protocols and management of the plan. The committee will continue to conduct oversight over USDA's surveillance plan during the 109th Congress.
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
THURSDAY, JANUARY 23, 2020
USDA Consolidates Regulations for NAHLN Laboratory Testing USDA Animal and Plant Health Inspection Service sent this bulletin at 01/23/2020 02:15 PM EST
SRM's TSE PRION CONSUMPTION IN THE USA
Wednesday, March 2, 2016
RANCHO He did not know that they were placing healthy cow heads next to suspect carcasses BSE TSE Prion
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion
Thursday, June 12, 2014
Missouri Firm Recalls Ribeye and Carcass Products That May Contain Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal root ganglia may not have been completely removed
Saturday, November 10, 2012
Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials Nov 9, 2012 WI Firm Recalls Beef Tongues
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle
SPECIFIED RISK MATERIALS SRMs
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
*** Monday, October 26, 2015 ***
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
In the USA, USDA et al sometimes serves SRM’s up as appetizers or horderves.
Thursday, November 28, 2013
Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows
seems USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ???
Saturday, September 21, 2013
Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???
this recall was not for the welfare of the animals. ...tss you can check and see here ; (link now dead, does not work...tss)
2017 – Alabama
TUESDAY, JULY 18, 2017
***> USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama
THURSDAY, JULY 20, 2017
***> USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589..200
2012 - California
2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
in the url that follows, I have posted
SRM breaches first, as late as 2011.
then
MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007, when they ceased posting them.
then,
MAD COW SURVEILLANCE BREACHES.
Friday, May 18, 2012
Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012
2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
SUNDAY, NOVEMBER 13, 2011
California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock
2006 - Alabama
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
TUESDAY, JULY 18, 2017
USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama
WEDNESDAY, JULY 19, 2017
OIE REPORT Bovine spongiform encephalopathy United States of America
Date: February 4, 2004 at 10:53 am PST
Alabama man dies of Creutzfeldt-Jakob disease, Alabama does not have to report CJD
The Associated Press
A DeKalb County resident who died last year was diagnosed with a form of a rare illness sometimes linked to mad cow disease, but it was unclear how he got the infection.
Doctors determined that a man who died in November while under hospice care suffered from Creutzfeldt-Jakob disease, Coroner Tom Wilson said Tuesday. The disease was listed as the cause of death on the death certificate, he said.
Health officials said the illness kills a few people each year in Alabama, but there has never been any sign of a link with mad cow disease, which has drawn wide attention since the Dec. 23 announcement that a cow in Washington state had tested positive for it.
Wilson declined further comment and referred questions to New Beacon Hospice, which cared for the victim in DeKalb County. Mary Colley of New Beacon refused comment, citing patient confidentiality laws.
Officials with the DeKalb County Public Health Department and the area health office covering northeast Alabama said they were unaware of the case. Doctors are not required to report cases of Creutzfeldt-Jakob to the state.
WHNT-TV of Huntsville reported that the man was diagnosed with sporadic Creutzfeldt-Jakob disease, a designation given cases where the source of the infection was unknown.
Researchers believe there is a connection between mad cow disease, or bovine spongiform encephalopathy, and a variation of Creutzfeldt-Jakob disease, a fatal disorder that causes rapid dementia and loss of muscle control.
Sharon Thompson, a nurse with the epidemiology office of the Alabama Department of Public Health in Montgomery, said four to five people die each year in Alabama of Creutzfeldt-Jakob disease.
None of those deaths have been from the variant of the disease sometimes linked to mad cow disease, she said. "There are cases of it that occur naturally," said Thompson.
About one person in 1 million died of Creutzfeldt-Jakob annually in the United States from 1979 through 1994, according to statistics from the Centers for Disease Control and Prevention in Atlanta.
ALABAMA CREUTZFELDT JAKOB DISEASE TSE PRION DISEASE REPORTING
***> cjd tse prion disease is not reportable apparently <***
2005 - Texas
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
THURSDAY, OCTOBER 22, 2015
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened
HOW TO COVER UP MAD COW DISEASE IN TEXAS
FRIDAY, DECEMBER 14, 2018
MAD COW USA FLASHBACK FRIDAY DECEMBER 14, 2018
2003 - Washington State
END...TSS
WEDNESDAY, OCTOBER 21, 2020
Human Prion Disease Surveillance in Washington State, 2006-2017
10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question...
''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data.
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison.
The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
snip...
The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
try this link ;
TUESDAY, AUGUST 18, 2020
Sheep Scrapie, Bovine BSE, Cervid CWD, ZOONOSIS, TSE Prion Roundup August 18, 2020
THURSDAY, AUGUST 20, 2020
Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?
MONDAY, AUGUST 24, 2020
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
SUNDAY, OCTOBER 4, 2020
Cattle Meat and Offal Imported from the United States of America, Canada and Ireland to Japan (Prions) Food Safety Commission of Japan
TUESDAY, MARCH 12, 2019
Early preclinical detection of prions in the skin of prion-infected animals
SUNDAY, OCTOBER 11, 2020
Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ
THURSDAY, SEPTEMBER 24, 2020
The emergence of classical BSE from atypical/ Nor98 scrapie
TUESDAY, SEPTEMBER 22, 2020
APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020
WEDNESDAY, MAY 29, 2019
Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!
THURSDAY, AUGUST 20, 2020
Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?
TUESDAY, SEPTEMBER 29, 2020
ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!
FRIDAY, OCTOBER 2, 2020
H.R.925 America's Conservation Enhancement Act 116th Congress 2019-2020 SEC 104 CHRONIC WASTING DISEASE TASK FORCE
MONDAY, OCTOBER 05, 2020
USA, UK, JAPAN, CJD TSE PRION STATISTICS UPDATE OCTOBER 2020
Monday, September 14, 2020
***> Assessing the aggregated probability of entry of a novel prion disease agent into the United Kingdom
WEDNESDAY, OCTOBER 28, 2020
***> North Iceland, A case of scrapie was confirmed in a sheep, strong suspicion that scrapie is present in sheep on three farms
FRIDAY, OCTOBER 23, 2020
***> Scrapie TSE Prion Zoonosis Zoonotic, what if?
MONDAY, JULY 27, 2020
BSE Inquiry DFA's a review
Chronic Wasting Disease CWD TSE Prion update
FRIDAY, AUGUST 7, 2020
National List of Reportable Animal Diseases (NLRAD) proposed rule CWD, Scrapie, BSE, TSE, Prion Disease Singeltary Submission Docket APHIS-2017-0002
SATURDAY, OCTOBER 24, 2020
Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%
TUESDAY, OCTOBER 20, 2020
Public ownership of Texas’ white-tailed deer re-affirmed
SUNDAY, AUGUST 30, 2020
Texas CWD TSE Prion 3 More Documented, 185 Cases To Date
FRIDAY, OCTOBER 16, 2020
TAHC Rules and Resources for Harvesting Exotic CWD Susceptible Species this 2020-21 Hunting Season
WEDNESDAY, SEPTEMBER 09, 2020
TEXAS TAHC CWD TSE Prion SUMMARY MINUTES OF THE 406th COMMISSION MEETING
FRIDAY, DECEMBER 20, 2019
TEXAS ANIMAL HEALTH COMMISSION EXECUTIVE DIRECTOR ORDER DECLARING A CHRONIC WASTING DISEASE HIGH RISK AREA CONTAINMENT ZONE FOR PORTIONS OF VAL VERDE COUNTY
TUESDAY, DECEMBER 31, 2019
In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus
SUNDAY, AUGUST 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
SUNDAY, FEBRUARY 16, 2020
***> Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion?
TUESDAY, FEBRUARY 04, 2020
TEXAS REPORTS 20 NEW CWD TSE PRION CASES 3 WILD 17 BREEDER 166 POSITIVE TO DATE
FRIDAY, MAY 22, 2020
TPW Commission has adopted rules establishing Chronic Wasting Disease (CWD) management zones to further detection and response efforts among WTD
SUNDAY, MARCH 01, 2020
Texas As one CWD investigation continues, another launches...THE FULL MONTY!
SATURDAY, DECEMBER 02, 2017
TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play
SUNDAY, JANUARY 22, 2017
Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry
*** TEXAS TAHC OLD STATISTICS BELOW FOR PAST CWD TESTING ***
CWD TEXAS TAHC OLD FILE HISTORY
updated from some of my old files, some of the links will not work.
*** Subject: CWD testing in Texas ***
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
To: flounder@wt.net
snip...see ;
MONDAY, AUGUST 14, 2017
*** Texas Chronic Wasting Disease CWD TSE Prion History ***
SATURDAY, OCTOBER 10, 2020
Utah As of October 7, 2020, 118 mule deer and two elk have tested positive for CWD TSE Prion
FRIDAY, OCTOBER 09, 2020
Maryland detects additional 28 positives from last year's CWD TSE Prion sampling, total stands at 80 confirmed cases to date
THURSDAY, SEPTEMBER 24, 2020
ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE 845 Cases Positive To Date
FRIDAY, JANUARY 24, 2020
Arkansas Chronic Wasting Disease CWD TSE Prion FY2020 211 Positive Cases as of January 17, 2020
SUNDAY, JANUARY 05, 2020
Arkansas Chronic Wasting Disease CWD TSE Prion 2019 to 2020 Totals As Of December 3, 2019 399 Confirmed with more pending results
SUNDAY, SEPTEMBER 20, 2020
Wisconsin Sinks Further Into the Abyss With CWD TSE Prion 2020
WEDNESDAY, OCTOBER 28, 2020
Wyoming Hunter-submitted CWD samples identify three new positive deer hunt areas
THURSDAY, OCTOBER 08, 2020
Wyoming Chronic wasting disease 2020 surveillance and monitoring
FRIDAY, SEPTEMBER 18, 2020
CWD found in new deer and elk hunt areas in northeast Wyoming
TUESDAY, SEPTEMBER 22, 2020
Michigan CWD TSE Prion 189 Positive To Date UPDATE September 2020
SATURDAY, JANUARY 04, 2020
Mississippi CWD TOTALS JUST ABOUT DOUBLE Since October 1, 2019 To Date Statewide Total is 37 Confirmed
WEDNESDAY, OCTOBER 28, 2020
Missouri MDC FINDS FIRST CASE OF CWD IN PULASKI COUNTY
WEDNESDAY, MAY 06, 2020
Missouri 46 new cases Chronic Wasting Disease found, total to date at 162 documented CWD
SUNDAY, JANUARY 19, 2020
Missouri CWD TSE Prion 2019-2020 SAMPLING RESULTS TO DATE 25 Positive
THURSDAY, JANUARY 02, 2020
Missouri MDC officially reports more than 20 new cases of Chronic Wasting Disease CWD TSE Prion
WEDNESDAY, OCTOBER 21, 2020
Montana 18 deer test positive for chronic wasting disease CWD TSE Prion
CWD positives from across the state, no new areas
TUESDAY, MAY 19, 2020
Montana White-tailed deer in Gallatin County suspected positive for CWD
FRIDAY, FEBRUARY 07, 2020
Montana 142 animals tested positive for CWD thus far during 2019/20 sampling
FRIDAY, JANUARY 17, 2020
Montana Moose Tests Positive for Chronic Wasting Disease CWD TSE PRION in Libby Area
Montana Fish, Wildlife & Parks 2019 CWD Surveillance Hunter Test Results CWD TSE PRION LOOKS LIKE 136 POSITIVE SO FAR, count them up...
WEDNESDAY, DECEMBER 25, 2019
Montana 16 more deer positive for CWD first time positive hunting district 705 in southeast
WEDNESDAY, MARCH 25, 2020
Michigan CWD TSE Prion Total Suspect Positive Deer Moves Up To 188 with total deer tested 80,687 to date
THURSDAY, JANUARY 30, 2020
Michigan CWD TSE Prion Total Suspect Positive Deer Jumps To 181 to date
MONDAY, JANUARY 27, 2020
updated
Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?
SUNDAY, DECEMBER 22, 2019
Illinois CWD TSE Prion 90 CWD-positive deer with 826 confirmed positive Total positives through June 30, 2019
TUESDAY, FEBRUARY 11, 2020
Missouri MDC 2019-2020 SAMPLING RESULTS CWD TSE PRION TO DATE 28 Positive
SUNDAY, APRIL 12, 2020
PENNSYLVANIA REVISED CWD RESPONSE PLAN DRAFT AVAILABLE FOR REVIEW
WEDNESDAY, MARCH 04, 2020
Politicians State Rep. David Maloney, R-Berks Helping to Spread Chronic Wasting Disease CWD TSE Prion
FRIDAY, OCTOBER 16, 2020
Minnesota CWD TSE Prion confirmed in Houston County farmed deer herd
SATURDAY, MARCH 14, 2020
Minnesota 4 More Farmed Deer and 1 wild positive for CWD TSE Prion
FRIDAY, FEBRUARY 28, 2020
Virginia DGIF say 21 new cases of CWD TSE Prion confirmed in white-tailed deer in northwest Virginia throughout 2019
TUESDAY, MARCH 03, 2020
North Dakota Eight deer taken during the 2019 deer gun season tested positive for chronic wasting disease CWD TSE Prion
TUESDAY, FEBRUARY 11, 2020
South Dakota Chronic Wasting Disease CWD TSE Prion Detected in New Areas
MONDAY, FEBRUARY 10, 2020
Iowa CWD TSE Prion 2019/20 (confirmed or suspect) 43 cases to date Wild Cervid
SATURDAY, FEBRUARY 01, 2020
Colorado confirmed CWD TSE Prion in 24 game management units in the state where it previously hadn’t been found
WEDNESDAY, JANUARY 29, 2020
Utah CWD TSE Prion Since July 1, 2019, the DWR confirmed 16 positive deer statewide Six of those, including Coal, were in the La Sal Unit, 59 test pending
TUESDAY, JANUARY 28, 2020
Mississippi MDWFP North MS CWD Management Zone Since October 2019, 25 CWD-positive deer have been detected from this zone
SATURDAY, JANUARY 25, 2020
Tennessee 2019-20 deer season 462 CWD TSE Prion Confirmed To Date
Fri, Jan 24, 2020 2:29 pm
Wyoming Game & Fish Discovers CWD-Positive Mule Deer in Pinedale, Discourages Feeding of Wildlife
''As of September 2019, CWD has been identified in 31 of 37 (84%) Wyoming mule deer herds, nine of 36 (25%) elk herds, and generally wherever white-tailed deer occur. Increasing prevalence and distribution of CWD has the potential to cause widespread and long-term negative impacts to Wyoming’s cervid populations. Prevalence of this disease in chronically infected Wyoming deer herds has exceeded 40%, with one elk herd exhibiting nearly 15% prevalence.''
''for the first time, there is clear evidence that CWD is adversely affecting the overall health and viability of some herds.''
MONDAY, FEBRUARY 03, 2020
Montana Chronic Wasting Disease CWD TSE Prion in Eastern Part of State Game Farm Elk
TUESDAY, JANUARY 07, 2020
Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive
THURSDAY, JULY 30, 2020
Ohio Deer Summary 2019 - 2020 CWD TSE Prion 24 Confirmed To Date All Captive Cervid
WEDNESDAY, JANUARY 29, 2020
Pennsylvania CWD TSE Prion 2019-20 hunting seasons as of January 14, 148 of the samples had tested positive for CWD in Wild Deer
WEDNESDAY, JANUARY 29, 2020
Pennsylvania CWD TSE Prion 2019-20 hunting seasons as of January 14, 148 of the samples had tested positive for CWD in Wild Deer
SUNDAY, DECEMBER 22, 2019
Pennsylvania Steady Climb of CWD TSE Prion Confirms 250 Positive To Date In Wild Cervid As At September 12, 2019
Pennsylvania Captive Cervid Industry Total CWD TSE Prion ??? anyone's guess...
SUNDAY, OCTOBER 11, 2020
Michigan Chronic Wasting Disease CWD TSE Prion increases to 191 positive to date
TUESDAY, SEPTEMBER 22, 2020
Michigan CWD TSE Prion 189 Positive To Date UPDATE September 2020
MONDAY, JANUARY 27, 2020
Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?
TUESDAY, JANUARY 07, 2020
Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 174 confirmed to date
TUESDAY, JANUARY 14, 2020
Michigan MDARD has confirmed chronic wasting disease (CWD) in 3 white-tailed deer from a Newaygo County deer farm
SATURDAY, JANUARY 25, 2020
Tennessee 2019-20 deer season 462 CWD TSE Prion Confirmed To Date
FRIDAY, JANUARY 24, 2020
Wyoming Game & Fish Discovers CWD-Positive Mule Deer in Pinedale, Discourages Feeding of Wildlife
''As of September 2019, CWD has been identified in 31 of 37 (84%) Wyoming mule deer herds, nine of 36 (25%) elk herds, and generally wherever white-tailed deer occur. Increasing prevalence and distribution of CWD has the potential to cause widespread and long-term negative impacts to Wyoming’s cervid populations. Prevalence of this disease in chronically infected Wyoming deer herds has exceeded 40%, with one elk herd exhibiting nearly 15% prevalence.''
''for the first time, there is clear evidence that CWD is adversely affecting the overall health and viability of some herds.''
THURSDAY, SEPTEMBER 24, 2020
ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE 845 Cases Positive To Date
FRIDAY, JANUARY 24, 2020
Arkansas Chronic Wasting Disease CWD TSE Prion FY2020 211 Positive Cases as of January 17, 2020
SUNDAY, JANUARY 05, 2020
Arkansas Chronic Wasting Disease CWD TSE Prion 2019 to 2020 Totals As Of December 3, 2019 399 Confirmed with more pending results
WEDNESDAY, JANUARY 29, 2020
Utah CWD TSE Prion Since July 1, 2019, the DWR confirmed 16 positive deer statewide Six of those, including Coal, were in the La Sal Unit, 59 test pending
FRIDAY, JANUARY 17, 2020
North Dakota 11 Positive Chronic Wasting Disease CWD TSE Prion detected since Sept 1, 2019
TUESDAY, JANUARY 21, 2020
Minnesota CWD update test results from deer harvested in the 2019 hunting season and the special hunts have returned 27 wild deer tested positive for CWD all from the southeast DMZ
FRIDAY, JANUARY 10, 2020
Minnesota Investigation leads to additional CWD positive deer on Pine County farm
THURSDAY, JANUARY 23, 2020
Canadian Food Inspection Agency (CFIA) has updated the following chapter of the Accredited Veterinarian's Manual: Chapter 13 Chronic Wasting Disease Herd Certification Programs
TUESDAY, JANUARY 21, 2020
2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020
SUNDAY, FEBRUARY 09, 2020
Management of chronic wasting disease in ranched elk: conclusions from a longitudinal three-year study
Although the herd owners were presented with additional management directives, including culling of CWD positive bulls and those animals positive by an amplification assay (RT-QuIC), they were not implemented due to concern regarding its potential impact on hunting revenue.
FRIDAY, DECEMBER 06, 2019
Estimating relative CWD susceptibility and disease progression in farmed white-tailed deer with rare PRNP alleles
THURSDAY, DECEMBER 19, 2019
TSE surveillance statistics exotic species and domestic cats Update December 2019
FRIDAY, NOVEMBER 15, 2019
Southwest Wisconsin CWD, Deer and Predator Study
FRIDAY, NOVEMBER 08, 2019
EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III
WEDNESDAY, OCTOBER 16, 2019
Australia Assessment of bulk wheat from Canada Part B: Animal biosecurity risk advice, CWD TSE Prion concerns are mounting
FRIDAY, MAY 24, 2019
Assessing chronic wasting disease strain differences in free-ranging cervids across the United States
TUESDAY, FEBRUARY 04, 2020
Predicting the spread-risk potential of chronic wasting disease to sympatric ungulate species
MONDAY, MAY 20, 2019
APHIS, USDA, Announces the Finalized Chronic Wasting Disease Herd Certification Program Standards Singeltary Submissions
SUNDAY, JANUARY 12, 2020 2019
USAHA-AAVLD Annual Meeting October 24-30, 2019 Transmissible Spongiform Encephalopathy TSE Prion CWD, Scrapie UPDATE
MONDAY, OCTOBER 07, 2019
Chronic Wasting Disease (CWD) and Government Response Congressional Research Service May 17, 2019
WEDNESDAY, OCTOBER 02, 2019
Chronic Wasting Disease In Cervids: Prevalence, Impact And Management Strategies
SATURDAY, SEPTEMBER 26, 2020
A nationwide trend analysis in the incidence and mortality of Creutzfeldt–Jakob disease in Japan between 2005 and 2014 with increasing trends of incidence and mortality
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Overall, the AAPCs of age-adjusted CJD-associated mortality rates rose significantly over the study period (3.2%; 95% confidence interval [CI] 1.4–5.1%). The AAPC of the age-adjusted incidence rates also increased (overall 6.4%; 95% CI 4.7–8.1%). The CJD-associated increases in the mortality and incidence rates were especially prominent among adults over the age of 70 years. Given this trend in aging of population, the disease burden of CJD will continue to increase in severity. Our findings thus recommend that policymakers be aware of the importance of CJD and focus on preparing to address the increasing prevalence of dementia.
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Volume 26, Number 8—August 2020
Sporadic Creutzfeldt-Jakob Disease among Physicians, Germany, 1993–2018 high proportion of physicians with sCJD were surgeons
THURSDAY, JULY 02, 2020
Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure
Terry S. Singeltary Sr.
