The naturally occurring lysine to glutamic acid substitution (E211K in the bovine prion protein) results in short incubation periods for H-type bovine spongioform encephalopathy (BSE)
The naturally occurring lysine to glutamic acid substitution (E211K in the bovine prion protein) results in short incubation periods for H-type bovine spongioform encephalopathy (BSE)
Component 6: Transmissible Spongiform Encephalopathies (TSEs)
Problem Statement 6A: Determine pathobiology of prion strains.
The naturally occurring lysine to glutamic acid substitution (E211K in the bovine prion protein) results in short incubation periods for H-type bovine spongioform encephalopathy (BSE).
Virus and Prion Research Unit, National Animal Disease Center, Ames, Iowa
Classical BSE (C-BSE) is a prion disease of cattle that was responsible for the "mad cow disease" epizootic in Europe in the 1980s. C-BSE was determined to cause the human prion disease vCJD. Since then, atypical spontaneous strains of BSE were identified. H-BSE is one of those strains. Much research has explored the origins of C-BSE, and strain emergence from atypical H-BSE is one hypothesis. An H-BSE case was determined to have a germline mutation, an E211K substitution in the prion protein gene, which is analogous to a hereditary human prion disease. ARS scientists in Ames, Iowa reported the transmission of H-BSE from cattle, with and without the germline prion protein amino acid substitution, to cattle with various prion genotypes: EE211 (wild-type), EK211, and KK211. Results indicated a significantly shorter incubation period in K containing cattle compared to prion wild-type cattle. The scientists also explored the possibility that the C-BSE strain might have occurred after serial passages of EK211 and KK211 containing H-BSE in cattle, but results did not support this concept. This information is important to prion researchers, veterinary diagnostic laboratories, and those involved with establishing regulatory guidelines.
https://www.ars.usda.gov/ARSUserFiles/np103/AnnualReports/Final%20NP103%20FY2024%20Annual%20Report.updated%205.30.25.pdf
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Cattle with the EK211 PRNP polymorphism are susceptible to the H-type bovine spongiform encephalopathy agent from either E211K or wild type donors after oronasal inoculation
Author item Greenlee, Justin item Cassmann, Eric item MOORE, SARA JO - Oak Ridge Institute For Science And Education (ORISE) item WEST GREENLEE, HEATHER - Iowa State University
Submitted to: Meeting Abstract Publication Type: Abstract Only Publication Acceptance Date: 6/24/2022 Publication Date: 9/16/2022 Citation: Greenlee, J.J., Cassmann, E.D., Moore, S., West Greenlee, H.M. 2022.
Cattle with the EK211 PRNP polymorphism are susceptible to the H-type bovine spongiform encephalopathy agent from either E211K or wild type donors after oronasal inoculation.
Prion 2022 Conference abstracts: pushing the boundaries. 16(1):150. https://doi.org/10.1080/19336896.2022.2091286.
DOI: https://doi.org/10.1080/19336896.2022.2091286
Interpretive Summary:
Technical Abstract: In 2006, a case of H-type bovine spongiform encephalopathy (H-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 the H-BSE agent from either the US 2004 case (wild type donor; n=3) or from the US 2006 case with the E211K polymorphism (n=4). Cattle were observed daily throughout the course of the experiment for the development of clinical signs. When signs were noted, animals were euthanized and necropsied. Cattle were confirmed positive for abnormal BSE prions by enzyme immunoassay (EIA; Idexx HerdChek BSE Ag Test), anti-PrP immunohistochemistry (IHC) on brainstem, and microscopic examination for vacuolation. Three-out-of-four (75%) calves with the EK211 genotype developed clinical signs of H-BSE including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and were euthanized. Two of the positive EK211 steers received H-BSE US 2004 inoculum (Incubation Period (IP): 59.3 and 72.3 months) while the other positive steer received the E211K H-BSE inoculum (IP: 49.7 months). EIA confirmed that abundant misfolded protein (O.D. 2.57-4.0) in the brainstem, and IHC demonstrated PrPSc throughout the brain. All cattle in the EE211 recipient group remain asymptomatic for the duration of the experiment (approximately 7 years post-inoculation).
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=395351
Highlights
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=395351
Title: A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation
Author item MOORE, S - Orise Fellow item WEST GREENLEE, M - Iowa State University item Smith, Jodi item Vrentas, Catherine item Nicholson, Eric item Greenlee, Justin
Submitted to: Frontiers in Veterinary Science Publication Type: Peer Reviewed Journal Publication Acceptance Date: 8/30/2016 Publication Date: 9/15/2016 Citation: Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016.
A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation.
Frontiers in Veterinary Science. 3:78. Interpretive
Summary: Cases of bovine spongiform encephalopathy (BSE) or mad cow disease can be subclassified into at least 3 distinct disease forms with the predominate form known as classical BSE and the others collectively referred to as atypical BSE. Atypical BSE can be further subdivided into H-type and L-type cases that are distinct from classical BSE and from each other. Both of the atypical BSE subtypes are believed to occur spontaneously, whereas classical BSE is spread through feeding contaminated meat and bone meal to cattle. Work by other research groups suggests that the stability of the distinguishing features of atypical BSE cases (phenotypical stability) can change to closely resemble classical BSE after experimental passage implicating atypical BSE as a possible origin of classical BSE. Interestingly, one case of H-type BSE in the US was associated with an inherited mutation in the prion protein gene referred to as E211K. The purpose of this work was to compare wild type and cattle with the E211K mutation after experimental inoculation with either classical BSE or H-BSE from the original E211K case. This study demonstrates that the disease features of E211K BSE-H remain stable when transmitted to cattle without the K211 polymorphism. In addition, passage of classical BSE to cattle with the K211 polymorphism results in disease with features consistent with classical BSE and not a switch to atypical BSE-H as a result of the K211 polymorphism. As the origin of classical, feedborne BSE remains unknown and low numbers of atypical BSE are diagnosed each year, parties with interest in the cattle and beef industries and regulatory officials responsible for safe feeding practices of cattle will be interested in this work.
Technical Abstract: In 2006, a case of H-type bovine spongiform encephalopathy (BSE-H) was diagnosed in a cow that was associated with a heritable polymorphism in the bovine prion protein gene (PRNP) resulting in a lysine for glutamine amino acid substitution at codon 211 (called E211K) of the prion protein. Although the prevalence of this polymorphism is low, cattle carrying the K211 allele may be predisposed to rapid onset of BSE-H when exposed or to the potential development of a genetic BSE. This study was conducted to better understand the relationship between the K211 polymorphism and its effect on BSE phenotype. BSE-H from the US 2006 case was inoculated intracranially (IC) in one PRNP wild type (EE211) calf and one EK211 calf. In addition, one wild type calf and one EK211 calf were inoculated IC with brain homogenate from a US 2003 classical BSE case. All cattle developed clinical disease. The survival times of the E211K BSE-H inoculated EK211 calf (10 months) was shorter than the wild type calf (18 months). This genotype effect was not observed in classical BSE inoculated cattle (both 26 months). Significant changes in retinal function were observed in H-type BSE challenged cattle only. Cattle challenged with the same inoculum showed similar severity and neuroanatomical distribution of vacuolation and disease-associated prion protein deposition in the brain, though differences in neuropathology were observed between E211K BSE-H and classical BSE inoculated animals. Western blot results for brain tissue from challenged animals were consistent with the inoculum strains. This study demonstrates that the phenotype of E211K BSE-H remains stable when transmitted to cattle without the K211 polymorphism, and exhibits a number of features that differ from classical BSE in both wild type and heterozygous EK211 animals.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326785
THURSDAY, JUNE 5, 2025
World Organisation for Animal Health (WOAH) downgrades UK’s BSE risk rating to negligible, what could go wrong?
https://bovineprp.blogspot.com/2025/06/world-organisation-for-animal-health.html
Title: Transmission of atypical BSE: a possible origin of Classical BSE in cattle
Authors: Sandor Dudas1, Samuel James Sharpe1, Kristina Santiago-Mateo1, Stefanie Czub1, Waqas Tahir1,2, * Affiliation: 1National and WOAH reference Laboratory for Bovine Spongiform Encephalopathy, Canadian Food inspection Agency, Lethbridge Laboratory, Lethbridge, Canada. 2Department of Biological Sciences, University of Lethbridge, Lethbridge, Alberta, Canada. *Corresponding and Presenting Author: waqas.tahir@inspection.gc.ca
Background: Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disease of cattle and is categorized into classical and atypical forms. Classical BSE (CBSE) is linked to the consumption of BSE contaminated feed whereas atypical BSE is considered to be spontaneous in origin. The potential for oral transmission of atypical BSE is yet to be clearly defined.
Aims: To assess the oral transmissibility of atypical BSE (H and L type) in cattle. Should transmission be successful, determine the biochemical characteristics and distribution of PrPSc in the challenge cattle.
Material and Methods: For oral transmission, calves were fed with 100 g of either H (n=3) or L BSE (n=3) positive brain material. Two years post challenge, 1 calf from each of the H and L BSE challenge groups exhibited behavioural signs and were euthanized. Various brain regions of both animals were tested by traditional and novel prion detection methods with inconclusive results. To detect infectivity, brain homogenates from these oral challenge animals (P1) were injected intra-cranially (IC) into steer calves. Upon clinical signs of BSE, 3/4 of IC challenged steer calves were euthanized and tested for PrPSc with ELISA, immunohistochemistry and immunoblot.
Results: After 6 years of incubation, 3/4 animals (2/2 steers IC challenged with brain from P1 L-BSE oral challenge and 1/2 steer IC challenged with brain from P1 H-BSE oral challenge) developed clinical disease. Analysis of these animals revealed high levels of PrPSc in their brains, having biochemical properties similar to that of PrPSc in C-BSE.
Conclusion: These results demonstrate the oral transmission potential of atypical BSE in cattle. Surprisingly, regardless of which atypical type of BSE was used for P1 oral challenge, PrPSc in the P2 animals acquired biochemical characteristics similar to that of PrPSc in C-BSE, suggesting atypical BSE as a possible origin of C-BSE in UK.
Presentation Type: Oral Presentation Funded by: CFIA, Health Canada, Alberta Livestock and Meat Agency, Alberta Prion Research Institute
Grant Number: ALMA/APRI: 201400006, HC 414250
Acknowledgement: TSE unit NCAD, Lethbridge (Jianmin Yang, Sarah Bogart, Rachana Muley, Yuanmu Fang, Keri Colwell, Renee Anderson, John Gray, Rakhi Katoch) (CFIA, Canada), Dr. Catherine Graham (NSDA, Canada), Dr. Michel Levy (UCVM, Canada), Dr. Martin Groschup (FLI, Germany), Dr. Christine Fast (FLI, Germany), Dr. Bob Hills (Health Canada, Canada) Theme: Animal prion diseases
"After 6 years of incubation, 3/4 animals (2/2 steers IC challenged with brain from P1 L-BSE oral challenge and 1/2 steer IC challenged with brain from P1 H-BSE oral challenge) developed clinical disease. Analysis of these animals revealed high levels of PrPSc in their brains, having biochemical properties similar to that of PrPSc in C-BSE. "
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PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
"Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material."
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
2023
OIE Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
https://www.oie.int/fileadmin/SST/adhocreports/Bovine%20spongiform%20encephalopathy/AN/A_AhG_BSEsurv_RiskAss_Mar2019.pdf
Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019
34 Scientific Commission/September 2019
3. Atypical BSE
The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below. With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.
4. Definitions of meat-and-bone meal (MBM) and greaves
http://web.oie.int/downld/PROC2020/A_SCAD_Sept2019.pdf
Title: Transmission of atypical BSE: a possible origin of Classical BSE in cattle
Authors: Sandor Dudas1, Samuel James Sharpe1, Kristina Santiago-Mateo1, Stefanie Czub1, Waqas Tahir1,2, *
Affiliation: 1National and WOAH reference Laboratory for Bovine Spongiform Encephalopathy, Canadian Food inspection Agency, Lethbridge Laboratory, Lethbridge, Canada. 2Department of Biological Sciences, University of Lethbridge, Lethbridge, Alberta, Canada.
*Corresponding and Presenting Author: waqas.tahir@inspection.gc.ca
Background: Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disease of cattle and is categorized into classical and atypical forms. Classical BSE (CBSE) is linked to the consumption of BSE contaminated feed whereas atypical BSE is considered to be spontaneous in origin. The potential for oral transmission of atypical BSE is yet to be clearly defined.
Aims: To assess the oral transmissibility of atypical BSE (H and L type) in cattle. Should transmission be successful, determine the biochemical characteristics and distribution of PrPSc in the challenge cattle.
Material and Methods: For oral transmission, calves were fed with 100 g of either H (n=3) or L BSE (n=3) positive brain material. Two years post challenge, 1 calf from each of the H and L BSE challenge groups exhibited behavioural signs and were euthanized. Various brain regions of both animals were tested by traditional and novel prion detection methods with inconclusive results. To detect infectivity, brain homogenates from these oral challenge animals (P1) were injected intra-cranially (IC) into steer calves. Upon clinical signs of BSE, 3/4 of IC challenged steer calves were euthanized and tested for PrPSc with ELISA, immunohistochemistry and immunoblot.
Results: After 6 years of incubation, 3/4 animals (2/2 steers IC challenged with brain from P1 L-BSE oral challenge and 1/2 steer IC challenged with brain from P1 H-BSE oral challenge) developed clinical disease. Analysis of these animals revealed high levels of PrPSc in their brains, having biochemical properties similar to that of PrPSc in C-BSE.
Conclusion: These results demonstrate the oral transmission potential of atypical BSE in cattle. Surprisingly, regardless of which atypical type of BSE was used for P1 oral challenge, PrPSc in the P2 animals acquired biochemical characteristics similar to that of PrPSc in C-BSE, suggesting atypical BSE as a possible origin of C-BSE in UK.
Presentation Type: Oral Presentation
Funded by: CFIA, Health Canada, Alberta Livestock and Meat Agency, Alberta Prion Research Institute
Grant Number: ALMA/APRI: 201400006, HC 414250
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Molecular phenotype shift after passage of low-type bovine spongiform encephalopathy (L-BSE).
Zoe J. Lambert, M. Heather West Greenlee, Jifeng Bian, Justin J. Greenlee Ames, USA
Aims: The purpose of this study is to compare the molecular phenotypes of L-BSE in wild type cattle and cattle with the E211K polymorphism to samples of other cattle TSEs, such as classical BSE (C-BSE), hightype BSE (H-BSE), and transmissible mink encephalopathy (TME).
Materials and Methods: Two wild type cattle (EE211 PRNP) and one steer with the E211K polymorphism (EK211) were intracranially inoculated with 1 mL of brain homogenate that originated from a 2005 French L-BSE case. Multiple assays were used to compare and differentiate tissues, including enzyme immunoassay, western blot (Sha31, 12B2, SAF84), stability (Sha31), and immunohistochemistry (F99/97).
Results: Approximately 16.6 months post-inoculation, Steer 6 (EK211 L-BSE) developed neurologic signs, including agitation, difficulty eating accompanied by weight loss, head tremor, ataxia, and fasciculations in the forelimbs, and was necropsied. Enzyme immunoassays demonstrated misfolded prion protein in the brainstem (4.0 O.D) but not in peripheral tissues, such as the retropharyngeal lymph node and palatine tonsil. When compared by western blot, the molecular phenotype of the brainstem of Steer 6 (EK211 L-BSE) is higher than that of wildtype cattle inoculated with L-BSE, requiring careful differentiation from C-BSE. Ongoing mouse studies in bovinized mice (K211 and TgBov) will provide data to compare to all other BSE strains available, including L-BSE, C-BSE, H-BSE, E211K H-BSE, and TME.
Conclusions: Further study of L-BSE in EK211 cattle with a higher molecular phenotype in the brainstem may give more insight into the origin of C-BSE.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript. This research was supported in part by an appointment to the Agricultural Research Service (ARS) Research Participation Program administered by the Oak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. All opinions expressed in this paper are the author’s and do not necessarily reflect the policies and views of USDA, ARS, DOE, or ORAU/ORISE.
Grant number: DOE contract number DE-SC0014664 Acknowledgements: NA Theme: Animal prion diseases
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PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
The L-type BSE prion is much more virulent in primates and in humanized mice than is the classical BSE prion, which suggests the possibility of zoonotic risk associated with the L-type BSE prion
https://wwwnc.cdc.gov/eid/article/16/7/09-1882_article
Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/
Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/
Atypical L-type bovine spongiform encephalopathy (L-BSE) transmission to cynomolgus macaques, a non-human primate
Fumiko Ono 1, Naomi Tase, Asuka Kurosawa, Akio Hiyaoka, Atsushi Ohyama, Yukio Tezuka, Naomi Wada, Yuko Sato, Minoru Tobiume, Ken'ichi Hagiwara, Yoshio Yamakawa, Keiji Terao, Tetsutaro Sata
Affiliations expand
PMID: 21266763
Abstract
A low molecular weight type of atypical bovine spongiform encephalopathy (L-BSE) was transmitted to two cynomolgus macaques by intracerebral inoculation of a brain homogenate of cattle with atypical BSE detected in Japan. They developed neurological signs and symptoms at 19 or 20 months post-inoculation and were euthanized 6 months after the onset of total paralysis. Both the incubation period and duration of the disease were shorter than those for experimental transmission of classical BSE (C-BSE) into macaques. Although the clinical manifestations, such as tremor, myoclonic jerking, and paralysis, were similar to those induced upon C-BSE transmission, no premonitory symptoms, such as hyperekplexia and depression, were evident. Most of the abnormal prion protein (PrP(Sc)) was confined to the tissues of the central nervous system, as determined by immunohistochemistry and Western blotting. The PrP(Sc) glycoform that accumulated in the monkey brain showed a similar profile to that of L-BSE and consistent with that in the cattle brain used as the inoculant. PrP(Sc) staining in the cerebral cortex showed a diffuse synaptic pattern by immunohistochemistry, whereas it accumulated as fine and coarse granules and/or small plaques in the cerebellar cortex and brain stem. Severe spongiosis spread widely in the cerebral cortex, whereas florid plaques, a hallmark of variant Creutzfeldt-Jakob disease in humans, were observed in macaques inoculated with C-BSE but not in those inoculated with L-BSE.
https://pubmed.ncbi.nlm.nih.gov/21266763/
see full text;
https://www.niid.go.jp/niid/images/JJID/64/81.pdf
THURSDAY, JUNE 25, 2020
First Report of the Potential Bovine Spongiform Encephalopathy (BSE)-Related Somatic Mutation E211K of the Prion Protein Gene (PRNP) in Cattle
https://bovineprp.blogspot.com/2020/06/first-report-of-potential-bovine.html
WEDNESDAY, AUGUST 15, 2018
The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
http://bovineprp.blogspot.com/2018/08/the-agent-of-h-type-bovine-spongiform.html
PRION 2018 CONFERENCE
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.
reading up on this study from Prion 2018 Conference, very important findings ;
***> 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
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094
https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf
WEDNESDAY, OCTOBER 24, 2018
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
https://bse-atypical.blogspot.com/2018/10/experimental-infection-of-cattle-with.html
WEDNESDAY, OCTOBER 24, 2018
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
https://bse-atypical.blogspot.com/2018/10/experimental-infection-of-cattle-with.html
let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156
http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF
THE last two mad cows documented in the USA were in Alabama and Texas, both of which were atypical h-BSE.
SINGE then, the surveillance for TSE in cattle in the USA has been reduced to a number of which detecting any TSE would almost impossible.
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
https://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/UPI-12841142465253/
Technical Abstract: In 2006, a case of H-type bovine spongiform encephalopathy (H-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 the H-BSE agent from either the US 2004 case (wild type donor; n=3) or from the US 2006 case with the E211K polymorphism (n=4). Cattle were observed daily throughout the course of the experiment for the development of clinical signs. When signs were noted, animals were euthanized and necropsied. Cattle were confirmed positive for abnormal BSE prions by enzyme immunoassay (EIA; Idexx HerdChek BSE Ag Test), anti-PrP immunohistochemistry (IHC) on brainstem, and microscopic examination for vacuolation. Three-out-of-four (75%) calves with the EK211 genotype developed clinical signs of H-BSE including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and were euthanized. Two of the positive EK211 steers received H-BSE US 2004 inoculum (Incubation Period (IP): 59.3 and 72.3 months) while the other positive steer received the E211K H-BSE inoculum (IP: 49.7 months). EIA confirmed that abundant misfolded protein (O.D. 2.57-4.0) in the brainstem, and IHC demonstrated PrPSc throughout the brain. All cattle in the EE211 recipient group remain asymptomatic for the duration of the experiment (approximately 7 years post-inoculation).
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=395351
Highlights
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=395351
Title: A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation
Author item MOORE, S - Orise Fellow item WEST GREENLEE, M - Iowa State University item Smith, Jodi item Vrentas, Catherine item Nicholson, Eric item Greenlee, Justin
Submitted to: Frontiers in Veterinary Science Publication Type: Peer Reviewed Journal Publication Acceptance Date: 8/30/2016 Publication Date: 9/15/2016 Citation: Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016.
A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation.
Frontiers in Veterinary Science. 3:78. Interpretive
Summary: Cases of bovine spongiform encephalopathy (BSE) or mad cow disease can be subclassified into at least 3 distinct disease forms with the predominate form known as classical BSE and the others collectively referred to as atypical BSE. Atypical BSE can be further subdivided into H-type and L-type cases that are distinct from classical BSE and from each other. Both of the atypical BSE subtypes are believed to occur spontaneously, whereas classical BSE is spread through feeding contaminated meat and bone meal to cattle. Work by other research groups suggests that the stability of the distinguishing features of atypical BSE cases (phenotypical stability) can change to closely resemble classical BSE after experimental passage implicating atypical BSE as a possible origin of classical BSE. Interestingly, one case of H-type BSE in the US was associated with an inherited mutation in the prion protein gene referred to as E211K. The purpose of this work was to compare wild type and cattle with the E211K mutation after experimental inoculation with either classical BSE or H-BSE from the original E211K case. This study demonstrates that the disease features of E211K BSE-H remain stable when transmitted to cattle without the K211 polymorphism. In addition, passage of classical BSE to cattle with the K211 polymorphism results in disease with features consistent with classical BSE and not a switch to atypical BSE-H as a result of the K211 polymorphism. As the origin of classical, feedborne BSE remains unknown and low numbers of atypical BSE are diagnosed each year, parties with interest in the cattle and beef industries and regulatory officials responsible for safe feeding practices of cattle will be interested in this work.
Technical Abstract: In 2006, a case of H-type bovine spongiform encephalopathy (BSE-H) was diagnosed in a cow that was associated with a heritable polymorphism in the bovine prion protein gene (PRNP) resulting in a lysine for glutamine amino acid substitution at codon 211 (called E211K) of the prion protein. Although the prevalence of this polymorphism is low, cattle carrying the K211 allele may be predisposed to rapid onset of BSE-H when exposed or to the potential development of a genetic BSE. This study was conducted to better understand the relationship between the K211 polymorphism and its effect on BSE phenotype. BSE-H from the US 2006 case was inoculated intracranially (IC) in one PRNP wild type (EE211) calf and one EK211 calf. In addition, one wild type calf and one EK211 calf were inoculated IC with brain homogenate from a US 2003 classical BSE case. All cattle developed clinical disease. The survival times of the E211K BSE-H inoculated EK211 calf (10 months) was shorter than the wild type calf (18 months). This genotype effect was not observed in classical BSE inoculated cattle (both 26 months). Significant changes in retinal function were observed in H-type BSE challenged cattle only. Cattle challenged with the same inoculum showed similar severity and neuroanatomical distribution of vacuolation and disease-associated prion protein deposition in the brain, though differences in neuropathology were observed between E211K BSE-H and classical BSE inoculated animals. Western blot results for brain tissue from challenged animals were consistent with the inoculum strains. This study demonstrates that the phenotype of E211K BSE-H remains stable when transmitted to cattle without the K211 polymorphism, and exhibits a number of features that differ from classical BSE in both wild type and heterozygous EK211 animals.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326785
THURSDAY, JUNE 5, 2025
World Organisation for Animal Health (WOAH) downgrades UK’s BSE risk rating to negligible, what could go wrong?
https://bovineprp.blogspot.com/2025/06/world-organisation-for-animal-health.html
Title: Transmission of atypical BSE: a possible origin of Classical BSE in cattle
Authors: Sandor Dudas1, Samuel James Sharpe1, Kristina Santiago-Mateo1, Stefanie Czub1, Waqas Tahir1,2, * Affiliation: 1National and WOAH reference Laboratory for Bovine Spongiform Encephalopathy, Canadian Food inspection Agency, Lethbridge Laboratory, Lethbridge, Canada. 2Department of Biological Sciences, University of Lethbridge, Lethbridge, Alberta, Canada. *Corresponding and Presenting Author: waqas.tahir@inspection.gc.ca
Background: Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disease of cattle and is categorized into classical and atypical forms. Classical BSE (CBSE) is linked to the consumption of BSE contaminated feed whereas atypical BSE is considered to be spontaneous in origin. The potential for oral transmission of atypical BSE is yet to be clearly defined.
Aims: To assess the oral transmissibility of atypical BSE (H and L type) in cattle. Should transmission be successful, determine the biochemical characteristics and distribution of PrPSc in the challenge cattle.
Material and Methods: For oral transmission, calves were fed with 100 g of either H (n=3) or L BSE (n=3) positive brain material. Two years post challenge, 1 calf from each of the H and L BSE challenge groups exhibited behavioural signs and were euthanized. Various brain regions of both animals were tested by traditional and novel prion detection methods with inconclusive results. To detect infectivity, brain homogenates from these oral challenge animals (P1) were injected intra-cranially (IC) into steer calves. Upon clinical signs of BSE, 3/4 of IC challenged steer calves were euthanized and tested for PrPSc with ELISA, immunohistochemistry and immunoblot.
Results: After 6 years of incubation, 3/4 animals (2/2 steers IC challenged with brain from P1 L-BSE oral challenge and 1/2 steer IC challenged with brain from P1 H-BSE oral challenge) developed clinical disease. Analysis of these animals revealed high levels of PrPSc in their brains, having biochemical properties similar to that of PrPSc in C-BSE.
Conclusion: These results demonstrate the oral transmission potential of atypical BSE in cattle. Surprisingly, regardless of which atypical type of BSE was used for P1 oral challenge, PrPSc in the P2 animals acquired biochemical characteristics similar to that of PrPSc in C-BSE, suggesting atypical BSE as a possible origin of C-BSE in UK.
Presentation Type: Oral Presentation Funded by: CFIA, Health Canada, Alberta Livestock and Meat Agency, Alberta Prion Research Institute
Grant Number: ALMA/APRI: 201400006, HC 414250
Acknowledgement: TSE unit NCAD, Lethbridge (Jianmin Yang, Sarah Bogart, Rachana Muley, Yuanmu Fang, Keri Colwell, Renee Anderson, John Gray, Rakhi Katoch) (CFIA, Canada), Dr. Catherine Graham (NSDA, Canada), Dr. Michel Levy (UCVM, Canada), Dr. Martin Groschup (FLI, Germany), Dr. Christine Fast (FLI, Germany), Dr. Bob Hills (Health Canada, Canada) Theme: Animal prion diseases
"After 6 years of incubation, 3/4 animals (2/2 steers IC challenged with brain from P1 L-BSE oral challenge and 1/2 steer IC challenged with brain from P1 H-BSE oral challenge) developed clinical disease. Analysis of these animals revealed high levels of PrPSc in their brains, having biochemical properties similar to that of PrPSc in C-BSE. "
=====end
PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
"Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material."
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
2023
OIE Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
https://www.oie.int/fileadmin/SST/adhocreports/Bovine%20spongiform%20encephalopathy/AN/A_AhG_BSEsurv_RiskAss_Mar2019.pdf
Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019
34 Scientific Commission/September 2019
3. Atypical BSE
The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below. With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.
4. Definitions of meat-and-bone meal (MBM) and greaves
http://web.oie.int/downld/PROC2020/A_SCAD_Sept2019.pdf
Title: Transmission of atypical BSE: a possible origin of Classical BSE in cattle
Authors: Sandor Dudas1, Samuel James Sharpe1, Kristina Santiago-Mateo1, Stefanie Czub1, Waqas Tahir1,2, *
Affiliation: 1National and WOAH reference Laboratory for Bovine Spongiform Encephalopathy, Canadian Food inspection Agency, Lethbridge Laboratory, Lethbridge, Canada. 2Department of Biological Sciences, University of Lethbridge, Lethbridge, Alberta, Canada.
*Corresponding and Presenting Author: waqas.tahir@inspection.gc.ca
Background: Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disease of cattle and is categorized into classical and atypical forms. Classical BSE (CBSE) is linked to the consumption of BSE contaminated feed whereas atypical BSE is considered to be spontaneous in origin. The potential for oral transmission of atypical BSE is yet to be clearly defined.
Aims: To assess the oral transmissibility of atypical BSE (H and L type) in cattle. Should transmission be successful, determine the biochemical characteristics and distribution of PrPSc in the challenge cattle.
Material and Methods: For oral transmission, calves were fed with 100 g of either H (n=3) or L BSE (n=3) positive brain material. Two years post challenge, 1 calf from each of the H and L BSE challenge groups exhibited behavioural signs and were euthanized. Various brain regions of both animals were tested by traditional and novel prion detection methods with inconclusive results. To detect infectivity, brain homogenates from these oral challenge animals (P1) were injected intra-cranially (IC) into steer calves. Upon clinical signs of BSE, 3/4 of IC challenged steer calves were euthanized and tested for PrPSc with ELISA, immunohistochemistry and immunoblot.
Results: After 6 years of incubation, 3/4 animals (2/2 steers IC challenged with brain from P1 L-BSE oral challenge and 1/2 steer IC challenged with brain from P1 H-BSE oral challenge) developed clinical disease. Analysis of these animals revealed high levels of PrPSc in their brains, having biochemical properties similar to that of PrPSc in C-BSE.
Conclusion: These results demonstrate the oral transmission potential of atypical BSE in cattle. Surprisingly, regardless of which atypical type of BSE was used for P1 oral challenge, PrPSc in the P2 animals acquired biochemical characteristics similar to that of PrPSc in C-BSE, suggesting atypical BSE as a possible origin of C-BSE in UK.
Presentation Type: Oral Presentation
Funded by: CFIA, Health Canada, Alberta Livestock and Meat Agency, Alberta Prion Research Institute
Grant Number: ALMA/APRI: 201400006, HC 414250
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Molecular phenotype shift after passage of low-type bovine spongiform encephalopathy (L-BSE).
Zoe J. Lambert, M. Heather West Greenlee, Jifeng Bian, Justin J. Greenlee Ames, USA
Aims: The purpose of this study is to compare the molecular phenotypes of L-BSE in wild type cattle and cattle with the E211K polymorphism to samples of other cattle TSEs, such as classical BSE (C-BSE), hightype BSE (H-BSE), and transmissible mink encephalopathy (TME).
Materials and Methods: Two wild type cattle (EE211 PRNP) and one steer with the E211K polymorphism (EK211) were intracranially inoculated with 1 mL of brain homogenate that originated from a 2005 French L-BSE case. Multiple assays were used to compare and differentiate tissues, including enzyme immunoassay, western blot (Sha31, 12B2, SAF84), stability (Sha31), and immunohistochemistry (F99/97).
Results: Approximately 16.6 months post-inoculation, Steer 6 (EK211 L-BSE) developed neurologic signs, including agitation, difficulty eating accompanied by weight loss, head tremor, ataxia, and fasciculations in the forelimbs, and was necropsied. Enzyme immunoassays demonstrated misfolded prion protein in the brainstem (4.0 O.D) but not in peripheral tissues, such as the retropharyngeal lymph node and palatine tonsil. When compared by western blot, the molecular phenotype of the brainstem of Steer 6 (EK211 L-BSE) is higher than that of wildtype cattle inoculated with L-BSE, requiring careful differentiation from C-BSE. Ongoing mouse studies in bovinized mice (K211 and TgBov) will provide data to compare to all other BSE strains available, including L-BSE, C-BSE, H-BSE, E211K H-BSE, and TME.
Conclusions: Further study of L-BSE in EK211 cattle with a higher molecular phenotype in the brainstem may give more insight into the origin of C-BSE.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript. This research was supported in part by an appointment to the Agricultural Research Service (ARS) Research Participation Program administered by the Oak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. All opinions expressed in this paper are the author’s and do not necessarily reflect the policies and views of USDA, ARS, DOE, or ORAU/ORISE.
Grant number: DOE contract number DE-SC0014664 Acknowledgements: NA Theme: Animal prion diseases
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PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
The L-type BSE prion is much more virulent in primates and in humanized mice than is the classical BSE prion, which suggests the possibility of zoonotic risk associated with the L-type BSE prion
https://wwwnc.cdc.gov/eid/article/16/7/09-1882_article
Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/
Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/
Atypical L-type bovine spongiform encephalopathy (L-BSE) transmission to cynomolgus macaques, a non-human primate
Fumiko Ono 1, Naomi Tase, Asuka Kurosawa, Akio Hiyaoka, Atsushi Ohyama, Yukio Tezuka, Naomi Wada, Yuko Sato, Minoru Tobiume, Ken'ichi Hagiwara, Yoshio Yamakawa, Keiji Terao, Tetsutaro Sata
Affiliations expand
PMID: 21266763
Abstract
A low molecular weight type of atypical bovine spongiform encephalopathy (L-BSE) was transmitted to two cynomolgus macaques by intracerebral inoculation of a brain homogenate of cattle with atypical BSE detected in Japan. They developed neurological signs and symptoms at 19 or 20 months post-inoculation and were euthanized 6 months after the onset of total paralysis. Both the incubation period and duration of the disease were shorter than those for experimental transmission of classical BSE (C-BSE) into macaques. Although the clinical manifestations, such as tremor, myoclonic jerking, and paralysis, were similar to those induced upon C-BSE transmission, no premonitory symptoms, such as hyperekplexia and depression, were evident. Most of the abnormal prion protein (PrP(Sc)) was confined to the tissues of the central nervous system, as determined by immunohistochemistry and Western blotting. The PrP(Sc) glycoform that accumulated in the monkey brain showed a similar profile to that of L-BSE and consistent with that in the cattle brain used as the inoculant. PrP(Sc) staining in the cerebral cortex showed a diffuse synaptic pattern by immunohistochemistry, whereas it accumulated as fine and coarse granules and/or small plaques in the cerebellar cortex and brain stem. Severe spongiosis spread widely in the cerebral cortex, whereas florid plaques, a hallmark of variant Creutzfeldt-Jakob disease in humans, were observed in macaques inoculated with C-BSE but not in those inoculated with L-BSE.
https://pubmed.ncbi.nlm.nih.gov/21266763/
see full text;
https://www.niid.go.jp/niid/images/JJID/64/81.pdf
THURSDAY, JUNE 25, 2020
First Report of the Potential Bovine Spongiform Encephalopathy (BSE)-Related Somatic Mutation E211K of the Prion Protein Gene (PRNP) in Cattle
https://bovineprp.blogspot.com/2020/06/first-report-of-potential-bovine.html
WEDNESDAY, AUGUST 15, 2018
The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
http://bovineprp.blogspot.com/2018/08/the-agent-of-h-type-bovine-spongiform.html
PRION 2018 CONFERENCE
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.
reading up on this study from Prion 2018 Conference, very important findings ;
***> 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
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094
https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf
WEDNESDAY, OCTOBER 24, 2018
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
https://bse-atypical.blogspot.com/2018/10/experimental-infection-of-cattle-with.html
WEDNESDAY, OCTOBER 24, 2018
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
https://bse-atypical.blogspot.com/2018/10/experimental-infection-of-cattle-with.html
let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156
http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF
THE last two mad cows documented in the USA were in Alabama and Texas, both of which were atypical h-BSE.
SINGE then, the surveillance for TSE in cattle in the USA has been reduced to a number of which detecting any TSE would almost impossible.
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
https://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/UPI-12841142465253/
In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
PLEASE SEE EVIDENCE imo, THAT THE USDA ET AL COVERED UP MAD COW DISEASE IN TEXAS ; PAGE 43; Section 2. Testing Protocols and Quality Assurance Controls snip... FULL TEXT 130 PAGES
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
TUESDAY, JULY 18, 2017
USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama
http://bovineprp.blogspot.com/2017/07/usda-announces-alabama-case-of-bovine.html
2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
http://transmissiblespongiformencephalopathy.blogspot.com/2012/08/final-feed-investigation-summary.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
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)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
TUESDAY, AUGUST 22, 2006
BSE ATYPICAL TEXAS AND ALABAMA UPDATE JANUARY 20, 2007
https://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine–human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA
NATURE|Vol 457|26 February 2009
https://www.nature.com/articles/4571079b.pdf
https://www.nature.com/articles/4571079b
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/EPI_Final5-2-06.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2525843/
''This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.''
LMAO!
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
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
http://web.archive.org/web/20080229052729/http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
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
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
http://web.archive.org/web/20070223174152/http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
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
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
http://web.archive.org/web/20060821195949/http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
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
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
http://web.archive.org/web/20070223180551/http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
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
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
http://web.archive.org/web/20091104111717/http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
***> The U.S. cases were animals born and raised in the U.S. (Texas, Alabama).
SEE HISTORY AT THE BOTTOM...TSS
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
THURSDAY, OCTOBER 18, 2007
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
http://madcowtesting.blogspot.com/2007/10/bse-base-mad-cow-testing-texas-usa-and.html
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)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY, what if?
BSE Case Associated with Prion Protein Gene Mutation
http://bovineprp.blogspot.com/2015/05/bse-case-associated-with-prion-protein.html
WEDNESDAY, AUGUST 15, 2018
***> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
http://bovineprp.blogspot.com/2018/08/the-agent-of-h-type-bovine-spongiform.html
From: TSS
USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama
http://bovineprp.blogspot.com/2017/07/usda-announces-alabama-case-of-bovine.html
2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
http://transmissiblespongiformencephalopathy.blogspot.com/2012/08/final-feed-investigation-summary.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
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)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
TUESDAY, AUGUST 22, 2006
BSE ATYPICAL TEXAS AND ALABAMA UPDATE JANUARY 20, 2007
https://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine–human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA
NATURE|Vol 457|26 February 2009
https://www.nature.com/articles/4571079b.pdf
https://www.nature.com/articles/4571079b
Epidemiological investigations conducted by USDA personnel failed to reveal any evidence of a feed source contaminated with TSE material fed to this animal
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/EPI_Final5-2-06.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2525843/
''This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.''
LMAO!
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
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
http://web.archive.org/web/20080229052729/http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
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
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
http://web.archive.org/web/20070223174152/http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
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
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
http://web.archive.org/web/20060821195949/http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
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
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
http://web.archive.org/web/20070223180551/http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
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
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
http://web.archive.org/web/20091104111717/http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
***> The U.S. cases were animals born and raised in the U.S. (Texas, Alabama).
SEE HISTORY AT THE BOTTOM...TSS
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
THURSDAY, OCTOBER 18, 2007
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
http://madcowtesting.blogspot.com/2007/10/bse-base-mad-cow-testing-texas-usa-and.html
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)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY, what if?
BSE Case Associated with Prion Protein Gene Mutation
http://bovineprp.blogspot.com/2015/05/bse-case-associated-with-prion-protein.html
WEDNESDAY, AUGUST 15, 2018
***> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
http://bovineprp.blogspot.com/2018/08/the-agent-of-h-type-bovine-spongiform.html
From: TSS
Subject: Transcript of Tele-News Conference regarding The inconclusive BSE Rapid Test Result With Chief Veterinary Officer Dr. John Clifford, March 13, 2006
Date: March 14, 2006 at 10:31 am PST
Transcript
Release No. 0084.06 Contact: Office of Communications (202) 720-4623
Transcript of Tele-News Conference regarding The inconclusive BSE Rapid Test Result With Chief Veterinary Officer Dr. John Clifford, March 13, 2006 MR. JIM ROGERS: Hi, everybody. This is Jim Rogers with the Animal Plant Health Inspection Service Legislative and Public Affairs Office. I appreciate you all calling in today. We have here the USDA chief veterinarian, Dr. John Clifford. He is also known as the deputy administrator for the Veterinary Services Program under APHIS. And at this time I will turn the call over to him.
DR. CLIFFORD: Thanks, Jim. Thanks, everybody for joining us this afternoon. We received a positive result on a Western blot confirmatory test conducted at our USDA laboratories in Ames, Iowa, on samples from an animal that had tested inconclusive on a rapid screening test performed on Friday, March 10.
The samples were taken of a nonambulatory animal on a farm in Alabama. A local private veterinarian euthanized and sampled the animal and sent the samples for further testing, which was conducted at one of our contract diagnostic laboratories at the University of Georgia.
The animal was buried on the farm and did not enter the animal or human food chains. We are now working with Alabama Animal Health officials to conduct an epidemiological investigation to gather any further information we can on the herd of origin of this animal.
The animal had only resided on the most recent farm in Alabama for less than a year. We will be working to locate animals from this cow's first cohort and any offspring. We will also work with Food and Drug Administration officials to determine any feed history that may be relevant to the investigation.
Experience worldwide has shown us that it's highly unusual to find BSE in more than one animal in a herd or in affected animal's offspring. Nevertheless, all animals of interest will be tested for BSE.
Under USDA's testing protocols, surveillance samples are sent to contract laboratories for screening tests. If the sample is found to be inconclusive on a screening test, it is then shipped to our National Veterinary Services Laboratory in Ames, Iowa, for an additional rapid test and two confirmatory tests-- the immunohistochemistry test which is conducted by APHIS scientists, and the Western blot test which is conducted by scientists with USDA's Agricultural Research Service.
USDA considers an animal positive if either of these two confirmatory tests returns a positive result. In this instance the inconclusive result from the contract lab in Georgia was confirmed through a second rapid test at NVSL. Now the Western blot test has returned a positive result, and that is sufficient for us to confirm this animal to be positive for BSE, which is why we are making the announcement today.
The IHC tests are still pending, and we will release those results as soon as they are available, which we expect to be later this week.
I want to emphasize that human and animal health in the United States are protected by a system of interlocking safeguards and we remain very confident in the safety of U.S. beef.
Again, this animal did not enter the human food or animal feed chains while epidemiological work to determine the animal's precise age is just getting underway and is ongoing, the attending veterinarian has indicated that based on dentition it was an older animal, quite possibly upwards of 10 years of age.
This would indicate that this animal would have been born prior to the implementation of the Food and Drug Administration's 1997 feed ban.
Older animals are more likely to have been exposed to contaminated feed circulating before FDA's '97 ban on ruminant-to-ruminant feed practices which scientific research has indicated is the most likely route for BSE transmission.
By any measure the incidence of BSE in this country is extremely low. Our enhanced surveillance program was designed as a one-time snapshot to provide information about the level of prevalence of BSE in the United States. Since June 2004 all sectors of the cattle industry have cooperated in this program by submitting samples from more than 640,000 animals from the highest risk populations and more than 20,000 from clinically normal older animals as part of our enhanced BSE surveillance program.
To date, including the animal in today's announcement, only two of these highest risk animals have tested positive for the disease, as part of our enhanced surveillance program.
As we approach the conclusion of our enhanced surveillance program, let me offer a few thoughts regarding surveillance going forward. I can assure you that we will continue to base our maintenance surveillance testing on international guidelines. Though the nature and extent of maintenance surveillance has not yet been finalized, the incidence of BSE in this country remains extremely low and our interlocking safeguards are working to protect both human and animal health, and we remain very confident in the safety of U.S. beef.
As we move forward with the epidemiological investigation that's been initiated today in this case of BSE, we will continue to be very transparent in sharing information with the public and with our trading partners around the world.
With that, I'm happy to take any questions that you may have.
OPERATOR: At this time we are ready to begin the question and answer session. If you'd like to ask a question, please press *1 on your touch-tone phone. You will be announced prior to asking your question and to withdraw your question you will press *2.
Our first question comes from Beth Grohem (sp). Your line is open.
REPORTER: Yes. Hi, there. I'm with the Canadian Press. Thanks for taking my question. You said you were investigating the herd of origin. I'm wondering if there's any idea yet whether the animal was born in Canada or the United States.
DR. CLIFFORD: Thank you for the question. At this time we don't, we'd not be able to indicate whether it's of U.S. origin or Canadian origin. As I'd indicated, the animal was really at this particular location for less than a year, and it will require us to complete our investigation before we can determine the actual farm of origin or birth origin.
MR. ROGERS: Next question, please.
OPERATOR: Catherine Hunter, your line is open.
REPORTER: Hi, there. I was wondering if you could tell me how you expect this result to impact your ongoing negotiations to open up the Japanese import beef market.
DR. CLIFFORD: We would not anticipate that this would impact our ongoing negotiations. As I'd indicated our product is safe, we've got a number of interlocking safeguards, and Japan themselves has had 20-plus cases of BSE. And we believe their product is safe with regards to the safeguards they've in place in that country. We have a ruminant-to-ruminant feed ban to protect animal health in this country as well.
MR. ROGERS: Next question, please.
OPERATOR: Peter Shinn, your line's open.
REPORTER: Yes, thank you. Peter Shinn with the National Association of Farm Broadcasting. My question is simply, at what point do you think that you will know more relative to specifics about this animal's life? Do you have any kind of timeline?
DR CLIFFORD: We'll work as quickly as we can. I really can't give you a specific timeline, but I can tell you that we're very transparent with our information, and as soon as we have the completion of that and more information we can share we will certainly do that.
MR. ROGERS: Next question, please.
OPERATOR: Philip Brasher, your line's open.
REPORTER: Yes. Can you say anything about the breed of this animal? Do you have any idea how many farms it was on? And what's the state of the record keeping associated with this animal?
DR. CLIFFORD: I missed the second part of that, that the breed itself -- it's a beef breed. It's actually a Santa Gertrubis, has been identified. As far as the record keeping, I can't really speak to any of the record keeping at this point in time other than the fact that we know this animal was at this location for less than a year.
MR. ROGERS: Next question, please.
OPERATOR: Pete Heisey, your line's open.
REPORTER: Hi. How about the effect on trade with South Korea? They've announced since this turned positive that they were likely to suspend their reopening, which is scheduled for a month from now.
DR. CLIFFORD: Again we would hope this wouldn't affect any trade. We have a number of safeguards based upon the estimation of age and based on dentition from the private veterinarian this animal should have been born before the feed ban went into place, and we have effective safeguards in the U.S. in the ruminant-to-ruminant feed ban as well as SRM removal.
So we would not anticipate that it would affect trade and as well, we would request other countries and our trading partners as well as ourselves to move to the international standards and OIE guidelines that are based upon safe trade in commodities.
MR. ROGERS: Next question, please.
OPERATOR: Jeff Wilson, your line's open.
REPORTER: Yes. I'd like to know whether or not it's standard practice to bury any of these dead animals on the farm at all times or are they supposed to be incinerated, or is there some other means of disposal?
DR. CLIFFORD: Actually with regards to disposal methods, there are several different possibilities and options. But with regards to burying on-farm, I think that's probably specific to state issue and possibly EPA guidelines as well with regards to particular states. So I couldn't speak to the state itself.
But with regards to disposal methods we use for animals, we would use incineration, burial in lime type of burial sites as well as alkaline tissue digestion. So there's more than one method that would be available.
MR. ROGERS: Before we go to the next question, Operator, I'd like to ask everybody please state your organization that you represent before asking your question. Next question, please.
OPERATOR: Chris Clayton, your line's open.
REPORTER: Hi. I'm with DTN in Omaha, Nebraska. I wanted to just clarify the animal had died on the farm, and that was this animal already had been buried or was in the process of being buried? And have you quarantined the farm that it was on? And what kind of herd was that, how big size, that sort of thing?
DR. CLIFFORD: This particular animal, as I'd indicated, was at this farm for less than a year. Obviously they did not get, would not have been born on that farm; so therefore would not likely to have other animals of interest. So therefore it's not necessary to quarantine the farm. But whether or not it is quarantined or not I'd have to check with state officials to see if they have put a quarantine in place.
With regard to the status of the animal itself, the animal was nonambulatory. I believe the animal was treated by the veterinarian initially and the veterinarian returned on the following day and actually euthanized the animal and took the sample.
MR. ROGERS: Next question, please.
OPERATOR: Daniel Goldstein, your line's open.
REPORTER: Yeah, hi, Dr. Clifford. Dan Goldstein with Bloomberg. You said that this animal is going to go through the IHC test or the brain tissue's going to go through the IHC test. Are there any plans to send the brain tissue to Weybridge, England, for a second confirmatory IHC test?
DR. CLIFFORD: No, there's not. We don't feel that would be necessary, and as I've indicated we use both now-- the Western blot as well as the IHC. And either one of those findings to be positive, we consider that to be a positive result. So we don't feel the need in sending the sample to Weybridge.
MR. ROGERS: Next question, please.
OPERATOR: Elizabeth Weiss with USA Today. Your line's open.
REPORTER: Hey. It's Beth Weiss with USA Today. So a 10-year-old. Can you spell the name of that breed, or at least say it slowly?
DR. CLIFFORD: Santa Gertrubis. I may have get the exact spelling. It's been awhile since I've spelled it. I think it's, the first name's Santa, which is S-A-N-T-A. And the last one is G-E-R-T-R-U-B-I-S.
MR. ROGERS: All right. Spelling questions. I guess that means we're going to probably wrap it up in about two more questions, Operator. Next question, please.
OPERATOR: Wyatt Andrews with CBS News. Your line's open.
REPORTER: Thanks. It's Wyatt Andrews from CBS. Doctor, could you go in a little deeper about how you were going to look for the offspring of this cow? I mean obviously it's a cow; she's 10 years old. She clearly must have had quite a bit of offspring. First of all, do you have the records to track all the young calves that this cow had over her lifespan, number one? And number two, would those cows be presumptively contagious, and how do you look for BSE in them?
DR. CLIFFORD: Let me start by talking about records. Basically we'll have to do an epi investigation as I indicated. This particular cow was on this farm for less than a year, so therefore we will have to do an epi investigation, which will require us to try to trace her back to her farm of origin.
Once we've determined the farm of origin and then through that we would determine what other locations she may have been as well. We would determine through that then if we're able to determine that we will determine animals of interest. We would go back to the farm of origin and talk to that particular owner about what records they have or may have relative to time of birth and her first year of life on that farm.
The offspring issue, let me point out while we would still trace her two last offspring if we're able to identify those animals, it's very highly unlikely and extremely rare that either of those animals would even have the potential of having BSE while it is part currently of the OIE code, there's little science that supports that that disease is transmitted from the dam to the offspring while in the womb. So basically there's very little -- or we'll have to complete our epi investigation before we can give you more details relative to that.
MR. ROGERS: Last and final question, please, Operator?
OPERATOR: Elizabeth Lee with Atlanta Journal Constitution, your line's open.
REPORTER: Hi. It's Elizabeth Lee with the Atlanta Journal Constitution. I wanted to ask about the conclusion of the expanded surveillance program, if you could talk a little bit about when that is supposed to end and what the proposals are, how many fewer animals might be tested going forward?
DR. CLIFFORD: I think, we indicated in our statement that I'd given earlier you know as we talk about the conclusion of our enhanced surveillance program I wanted to reiterate and state that program was to take a snapshot in time to give us an estimate of prevalence.
Having said that, we will be continuing to do a level of surveillance for a long period of time within the U.S. So we will make sure that those standards meet international standards. We'll be working with scientists and others and having input in that, but at this point in time the nature and extent of that surveillance program has not yet been finalized. And when we do that we'll certainly share that publicly.
MR. ROGERS: I'd like to thank everybody very much for attending the call today. Just a few points of clarification. There's been some confusion out there about the number of inconclusives that have been found under the enhanced surveillance program. That number is four.
All of that testing data is available on our website at WWW.APHIS.USDA.GOV.
There's a picture of a cow down at the bottom, click on that and it will tell you everything you need to know.
And before we go, Dr. Clifford has one final statement.
DR. CLIFFORD: I also want to clarify for you there may be some confusion relative to the number of cases found within the U.S. for BSE. The Washington state cow, which was a Canadian origin animal, was actually found prior to our enhanced surveillance effort. So that's why when we talk about two cases, that's during the enhanced surveillance program.
MR. ROGERS: Then I guess just because I always have to have the last word, the testing numbers are now over 650,000, the new numbers are posted today.
Thank you everybody. There will be a transcript posted on our website as soon as we can make one available. This concludes our call.
Last Modified 3/14/2006
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retrievecontent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/2/_th/J_2_9D/_s.7_0_A/7_0_1OB?PC_7_2_5JM_contentid=2006%2F03%2F0084.xml&PC;_7_2_5JM_navtype=RT&PC;_7_2_5JM_parentnav=TRANSCRIPTS_SPEECHES&PC;_7_2_5JM_navid=TRANSCRIPT#7_2_5JM
Transcript
Release No. 0084.06 Contact: Office of Communications (202) 720-4623
Transcript of Tele-News Conference regarding The inconclusive BSE Rapid Test Result With Chief Veterinary Officer Dr. John Clifford, March 13, 2006 MR. JIM ROGERS: Hi, everybody. This is Jim Rogers with the Animal Plant Health Inspection Service Legislative and Public Affairs Office. I appreciate you all calling in today. We have here the USDA chief veterinarian, Dr. John Clifford. He is also known as the deputy administrator for the Veterinary Services Program under APHIS. And at this time I will turn the call over to him.
DR. CLIFFORD: Thanks, Jim. Thanks, everybody for joining us this afternoon. We received a positive result on a Western blot confirmatory test conducted at our USDA laboratories in Ames, Iowa, on samples from an animal that had tested inconclusive on a rapid screening test performed on Friday, March 10.
The samples were taken of a nonambulatory animal on a farm in Alabama. A local private veterinarian euthanized and sampled the animal and sent the samples for further testing, which was conducted at one of our contract diagnostic laboratories at the University of Georgia.
The animal was buried on the farm and did not enter the animal or human food chains. We are now working with Alabama Animal Health officials to conduct an epidemiological investigation to gather any further information we can on the herd of origin of this animal.
The animal had only resided on the most recent farm in Alabama for less than a year. We will be working to locate animals from this cow's first cohort and any offspring. We will also work with Food and Drug Administration officials to determine any feed history that may be relevant to the investigation.
Experience worldwide has shown us that it's highly unusual to find BSE in more than one animal in a herd or in affected animal's offspring. Nevertheless, all animals of interest will be tested for BSE.
Under USDA's testing protocols, surveillance samples are sent to contract laboratories for screening tests. If the sample is found to be inconclusive on a screening test, it is then shipped to our National Veterinary Services Laboratory in Ames, Iowa, for an additional rapid test and two confirmatory tests-- the immunohistochemistry test which is conducted by APHIS scientists, and the Western blot test which is conducted by scientists with USDA's Agricultural Research Service.
USDA considers an animal positive if either of these two confirmatory tests returns a positive result. In this instance the inconclusive result from the contract lab in Georgia was confirmed through a second rapid test at NVSL. Now the Western blot test has returned a positive result, and that is sufficient for us to confirm this animal to be positive for BSE, which is why we are making the announcement today.
The IHC tests are still pending, and we will release those results as soon as they are available, which we expect to be later this week.
I want to emphasize that human and animal health in the United States are protected by a system of interlocking safeguards and we remain very confident in the safety of U.S. beef.
Again, this animal did not enter the human food or animal feed chains while epidemiological work to determine the animal's precise age is just getting underway and is ongoing, the attending veterinarian has indicated that based on dentition it was an older animal, quite possibly upwards of 10 years of age.
This would indicate that this animal would have been born prior to the implementation of the Food and Drug Administration's 1997 feed ban.
Older animals are more likely to have been exposed to contaminated feed circulating before FDA's '97 ban on ruminant-to-ruminant feed practices which scientific research has indicated is the most likely route for BSE transmission.
By any measure the incidence of BSE in this country is extremely low. Our enhanced surveillance program was designed as a one-time snapshot to provide information about the level of prevalence of BSE in the United States. Since June 2004 all sectors of the cattle industry have cooperated in this program by submitting samples from more than 640,000 animals from the highest risk populations and more than 20,000 from clinically normal older animals as part of our enhanced BSE surveillance program.
To date, including the animal in today's announcement, only two of these highest risk animals have tested positive for the disease, as part of our enhanced surveillance program.
As we approach the conclusion of our enhanced surveillance program, let me offer a few thoughts regarding surveillance going forward. I can assure you that we will continue to base our maintenance surveillance testing on international guidelines. Though the nature and extent of maintenance surveillance has not yet been finalized, the incidence of BSE in this country remains extremely low and our interlocking safeguards are working to protect both human and animal health, and we remain very confident in the safety of U.S. beef.
As we move forward with the epidemiological investigation that's been initiated today in this case of BSE, we will continue to be very transparent in sharing information with the public and with our trading partners around the world.
With that, I'm happy to take any questions that you may have.
OPERATOR: At this time we are ready to begin the question and answer session. If you'd like to ask a question, please press *1 on your touch-tone phone. You will be announced prior to asking your question and to withdraw your question you will press *2.
Our first question comes from Beth Grohem (sp). Your line is open.
REPORTER: Yes. Hi, there. I'm with the Canadian Press. Thanks for taking my question. You said you were investigating the herd of origin. I'm wondering if there's any idea yet whether the animal was born in Canada or the United States.
DR. CLIFFORD: Thank you for the question. At this time we don't, we'd not be able to indicate whether it's of U.S. origin or Canadian origin. As I'd indicated, the animal was really at this particular location for less than a year, and it will require us to complete our investigation before we can determine the actual farm of origin or birth origin.
MR. ROGERS: Next question, please.
OPERATOR: Catherine Hunter, your line is open.
REPORTER: Hi, there. I was wondering if you could tell me how you expect this result to impact your ongoing negotiations to open up the Japanese import beef market.
DR. CLIFFORD: We would not anticipate that this would impact our ongoing negotiations. As I'd indicated our product is safe, we've got a number of interlocking safeguards, and Japan themselves has had 20-plus cases of BSE. And we believe their product is safe with regards to the safeguards they've in place in that country. We have a ruminant-to-ruminant feed ban to protect animal health in this country as well.
MR. ROGERS: Next question, please.
OPERATOR: Peter Shinn, your line's open.
REPORTER: Yes, thank you. Peter Shinn with the National Association of Farm Broadcasting. My question is simply, at what point do you think that you will know more relative to specifics about this animal's life? Do you have any kind of timeline?
DR CLIFFORD: We'll work as quickly as we can. I really can't give you a specific timeline, but I can tell you that we're very transparent with our information, and as soon as we have the completion of that and more information we can share we will certainly do that.
MR. ROGERS: Next question, please.
OPERATOR: Philip Brasher, your line's open.
REPORTER: Yes. Can you say anything about the breed of this animal? Do you have any idea how many farms it was on? And what's the state of the record keeping associated with this animal?
DR. CLIFFORD: I missed the second part of that, that the breed itself -- it's a beef breed. It's actually a Santa Gertrubis, has been identified. As far as the record keeping, I can't really speak to any of the record keeping at this point in time other than the fact that we know this animal was at this location for less than a year.
MR. ROGERS: Next question, please.
OPERATOR: Pete Heisey, your line's open.
REPORTER: Hi. How about the effect on trade with South Korea? They've announced since this turned positive that they were likely to suspend their reopening, which is scheduled for a month from now.
DR. CLIFFORD: Again we would hope this wouldn't affect any trade. We have a number of safeguards based upon the estimation of age and based on dentition from the private veterinarian this animal should have been born before the feed ban went into place, and we have effective safeguards in the U.S. in the ruminant-to-ruminant feed ban as well as SRM removal.
So we would not anticipate that it would affect trade and as well, we would request other countries and our trading partners as well as ourselves to move to the international standards and OIE guidelines that are based upon safe trade in commodities.
MR. ROGERS: Next question, please.
OPERATOR: Jeff Wilson, your line's open.
REPORTER: Yes. I'd like to know whether or not it's standard practice to bury any of these dead animals on the farm at all times or are they supposed to be incinerated, or is there some other means of disposal?
DR. CLIFFORD: Actually with regards to disposal methods, there are several different possibilities and options. But with regards to burying on-farm, I think that's probably specific to state issue and possibly EPA guidelines as well with regards to particular states. So I couldn't speak to the state itself.
But with regards to disposal methods we use for animals, we would use incineration, burial in lime type of burial sites as well as alkaline tissue digestion. So there's more than one method that would be available.
MR. ROGERS: Before we go to the next question, Operator, I'd like to ask everybody please state your organization that you represent before asking your question. Next question, please.
OPERATOR: Chris Clayton, your line's open.
REPORTER: Hi. I'm with DTN in Omaha, Nebraska. I wanted to just clarify the animal had died on the farm, and that was this animal already had been buried or was in the process of being buried? And have you quarantined the farm that it was on? And what kind of herd was that, how big size, that sort of thing?
DR. CLIFFORD: This particular animal, as I'd indicated, was at this farm for less than a year. Obviously they did not get, would not have been born on that farm; so therefore would not likely to have other animals of interest. So therefore it's not necessary to quarantine the farm. But whether or not it is quarantined or not I'd have to check with state officials to see if they have put a quarantine in place.
With regard to the status of the animal itself, the animal was nonambulatory. I believe the animal was treated by the veterinarian initially and the veterinarian returned on the following day and actually euthanized the animal and took the sample.
MR. ROGERS: Next question, please.
OPERATOR: Daniel Goldstein, your line's open.
REPORTER: Yeah, hi, Dr. Clifford. Dan Goldstein with Bloomberg. You said that this animal is going to go through the IHC test or the brain tissue's going to go through the IHC test. Are there any plans to send the brain tissue to Weybridge, England, for a second confirmatory IHC test?
DR. CLIFFORD: No, there's not. We don't feel that would be necessary, and as I've indicated we use both now-- the Western blot as well as the IHC. And either one of those findings to be positive, we consider that to be a positive result. So we don't feel the need in sending the sample to Weybridge.
MR. ROGERS: Next question, please.
OPERATOR: Elizabeth Weiss with USA Today. Your line's open.
REPORTER: Hey. It's Beth Weiss with USA Today. So a 10-year-old. Can you spell the name of that breed, or at least say it slowly?
DR. CLIFFORD: Santa Gertrubis. I may have get the exact spelling. It's been awhile since I've spelled it. I think it's, the first name's Santa, which is S-A-N-T-A. And the last one is G-E-R-T-R-U-B-I-S.
MR. ROGERS: All right. Spelling questions. I guess that means we're going to probably wrap it up in about two more questions, Operator. Next question, please.
OPERATOR: Wyatt Andrews with CBS News. Your line's open.
REPORTER: Thanks. It's Wyatt Andrews from CBS. Doctor, could you go in a little deeper about how you were going to look for the offspring of this cow? I mean obviously it's a cow; she's 10 years old. She clearly must have had quite a bit of offspring. First of all, do you have the records to track all the young calves that this cow had over her lifespan, number one? And number two, would those cows be presumptively contagious, and how do you look for BSE in them?
DR. CLIFFORD: Let me start by talking about records. Basically we'll have to do an epi investigation as I indicated. This particular cow was on this farm for less than a year, so therefore we will have to do an epi investigation, which will require us to try to trace her back to her farm of origin.
Once we've determined the farm of origin and then through that we would determine what other locations she may have been as well. We would determine through that then if we're able to determine that we will determine animals of interest. We would go back to the farm of origin and talk to that particular owner about what records they have or may have relative to time of birth and her first year of life on that farm.
The offspring issue, let me point out while we would still trace her two last offspring if we're able to identify those animals, it's very highly unlikely and extremely rare that either of those animals would even have the potential of having BSE while it is part currently of the OIE code, there's little science that supports that that disease is transmitted from the dam to the offspring while in the womb. So basically there's very little -- or we'll have to complete our epi investigation before we can give you more details relative to that.
MR. ROGERS: Last and final question, please, Operator?
OPERATOR: Elizabeth Lee with Atlanta Journal Constitution, your line's open.
REPORTER: Hi. It's Elizabeth Lee with the Atlanta Journal Constitution. I wanted to ask about the conclusion of the expanded surveillance program, if you could talk a little bit about when that is supposed to end and what the proposals are, how many fewer animals might be tested going forward?
DR. CLIFFORD: I think, we indicated in our statement that I'd given earlier you know as we talk about the conclusion of our enhanced surveillance program I wanted to reiterate and state that program was to take a snapshot in time to give us an estimate of prevalence.
Having said that, we will be continuing to do a level of surveillance for a long period of time within the U.S. So we will make sure that those standards meet international standards. We'll be working with scientists and others and having input in that, but at this point in time the nature and extent of that surveillance program has not yet been finalized. And when we do that we'll certainly share that publicly.
MR. ROGERS: I'd like to thank everybody very much for attending the call today. Just a few points of clarification. There's been some confusion out there about the number of inconclusives that have been found under the enhanced surveillance program. That number is four.
All of that testing data is available on our website at WWW.APHIS.USDA.GOV.
There's a picture of a cow down at the bottom, click on that and it will tell you everything you need to know.
And before we go, Dr. Clifford has one final statement.
DR. CLIFFORD: I also want to clarify for you there may be some confusion relative to the number of cases found within the U.S. for BSE. The Washington state cow, which was a Canadian origin animal, was actually found prior to our enhanced surveillance effort. So that's why when we talk about two cases, that's during the enhanced surveillance program.
MR. ROGERS: Then I guess just because I always have to have the last word, the testing numbers are now over 650,000, the new numbers are posted today.
Thank you everybody. There will be a transcript posted on our website as soon as we can make one available. This concludes our call.
Last Modified 3/14/2006
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retrievecontent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/2/_th/J_2_9D/_s.7_0_A/7_0_1OB?PC_7_2_5JM_contentid=2006%2F03%2F0084.xml&PC;_7_2_5JM_navtype=RT&PC;_7_2_5JM_parentnav=TRANSCRIPTS_SPEECHES&PC;_7_2_5JM_navid=TRANSCRIPT#7_2_5JM
WONDER if it was typical BSE or atypical BSE/BASE/TSE ??? where is the pathology, or is burying them on the farm and no weybridge going to be the norm now?
must give them credit for confirming the cow though, i am still in shock over that. ...TSS
2025, PLEASE NOTE, the above link told me ;
Forbidden
You don't have permission to access this resource.
Rather infuriating if you ask me…terry
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle
03-025IFA 03-025IFA-2 Terry S. Singeltary
Page 1 of 17
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Thursday, September 08, 2005 6:17 PM
To: fsis.regulationscomments@fsis.usda.gov
Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements
for the Disposition of Non-Ambulatory Disabled Cattle
Greetings FSIS,
I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and
Requirements for the Disposition of Non-Ambulatory Disabled Cattle
THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle
Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;
snip...FULL TEXT ;
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
http://web.archive.org/web/20060316114732/http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
=====
From: TSS
=====
From: TSS
Subject: TRANSCRIPT FROM ALABAMA AI COMMISSIONER RON SPARKS ON BSE
(a must see)
Date: March 14, 2006 at 11:39 am PST
March 13, 2006 - Second BSE Results Show Positive, Cow on Alabama Farm MONTGOMERY – Agriculture & Industries Commissioner Ron Sparks has confirmed that a second test for bovine spongiform encephalopathy (BSE) is positive. The cow was a downed animal and did not enter the human or animal food supply. The samples were taken from a cow that was on an Alabama farm within the last year.
http://www.agi.state.al.us/press_releases
March 13, 2006 - Second BSE Results Show Positive, Cow on Alabama Farm
Videos from yesterdays BSE news conference: WATCH AND LISTEN TO THIS LOAD OF BSeee, BEEF IS SAFE PR at it's finest. NO more animals are at risk on this farm? COW was 10 years old, and in Alabama for less than a year? was it ever in TEXAS and did it feed from TEXAS? mama cow. only transmitted through spinal cord and brain, firewalls in place and working. cannot be passed on to other cattle, and be very clear, IS NOT IN MUSCLE. NO COWS EATING THIS PARTICULAR TYPE FOOD. she was a DOWNER. it is not a contagious disease, no way any of the other animals can contact this disease. absolutely as safe today as it is tomorrow. nvCJD bull sh!t, and cjd in the USA is different. safe, safe, safe, safe, safe i bet this guy says it 20 times. lets compliment the cattleman, this guy, that guy, enhanced surveillance is working all the time (he does not have a clue), call in, more pats on the back. (this is the biggest hoot i have heard in a while, you must listen, safe, safe, safe). we been talking about bse in Alabama for a few years, and i have to be honest, i feel good about finding it, firewalls in place. not under quarantine, but no animals will go or come for now. not contagious. muscle tissue is safe again. cow is not shedding any organism that is dangerous to other cows. somebody in background whispering answers to commissioner sparks. Alabama food supply is safe. safe safe safe. animals cannot eat materials that they ate in 1997.............huh????? again, safe, safe, safe. (holy mad cow, these folks are oblivious) Canada has same feed ban, safe, safe, safe (commissioner is more whispers and answers, he is oblivious). we will possibly give the location of the farm later. for the security of the farmer, we will not release that information now. consumers by 93% in food supply, they vote with there pocket book (it's time the consumer showed them finally just what that is all about, show them we demand safer beef, TEST ALL CATTLE...TSS). another person speaking about the firewalls, and no risk to human health. random testing, why would i test you for flu, if bse is not contagious. clear message. transmission of cow to cow is not possible. speaker confuses himself on program and has to get someone else, he is not sure either, but insists brain and spinal is not going into feed chain. there is a testing for normal animals, we tested 20,000. (WHOOPY...tss)
Windows Media Player:
http://video1.adph.state.al.us/alphtn/newscasts/agnewscast.wmv.asx
Real Player:
http://video1.adph.state.al.us/alphtn/newscasts/agnewscast.ram
“I was very concerned to find out that the samples that tested positive for BSE were from a cow in Alabama, but this is exactly the reason that we emphasis the importance of BSE surveillance,” said Sparks. “The cow was tested as part of the enhanced BSE surveillance program that has been in place in Alabama,” said Sparks. “Even cows brought in from other states get tested for BSE before they would have a chance to be sold as food. I cannot stress enough how important this testing is to protect consumers. Also, having the Premises ID program in place in Alabama means we are able to trace the origin of a diseased animal. The cattle producers of Alabama understand the need for these precautions as well and we will continue to work together closely to protect consumers.”
The cow had been purchased by an Alabama producer and was examined and treated by a local veterinarian. After failing to respond to medication, the cow was humanely euthanized by the veterinarian and a routine sample was collected to test for BSE. Following an inconclusive test result from a rapid BSE test, the samples were tested at the National Veterinary Services Laboratories in Ames, Iowa, . The Western blot test produced a positive result. A third test, the immunohistochemistry test, is in progress and will be completed later this week. BSE is not a contagious disease that spreads animal to animal, or animal to human. BSE spreads in cattle through feed containing meat and bone meal derived from BSE infected cattle. The United States banned the use of such protein supplements in cattle feed since 1997. Commissioner Sparks stresses that beef consumption in this country is safe and there are measures in place to see that they continue. For example, downer animals are not allowed to enter commerce for human consumption and there is a ban on feeding ruminant derived protein to cattle.
http://www.agi.state.al.us/press_releases/second-bse-results-show-positive-cow-on-alabama-farm?pn=2
http://web.archive.org/web/20060604180930/http://www.agi.state.al.us/press_releases/second-bse-results-show-positive-cow-on-alabama-farm?pn=2
TSS
=====
From: TSS
Subject: USDA/Alabama BSE Epidemiological Update
Date: March 16, 2006 at 5:51 pm PST
Jim Rogers (202) 690-4755 U.S. Department of Agriculture
Christy Rhodes (334) 240-7103 Alabama Department of Agriculture & Industries
USDA/Alabama BSE Epidemiological Update
WASHINGTON , March 16, 2006 --Today, officials with the state of Alabama and the U.S. Department of Agriculture have completed work at the farm in Alabama to recover the remains of the cow that tested earlier this week as positive for BSE.
Federal and state agriculture workers excavated the remains of the animal, which had been buried on the farm and did not enter the animal or human food chain, in accordance with USDA protocols. While the carcass matches the description provided by the owner, samples are being sent to USDA's National Veterinary Services Laboratory (NVSL) in Ames , Iowa to match DNA with the positive sample. The DNA will also be used to match suspected siblings and offspring found during the epidemiological investigation.
After further examination, experts confirmed through dentition that the animal was at least 10 years of age. This means the animal would have been born prior to the implementation of the Food and Drug Administration's 1997 feed ban. Human and animal health in the United States is protected by a system of interlocking safeguards, which ensure the safety of U.S. beef. The most important of these safeguards is the ban on specified risk materials from the food supply and the FDA's ruminant-to-ruminant feed ban.
In addition to the carcass, federal agriculture officials located a six-week-old calf belonging to the BSE positive animal. The calf has been quarantined and is being moved to NVSL for further observation.
The USDA's Animal and Plant Health Inspection Service will begin tomorrow to post daily updates on the progress of the epidemiological investigation on its website between 4 and 5 p.m. EST. The updates will be available at:
Jim Rogers (202) 690-4755 U.S. Department of Agriculture
Christy Rhodes (334) 240-7103 Alabama Department of Agriculture & Industries
USDA/Alabama BSE Epidemiological Update
WASHINGTON , March 16, 2006 --Today, officials with the state of Alabama and the U.S. Department of Agriculture have completed work at the farm in Alabama to recover the remains of the cow that tested earlier this week as positive for BSE.
Federal and state agriculture workers excavated the remains of the animal, which had been buried on the farm and did not enter the animal or human food chain, in accordance with USDA protocols. While the carcass matches the description provided by the owner, samples are being sent to USDA's National Veterinary Services Laboratory (NVSL) in Ames , Iowa to match DNA with the positive sample. The DNA will also be used to match suspected siblings and offspring found during the epidemiological investigation.
After further examination, experts confirmed through dentition that the animal was at least 10 years of age. This means the animal would have been born prior to the implementation of the Food and Drug Administration's 1997 feed ban. Human and animal health in the United States is protected by a system of interlocking safeguards, which ensure the safety of U.S. beef. The most important of these safeguards is the ban on specified risk materials from the food supply and the FDA's ruminant-to-ruminant feed ban.
In addition to the carcass, federal agriculture officials located a six-week-old calf belonging to the BSE positive animal. The calf has been quarantined and is being moved to NVSL for further observation.
The USDA's Animal and Plant Health Inspection Service will begin tomorrow to post daily updates on the progress of the epidemiological investigation on its website between 4 and 5 p.m. EST. The updates will be available at:
http://www.aphis.usda.gov/newsroom/hot_issues/bse.shtml
http://web.archive.org/web/20061027224321/http://www.aphis.usda.gov/newsroom/hot_issues/bse.shtml
http://www.aphis.usda.gov/newsroom/content/2006/03/bse_al-epi_vs.shtml
http://www.aphis.usda.gov/newsroom/content/2006/03/bse_al-epi_vs.shtml
http://web.archive.org/web/20060922193758/http://www.aphis.usda.gov/newsroom/content/2006/03/bse_al-epi_vs.shtml
=====
From: TSS
=====
From: TSS
Subject: SECOND USDA CONFIRMATORY TEST RESULTS POSITIVE FOR BSE Date: March 16, 2006 at 7:22 am PST
Release No. 0090.06 Contact: Jim Rogers (202) 690-4755 USDA Press Office (202) 720-4623
SECOND USDA CONFIRMATORY TEST RESULTS POSITIVE FOR BSE
WASHINGTON, March 15, 2006- The U.S. Department of Agriculture's Animal and Plant Health Inspection Service (APHIS) today announced that the second of two bovine spongiform encephalopathy (BSE) confirmatory tests conducted on an Alabama cow has returned a positive result.
Earlier this week, USDA announced that an Alabama cow was positive for BSE after receiving the results of a Western blot confirmatory test. APHIS' National Veterinary Services Laboratories in Ames, Iowa, which conducted a second confirmatory test, the immunohistochemistry (IHC), received positive results today. Under APHIS protocols, if either the IHC or the Western blot returns a positive result the animal is considered positive for BSE.
APHIS is currently conducting an epidemiological investigation into the animal's origin in order to attempt to trace the animal to its place of birth. It had been on the Alabama farm less than a year. One of the first steps in this investigation will be the recovery of the carcass for examination to allow APHIS investigators to directly examine the breed and age of the animal as well as check the animal for any form of identification such as ear-tags. The recovery will be completed within the next day.
The cow, initially reported to be a Santa Gertrudis, is now believed to be a red crossbred (possibly crossed with a Santa Gertrudis or similar breed). This animal was non-ambulatory on the farm and examined by a local, private veterinarian. The veterinarian returned to the farm the following day, euthanized the animal and collected a sample, which was submitted for testing. The animal was buried on the farm at that time.
This animal did not enter the animal or human food chain, in accordance with USDA protocols. Human and animal health in the United States is protected by a system of interlocking safeguards, which ensure the safety of U.S. beef. The most important of these safeguards is the ban on specified risk materials from the food supply and the Food and Drug Administration's ruminant-to-ruminant feed ban.
As part of USDA's BSE enhanced surveillance program, more than 650,000 samples have been tested since June 2004. Throughout this effort, APHIS has noted the likelihood of finding additional cases of BSE. To date, only two of these highest risk animals has tested positive for the disease as part of the surveillance program, for a total of three cases of BSE in the United States. The enhanced surveillance program was designed as a one-time, intensive effort to provide a snap shot of the U.S. cattle population, in order to determine the prevalence of BSE in this country. This second case does not change the fact that BSE prevalence in the United States remains extremely low.
APHIS will continue to work closely with the state of Alabama to learn more about this animal's history, and the results of our epidemiological investigation will be shared with the public. All animals of interest will be tested for BSE.
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retrievecontent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/3/_th/J_2_9D/_s.7_0_A/7_0_1OB?PC_7_2_5JM_contentid=2006%2F03%2F0090.xml&PC;_7_2_5JM_navtype=RT&PC;_7_2_5JM_parentnav=LATEST_RELEASES&PC;_7_2_5JM_navid=NEWS_RELEASE#7_2_5JM
TSS
Release No. 0090.06 Contact: Jim Rogers (202) 690-4755 USDA Press Office (202) 720-4623
SECOND USDA CONFIRMATORY TEST RESULTS POSITIVE FOR BSE
WASHINGTON, March 15, 2006- The U.S. Department of Agriculture's Animal and Plant Health Inspection Service (APHIS) today announced that the second of two bovine spongiform encephalopathy (BSE) confirmatory tests conducted on an Alabama cow has returned a positive result.
Earlier this week, USDA announced that an Alabama cow was positive for BSE after receiving the results of a Western blot confirmatory test. APHIS' National Veterinary Services Laboratories in Ames, Iowa, which conducted a second confirmatory test, the immunohistochemistry (IHC), received positive results today. Under APHIS protocols, if either the IHC or the Western blot returns a positive result the animal is considered positive for BSE.
APHIS is currently conducting an epidemiological investigation into the animal's origin in order to attempt to trace the animal to its place of birth. It had been on the Alabama farm less than a year. One of the first steps in this investigation will be the recovery of the carcass for examination to allow APHIS investigators to directly examine the breed and age of the animal as well as check the animal for any form of identification such as ear-tags. The recovery will be completed within the next day.
The cow, initially reported to be a Santa Gertrudis, is now believed to be a red crossbred (possibly crossed with a Santa Gertrudis or similar breed). This animal was non-ambulatory on the farm and examined by a local, private veterinarian. The veterinarian returned to the farm the following day, euthanized the animal and collected a sample, which was submitted for testing. The animal was buried on the farm at that time.
This animal did not enter the animal or human food chain, in accordance with USDA protocols. Human and animal health in the United States is protected by a system of interlocking safeguards, which ensure the safety of U.S. beef. The most important of these safeguards is the ban on specified risk materials from the food supply and the Food and Drug Administration's ruminant-to-ruminant feed ban.
As part of USDA's BSE enhanced surveillance program, more than 650,000 samples have been tested since June 2004. Throughout this effort, APHIS has noted the likelihood of finding additional cases of BSE. To date, only two of these highest risk animals has tested positive for the disease as part of the surveillance program, for a total of three cases of BSE in the United States. The enhanced surveillance program was designed as a one-time, intensive effort to provide a snap shot of the U.S. cattle population, in order to determine the prevalence of BSE in this country. This second case does not change the fact that BSE prevalence in the United States remains extremely low.
APHIS will continue to work closely with the state of Alabama to learn more about this animal's history, and the results of our epidemiological investigation will be shared with the public. All animals of interest will be tested for BSE.
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retrievecontent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/3/_th/J_2_9D/_s.7_0_A/7_0_1OB?PC_7_2_5JM_contentid=2006%2F03%2F0090.xml&PC;_7_2_5JM_navtype=RT&PC;_7_2_5JM_parentnav=LATEST_RELEASES&PC;_7_2_5JM_navid=NEWS_RELEASE#7_2_5JM
TSS
2025 link is Forbidden…terry
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
<<Asante et al 2002.pdf>>
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
____________________________________
''This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.''
***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.
https://www.nature.com/articles/srep11573
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.
==============
PRION 2015 CONFERENCE
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019500/
***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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
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
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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
Sunday, January 10, 2021 APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with 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. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
https://www.regulations.gov/comment/APHIS-2018-0087-0002
https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.230.8886&rep=rep1&type=pdf
https://bovineprp.blogspot.com/2020/12/bse-research-project-final-report-2005.html
http://bovineprp.blogspot.com/2020/12/
Control of Chronic Wasting Disease OMB Control Number: 0579-0189APHIS-2021-0004 Singeltary Submission
https://www.regulations.gov/comment/APHIS-2021-0004-0002
https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
https://www.regulations.gov/document/APHIS-2018-0011-0003
https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
<<Asante et al 2002.pdf>>
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
____________________________________
''This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.''
***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.
https://www.nature.com/articles/srep11573
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.
==============
PRION 2015 CONFERENCE
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019500/
***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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
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
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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
Sunday, January 10, 2021 APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with 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. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
https://www.regulations.gov/comment/APHIS-2018-0087-0002
https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.230.8886&rep=rep1&type=pdf
https://bovineprp.blogspot.com/2020/12/bse-research-project-final-report-2005.html
http://bovineprp.blogspot.com/2020/12/
Control of Chronic Wasting Disease OMB Control Number: 0579-0189APHIS-2021-0004 Singeltary Submission
https://www.regulations.gov/comment/APHIS-2021-0004-0002
https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
https://www.regulations.gov/document/APHIS-2018-0011-0003
https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf
Tennessee State Veterinarian Alerts Cattle Owners to Disease Detection Mad Cow atypical L-Type BSE
Friday, May 19, 2023 | 04:12pm NASHVILLE — The Tennessee State Veterinarian is confirming a case of atypical bovine spongiform encephalopathy (BSE) in a cow with ties to Tennessee.
The cow appeared unwell after arriving at a packing company in South Carolina. In alignment with the United States Department of Agriculture’s BSE surveillance program, the animal was isolated and euthanized. It did not enter the food supply. Preliminary investigation has determined the cow originated in southeast Tennessee.
“We are working closely with our federal partners and animal health officials in South Carolina for this response,” State Veterinarian Dr. Samantha Beaty said. “That includes determining prior owners and locations where the affected cow lived in Tennessee and tracing siblings and offspring for testing.”
BSE is a chronic degenerative disease affecting the central nervous system of cattle. It is caused by an abnormal prion protein. The atypical form occurs spontaneously at very low levels in all cattle populations, particularly in older animals. Atypical BSE poses no known risk to human health. It is different from the classical form of BSE, which has not been detected in the U.S. since 2003.
BSE is not contagious and therefore is not spread through contact between cattle or with other species. There is no treatment for or vaccine to prevent BSE. The U.S. has a strong surveillance program in place for early detection and to prevent suspect cattle from entering the food supply chain.
Cattle owners are always advised to monitor their herds for health. Cattle affected by BSE may display changes in temperament, abnormal posture, poor coordination, decreased milk production, or loss of condition without noticeable loss of appetite. Owners should report any herd health concerns to their veterinarian or to the State Veterinarian’s office at 615-837-5120.
The Tennessee Department of Agriculture Animal Health Division is responsible for promoting animal health in Tennessee. The State Veterinarian’s office seeks to prevent the spread of disease through import and movement requirements, livestock traceability, disaster mitigation, and the services of the C.E. Kord Animal Health Diagnostic Laboratory. The division collaborates with other health-related stakeholders, academic institutions, and extension services to support One Health, an initiative to improve health for people and animals.
USDA Announces Atypical L-Type Bovine Spongiform Encephalopathy BSE Detection
The U.S. Department of Agriculture (USDA) is announcing an atypical case of Bovine Spongiform Encephalopathy (BSE), a neurologic disease of cattle, in an approximately five-year-old or older beef cow at a slaughter plant in South Carolina. This animal never entered slaughter channels and at no time presented a risk to the food supply or to human health in the United States. Given the United States’ negligible risk status for BSE, we do not expect any trade impacts as a result of this finding.
USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Laboratories (NVSL) confirmed that this cow was positive for atypical L-type BSE. The animal was tested as part of APHIS’s routine surveillance of cattle that are deemed unsuitable for slaughter. The radio frequency identification tag present on the animal is associated with a herd in Tennessee. APHIS and veterinary officials in South Carolina and Tennessee are gathering more information during this ongoing investigation.
Atypical BSE generally occurs in older cattle and seems to arise rarely and spontaneously in all cattle populations.
This is the nation’s 7th detection of BSE. Of the six previous U.S. cases, the first, in 2003, was a case of classical BSE in a cow imported from Canada; the rest have been atypical (H- or L-type) BSE.
The World Organization for Animal Health (WOAH) recognizes the United States as negligible risk for BSE. As noted in the WOAH guidelines for determining this status, atypical BSE cases do not impact official BSE risk status recognition as this form of the disease is believed to occur spontaneously in all cattle populations at a very low rate. Therefore, this finding of an atypical case will not change the negligible risk status of the United States, and should not lead to any trade issues.
The United States has a longstanding system of interlocking safeguards against BSE that protects public and animal health in the United States, the most important of which is the removal of specified risk materials - or the parts of an animal that would contain BSE should an animal have the disease - from all animals presented for slaughter. The second safeguard is a strong feed ban that protects cattle from the disease. Another important component of our system - which led to this detection - is our ongoing BSE surveillance program that allows USDA to detect the disease if it exists at very low levels in the U.S. cattle population.
More information about this disease is available in the BSE factsheet.
#
May 2, 2023
Docket No. APHIS–2023–0027 Notice of Request for Revision to and Extension of Approval of an Information Collection; National Veterinary Services Laboratories; Bovine Spongiform Encephalopathy Surveillance Program Singeltary Submission
ONLY by the Grace of God, have we not had a documented BSE outbreak, that and the fact the USDA et al are only testing 25K cattle for BSE, a number too low to find mad cow disease from some 28.9 million beef cows in the United States as of Jan. 1, 2023, down 4% from last year. The number of milk cows in the United States increased to 9.40 million. U.S. calf crop was estimated at 34.5 million head, down 2% from 2021. Jan 31, 2023.
ALL it would take is one BSE positive, yet alone a handful of BSE cases, this is why the Enhanced BSE was shut down, and the BSE testing shut down to 25k, and the BSE GBRs were replaced with BSE MRRs, after the 2003 Christmas Mad cow, the cow that stole Christmas, making it legal to trade BSE, imo.
Document APHIS-2023-0027-0001 BSE Singeltary Comment Submission
see full submission;
Mission, Texas, scrapie transmission to cattle atypical BSE.
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT
PLOS ONE Journal
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT
***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.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
WEDNESDAY, DECEMBER 23, 2020
Idiopathic Brainstem Neuronal Chromatolysis IBNC BSE TSE Prion a Review 2020
***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.
***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice
Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2
1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO
Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.
Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.
Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.
Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
snip...
In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.
CH1641
WEDNESDAY, JULY 31, 2019
The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
49. The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
E. D. Cassmanna,b, S. J. Moorea,b, R. D. Kokemullera, A. Balkema-Buschmannc, M. H. Groschupcand J. J. Greenleea
aVirus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, USA (EDC, SJM, RDK, JJG); bOak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. (EDC, SJM), Department of Veterinary Pathology, Iowa State University, Ames, IA, USA (JDS); cInstitute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Greifswald – Isle of Riems, Germany (ABB, MHG)
CONTACT E. D. Cassmann eric.cassmann@usda.gov
ABSTRACT
Introduction: Transmissible mink encephalopathy (TME) is a fatal neurologic prion disease of farmed mink. Epidemiologic and experimental evidence following a Wisconsin outbreak in 1985 has linked TME to low-type bovine spongiform encephalopathy (BSE-L). Evidence suggests that farmed mink were likely exposed through feeding of BSE-L infected downer cattle. The interspecies transmission of TME to cattle has been documented. Recently, we demonstrated the susceptibility of sheep to cattle passaged TME by intracranial inoculation. The aim of the present study was to compare ovine passaged cattle TME to other prion diseases of food-producing animals. Using a bovine transgenic mouse model, we compared the disease phenotype of sheep TME to BSE-C and BSE-L.
Materials and Methods: Separate inoculants of sheep passaged TME were derived from animals with the VRQ/VRQ (VV136) and ARQ/VRQ (AV136) prion protein genotype. Transgenic bovinized mice (TgBovXV) were intracranially inoculated with 20 µl of 1% w/v brain homogenate. The disease phenotypes were characterized by comparing the attack rates, incubation periods, and vacuolation profiles in TgBovXV mice.
Results: The attack rate for BSE-C (13/13), BSE-L (18/18), and TMEVV (21/21) was 100%; whereas, the TMEAV group (15/19) had an incomplete attack rate. The average incubation periods were 299, 280, 310, and 541 days, respectively. The vacuolation profiles of BSE-L and TMEVV were most similar with mild differences observed in the thalamus and medulla. Vacuolation profiles from the BSE-C and TMEAV experimental groups were different than TMEVVand BSE-L.
Conclusion: Overall the phenotype of disease in TME inoculated transgenic mice was dependent on the sheep donor genotype (VV vs AV). The results of the present study indicate that TME isolated from VRQ/VRQ sheep is similar to BSE-L with regards to incubation period, attack rate, and vacuolation profile. Our findings are in agreement with previous research that found phenotypic similarities between BSE-L and cattle passaged TME in an ovine transgenic rodent model. In this study, the similarities between ovine TME and BSE-L are maintained after multiple interspecies passages.
Prion2019 Conference
2007
August 1988
Evidence That Transmissible Mink Encephalopathy Results From Feeding Infected Cattle
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
NOW, in 1979, it was proven that indeed U.S. scrapie strain that was transmitted to U.S. cattle, did NOT produce a Transmissible Spongiform Encephalopathy (TSE) like the U.K. B.S.E., but a TSE unlike the U.K. B.S.E. SO what does all this tell us? it tells me that there is a possibility that a strain of mad cow disease was circulating in the U.S.A. long, long, before originally thought, only left to be ignored, while incubating and spreading.
3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to DrWatson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.
3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA.343 It was also felt that the results of such an experiment would be hard to interpret. While a negative result would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE.344 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest.345
3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility.
337 Fraser, H., Bruce, M., Chree, A., McConnell, I. and Wells, G. (1992) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice, Journal of General Virology, 73, 1891–7; Bruce, M., Chree, A., McConnell, I., Foster, J., Pearson, G. and Fraser, H. (1994) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice: Strain Variation and the Species Barrier, Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, 343, 405–11 338 Bruce, M., Will, R., Ironside, J., McConell, I., Drummond, D., Suttie, A., McCordie, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. (1997) Transmissions to Mice Indicate that ‘New Variant’ CJD is Caused by the BSE Agent, Nature, 389, 498–501 339 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606–12 340 YB88/10.00/1.1 341 Cutlip, R., Miller, J., Race, R., Jenny, A., Katz, J., Lehmkuhl, H., Debey, B. and Robinson, M. (1994) Intracerebral Transmission of Scrapie to Cattle, Journal of Infectious Diseases, 169, 814–20 342 YB88/6.21/1.2 343 YB88/11.17/2.4
31
Appendix I VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE
Dr Clark lately of the scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The
experimental results have not been published but there are plans to do
this. This work was initiated in 1978. A summary of it is:-
Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with
a 2nd Suffolk scrapie passage:-
i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BSE-like disease.
Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat
virus 2/6 went down similarly after 36 months.
Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.
Diagnosis in A, B, C was by histopath. No reports on SAF were given.
Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally— (and naturally) infected sheep by ET. He had found difficulty in obtaining embryos from naturally infected sheep (cf SPA).
Prof. A Robertson gave a brief accout of BSE. The us approach was to
32
accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.
BSE was not reported in USA.
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.
5. Scrapie agent was reported to have been isolated from a solitary fetus.
6. A western blotting diagnostic technique (? on PrP) shows some promise.
7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated
17/33 wished to drop it
6/33 wished to develop it
8/33 had few sheep and were neutral
Information obtained from Dr Wrathall‘s notes of a meeting of the u.s.
Animal Health Association at Little Rock, Arkansas Nov. 1988.
33
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
VISIT TO USA - DR AE WRATHALL - INFO ON BSE AND SCRAPIE
1. Dr. Clark lately of the Scrapie Research Unit, Mission Texas has successfully transmitted ovine & caprine Scrapie to cattle. The experimental results have not been published but there are plans to do this. This work was initiated in 1978. A summary of it is;
snip...see handwritten notes from this here;
http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf
IN CONFIDENCE
Perceptions of an unconventional slow virus diseases of animals in the U.S.A. G A H Wells
Report of a Visit to the USA April-May 1989
http://bseusa.blogspot.com/2018/
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Confucius ponders...
Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?
Epidemiology of Scrapie in the United States 1977
snip...
Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas.
It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.
The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds.
They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed.
Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary.
The station was divided into 2 areas:
(1) a series of pastures and-pens occupied by male animals only, and
(2) a series of pastures and pens occupied by females and young progeny of both sexes.
... snip...
see full text ;
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964 How Did CWD Get Way Down In Medina County, Texas?
doi:10.1016/S0021-9975(97)80022-9 Copyright © 1997 Published by Elsevier Ltd.
Second passage of a US scrapie agent in cattle
R.C. Cutlip, J.M. Miller and H.D. Lehmkuhl
United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Ames, Iowa, USA
Received 10 September 1996; accepted 31 July 1997. Available online 25 May 2006.
Summary
Scrapie and bovine spongiform encephalopathy are similar chronic neurodegenerative diseases of sheep and cattle. An earlier study showed that, on first passage in cattle, a US scrapie agent caused an encephalopathy that was distinct from bovine spongiform encephalopathy (BSE). The present report describes a second passage in cattle, carried out because diseases caused by the spongiform encephalopathy agents often change in character with additional passages in abnormal hosts. For this work, young calves were inoculated intracerebrally with a pooled suspension of brain from cattle that had died of encephalopathy after experimental inoculation with brain from scrapie-affected sheep. The second passage disease was essentially identical with the first passage disease, as judged by clinical signs, histopathological findings and distribution of "prion protein scrapie" (PrPsc). This represents additional evidence to suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.
(b) the epidemiological and laboratory studies in the USA suggest the possibility of an occurrence of BSE infection in cattle as the origin of outbreaks of TME.
{c) there is also evidence from two experiments conducted in the USA that cattle, though susceptible to scrapie inocula prepared from sheep, express a pathology quite different from that of BSE and not convincingly diagnostic of an SE by histopathological criteria. Furthermore, neither of these studies can be regarded as a basis for extrapolation to the situation in the UK because the inocula used were either experimentally passaged or natural scrapie originating from Suffolk sheep; a minority breed in this country.
Is There a Scrapie-Like Disease in Cattle? R.F. Marsh*, DVM, PhD and G.R. Hartsough, DVM
Transmissible mink encephalopathy (TME) is a rare disease of ranch-reared mink which is indistinguishable from sheep scrapie. Previous studies on the epidemiology of TME have not identified a definite source of infection for mink. Studies on experimental transmission have shown that mink are susceptible to intracerebral inoculation of American Suffolk scrapie, but that the incubation periods are longer (>1 year) than those observed in natural outbreaks of TME (<1 year).
In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a “dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.
We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.
* Department of Veterinary Science, University of Wisconsin-
- Madison, Madison, WI 53706, .
* Director of the GLMA/EMBA Ranch Service, P.0. Box 342, Thiensville, WI 53092.
PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986
August 1988
Evidence That Transmissible Mink Encephalopathy Results From Feeding Infected Cattle
Mission, Texas, scrapie transmission to cattle atypical BSE.
THURSDAY, JUNE 5, 2025
World Organisation for Animal Health (WOAH) downgrades UK’s BSE risk rating to negligible, what could go wrong?
https://bovineprp.blogspot.com/2025/06/world-organisation-for-animal-health.html
World Organisation for Animal Health (WOAH) downgrades UK’s BSE risk rating to negligible, what could go wrong?
https://bovineprp.blogspot.com/2025/06/world-organisation-for-animal-health.html
terry
posted by Terry S. Singeltary Sr. at
10:41 AM
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