2017
Subject: JAVMA NEWS Atypical BSE found in Alabama cow September 01, 2017 (ATYPICAL L-TYPE BASE BSE)
Atypical BSE found in Alabama cow
Posted Aug. 16, 2017
Health authorities found in July that an 11-year-old beef cow in Alabama had bovine spongiform encephalopathy, a degenerative prion disease.
"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," Department of Agriculture officials said in an announcement.
The cow had an atypical—or spontaneously developing—form of the disease, which differs from the classical form that is contracted through infected feed ingredients, according to the announcement from the USDA Animal and Plant Health Inspection Service. The cow is the fifth known to be infected in the U.S., the first one having been discovered in 2003. That cow had a classical form of BSE, and the rest had atypical forms.
BSE spreads among cattle and to some other animals through consumption of transmissible prion proteins. Consumption of BSE-contaminated materials has been linked with a variant of Creutzfeldt-Jakob disease, a prion disease in humans. But APHIS officials have noted that animal tissues that could contain the BSE agent are prohibited from use in human and animal foods.
Atypical forms of BSE have been identified as L-type—the form found in the Alabama cow—or H-type.
Ryan Maddox, PhD, an epidemiologist in the Prion and Public Health Office of the Centers for Disease Control and Prevention, said L-type atypical BSE has been shown in laboratory conditions to infect both primates and humanized transgenic mice more efficiently than H-type atypical BSE or classical BSE. But he noted that there is no evidence of direct transmission of the L-type form to humans.
Dr. Maddox also said that BSE infections since the 1980s have been associated with disease in about 230 people worldwide, so he would not consider the risk to be extremely high. He also noted that the U.S. has regulations to reduce the risk to humans and animals.
Regulations from the Food and Drug Administration and the USDA prohibit inclusion of mammalian protein in ruminant feed or inclusion of high-risk materials in any animal feed. Examples of materials presenting the highest risk of transmission are the brains and spinal cords of cattle ages 2.5 years and older.
The USDA announcement states that atypical BSE occurs at a low rate in all cattle populations, usually in cattle age 8 years and older. At press time, the World Animal Health Organisation (OIE) had received three other reports of atypical BSE in cattle during 2017, two of them in Spain and one in Ireland.
The OIE lists the United States and Spain among countries considered to have a negligible risk of BSE, and Ireland is considered to have a controlled risk.
*** 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.
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.
''To assess and monitor for compliance with the feed ban, the FDA established the ruminant feed ban inspection program and guidance to assist both the FDA and State investigators. Feed mill and rendering plant inspections conducted since 1998 indicate a very high level of compliance with the feed ban.''
THERE HAS BEEN LITERALLY 100s if not 1000s OF TONNAGE OF BANNED MAD COW FEED FED OUT INTO COMMERCE AS LATE AS 10 YEARS POST FEED BAN 2007, AND AS RECENTLY AS LAST YEAR 2016 the breach of the mad cow feed ban continued. these are the facts...
P56 Detection of classical BSE prions in the ileal Peyer’s patch of unweaned calves from two months after oral challenge
Ivett Ackermann1, Dr. Anne Balkema-Buschmann1, Dr. Reiner Ulrich2, Dr. Kerstin Tauscher2, Dr. Christine Fast1, Dr. Markus Keller1, James C. Shawulu1, Prof. Dr. Martin H. Groschup1 1Friedrich-Loeffler-Institut, INEID, Greifswald-Insel Riems, Germany, 2Friedrich-Loeffler-Institut, ATB, Greifswald-Insel Riems, Germany
Aims: In cattle the ileal Peyer’s patch (IPP) functions as the entry port for classical BSE prions, as these were detectable from 4 months post experimental challenge of cattle that were 4 to 6 months of age at infection. However, the earliest time point of prion detection in bovines may also be a matter of age, as a recently reported experiment indicated that BSE challenged unweaned lambs are more susceptible than older weaned lambs or adults. To prove this hypothesis and to clarify the dynamics of pathological prion protein (PrPSc) spread during the first 8 months of infection, young unweaned calves were challenged orally with classical BSE prions and the progress of the infection was monitored by assessing the ileal Peyer’s patches to determine – as a proxy of their susceptibility - the earliest time point at which pathological prion protein (PrPSc) and prion infectivity are detectable.
Methods: 18 unweaned Simmental calves aged 4 to 6 weeks were orally challenged with classical BSE, while 2 calves served as negative controls. The animals were euthanized and necropsied at predetermined time points of 1 week as well as 2, 4, 6 and 8 months post infection. To serve as positive controls 2 infected cattle were kept until the development of clinical symptoms of BSE. For each of the 18 infected and 2 negative control calves, samples of the ileal Peyer’s patch were examined by immunohistochemistry (IHC), protein misfolding cyclic amplification (PMCA) and transgenic Tgbov XV mouse bioassay.
Results: In the ileal Peyer’s patches newly generated BSE prions were detectable as early as 2 months post infection (mpi) by PMCA and transgenic mouse bioassay. From 4 mpi, PrPSc accumulation was detectable by IHC in tingible body macrophages (TBMs) of the IPP follicles and already in follicular dendritic cells (FDCs). The positive control animals developed clinical signs of BSE after incubation periods of 32 mpi and 36 mpi, respectively.
Conclusions: The earlier detection of BSE prions in the ileal Peyer’s patches may result from using improved assay protocols for the sample analysis. However, the presented data rather indicate an earlier propagation of BSE prions in the ileal Peyer’s patches as a result of challenging unweaned calves. This is also supported by the observation that the 2 BSE-challenged control animals came down after short incubation times.
P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE.
We are further examining explanations for the unusual disease presentation in the third challenged animal.
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplifi- cation (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada
Keywords: Atypical BSE, oral transmission, RT-QuIC
The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.
The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.
Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.
SATURDAY, JANUARY 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
To see a printable version of the article in the Adobe file format, click this [PDF] link.
Short Communication
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Fumiko Ono, Naomi Tase1, Asuka Kurosawa3, Akio Hiyaoka, Atsushi Ohyama, Yukio Tezuka, Naomi Wada2, Yuko Sato3, Minoru Tobiume3, Ken'ichi Hagiwara4, Yoshio Yamakawa4*, Keiji Terao1, and Tetsutaro Sata3
The Corporation for Production and Research of Laboratory Primates, Tsukuba 305-0843; 1Tsukuba Primate Research Center, National Institute of Biomedical Innovation, Tsukuba 305-0843; 2Department of Veterinary Medicine, Yamaguchi University, Yamaguchi 753-8515; and 3Department of Pathology and 4Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan
(Received December 9, 2010. Accepted December 22, 2010)
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*Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan. Tel: +81-3-5285-1111 ext. 2127, Fax: +81-3-5285-1157, E-mail: yamakawa@nih.go.jp
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SUMMARY: 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 (PrPSc) was confined to the tissues of the central nervous system, as determined by immunohistochemistry and Western blotting. The PrPSc 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. PrPSc 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.
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To date, 27 cases of L-BSE and 24 cases of H-BSE have been reported worldwide (16), thus meaning that the prevalence of atypical BSE is considerably lower than that of C-BSE. However, recent studies showed that L-BSE is easily transmissible to transgenic mice expressing human (17,18) or bovine (19,20) prion protein, as well as to non-human primates (21), with shorter incubation periods than for the transmission of C-BSE to these animals. The virulent nature of L-BSE has stimulated new concern for human public health since the transmission of C-BSE to humans resulted in variant Creutzfeldt-Jakob disease (vCJD) (4-7), a new emergent prion disease.
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Two macaques simultaneously developed neurological signs and symptoms 19-20 months post-inoculation (mpi) with the brain homogenate of BSEI JP24. The monkeys entered the terminal stage of the disease (total paralysis) at 24-25 mpi, Both the onset and duration of the disease were shorter than those reported for the transmission of C-BSE to macaques by us and other groups (27,28). The clinical manifestations such as tremor, myoclonic jerking, and paralysis were similar to those observed during the transmission of C-BSE to ma- caques, whereas the premonitory abnormal behaviors, such as hyperekplexia and depression, seen upon transmission of C-BSE to macaques were not evident (27).
Histopathological analysis and IHC, performed as described previously (29), showed that severe spongiform changes and the accumulation of Prpsc with various patterns were detectable in the brains of both monkeys (Fig. 1). Vacuolization was profound throughout the cerebral cortex, from the frontal to the occipital lobes (Fig. la). Likewise, synaptic-type Prpsc precipitation (30) was observed in the whole cerebral cortex and basal ganglia by IHC (Figs. Ib and c). Dense precipitates and plaques of Prpsc, which had been observed in cattle (JP24) brain (13), were not detected in the cerebrum of the monkeys. Prpsc, in the form of small plaques or coarse granules, was, however, detected in the molecular layer of the cerebellum (Fig. Ie). Despite the severe spongiosis in the cerebral cortex, florid plaques, which are large Prpsc plaques surrounded by vacuoles, a hallmark ofvCJD (4-7,30) and C-BSE transmission to macaques (27,28), were not observed. The histopathology of the brain was therefore similar to that reported for the brain of L-BSE (BASE)-transmitted macaques (21).
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see full text ;
Monday, September 13, 2010
atypical BSE strains and sporadic CJD strains, is there a connection and why shouldn't there be $
Monday, September 13, 2010
atypical BSE strains and sporadic CJD strains, is there a connection and why shouldn't there be $ A Surprisingly High Number of the Plaque-Like VV sCJD Subtype Among the Polish sCJD-is There a Connection with BASE?
PPo4-15:
A Surprisingly High Number of the Plaque-Like VV sCJD Subtype Among the Polish sCJD—is There a Connection with BASE?
Beata Sikorska and Pawel P. Liberski Department of Molecular Pathology and Neuropathology; Medical University of Lodz; Lodz, Poland
Recently described bovine amyloidotic spongiform encephalopathy (BASE) or L type BSE—was is overrepresented in Poland (15% of all cases of BSE). Moreover, the number of BASE cases in Poland per million bovines is the highest in Europe. A potential human risk from BASE is evident from experimental transmission to “humanized” transgenic animals and primates. Taking into consideration that non-human primate inoculated with BASE had a shorter incubation period than monkeys infected with classical BSE, and that humanized Tg mice have been found to be highly susceptible to infection with atypical form of BSE, it seems probable that BASE may be more pathogenic for humans than BSE, but the transmitted disease may differ from BSE-derived vCJD. Among 47 cases which have been diagnosed as definite in our laboratory, in 19 cases complete histopathological examination and codon 129 status were available. On the basis of the histological pattern and codon 129 status the cases of sCJD were divided into subtypes according to the Parchi&Gambetti classification. The results are as follows: type 1 (MMorMV)- 42%, type 2 (VV)-32%, type 3 (MV)-10.5%, type 4c (MM)- 10.5% and type 5 (VV)-5 %. Although the number of cases is too low to conclude a significantly different distribution of sCJD subtypes in Polish population those data show surprisingly high number of the plaque-like VV sCJD subtype. Interestingly, it was shown before that Tg mice inoculated with BASE showed granular and plaque-like aggregates or PrPSc in brains resembling those observed in VV2 subtype of sCJD.
PPo2-26:
Transmission of Classical and Atypical (L-type) Bovine Spongiform Encephalopathy (BSE) Prions to Cynomolgus macaques
Fumiko Ono,1 Yoshio Yamakawa,2 Minoru Tobiume,3 Yuko Sato,3 Harutaka Katano,3 Kenichi Hagiwara,2 Iori Itagaki,1 Akio Hiyaoka,1 Katuhiko Komatuzaki,1 Yasunori Emoto,1 Hiroaki Shibata,4 Yuichi Murayama,5 Keiji Terao,4 Yasuhiro Yasutomi4 and Tetsutaro Sata3
1The Corporation for Production and Research of Laboratory Primates; Tsukuba City, Japan; 2Departments of Cell Biology and Biochemistry; and 3Pathology; National Institute of Infectious Diseases; Tokyo, Japan; 4Tsukuba Primate Research Center; National Institute of Biomedical Innovation; Tsukuba City, Japan; 5Prion Disease Research Team; National Institute of Animal Health; Tsukuba City, Japan
Key words: L-type BSE, cBSE, cynomolgus macaques, transmission
BSE prion derived from classical BSE (cBSE) or L-type BSE was characterized by inoculation into the brain of cynomolgus macaques. The neurologic manifestation was developed in all cynomolgus macaques at 27–43 months after intracerebral inoculation of brain homogenate from cBSE-affected cattle (BSE JP/6). Second transmission of cBSE from macaque to macaque shortened incubation period to 13–18 months. cBSE-affected macaques showed the similar clinical signs including hyperekplexia, tremor and paralysis in both primary and second transmission.
Two macaques were intracerebrally inoculated brain homogenate from the L-type BSE-affected cattle (BSE JP/24). The incubation periods were 19–20 months in primary transmission.
The clinical course of the L-type BSE-affected macaques differed from that in cBSE-affected macaques in the points of severe myoclonus without hyperekplexia. The glycoform profile of PrPSc detected in macaque CNS was consistent with original pattern of either cBSE or L-typeBSE PrPSc, respectively. Although severe spongiform change in the brain was remarkable in all BSE-affected macaques, severe spongiform spread widely in cerebral cortex in L-type BSE-affected macaques. Heavy accumulation of PrPSc surrounded by vacuola formed florid plaques in cerebral cortex of cBSE-affected macaques. Deposit of PrPSc in L-type BSE-affected macaque was weak and diffuse synaptic pattern in cerebrum, but large PrPSc plaques were evident at cerebellum. MRI analysis, T2, T1, DW and flair sequences, at the time of autopsy revealed that brain atrophy and dilatation of cerebral ventricles were significantly severe in L-type BSE-affected macaques. These results suggest that L-type BSE is more virulent strain to primates comparing to cBSE.
SP1-4:
Evidence from Molecular Strain Typing
Gianluigi Zanusso Department of Neurological and Visual Sciences; Section of Clinical Neurology; University of Verona; Verona, Italy
Key words: molecular analysis, strain typing, atypical BSE, CJD
In 2001, active surveillance for bovine spongiform encephalopathy (BSE) led to the discovery of atypical BSE phenotypes in aged cattle distinct from classical BSE (C-type). These atypical BSE cases had been classified as low L-type (BASE) or high H-type BSE based on the molecular mass and the degree of glycosylation of of the pathological prion protein (PrPSc). Transmission studies in TgBov mice showed that H-type BSE, C-type BSE and BASE behave as distinct prion strains with different incubation periods, PrPSc molecular patterns and pathological phenotypes. A still unclear issue concerns the potential transmissibility and phenotypes of atypical BSEs in humans. We previously indicated that BASE was similar to a distinct subgroup of sporadic form of Creutzfeldt-Jakob disease (sCJD) MV2, based on molecular similarities and on neuropathological pattern of PrP deposition. To investigate a possible link between BASE and sCJD, Kong et al. and Comoy et al. experimentally inoculated TgHu mice (129MM) and a non-human primate respectively, showing in both models that BASE was more virulent compare to BSE. Further, non-human primate reproduced a clinical phenotype resembling to that of sCJD subtype MM2. Here, we presented a comparative analysis of the biochemical fingerprints of PrPSc between the different sCJD subtypes and animal TSEs and after experimental transmission to animals.
Opinion of the Scientific Steering Committee on the GEOGRAPHICAL RISK OF BOVINE SPONGIFORM ENCEPHALOPATHY (GBR) in POLAND Adopted on 30/03/2001
It is concluded that it is likely but not confirmed that one or several cattle that are (pre-clinically or clinically) infected with the BSE agent are currently present in the domestic herd of Poland (GBR III).
Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate
Emmanuel E. Comoy1*, Cristina Casalone2, Nathalie Lescoutra-Etchegaray1, Gianluigi Zanusso3, Sophie Freire1, Dominique Marcé1, Frédéric Auvré1, Marie-Magdeleine Ruchoux1, Sergio Ferrari3, Salvatore Monaco3, Nicole Salès4, Maria Caramelli2, Philippe Leboulch1,5, Paul Brown1, Corinne I. Lasmézas4, Jean-Philippe Deslys1
1 Institute of Emerging Diseases and Innovative Therapies, CEA, Fontenay-aux-Roses, France, 2 Istituto Zooprofilattico Sperimentale del Piemonte, Turin, Italy, 3 Policlinico G.B. Rossi, Verona, Italy, 4 Scripps Florida, Jupiter, Florida, United States of America, 5 Genetics Division, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
Abstract Top Background Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.
Methodology/Principal Findings Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.
Conclusion/Significance Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.
Citation: Comoy EE, Casalone C, Lescoutra-Etchegaray N, Zanusso G, Freire S, et al. (2008) Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate. PLoS ONE 3(8): e3017. doi:10.1371/journal.pone.0003017
Editor: Neil Mabbott, University of Edinburgh, United Kingdom
Received: April 24, 2008; Accepted: August 1, 2008; Published: August 20, 2008
Copyright: © 2008 Comoy et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work has been supported by the Network of Excellence NeuroPrion.
Competing interests: CEA owns a patent covering the BSE diagnostic tests commercialized by the company Bio-Rad.
* E-mail: emmanuel.comoy@cea.fr
Session I - Prions: Structure, Strain and Detection (II)
Searching for BASE Strain Signature in Sporadic Creutzfedlt-Jakob Disease
Gianluigi Zanusso
Department of Neurological and Visual Sciences, Section of Clinical Neurology University of Verona, Verona, Italy.
Bovine amyloidotic spongiform encephalopathy (BASE) is a newly recognized form of bovine prion disease, which was originally detected in Italy in 2004 as an effect of active surveillance. BASE or BSE L-type (L is referred to the lower electrophoretic PrPSc migration than classical BSE) has now been reported in several countries, including Japan. All field cases of BASE were older than 8 years and neurologically normal at the time of slaughtered. By experimental transmission, we defined the disease phenotype of cattle BASE, which is quite distinct from that seen in typical BSE and characterized by mental dullness and amyotrophy. Surprisingly, following intraspecies and interspecies transmission the incubation period of BASE was shorter than BSE. The relatively easy transmission of BASE isolate as well as the molecular similarity with sporadic Creutzfeldt-Jakob disease (sCJD) have raised concern regarding its potential passage to humans. Tg humanized mice Met/Met at codon 129 challenged with both BSE and BASE isolates, showed a resistance to BSE but a susceptibility to BASE at a 60% rate; in addition, BASE-inoculated Cynomolgus (129 Met/Met) had shorter incubation periods than BSE-inoculated primates. In this study we compared the biochemical properties of PrPSc in Cynomolgus and in TgHu Met/Met mice challenged with BSE and BASE strains, by conventional SDS-PAGE analysis and 2D separation. The results obtained disclose distinct conformational changes in PrPSc, which are dependent on the inoculated host but not on the codon 129 genotype.
This work was supported by Neuroprion contract n. FOOD CT 2004 -506579 (NOE)
SEE OTHER YEARS OF PRION CONFERENCE ABSTRACTS
P02.35
Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden
Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
Thursday, October 07, 2010
Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice
Thursday, October 07, 2010 Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice
Vet Pathol 0300985810382672, first published on October 4, 2010
Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice
H. Okada okadahi@affrc.go.jp Prion Disease Research Center, National Institute of Animal Health, Tsukuba, K. Masujin Prion Disease Research Center, National Institute of Animal Health, Tsukuba, Y. Imamaru Prion Disease Research Center, National Institute of Animal Health, Tsukuba, M. Imamura Prion Disease Research Center, National Institute of Animal Health, Tsukuba, Y. Matsuura Prion Disease Research Center, National Institute of Animal Health, Tsukuba, S. Mohri Prion Disease Research Center, National Institute of Animal Health, Tsukuba, S. Czub Animal Disease Research Institute, Canadian Food Inspection Agency, T. Yokoyama Prion Disease Research Center, National Institute of Animal Health, Tsukuba,
Abstract
To characterize the biological and biochemical properties of H-type bovine spongiform encephalopathy (BSE), a transmission study with a Canadian H-type isolate was performed with bovinized transgenic mice (TgBoPrP), which were inoculated intracerebrally with brain homogenate from cattle with H-type BSE. All mice exhibited characteristic neurologic signs, and the subsequent passage showed a shortened incubation period. The distribution of disease-associated prion protein (PrPSc) was determined by immunohistochemistry, Western blot, and paraffin-embedded tissue (PET) blot. Biochemical properties and higher molecular weight of the glycoform pattern were well conserved within mice. Immunolabeled granular PrPSc, aggregates, and/or plaque-like deposits were mainly detected in the following brain locations: septal nuclei, subcallosal regions, hypothalamus, paraventricular nucleus of the thalamus, interstitial nucleus of the stria terminalis, and the reticular formation of the midbrain. Weak reactivity was detected by immunohistochemistry and PET blot in the cerebral cortex, most thalamic nuclei, the hippocampus, medulla oblongata, and cerebellum. These findings indicate that the H-type BSE prion has biological and biochemical properties distinct from those of C-type and L-type BSE in TgBoPrP mice, which suggests that TgBoPrP mice constitute a useful animal model to distinguish isolates from BSE-infected cattle.
© 2010 Sage Publications, Inc.
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain▿ Qingzhong Kong1,*, Mengjie Zheng1, Cristina Casalone2, Liuting Qing1, Shenghai Huang1,†, Bikram Chakraborty1, Ping Wang1, Fusong Chen1, Ignazio Cali1, Cristiano Corona2, Francesca Martucci2, Barbara Iulini2, Pierluigi Acutis2, Lan Wang1, Jingjing Liang1, Meiling Wang1, Xinyi Li1, Salvatore Monaco3, Gianluigi Zanusso3, Wen-Quan Zou1, Maria Caramelli2 and Pierluigi Gambetti1,* + Author Affiliations
1Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106 2CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy 3Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy ABSTRACT
Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to be caused by only one strain, BSE-C. BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE strains by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE strain-infected cattle. Sixty percent of the inoculated Tg mice became infected after 20 to 22 months of incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE strain-infected Tg mice, but none of the Tg mice infected with prions causing a sporadic human prion disease, showed the presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE strain-infected humanized Tg mouse brains are different from those from the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation times are observed for the BASE strain-infected Tg mice. These results suggest that in humans, the BASE strain is a more virulent BSE strain and likely lymphotropic.
SNIP...
DISCUSSION We have shown that 60% of our Tg40 mice (in an inbred FVB background) that express normal levels of human PrP-129M became infected 20 to 22 months after i.c. inoculation with 0.3 mg of brain tissue from the two BASE isolates, suggesting a titer of approximately 3 50% infective dose units per milligram of brain tissue in the Tg40 line. An approximately 20% attack rate has been reported for the Tg650 line (in a mixed 129/Sv × C57BL/6 background) after i.c. inoculation with 2 mg brain tissues from BSE-C-infected cattle (2). It is noteworthy that the Tg650 mice express human PrP-129M at five to eight times the normal level, and high PrP levels are known to increase prion transmissibility (9, 17, 22). Inefficient BSE-C transmissions (0 to 30%) in Tg mouse lines of other genetic backgrounds expressing human PrP-129M at one or two times the normal level have also been reported by different groups (1, 4). Although it is difficult to compare results from different mouse lines, these findings suggest that the BASE strain has higher transmissibility than BSE-C does for humanized Tg mice with PrP-129M and possibly for humans with PrP-129MM. The BASE strain also appears to be more virulent than BSE-C in bovinized Tg mice, since the incubation time for the BASE strain is 185 ± 12 days, whereas that for BSE-C is 230 ± 7 days (7). Nevertheless, compared with the 100% attack rate and incubation times of ∼9 months for sCJDMM1 and sCJDMM2 in the Tg40 line (Table 1), the 60% attack rate and unusually long incubation times (20 to 22 months) for the BASE strain in the same Tg line suggest that the transmission barrier from the BASE strain to humans with PrP-129MM is still quite significant.
PK-resistant PrPSc was also detected in the spleen in 4 out of 18 BASE strain-infected Tg40 mice. In contrast, no spleen involvement could be demonstrated for the Tg40 mice following i.c. inoculation with human PrPSc from sCJDMM1. This is the first report of the presence of PrPSc in the spleens of humanized Tg mice after i.c. inoculation with a BSE strain, suggesting that the BASE strain, like BSE-C, where at least in vCJD-infected subjects PrPSc and prion infectivity have been detected in spleens and tonsils (6, 11), is intrinsically lymphotropic. Therefore, lymphoid tissues of BASE strain-infected individuals might also carry prion infectivity.
The gel mobility of the PK-resistant PrPSc recovered from the BASE strain-inoculated Tg40 mice was consistently slightly faster than the mobility of BSE-C, as originally reported for the BASE strain (8). The computed difference in gel mobilities between BASE and BSE-C PrPSc is 0.29 ± 0.12 kDa, corresponding to 2 to 4 amino acid residues. In contrast, the gel mobilities of the PK-resistant PrPSc species from the BASE strain, BASE strain-infected Tg40 mice, and sCJDMM2, which was used as representative of human PrPSc of type 2, were indistinguishable. This finding suggests that the PK-resistant PrPSc electrophoretic heterogeneity between the BASE strain and BSE-C falls well within the 7-amino-acid variability of the N terminus (positions 92 to 99) that is consistently found in PK-resistant PrPSc of type 2 (16). Therefore, despite their minor but distinct variability in gel mobility, both the BASE strain and BSE-C PrPSc species appear to belong to the PrPSc of type 2. However, the PrPSc glycoform ratios of BASE strain-infected Tg40 mice and the BASE strain inocula display a small but statistically significant difference (Fig. 1). Therefore, PrPSc in BASE strain-infected human subjects may be expected to display a different glycoform ratio from that of the BASE strain. It is worth noting that the electrophoretic characteristics of the PK-resistant PrPSc of some human prion strains has been faithfully reproduced by our Tg40 line as well as by other humanized mouse lines (10, 13, 21).
Two distinct histopathological and PrP immunohistochemical phenotypes have been reported following BSE-C inoculation: one reproduced the distinctive features of vCJD with the “florid” plaques that intensely immunostained for PrP, and the other was reminiscent of sCJDMM1, with prominent spongiform degeneration and no plaque PrP immunostaining (1, 23). The brain histopathology, the PrPSc distribution, and the PrP immunostaining pattern of BASE strain-inoculated Tg40 mice were definitely distinct from such features described above (1, 23), further supporting the notion that BASE and classical BSE are associated with two distinct prion strains (8).
The relatively easy transmission of BASE to humanized Tg mice indicates that effective cattle prion surveillance should be maintained until the extent and origin of this and other atypical forms of BSE are fully understood.
Previous Section Next Section ACKNOWLEDGMENTS
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang 1 , Sandor Dudas 2 , Catherine Graham 2 , Markus Czub 3 , Tim McAllister 1 , Stefanie Czub 1 1 Agriculture and Agri-Food Canada Research Centre, Canada; 2 National and OIE BSE Reference Laboratory, Canada; 3 University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle. Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.
Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal-specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.
see page 176 of 201 pages...tss
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;
***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 ***
Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?
USDA announces Alabama case of Atypical L-type BASE Bovine Spongiform Encephalopathy and BANNED FEED
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
It is clear that the designing scientists must
also have shared Mr Bradley's surprise at the results because all the dose
levels right down to 1 gram triggered infection.
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams.
***It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
2) Infectious dose:
To cattle: 1 gram of infected brain material (by oral ingestion)
SUNDAY, JULY 30, 2017
*** PRION2017 Low levels of classical BSE infectivity in rendered fat tissue
***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
The Presence of Disease-Associated Prion Protein in Skeletal Muscle of Cattle Infected with Classical Bovine Spongiform Encephalopathy
Hiroyuki OKADA,1,* Kohtaro MIYAZAWA,1 Shigeo FUKUDA,2 Yoshifumi IWAMARU,1 Morikazu IMAMURA,1 Kentaro MASUJIN,1 Yuichi MATSUURA,1 Takashi FUJII,2 Kei FUJII,2 Soichi KAGEYAMA,2 Miyako YOSHIOKA,1 Yuichi MURAYAMA,1 and Takashi YOKOYAMA1
Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy
Silvia Suardi , Chiara Vimercati , Cristina Casalone , Daniela Gelmetti, Cristiano Corona, Barbara Iulini, Maria Mazza, Guerino Lombardi, Fabio Moda, Margherita Ruggerone, Ilaria Campagnani, Elena Piccoli, Marcella Catania, [ ... ], Fabrizio Tagliavini [ view all ] Published: February 21, 2012 https://doi.org/10.1371/journal.pone.0031449
The present data offer novel information on the tropism of the BASE agent and highlight relevant public health issues. While the transmission barrier for classical BSE is high in most species, BASE prions are readily transmissible to a variety of mammals including non-human primates [11]–[13], [35]. Accordingly, the possibility of spreading of BASE prions through skeletal muscle to other species should be taken into account and evaluated in risk analysis studies.
P169 Low levels of classical BSE infectivity in rendered fat tissue
Dr. Christine Fast1, Dr. Markus Keller2, Dr. Ute Ziegler3, Prof. Dr. Martin Groschup4 1Friedrich-Loeffler-Institut, Greifswald, Germany, 2Friedrich-Loeffler-Institut, Greifswald, Germany, 3Friedrich-Loeffler-Institut, Greifswald, Germany, 4Friedrich-Loeffler-Institut, Greifswald, Germany
Aims: Specified Risk Materials (SRM) are the animal tissues potentially containing the highest levels of Bovine Spongiform Encephalopathy (BSE) prions; and their removal is the most important consumer protection measure against BSE. BSE infectivity in the mesentery fat is most likely associated with embedded nervous tissue. To date, it is unclear if contamination of the rendered fat could have occurred during tallow production at a slaughterhouse.
Methods: Samples were taken from five cattle originating from the German BSE pathogenesis study. Two animals were at preclinical, one at late preclinical and one animal at clinical stage of disease; one control animal was included. For all cattle, mouse bioassay results for the celiac and mesenteric ganglion complex (CMGC) were generated previously, showing either no, mild, moderate or substantial infectivity loads. Fat was rendered from CMGC samples embedded in mesentery fat by incubating for 20 minutes at 95°C, according to standard tallow production methods. Subsequently, the melted fat was 1:5 diluted in physiological saline and thoroughly vortexed. The liquid fat was cleaned by a short centrifugation at 10.000 rpm. Finally, 7-12 bovine prion protein overexpressing transgenic mice (Tgbov XV) were i.c. inoculated with 25-30 μl of the supernatant. Mice were sacrificed after 730 days or when showing clinical symptoms and mouse brains were subsequently examined by biochemical and immunohistochemical methods.
Results: Neither the control and the preclinical nor the late preclinical animals showed signs of infectivity in mouse bioassay of the fat samples after up to 730 days p.i. In contrast, low levels of infectivity were detected in the fat of the clinical animal as one mouse displayed a clear accumulation of pathological prion protein in the brain after an incubation period of 598 days p.i.
Conclusions: Our results clearly indicate the potential contamination of melted mesenteric fat by embedded nervous structures during standard tallow production. However, the BSE infectivity level was weak and detectable only in the fat rendered from one sample with documented high infectivity load in the ganglion itself (Kaatz et al. 2012). Albeit, this study is not representative as only one clinical animal was included, it provides a proof of principle. A broader examination would allow a better insight into temporal and spatial distribution pattern of BSE infectivity in rendered fat tissues of different origins.Such estimates have a critical role in qualitative and quantitative risk assessments and in providing advice on the designation and removal of certain SRM tissues.
=====
http://prion2017.org/programme/
Dr. Christine Fast1, Dr. Markus Keller2, Dr. Ute Ziegler3, Prof. Dr. Martin Groschup4 1Friedrich-Loeffler-Institut, Greifswald, Germany, 2Friedrich-Loeffler-Institut, Greifswald, Germany, 3Friedrich-Loeffler-Institut, Greifswald, Germany, 4Friedrich-Loeffler-Institut, Greifswald, Germany
Aims: Specified Risk Materials (SRM) are the animal tissues potentially containing the highest levels of Bovine Spongiform Encephalopathy (BSE) prions; and their removal is the most important consumer protection measure against BSE. BSE infectivity in the mesentery fat is most likely associated with embedded nervous tissue. To date, it is unclear if contamination of the rendered fat could have occurred during tallow production at a slaughterhouse.
Methods: Samples were taken from five cattle originating from the German BSE pathogenesis study. Two animals were at preclinical, one at late preclinical and one animal at clinical stage of disease; one control animal was included. For all cattle, mouse bioassay results for the celiac and mesenteric ganglion complex (CMGC) were generated previously, showing either no, mild, moderate or substantial infectivity loads. Fat was rendered from CMGC samples embedded in mesentery fat by incubating for 20 minutes at 95°C, according to standard tallow production methods. Subsequently, the melted fat was 1:5 diluted in physiological saline and thoroughly vortexed. The liquid fat was cleaned by a short centrifugation at 10.000 rpm. Finally, 7-12 bovine prion protein overexpressing transgenic mice (Tgbov XV) were i.c. inoculated with 25-30 μl of the supernatant. Mice were sacrificed after 730 days or when showing clinical symptoms and mouse brains were subsequently examined by biochemical and immunohistochemical methods.
Results: Neither the control and the preclinical nor the late preclinical animals showed signs of infectivity in mouse bioassay of the fat samples after up to 730 days p.i. In contrast, low levels of infectivity were detected in the fat of the clinical animal as one mouse displayed a clear accumulation of pathological prion protein in the brain after an incubation period of 598 days p.i.
Conclusions: Our results clearly indicate the potential contamination of melted mesenteric fat by embedded nervous structures during standard tallow production. However, the BSE infectivity level was weak and detectable only in the fat rendered from one sample with documented high infectivity load in the ganglion itself (Kaatz et al. 2012). Albeit, this study is not representative as only one clinical animal was included, it provides a proof of principle. A broader examination would allow a better insight into temporal and spatial distribution pattern of BSE infectivity in rendered fat tissues of different origins.Such estimates have a critical role in qualitative and quantitative risk assessments and in providing advice on the designation and removal of certain SRM tissues.
=====
http://prion2017.org/programme/
SUNDAY, JULY 30, 2017
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840 Next Section ABSTRACT
Chronic wasting disease (CWD) is a neurodegenerative prion disease of cervids. Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, human susceptibility to CWD is unknown. In ruminants, prion infectivity is found in central nervous system and lymphoid tissues, with smaller amounts in intestine and muscle. In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
http://jvi.asm.org/content/83/18/9608.full
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ ↵* These authors contributed equally to this work. ↵† Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA. ↵‡ Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. + See all authors and affiliations Science 24 Feb 2006: Vol. 311, Issue 5764, pp. 1117 DOI: 10.1126/science.1122864 Article Figures & Data Info & Metrics eLetters PDF You are currently viewing the abstract.
View Full Text
Abstract
The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
http://science.sciencemag.org/content/311/5764/1117.long
*** PRION2017 CONFERENCE ***
*** Low levels of classical BSE infectivity in rendered fat tissue ***
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840 Next Section ABSTRACT
Chronic wasting disease (CWD) is a neurodegenerative prion disease of cervids. Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, human susceptibility to CWD is unknown. In ruminants, prion infectivity is found in central nervous system and lymphoid tissues, with smaller amounts in intestine and muscle. In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
http://jvi.asm.org/content/83/18/9608.full
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ ↵* These authors contributed equally to this work. ↵† Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA. ↵‡ Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. + See all authors and affiliations Science 24 Feb 2006: Vol. 311, Issue 5764, pp. 1117 DOI: 10.1126/science.1122864 Article Figures & Data Info & Metrics eLetters PDF You are currently viewing the abstract.
View Full Text
Abstract
The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
http://science.sciencemag.org/content/311/5764/1117.long
Scientists investigate origin of isolated BSE cases
The European response to bovine spongiform encephalopathy (BSE) after the crisis of the 1980s has significantly reduced prevalence of the disease in cattle. However, isolated cases are still being reported in the EU and for this reason the European Commission asked EFSA to investigate their origin.
The key measure for controlling BSE in the EU is a ban on the use of animal proteins in livestock feed. This is because BSE can be transmitted to cattle through contaminated feed, mainly in the first year of life.
Sixty cases of classical BSE have been reported in cattle born after the EU ban was enforced in 2001. None of these animals entered the food chain. Classical BSE is the type of BSE transmissible to humans. The Commission asked EFSA to determine if these cases were caused by contaminated feed or whether they occurred spontaneously, i.e. without an apparent cause.
EFSA experts concluded that contaminated feed is the most likely source of infection. This is because the infectious agent that causes BSE has the ability to remain active for many years. Cattle may have been exposed to contaminated feed because the BSE infectious agent was present where feed was stored or handled. A second possibility is that contaminated feed ingredients may have been imported from non-EU countries.
Experts could not rule out other causes due to the difficulty of investigating individual cases. Some constraints are the long incubation period of the disease and the lack of detailed information available from farms at the time of the trace-back investigation.
EFSA experts made a series of recommendations to maintain and strengthen the EU monitoring and reporting system, and to evaluate new scientific data that become available.
The European response to BSE
The coordinated European response to BSE has succeeded in reducing the prevalence of the disease. Between 2005 and 2015 about 73,000,000 cattle were tested for BSE in the EU, out of which 60 born after the ban tested positive for classical BSE. The number of affected animals rises to 1,259 if cattle born before the ban are included. The number of classical BSE cases has dropped significantly in the EU over time, from 554 cases reported in 2005 to just two in 2015 (both animals born after the ban). Moreover the EU food safety system is designed to prevent the entry of BSE-contaminated meat into the food chain.
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
___________________________________
PRODUCT
Custom dairy premix products:
MNM ALL PURPOSE Pellet,
HILLSIDE/CDL Prot- Buffer Meal,
LEE, M.-CLOSE UP PX Pellet,
HIGH DESERT/ GHC LACT Meal,
TATARKA,
M CUST PROT Meal,
SUNRIDGE/CDL PROTEIN Blend,
LOURENZO, K PVM DAIRY Meal,
DOUBLE B DAIRY/GHC LAC Mineral,
WEST PIONT/GHC CLOSEUP Mineral,
WEST POINT/GHC LACT Meal,
JENKS,
J/COMPASS PROTEIN Meal,
COPPINI - 8# SPECIAL DAIRY Mix,
GULICK, L-LACT Meal (Bulk),
TRIPLE J - PROTEIN/LACTATION,
ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN,
BETTENCOURT #1/GHC MILK MINR,
V&C DAIRY/GHC LACT Meal,
VEENSTRA, F/GHC LACT Meal,
SMUTNY, A- BYPASS ML W/SMARTA,
Recall # V-025-2007
CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete.
REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs.
DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
ALABAMA MAD COW FEED IN COMMERCE 2006
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
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
______________________________
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE
None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
?????
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
=====
PRODUCT
Bulk Whole Barley, Recall # V-256-2009
CODE
No code or lot number.
RECALLING FIRM/MANUFACTURER
Mars Petcare US, Clinton, OK, by telephone on May 21, 2009. Firm initiated recall is complete.
REASON
Product may have contained prohibited materials without cautionary statement on the label.
VOLUME OF PRODUCT IN COMMERCE
208,820 pounds
DISTRIBUTION
TX
END OF ENFORCEMENT REPORT FOR AUGUST 26, 2009
###
Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ?????
Date: August 6, 2006 at 6:19 pm PST
PRODUCT Bulk custom made dairy feed, Recall # V-114-6
CODE None
RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006.
Firm initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE ?????
DISTRIBUTION KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
CODE a) Bulk b) None c) Bulk d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006.
Firm initiated recall is ongoing.
REASON Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006
Date: June 27, 2006 at 7:42 am PST Public Health Service Food and Drug Administration
New Orleans District 297 Plus Park Blvd. Nashville, TN 37217
Telephone: 615-781-5380 Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO. 2006-NOL-06
FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.
You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.
You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez Acting District Director New Orleans District
PLEASE NOTE, THE FDA URLS FOR OLD WARNING LETTERS ARE OBSOLETE AND DO NOT WORK IN MOST CASES. I LOOKED UP THE OLD ONE ABOVE AND FOUND IT, BUT HAVE NOT DONE THAT FOR THE OTHERS TO FOLLOW. THE DATA IS VALID THOUGH!
Subject: MAD COW PROTEIN IN COMMERCE USA 2006 RECALL UPDATE
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Reply-To: SAFETY <[log in to unmask]>
Date: Mon, 9 Oct 2006 14:10:37 -0500
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS
IN COMMERCE AL, TN, AND WV
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
______________________________
snip...
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________
snip...
______________________________
PRODUCT Bulk custom dairy pre-mixes, Recall # V-120-6
CODE None
RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.
REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS
Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006 RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
CODE a) Bulk b) None c) Bulk d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006.
Firm initiated recall is ongoing.
REASON Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
___________________________________
PRODUCT
Custom dairy premix products:
MNM ALL PURPOSE Pellet,
HILLSIDE/CDL Prot- Buffer Meal,
LEE, M.-CLOSE UP PX Pellet,
HIGH DESERT/ GHC LACT Meal,
TATARKA,
M CUST PROT Meal,
SUNRIDGE/CDL PROTEIN Blend,
LOURENZO, K PVM DAIRY Meal,
DOUBLE B DAIRY/GHC LAC Mineral,
WEST PIONT/GHC CLOSEUP Mineral,
WEST POINT/GHC LACT Meal,
JENKS,
J/COMPASS PROTEIN Meal,
COPPINI - 8# SPECIAL DAIRY Mix,
GULICK, L-LACT Meal (Bulk),
TRIPLE J - PROTEIN/LACTATION,
ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN,
BETTENCOURT #1/GHC MILK MINR,
V&C DAIRY/GHC LACT Meal,
VEENSTRA, F/GHC LACT Meal,
SMUTNY, A- BYPASS ML W/SMARTA,
Recall # V-025-2007
CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete.
REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs.
DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
ALABAMA MAD COW FEED IN COMMERCE 2006
Office of Inspector General Semiannual Report to Congress FY 2007 - 2nd Half
Two Texas Companies Sentenced and Fined for Misbranding Meat Products In April 2007, two closely held and related Texas companies pled guilty in Federal court and were sentenced to 12 months of probation and ordered to pay $10,250 in fines for misbranding meat products. One of the companies sold adulterated meat products to a retail store in New Mexico. Additionally, portions of the invoices failed to properly and consistently identify the meat products as being from cattle more than 30 months old at time of slaughter. This information is required to be disclosed because of bovine spongiform encephalopathy (BSE, or "mad cow disease") concerns. No adulterated meat reached consumers.
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
16 years post mad cow feed ban August 1997 2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
Thursday, November 16, 2017
Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination
MONDAY, NOVEMBER 06, 2017
Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque
''On secondary and tertiary transmissions, however, the proportion of PrPres positive animals gradually increased to almost 100%.
''Recent communications suggest that a similar situation might exist in other models of experimental exposure to prions involving swine32 and cattle33.''
''Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque''
i am thinking of that 10,000,000 POUNDS OF BLOOD LACED MEAT AND BONE MEAL IN COMMERCE WARNING LETTER back in 2007, see;
SATURDAY, NOVEMBER 4, 2017
FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006
FRIDAY, NOVEMBER 3, 2017
BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW
''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''
IN CONFIDENCE
CWD TRANSMITS TO PIGS ORALLY
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
MONDAY, AUGUST 14, 2017
Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
MONDAY, SEPTEMBER 25, 2017
Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosisF
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
CWD TO CATTLE
***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.
SNIP...
price of prion poker goes up for cwd to cattle;
Monday, April 04, 2016
*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***
*USA USDA CWD BSE SCRAPIE TSE PRION?
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. ...
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...
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. ...
The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province! ...page 26.
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
2017
TUESDAY, JULY 18, 2017
USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
SUNDAY, JULY 23, 2017
atypical L-type BASE Bovine Amyloidotic Spongiform Encephalopathy BSE TSE PRION
SUNDAY, JULY 23, 2017
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***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.***
Wednesday, December 21, 2016
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH
Tuesday, September 06, 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
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
TUESDAY, JULY 18, 2017
MINK FARMING USA TRANSMISSIBLE MINK ENCEPHALOPATHY TSE PRION DISEASE SURVEILLANCE AND TESTING
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
Saturday, April 23, 2016
Scrapie ZOONOSIS PRION CONFERENCE TOKYO 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
Thursday, June 9, 2016
Advisory Committee; Transmissible Spongiform Encephalopathies Advisory Committee; Termination
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
TUESDAY, AUGUST 8, 2017
Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2016-0092]
WEDNESDAY, JULY 26, 2017
APHIS USDA Emerging Animal Disease Preparedness and Response Plan July 2017
THURSDAY, JUNE 22, 2017
World Organisation for Animal Health (OIE) to establish liaison office in College Station, Texas
MONDAY, JANUARY 4, 2016
Long live the OIE, or time to close the doors on a failed entity?
WEDNESDAY, MARCH 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
MONDAY, MAY 05, 2014
Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing
OIE STILL FLOUNDERING WITH TSE PRION DISEASE, letting it spread around the globe with the bse mrr policy, and still ignoring cwd, and making atypical scrapie a legal trading commodity.
THURSDAY, MAY 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease
TUESDAY, JULY 17, 2012
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012
2001 FDA CJD TSE Prion Singeltary Submission
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
BSE YOUNGEST DOCUMENTED TO DATE 20 MONTHS
1992 20 26 15.02 16.02
1.6. YOUNGEST AND OLDEST CASES BY YEAR OF ONSET (FOR PASSIVE SURVEILLANCE CASES) AND ON YEAR OF SLAUGHTER (FOR ACTIVE SURVEILLANCE CASES) AS AT 03/09/2007 NB The last case in an animal aged 30 months or less was in 1996
YR OF ONSET AGE YOUNGEST CASE (mths) AGE 2nd YOUNGEST CASE (mths) AGE 2nd OLDEST (yrs.mths) OLDEST CASE (yrs.mths)
1986 30 33 5.03 5.07
1987 30 31 9.09 10
1988 24 27 10.02 11.01(2)
1989 21 24(4) 12(2) 15.04
1990 24(2) 26 13.03 14
1991 24 26(3) 14.02 17.05
1992 20 26 15.02 16.02
1993 29 30(3) 14.1 18.1
1994 30(2) 31(2) 14.05 16.07
995 24 32 14.09 15.05
1996 29 30 15.07 17.02
1997 37(7) 38(3) 14.09 15.01
1998 34 36 14.07 15.05
1999 39(2) 41 13.07 13.1
2000 40 42 17.08 19.09
2001 45 48 16.01 20.08
2002 47 48(2) 18.04 22.07
2003 46 49 18.07(2) 20.06
2004 49 52 17.04 22.07
2005 36 38 18.01 19.04
2006 48 58 17.05 19.09
2007 81(2) 88 15(02) 17.03
PAGE 5
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
MONDAY, JULY 17, 2017
National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017
TUESDAY, SEPTEMBER 19, 2017
*** USDA APHIS Notice: Animal Disease Traceability (ADT) Summary of Feedback on the ADT Program
TEXAS HISTORY OF COVERING UP MAD COW DISEASE BSE TYPICAL AND ATYPICAL
Statement of Gov. Rick Perry on BSE Announcement
Thursday, June 30, 2005 • Press Release
AUSTIN – Gov. Rick Perry issued the following statement today on the announcement by the U.S. Department of Agriculture that a cow recently tested for Bovine Spongiform Encephalopathy – commonly known as mad cow disease – is from a Texas herd.
“I want to urge calm and reassure the public that they can have the highest confidence in our beef supply, and the safeguards we have in place to protect the public from the spread of BSE. There is not, nor has there ever been, a known instance of BSE contaminating the food supply in Texas or anywhere else in the United States.
The animal in question was not processed into food or any other product. Texans can be sure that the beef they buy at their local supermarkets or restaurants is as safe today as it was yesterday, and I encourage Texans to continue to enjoy Texas beef products.”
Section 2. Testing Protocols and Quality Assurance Controls
In November 2004, USDA announced that its rapid screening test, Bio-Rad Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test result as part of its enhanced BSE surveillance program. The ELISA rapid screening test performed at a BSE contract laboratory produced three high positive reactive results.40 As required,41 the contract laboratory forwarded the inconclusive sample to the APHIS National Veterinary Services Laboratories (NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again produced three high positive reactive results.42 In accordance with its established protocol, NVSL ran its confirmatory test, an immunohistochemistry (IHC) test, which was interpreted as negative for BSE. In addition, NVSL performed a histological43 examination of the tissue and did not detect lesions44 consistent with BSE.
Faced with conflicting results, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded no further testing was necessary because testing protocols were followed. In our discussions with APHIS officials, they justified their decision not to do additional testing because the IHC is internationally recognized as the "gold standard." Also, they believed that conducting additional tests would undermine confidence in USDA’s established testing protocols.
CANADIAN STYLE MAD COW SURVEILLANCE IN TEXAS I.E. SSS POLICY SHOOT, SHOVEL, AND SHUT THE HELL UP
EDMONTON - Some of former Alberta premier Ralph Klein's most colourful quotes — and the reactions they elicited:
SNIP...
"This all came about through the discovery of a single, isolated case of mad cow disease in one Alberta cow on May 20th. The farmer — I think he was a Louisiana fish farmer who knew nothing about cattle ranching. I guess any self-respecting rancher would have shot, shovelled and shut up, but he didn't do that." — Klein recalls how the mad cow crisis started and rancher Marwyn Peaster's role. The premier was speaking at the Western Governors Association meeting in Big Sky, Mont. September 2004...
USDA orders silence on mad cow in Texas
Susan Combs by no means has public and consumer health at heart while she is protecting the cattle industry. She is oblivious to mad cow disease. Her soul purpose is to protect the cattle industry at all cost, including my mothers life (DOD 12/14/97), or maybe one of your family members from any strain of mad cow disease in TEXAS. SHE helped cover-up mad cow disease in TEXAS both on that inconclusive that was positive so many times it will make your head spin. PLUS, the other mad cow in TEXAS they rendered without testing at all, that came from the top out of Austin. THEY should be tried for murder. corporate homicide is what i call it. they knew for years, but kept on keeping on.
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE)
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
Texas BSE Investigation Final Epidemiology Report August 2005
Executive Summary
In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.
Background of the Investigation
On June 10, 2005, USDA announced that the November 2004 inconclusive BSE sample tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s National Animal Disease Center (NADC) upon the recommendation of USDA’s Office of the Inspector General. Samples were sent to a World Organization for Animal Health (OIE) reference laboratory for BSE in Weybridge, England, for confirmatory tests. Farm A, located in Texas, was the suspected farm of origin for the index cow and was placed under hold order on June 20, 2005 pending confirmation of the positive results and DNA analysis of the herd. Weybridge confirmed the BSE positive on June 24, 2005. The carcass of the index cow had been disposed of by incineration in November 2004.
News Release
Texas Animal Health Commission
Box l2966 * Austin, Texas 78711 * (800) 550-8242 * FAX (512) 719-0719
Bob Hillman, DVM * Executive Director
For info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710, or mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:mailto:ceverett@tahc.state.tx.us
For immediate release---
State-Federal Team Responds to Texas BSE Case
The US Department of Agriculture announced June 29 that genetic testing has verified that an aged cow that tested positive for Bovine Spongiform Encephalopathy or BSE originated from a Texas beef cattle herd. Tissues for laboratory testing were initially collected from the animal in November 2004, and the carcass was incinerated and did not enter the human food, animal feed or fertilizer supply system. While tests in November indicated the animal did not have BSE, retesting in England in June confirmed the animal had the disease. The Texas Animal Health Commission (TAHC), the state’s livestock and poultry health regulatory agency, and USDA have jointly assigned a state-federal team to conduct the epidemiological investigation and response.
“The TAHC and US Department of Agriculture’s Veterinary Services are working with a complement of experts from federal and state animal health, food safety, public health and feed regulatory agencies to ensure the continued safety and wholesomeness of our meat supply,” said Dr. Bob Hillman, Texas state veterinarian and executive director of the TAHC, the state’s livestock and poultry health regulatory agency. “Epidemiological investigations are thorough and focus on verifying the herd of origin, and when, where and how the animal and potentially, any herd mates, were exposed to the abnormal prion, or disease agent, that causes BSE. Additionally, epidemiology investigations trace the infected animal’s movement and herd mates. Animals potentially exposed to the disease will be depopulated, with proper disposal. The animals will not be introduced into the human or animal food chain.”
The USDA’s BSE testing protocol requires testing of emaciated or injured cattle, cattle that exhibit central nervous system disorder, cattle unable to rise or to walk normally, and cattle that die of unknown causes. Since June 1, 2004, brain tissue samples from more than 394,000 cattle have been tested in the U.S. and were negative for BSE. Of those, 38,320 were tested in Texas, Dr. Hillman noted. BSE surveillance has been conducted in the U.S. since l990.
The U.S. has taken preventive measures against the introduction of BSE since l989, when prohibitions were placed on cattle and other ruminants from BSE-affected countries, noted Dr. Hillman. In 1997, the importation ban was extended to all of Europe.
Dr. Hillman said the U.S. Food and Drug Administration (FDA) in 1997 banned the use of ruminant-derived protein (from animals such as cattle and sheep) in feed for cattle and other ruminants. There is no evidence that BSE spreads from live animal to animal in the herd, but cattle can be exposed by eating feed that contains rendered protein from infected animals. “These measures taken by the USDA and the FDA are safeguards that work to protect livestock, and ultimately, our meat supply,” he said.
--30--
Second BSE case occurred in Texas, USDA says Jun 30, 2005 (CIDRAP News) – The United States' second case of bovine spongiform encephalopathy (BSE) was in a 12-year-old cow that came from a Texas herd and would have been made into pet food if it hadn't been flagged for BSE testing, federal officials announced yesterday evening.
US Department of Agriculture (USDA) officials said the cow was to be processed at a pet food plant in Waco, Tex., when it was diverted for testing because it couldn't walk. Officials didn't name the plant or say exactly where the cow came from. But an Associated Press (AP) report today identified the plant as Champion Pet Food in Waco and said the cow was already dead when brought there last November.
"The source herd is now under a hold order as we identify animals of interest within the herd," USDA Chief Veterinarian John Clifford said in a prepared statement. Investigators will look for cattle born within a year before or after the BSE-infected cow and any of the cow's offspring born within the past 2 years, he explained.
"If the age of the animal cannot be pinpointed, then we may expand our inquiry to include all animals in this herd before the feed ban went into place in 1997," Clifford said. To prevent BSE, the government banned putting cattle protein into cattle feed in August 1997.
The infected cow was incinerated, and no parts were used in human food or animal feed, according to the USDA. "The safety of our food supply is not in question," Clifford stated.
Because of the cow's age, the USDA suspects it became infected by eating contaminated feed before the government ban began in 1997. The USDA and the Food and Drug Administration (FDA) will try to trace the source herd's feed history, officials said.
The FDA will also check whether firms that may have processed meat-and-bone meal from animals from that herd have complied with the 1997 feed ban, Dr. Steve Sundlof, director of the FDA's Center for Veterinary Medicine, said at a news conference last night.
The Texas case is the first US BSE case in a native-born animal; Clifford said the cow lived on one farm all its life. The previous US case, found in December 2003, involved a Canadian-born dairy cow in Washington state.
An initial screening test on the Texas cow last November was inconclusive, and two confirmatory immunohistochemistry tests were negative. But early this month the USDA's inspector general ordered a Western blot test, which came back positive. Further confirmatory tests at an international reference lab in Britain were also positive, prompting the USDA to announce the findings last week.
The USDA waited for the results of DNA tests before announcing that the infected cow came from Texas. The step was necessary because parts of the infected cow were stored with those of four other cattle, causing some uncertainty, officials said.
"We felt that we had the correct herd; we wanted to identify that appropriately with DNA," Clifford said at the news conference. Investigators analyzed DNA from the infected animal and then looked for relatives in the presumed source herd by analyzing DNA from members of the herd, he said. The investigation turned up two cattle that are related to the infected cow, he added.
The AP report said Champion Pet Food is under contract to take samples from animals in poor health. The company's owner, Benjy Bauer, told the AP that his workers took samples from the cow and sent them to the Texas Veterinary Diagnostic Laboratory at Texas A&M University. The lab is one of several the USDA uses to screen cattle for BSE, the story said.
See also:
USDA news release http://www.aphis.usda.gov/lpa/issues/bse/BSE_statement6-29-05.pdf
USDA fact sheet on BSE epidemiologic investiation
USDA press conference transcript
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.
"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."
USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.
Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
OR, what the Honorable Phyllis Fong of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
FDA STATEMENT FOR IMMEDIATE RELEASE May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
#
TSS REPORT ON 2ND TEJAS MAD COW
Mon, 22 Nov 2004 17:12:15 -0600
(the one that did NOT get away, thanks to the Honorable Phyllis Fong)
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???terry
==============================
==============================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 -0600
From: Carla Everett To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no informationabout the animal being in Texas. CarlaAt 09:44 AM 11/19/2004, you wrote:
>Greetings Carla,
>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from
>TEXAS. can you comment on this either way please?
>>thank you,
>Terry S. Singeltary Sr
.>>
===================
===================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600
From: Carla Everett To: "Terry S. Singeltary Sr."
References: <[log in to unmask]> <[log in to unmask] us> <[log in to unmask]> <[log in to unmask] us> <[log in to unmask]>
our computer department was working on a place holder we could postUSDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.
At 06:05 PM 11/22/2004, you wrote:
>why was the announcement on your TAHC site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
> no confirmation on the U.S.'inconclusive test...
> no confirmation on location of animal. ;
THEN, 7+ MONTHS OF COVER-UP BY JOHANN ET AL! no doubt about it now $$$
NO, it's not pretty, hell, im not pretty, but these are the facts, take em or leave em, however, you cannot change them.
with kindest regards,
I am still sincerely disgusted and tired in sunny Bacliff, Texas USA 77518
Terry S. Singeltary Sr.
FULL 130 LASHINGS TO USDA BY OIG again http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Link: TSS
Feb 06, 2004 Washington State Investigation—Final Epidemiology Report
Secretary's Advisory Committee Recommendations
Feb 13, 2004 Secretary’s Advisory Committee Report
Feb 02, 2004 International Review Team (IRT) Report
Subject: Re: USDA/APHIS JUNE 2004 'ENHANCED' BSE/TSE COVER UP UPDATE DECEMBER 19, 2004 USA
Date: Thu, 30 Dec 2004 12:27:06 -0600
From: "Terry S. Singeltary Sr.
BSE-L
snip...
> > OH, i did ask Bio-Rad about this with NO reply to date;
> > > -------- Original Message --------
> Subject: USA BIO-RADs INCONCLUSIVEs
> Date: Fri, 17 Dec 2004 15:37:28 -0600
> From: "Terry S. Singeltary Sr."
> To: susan_berg@bio-rad.com
> > > > Hello Susan and Bio-Rad,
> > Happy Holidays!
> > I wish to ask a question about Bio-Rad and USDA BSE/TSE testing
> and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated,
> or is there most likely some human error we are seeing here?
> > HOW can Japan have 2 positive cows with
> No clinical signs WB+, IHC-, HP- ,
> BUT in the USA, these cows are considered 'negative'?
> > IS there more politics working here than science in the USA?
> > What am I missing?
> > > > -------- Original Message --------
> Subject: Re: USDA: More mad cow testing will demonstrate beef's safety
> Date: Fri, 17 Dec 2004 09:26:19 -0600
> From: "Terry S. Singeltary Sr."
> snip...end
> > > Experts doubt USDA's mad cow results
snip...END
WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;
Bio-Rad, TSS phone conversation 12/28/04
Finally spoke with ;
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX
at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.
my question;
Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???
ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.
again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there. "very difficult to answer"
"very political"
"very loaded question"
outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing. said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives? said something about ''just look at the sheep that tested IHC- but were positive''. ...
TSS
-------- Original Message --------
Subject: Your questions
Date: Mon, 27 Dec 2004 15:58:11 -0800
From: To: flounder@wt.net
Hi Terry:
............................................
snip Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you
Regards
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email:
=================================
snip...end...TSS
SEE FULL TEXT OF ALL THIS HERE ;
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
ALABAMA MAD COW CASE
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see COPIOUS AMOUNTS OF mad cow feed in COMMERCE IN ALABAMA...TSS)
Texas BSE Investigation Final Epidemiology Report August 2005
State-Federal Team Responds to Texas BSE Case
JUNE 30, 2005
(please note 7+ month delay in final confirmation so the BSE MRR policy could be set in stone first. $$$...tss)
SEE ATTEMPTED COVER-UP BEFORE THE END AROUND BY FONG ET AL OF THE O.I.G
The U.S. Department of Agriculture confirmed June 29 that genetic testing had verified bovine spongiform encephalopathy (mad cow disease) in a 12-year-old cow that was born and raised in a Texas beef cattle herd.
Subsequent epidemiological investigations resulted in the culling and testing of 67 adult animals from the index herd. Bio-Rad tests for BSE were conducted on all 67 animals by the National Veterinary Services Laboratory (NVSL) in Ames, Iowa. All tests were negative.
On July 12, Texas officials lifted the quarantine on the source herd. At press time, USDA's Animal and Plant Health Inspection Service was tracing animals of the same age that had left the ranch.
Timeline
The BSE-positive animal was a Brahman-cross cow born and raised in a single Texas herd. The location of the ranch was not disclosed.
On Nov. 11, 2004, the 12-year-old cow was taken to a Texas auction market. Because of its condition, the cow was sent to Champion Pet Foods in Waco, Texas. The company produces several blends of dog food, primarily for the greyhound industry.
On Nov. 15, the animal arrived dead at Champion. Under procedures established by USDA's intensive surveillance program, a sample was sent to the USDA-approved Texas Veterinary Medical Diagnostic Testing Laboratory (TVMDL) at Texas A&M University.
Between June 1, 2004, and June 1, 2005, TVMDL tested nearly 34,000 samples from Texas, New Mexico, Arkansas and Louisiana. They tested the sample from Champion on Nov. 19 using a Bio-Rad ELISA rapid test for BSE. Initial results were inconclusive.
Because of the inconclusive results, a representative from USDA took the entire carcass to TVMDL where it was incinerated. USDA's Animal and Plant Health Inspection Service (APHIS) began tracing the animal and herd.
The sample was then sent to the National Veterinary Services Laboratory for further testing. Two Immunohistochemistry (IHC) tests were conducted and both were negative for BSE. At that point APHIS stopped their trace.
USDA scientists also ran an additional, experimental IHC "rapid" tissue fixation test for academic purposes. This test has not been approved internationally.
Some abnormalities were noted in the experimental test, but because the two approved tests came back negative, the results were not reported beyond the laboratory.
Monitoring by OIG
USDA's Office of Inspector General (OIG) has been monitoring implementation of the BSE expanded surveillance program and evaluating the following:
* Effectiveness of the surveillance program;
* Performance of BSE laboratories in complying with policies and procedures for conducting tests and reporting results;
* Enforcement of the ban on specified risk materials in meat products;
* Controls to prevent central nervous system tissue in advanced meat recovery products;
* Ante mortem condemnation procedures; and
* Procedures for obtaining brain tissue samples from condemned cattle.
While reviewing voluminous records, OIG auditors noticed conflicting test results on one sample-rapid inconclusive, IHC negative, experimental reactive.
Sample retested
At the recommendation of the Inspector General, the sample was retested during the week of June 5 with a second confirmatory test, the Western Blot. The results were reactive.
USDA scientists then conducted an additional IHC confirmatory test, using different antibodies from the November 2004 test. On Friday, June 10, Secretary of Agriculture Mike Johanns publicly announced the results as a "weak positive."
On June 16 an official with USDA's National Veterinary Services Laboratory hand-carried samples for further testing to the Veterinary Laboratory Agency (VLA) in Weybridge, England. Since 1991, the VLA has been a BSE reference laboratory for the World Organization for Animal Health (OIE).
Experts from the Weybridge lab confirmed the accuracy of the results of USDA's November confirmatory IHC test, concurring that the case could not have been confirmed on the basis of this sample. They also examined the November experimental IHC test and interpreted the results to be positive.
Weybridge also conducted additional tests, including IHC, OIE-prescribed Western Blot, NaTTA Western Blot and Prionics Western Blot tests.
To better understand the conflicting results, USDA also conducted Bio-Rad and IDEXX rapid screening tests, IHC and OIE-prescribed Western Blot. USDA also used DNA sequencing to determine the prion protein gene sequence of the animal.
http://findarticles.com/p/articles/mi_qa5420/is_200508/ai_n21377094
Texas even had a 'secret' test that showed that mad cow positive; experimental IHC test results, because the test was not a validated procedure, and because the two approved IHC tests came back negative, the results were not considered to be of regulatory significance and therefore were not reported beyond the laboratory. . A Western blot test conducted the week of June 5, 2005, returned positive for BSE.
48 hr BSE confirmation turnaround took 7+ months to confirm this case, so the BSE MRR policy could be put into place. ...TSS
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to:
Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results
posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004. ...TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 -0600
From: "Terry S. Singeltary Sr."
To: Carla EverettReferences: [log in to unmask]; [log in to unmask] ;
Greetings Carla, still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...
can you confirm??? terry
============================================================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."References;[log in to unmask];
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas.
Carla
At 09:44 AM 11/19/2004, you wrote:
Greetings Carla,
i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from
TEXAS. can you comment on this either way please?
thank you,
Terry S. Singeltary Sr
======================================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."References: <[log in to unmask]><[log in to unmask] us><[log in to unmask]> <[log in to unmask]us> <[log in to unmask]>
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.
At 06:05 PM 11/22/2004,
you wrote:
why was the announcement on your TAHC site removed?
Bovine Spongiform Encephalopathy:
November 22: Press Release title here
star image More BSE information
terry
Carla Everett wrote:
no confirmation on the U.S.'inconclusive test...
no confirmation on location of animal. ;
FROM HERE, IT TOOK 7 MONTHS TO CONFIRM THIS MAD COW, while the BSE MRR policy was being bought and sold...(in my opinion...tss)
Saturday, August 16, 2008
Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)
TEXAS OFFICIALS DEAD WRONG ON AMOUNT OF INFECTIVITY TO CAUSE A TSE PRION DISEASE ;
"FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds."
5.5 GRAMS OF INFECTIOUS PROHIBITED MAD COW FEED FOR EACH OF THE 1,222 ANIMALS (5.5 GRAMS X 1,222 ANIMALS) IS ENOUGH INFECTIOUS MAD COW FEED TO KILL A SMALL HERD OF COWS...TSS
U.S. Food and Drug Administration FDA News | Today the Food and Drug Administ…U.S. Food and Drug Administration FDA News
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle — a violation of FDA’s 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.
According to Dr. Bernard Schwetz, FDA’s Acting Principal Deputy Commissioner, “The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture’s (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE.”
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
PRION 2009 CONGRESS BOOK OF ABSTRACTS
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfillment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........
It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
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...
FOR OVER 4 YEARS, USDA et al decided they should supply the National School Lunch Program with the most high risk cattle for mad cow disease i.e. dead stock downer cows. i'm not making this stuff up folks. they hid what at the time was the largest beef recall ever, they hid the cause of the recall, and listed it as 'animal abuse'. yes, yes, you read that right. they largest beef recall at the time in history, and the reason was animal abuse, NOT THE FACT THE DEAD STOCK DOWN COWS ARE THE MOST HIGH RISK FOR TSE PRION...TSS
Saturday, September 21, 2013
Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???
this recall was not for the welfare of the animals. ...tss
you can check and see here ;
(link now dead, does not work...tss)
http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf
try this link ;
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Subject: Prion 2017 Conference Abstracts CWD
https://ec.europa.eu/food/sites/food/files/safety/docs/sci-com_ssc_out324_en.pdf
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.
Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.
Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.
To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:
Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.
Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
*** Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT ***
OLD DOCUMENT, BUT SOME INTERESTING STUFF...TSS
MONDAY, SEPTEMBER 25, 2017
Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis
(see origin of cwd in Colorado debate and evidence there from...tss)
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)
Last updated: 08 September 2004
Adopted July 2004 (Question N� EFSA-Q-2003-083)
Report
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90�s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases. Publication date: 20 August 2004
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
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Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE-Risk (GBR) of United States of America (USA).
Question N° EFSA-Q-2003-083
Adopted July 2004
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
Key words: BSE, geographical risk assessment, GBR, USA, third countries
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
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Background
History
In 1998, the EC asked the Scientific Steering Committee (SSC) to perform a risk assessment in order to establish the GBR of a country. In July 2000 the SSC adopted its final opinion on "The Geographical Risk of Bovine Spongiform Encephalopathy (GBR)" (as updated in January 2002). It describes a method and a process for the assessment of the GBR and summarises the outcome of its application. Detailed reports on the GBR-assessments were published on the Internet for each of these countries.
Determination of BSE status
In 2001, Regulation (EC) No 999/20011 established the rules for the determination of BSE status of a country. It determines certain measures concerning the control of BSE and concerning trade and importation of certain live animals and animal products.
Annex II of this Regulation lays down the method for the determination of BSE status. This includes two steps: an initial risk assessment, and the evaluation of additional criteria. The method is similar to that laid down in the International Animal Health Code of the International Animal Health Organisation (OIE).
The categorisation of countries has been deferred until July 2005 awaiting a review of the OIE categorisation system. In the meantime a number of transitional measures are in place, in particular concerning specified risk material and import conditions.
State of play
The Scientific Steering Committee issued an opinion on GBR (using the methodology established by the SSC in June 2000 and updated January 2002) for one third of the countries requesting the determination of their BSE status.
Prioritisation
The first priority is the re-assessment of GBR I countries, as currently no TSE related import restrictions (certification of absence of specific risk material (SRM)) apply to GBR I countries.
If the preliminary re-assessment indicates that the current GBR I will not be confirmed, any delay might have negative consequences on consumer health protection. Furthermore, the GBR assessment of neighbouring countries with intensive trade contacts should be dealt with at the same time, because the outcomes are interdependent.
The major trading partners with a GBR II classification should be dealt with as second priority, in view of the SSC opinion on tallow derivatives and the draft guidance note of EMEA.
Terms of reference
In view of the above, the European Commission asks the EFSA to advice on the risk assessment for the appearance of BSE in USA.
1
Regulation (EC) No 999/2001 of the European Parliament and of the Council laying down rules for the prevention, control and eradication of certain transmissible spongiform encephalopathies OJ L 147, 31.5.2001 and updates.
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
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Assessment
EFSA refers to the Working Group Report (annex) prepared by the EFSA Scientific Expert Working Group on GBR for full details on the assessment.
External Challenge
USA was exposed to a moderate external challenge for the period 1980-1990, a very high external challenge for the period 1991-1995, and an extremely high external challenge for period 1996-2003.
Stability
For the overall assessment of the stability, the impact of the three main stability factors, (i.e. feeding, rendering and SRM-removal) and of the additional stability factor surveillance has to be estimated. Again, the guidance provided by the SSC in its opinion on the GBR of July 2000 (as updated in 2002) is applied. On the basis of the available information, it has to be concluded that the country's BSE/cattle system was extremely unstable until today, i.e., it would have recycled and amplified BSE-infectivity very fast, should it have entered the system.
Feeding
Until August 1997, ruminant meat and bone meal (RMBM) was legally fed to cattle. Feeding was therefore "not OK". In August 1997, an RMBM-ban was introduced but feeding of nonruminant MBM to cattle remained legal as well as feeding of RMBM to non-ruminant animals (farm animals and pets). An RMBM ban is difficult to maintain, as only labels can distinguish the various MMBMs. This makes control of the feed ban very difficult because analytical differentiation between ruminant and non-ruminant MBM is difficult. Due to the highly specialized production system in the USA, various mammalian MBM streams can be separated. Such a feed ban would therefore be assessed as "reasonably OK", for all regions where this highly specialized system exists. However, several areas in the USA do have mixed farming and mixed feed mills, and in such regions an RMBM ban would not suffice. Additionally, official controls for cattle feeds to control for compliance with the ban started in 2002. Thus, for the whole country, the assessment of the feeding after 1997 remains "not OK", but improving.
Rendering
The rendering industry is operating with processes that are not known to reduce infectivity. It is therefore concluded that rendering was and is "not OK".
SRM-removal
SRM were and are still rendered for feed, as are (parts of) the fallen stock. SRM-removal is therefore regarded as "not OK".
BSE surveillance
Before 1989, the ability of the system to identify (and eliminate) BSE-cases was limited.
Since 1990 this ability is improved, thanks to a specific (passive) BSE surveillance. The initiated introduction of active surveillance in risk populations should improve the system significantly.
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA). http://www.efsa.eu.int
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Conclusions
The European Food Safety Authority concludes:
1. The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. This cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that meat and bone meal (MBM) imported into the USA reached domestic cattle and lead to an internal challenge in the early nineties.
2. A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
3. The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
4. This assessment deviates from the previous assessment (SSC opinion, 2000) because at that time several exporting countries were not considered a potential risk.
5. It is also worth noting that the current GBR conclusions are not dependent on the large exchange of imports between USA and Canada. External challenge due to exports to the USA from European countries varied from moderate to high. These challenges indicate that it was likely that BSE infectivity was introduced into the North American continent.
6. EFSA and its Scientific Expert Working group on GBR are concerned that the available information was not confirmed by inspection missions as performed by the Food and Veterinary office (FVO – DG SANCO) in Member States and other third countries. They recommend including, as far as feasible, BSE-related aspects in future inspection missions.
Expected development of the GBR
As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
A table summarising the reasons for the current assessment is given in the table below Documentation provided to EFSA
• Letter with the ref D (2003) KVD/ip/420722 from the European Commission requesting a geographical risk assessment for the appearance of BSE in a country.
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
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• Country Dossier as prepared by the country in response to the EC and EFSA data collection request.
• Other sources of data information i.e. exports from third countries and Eurostat data.
• SSC, July 2000. Final opinion on the Geographical Risk of Bovine Spongiform Encephalopathy (GBR).
• SSC, January 2002. Updated opinion on the Geographical Risk of Bovine Spongiform Encephalopathy (GBR).
Acknowledgment
Members of the EFSA Scientific Working Group are acknowledged for their valuable contribution to this mandate. The members are: Didier Calavas, Aline De Koeijer, Michael Gravenor, John Griffin, Dagmar Heim, Matthias Kramer, Riitta Maijala, Mo Salman, Vittorio Silano, Emmanuel Vanopdenbosch, and Stig Widell.
Annex
Details of the assessment are presented in the report as prepared by the EFSA Scientific
Expert Working Group on GBR:
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
http://www.efsa.eu.int 6 of 6
USA, Summary of the GBR Assessment, July 2004 GBR Level : III**
EXTERNAL CHALLENGE STABILITY INTERACTION of EXTERNAL CHALLENGE and STABILITY
1980-1990: Moderate
1991-1995: Very High
1996-2003: Extremely high
1980-2003: Extremely unstable
Live Cattle imports MBM imports Feeding Rendering SRM-removal BSE surveillance
Any external challenge would have met the extremely unstable system and infectivity would have been recycled.
INTERNAL CHALLENGE
An internal challenge was possibly present from 1980 to 1990 and was likely to be present and growing from 1991 to 2003
EXPECTED DEVELOPMENT OF THE GBR
From UK: 323 (CD*) or 327 (other sources of data) From other BSE risk countries: 16.656.490 (CD) or 15.496.449 (other sources of data). *CD: country dossier
From UK: 5 tons (CD) or 101 tons (other sources of data) From other BSE risk countries: 406.547 tons (CD) or 229.701 tons (other sources of data)
1980-2003: Not OK. Feeding of ruminant MBM to cattle legally possible until August 1997.
1980-2003: Not OK. No proof of an effective process in reducing BSEinfectivity is given.
1980-2003: Not OK. SRM are still rendered for feed.
Passive but improving with some testing of risk groups.
As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
** GBR level III: ‘it is likely but not confirmed’ that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 1 - European Food Safety
Authority Scientific Expert Working Group on GBR Working Group Report on the Assessment of the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
NOTE TO THE READER Independent experts of the EFSA Scientific Expert Working Group on GBR have produced this report, applying an innovative methodology by a complex process to data that were supplied by the responsible country authorities. Both, the methodology and the process are described in detail in the final opinion of the Scientific Steering Committee (SSC) on "the Geographical Risk of Bovine Spongiform Encephalopathy (GBR)" of 6 July 2000 and its update of 11 January 2002. These opinions are available at the following Internet address: Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 2 - 1. DATA • The available information was sufficient to carry out the qualitative assessment of the GBR.
• Reasonable worst case assumptions have been used in cases where the available information was not fully adequate. Sources of data • Country dossier (CD) consisting of information provided from the country’s authorities in 1997-2004, including the study entitled “Harvard Risk Assessment” (hereafter abbreviated as HRS). Other sources:
• EUROSTAT data on export of "live bovine animals" and on "flour, meal and pellets of meat or offal, unfit for human consumption; greaves" (customs code 230110), covering the period 1980 to 2003.
• UK-export data (UK) on "live bovine animals", and on "Mammalian Flours, Meals and Pellets" MBM1 , 1980-1996.
• Available export data from other BSE-risk countries.
2. EXTERNAL CHALLENGES
2.1 Import of cattle from BSE-Risk2 countries An overview of the data on live cattle imports is presented in table 1 and is based on data as provided in the country dossier (CD) and corresponding data on relevant exports as available from BSE risk countries that exported to the USA. Only data from risk periods are indicated, i.e. those periods when exports from a BSE risk country already represented an external challenge, according to the SSC opinion on the GBR (SSC July 2000 and updated January 2002).
• According to the country dossier, 323 cattle were imported directly from the UK, all between 1980 and 1989, and 10 via Canada in 90, 91 and 92. According to Eurostat, 327 cattle were imported from UK. Of these cattle 96% were beef breeding cattle, 4% were dairy cattle. After 1989 an import stop for UK cattle was in effect. 1 For the purpose of the GBR assessment the abbreviation “MBM” refers to rendering products, in particular the commodities Meat and Bone Meal as such; Meat Meal; Bone Meal; and Greaves. With regard to imports it refers to the customs code 230110 “flours, meals and pellets, made from meat or offal, not fit for human consumption; greaves”. 2 BSE-Risk countries are all countries already assessed as GBR III or IV or with at least one confirmed domestic BSE case.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
- 3 -
• Cattle imported from the UK were traced-back in 1995. This trace back exercise provided the details on which the assessment of the HRS of the import risk assessment is based. The animals still alive in 1995 (117 cattle) have been purchased, diagnostic samples were taken, and the carcasses were incinerated. These animals were not taken into account for the external challenge. All these animals tested negative for BSE (histopathology and IHC). Of these 117 cattle 52 came from UK-herds in which one or more cases of BSE later on developed. • For 173 cattle imported from the UK in the 80s, information on their final use is, according to the HRS, lacking and it is indicated that it is possible that some of these animals could have been rendered. In the HRS it is also noted that these animals were imported before the peak of the epidemic and none came from a birth cohort in which a BSE case is known to be developed. However, based on realistic worst case assumptions it has to be assumed that they created a risk if rendered for feed.
• EU export data show that from the EU (excluding UK), 1,663 cattle were exported to the USA since 1980; according to the CD only 460 cattle have been imported from the EU.
• According to the CD, 162 cattle were imported from Ireland between 1980 and 1988 (according to Eurostat 233). The trace back of these animals showed that 22 were found as being excluded from rendering in the US system and 4 were born in US quarantine and were therefore not taken into account for the external challenge.
• According to the CD, 6 cattle from Belgium (Eurostat also 6), 46 from Germany (Eurostat 430), 3 from Austria (Eurostat 0) and 8 from Italy (Eurostat 21) have been imported. The 40 breeding-cattle imported from these countries in 1996 and 1997 were all traced back and none of them entered the US system.
• According to Eurostat, 12 cattle from Denmark and 558 cattle from the Netherlands were imported to the USA. These imports were not indicated in the CD.
• Additionally according to the CD, 235 cattle have been imported from France (403 according to Eurostat) and 103 cattle from Switzerland (48 according to other sources).
• The discrepancy in the EU export data and the import data in the CD (See table 1) can in some cases, be explained by the use of the fiscal year data (from October to September) in the CD.
• Between 235.000 and 1.7 Million (CD and Other sources) cattle per year are imported to the USA from Canada. According to the CD, feeder/slaughter cattle represent typically more around 80% of the imported cattle from Canada; therefore, only 20% of the imported cattle have been taken into account.
• From Japan, 242 animals from a special beef breed were imported. These animals were traced, and were mostly excluded from the US rendering system. At most 39 of these animals have been rendered.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
SNIP...
Table 1: Live cattle imports into the USA (CD) and corresponding exports from BSE risk countries. Source for export data: Eurostat and UK export statistics and, where available, export statistics from other BSE risk countries. Note: Only imports in risk periods (shaded) are taken into account for assessing the external challenge. Risk periods are defined according to the SSC opinion of January 2002. The numbers shown in the table are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 5 - 2.2 Import of MBM or MBM-containing feedstuffs from BSE-Risk countries An overview of the data on MBM imports is presented in table 2 and is based on data provided in the country dossier (CD) and corresponding data on relevant exports as available from BSE risk countries that exported to the USA. Only data from risk periods are indicated, i.e. those periods when exports from a BSE risk country already represented an external challenge, according to the SSC opinion on the GBR (SSC, July 2000 and updated January 2002).
• The CD reports import of 5 tons of MBM from the UK. According to Eurostat, 63 tons have been exported from the UK to the USA between 1980 and 1996; however, according the updated MBM statistics from the UK (August 2001) 24 tons of MBM were exported from the UK to the USA between 1980 and 1996; 39 tons exported in 1989 were not confirmed by the updated UK export statistic and therefore not taken into account. A further 38 tons were exported in 1997-1998 and 39 tons in 1999. As it was illegal to export mammalian meat meal, bone meal and MBM from UK since 27/03/1996, exports indicated after that date should only have included non-mammalian MBM. Therefore, these imports were not taken into account.
• According to the CD, MBM was imported from Denmark, France, Italy and the Netherlands. It was claimed but not substantiated that these imports were not from ruminant origin, and therefore did not contribute to the BSE risk of the USA.
• The Eurostat export statistics indicated additional exports from Belgium, Greece, Ireland and Spain.
• Very large amounts of MBM (CD and other sources) between 18.000 and 44.000 tons annually were imported from Canada.
SNIP...
Table 2: MBM imports into the USA (CD) and corresponding exports from BSE risk countries. Source for export data: Eurostat and UK export statistics and, where available, export statistics from other BSE risk countries. Note:
Only imports in risk periods (shaded) are taken into account for assessing the external risk. Risk periods are defined according to the SSC opinion of January 2002.The numbers shown in the table are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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2.3 Overall assessment of the external challenge
The level of the external challenge that has to be met by the BSE/cattle system is estimated according to the guidance given by the SSC in its final opinion on the GBR of July 2000 (as updated in January 2002).
Live cattle imports:
In total the country imported 2038 (other sources) or 1128 (CD) live cattle from BSE risk countries other than Canada, of which 327 (other sources) or 323 (CD) came from the UK. From Canada the imports were >500,000 animals per year. The numbers shown in table 1 are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge. Broken down to 5 year periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow to assume that certain imported cattle did not enter the domestic BSE-cattle system, i.e. were not rendered into feed. In the case of the USA, all the animals for which tracing information showed that they were not rendered were excluded from the external challenge.
MBM imports:
In total the country imported 689 tons MBM (CD) or 2,230 tons MBM (other sources) from BSE risk countries other than Canada, of which 5 tons (CD) or 101 tons (other sources) were exported from the UK (UK export data). From Canada, the imports were about 30 000 tons per year. The numbers shown in table 2 are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge. Broken down to 5 year periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow to assume that certain imported MBM did not enter the domestic BSE/cattle system or did not represent an external challenge for other reasons. As it was illegal to export mammalian MBM from UK since 27/03/1996, exports indicated after that date should only have included non-mammalian MBM. In the case of the USA imported MBM from UK in 1989 and between 1997 and 1999 was not taken into account.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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External Challenge experienced by the USA
External challenge Reason for this external challenge
Period Overall Level Cattle imports MBM imports Comment
1980 to 1985 Moderate Negligible
1986 to 1990
Moderate
Negligible Low
1991 to 1995 Very high High High
1996 to 2000 Very high
2001 to 2003
Extremely high Very high
Extremely high When Canadian import data are excluded from the assessment, the overall level varies from low to high.
Table 3: External challenge resulting from live cattle and/or MBM imports from the UK and other BSE risk countries. The challenge level is determined according to the SSC-opinion on the GBR of July 2000 (as updated in January 2002).
On the basis of the available information, the overall assessment of the external challenge is as given in table 3.
3. STABILITY
3.1 Overall appreciation of the ability to avoid recycling of BSE infectivity, should it enter processing
Feeding
Use of MBM in cattle feed
• Until 1997 ruminant MBM (RMBM) could legally be included in cattle feed and was indeed commonly fed to cattle of different age and type. Prior to the feed ban the US authorities estimated that 10% of all MBM would deliberately have been fed to cattle.
Feed bans
• A ban to feed (several types of) MMBM to ruminants was put in place in August 1997. Derogation from the ban was granted for pure porcine and equine protein (MBM) coming from designated (single species) rendering plants. This MMBM might still be fed to cattle. Therefore this feed ban is a ruminant to ruminant ban.
• It is planned to prohibit the use of all mammalian and poultry protein in ruminant feed and prohibiting materials from non-ambulatory disabled cattle and dead stock from use in all animal feed.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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Potential for cross-contamination and measures taken against
• The animal production chain in the USA is large-scale industry, which allows for a high level of specialisation and many farm and factories for slaughter, rendering and feed production are dedicated to one species only. This reduces the risk of cross-contamination to a large extend, but this does not apply to regions with a lot of mixed farming.
• Cross-contamination of non-ruminant MBM with RMBM is theoretically possible whenever transport of this material from rendering to feed plants is done in bulk and with the same means of transport. It is unknown if this can be excluded.
• Cross-contamination in feed mills is possible as many feed mills produce compound feeds for different species on the same production line. No data on the structure of the feed industry in the USA were provided by the US authorities that would allow estimating the amount of cattle feed annually produced in mixed feed mills throughout the period 1980-2001. Information on inspection of feed mills shows that this problem is still found, by 2003, in a very small fraction of the industry.
• Since 1997, FDA regulations provide for either the use of separate lines in the production of ruminant feed or specify detailed clean-out procedures to be used between production batches. However, experience in Europe shows that flushing batches etc are not capable to eliminate cross-contamination, even though they reduce it. The efficiency of the required measures cannot be assessed as detailed control data are lacking and samples are not taken for this purpose.
• Feed containing RMBM has labels not to be fed to ruminants, but “on-farm” cross-contamination is regarded to be possible.
• Hence, as reasonable worst case scenario, it is assumed that cattle, in particular dairy cattle, can still be exposed to RMBM and hence to BSE-infectivity, should it enter the feed chain.
• Rendering plants and feed mills are, according to the CD, regularly inspected for compliance with the regulations, throughout the country.
• It is planned to require dedicated equipment or facilities for handling and storing feed and ingredients during manufacturing and transportation, to prevent cross contamination.
Control of Feed bans and cross-contamination
• Since 1997, feed mills that are allowed to use RMBM, and also produce cattle feed (without RMBM), are inspected annually, other may also be inspected. Two types of violations were registered. One type not involving RMBM, the others involving this, this mainly concerns cross-contamination problems. These firms were re-inspected soon. In several cases, products were recalled, sales were closed and/or products were destroyed. Cattle feed is not sampled to test for presence of illegal MBM.
• According to information provided in 1999/2000 by the feed producers, the compliance is assumed by the US authorities to be in the order of magnitude of 70% to ≤90% since 1998, and 30% to ≤70% before. Official control data concerning rendering and feed mill industries were provided and show that action at shortcomings in the production processes (a few percent of the firms) have Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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become severe by the beginning of 2003. However, samples from ruminant feed are not regularly tested for the inclusion of MMBM. Reports from the feed industry in 2000 and 2001 indicate significant shortcomings in the implementation of the ban in that period. This does confirm the known difficulty of implementing and enforcing such a feed ban.
• No examinations are performed to assess cross-contamination with RMBM of the protein (e.g. through non ruminant MBM) that enters cattle feed. Rendering
• The domestic MBM production averages 3 million metric tons per year.
• Almost 60% of the MBM produced originate from ruminants (cattle 59%, sheep 0.6%), 20% from pigs and 20% from poultry.
Raw material used for rendering
• Ruminant material is rendered together with material from other species (approx. 50% of all plants). This is particular significant as SRM will be included. "Free renderers" are known to also process fallen stock.
• Slaughter by-products from different species, including SRM, is the raw material for most rendering plants that are associated with slaughterhouses.
• Some plants process material from one species, e.g. pigs or horses or poultry only.
• The CD does not provide the numbers of plants falling under each category nor of their respective annual production.
Rendering processes
• Four major rendering systems are used in the approximately 280 rendering plants in the USA. All systems operate under atmospheric pressure with temperatures ranging between 100 and 150 °C and different heating times:
- Batch cooker plants (46): 115-125 C°, 30-240 min.
- Continuous tube and disc cooker systems (220): 131-150 °C, 45-90 min.
- Continuous multi-stage evaporator systems (10): 115-125 °C, 20-40 min.
- Continuous preheat/press/evaporator systems (4): 87-120 °C, 240-270 min.
Due to the fact that they operate under atmospheric pressure only, none of the described rendering processes are assumed to reduce BSE-infectivity significantly, should it enter the processing.
SRM and fallen stock
• An SRM-ban for human food has been introduced in 2004. There was however never an SRM ban for the feed chain.
• SRM are rendered together with other slaughter by-products and, in case of independent renderers, together with fallen stock.
• It is planned to remove SRM from all animal feed, including pet-food. Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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Conclusion on the ability to avoid recycling
• Before 1997, US system would not have been able to avoid recycling of the BSEagent to any measurable extent. If the BSE-agent was introduced into the feed chain, it could have reached cattle.
• After the introduction of the 1997 ban in August 1997, the ability to avoid recycling of BSE-infectivity was somewhat improved. However, the rendering of ruminant material (including SRM and fallen stock) is inadequate (non pressurized), and cross-contamination potentials of cattle feed with other feeds remain.
• Therefore, the system is still unable to avoid recycling of BSE-infectivity if already present in the system or incoming.
3.2 Overall appreciation of the ability to identify BSE-cases and to eliminate animals at risk of being infected before they are processed
Cattle population structure
• The total cattle population of the USA was approximately 111 Million cattle in 1980, 99 Million in 1990, 102.8 Million cattle in 1995 and 99.5 Million cattle in 1998. Of these, approximately 17.6 % (17.5 Million) were dairy cattle and 82.4% beef cattle (based on data 1995-1998). However, the HRS recognised that the official slaughter figures were only compatible with a stable total cattle population of about 140 million.
• Between 17% and 19% of all cattle slaughtered were >2 years of age. The average age at slaughter for dairy cattle is between 4 and 5 years.
Husbandry systems
• According to the country experts it was assumed that mixed farming did exist in the USA, but at a low (and decreasing) level. No figures were provided.
• The two main cattle husbandry systems are beef (82.4%) and dairy (17.6%). Within both systems all levels of intensity are existing, however, both segments are now characterised by large, intensive operations. For dairy cattle a clear trend towards larger, more efficient holdings can be seen.
Maps were presented by the country experts in 1999 that indicate an overlap of intensive cattle, swine and poultry industry in certain geographic regions of the USA.
Cattle identification and monitoring system
• The existing animal identification system is jointly operated by State and Federal representatives and is maintained individually for each State. No centralised USwide animal identification system is in place.
• It was estimated by the country experts that this system ensures that approx. 95% of all cattle are officially tagged and registered in State databases.
• A trace-back of individual animals is possible whenever the animal has not moved several times (through several herds) within a particular State. Intra-State Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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movements are not recorded in any type of database, and any follow-up would rely on the documentation (records) or the memory of the respective owners.
BSE surveillance
• All foreign animal diseases (exotic diseases) have been and are notifiable by Federal legislation. BSE, as an exotic disease, was notifiable since it first was described as a disease (1986).
• A surveillance targeting animals with clinical signs that could be consistent with BSE is in place since 1989/1990 and operating with larger sample sizes (900-1600 per year) since 1997. This program officially started in 1990 but some samples examined under this system go back to 1986. The samples come from:
- Cattle exhibiting signs of neurological disease;
- Cattle condemned at ante-mortem examination in slaughterhouses for neurological signs;
- Rabies-negative cattle submitted to public-health laboratories (the country experts confirmed that samples were appropriately taken and should have allowed finding BSE if present);
- Neurological cases submitted to veterinary diagnostic laboratories and veterinary schools/teaching hospitals;
- Between 25% and 33% of the animals in the sample were supposed to be aged dairy cattle which are non-ambulatory (“downer cows”) at slaughter. Detailed information on the age distribution of those animals was not available.
• In addition to histopathology, immunhistochemistry is applied since 1994, initially on those animals for which a differential diagnosis could not be established. Since 1997 it is fully incorporated in the surveillance scheme and approx. 900-1.600 samples are examined annually by both tests. In 2000, a total of 2 870 submissions were examined.
• In 2001, the number of submissions doubled, and in 2002 and 2003, submissions totalled 19.777 and 20.277 respectively. The total number of samples examined through April 2004 is more than 72.500.
• A BSE case has been detected in December 2003. Intensive research showed that it was born and raised in Canada, and therefore, it is not a domestic case.
• In addition, since 1 June 2004, an extensive testing of the risk population is initiated. It is planned to test as many cattle from the risk population (the target is 268.000 cattle) in a 12–to–18–month period. The following categories will be tested: non-ambulatory cattle, cattle exhibiting signs of a central nervous system disorder, cattle exhibiting other signs that may be associated with BSE and dead cattle. The surveillance program will also include a limited number of random samples from apparently normal, aged animals.
3.3 Overall assessment of the stability
For the overall assessment of the stability, the impact of the three main stability factors, (i.e. feeding, rendering and SRM-removal) and of the additional stability factor surveillance has to be estimated. Again, the guidance provided by the SSC in its opinion on the GBR of July 2000 (as updated in 2002) is applied.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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Feeding
Until August 1997, RMBM was legally fed to cattle. Feeding was therefore "not OK". In August 1997 an RMBM-ban was introduced but feeding of non-ruminant MBM to cattle remained legal as well as feeding of RMBM to non-ruminant animals (farm animals and pets). An RMBM ban is difficult to maintain, as only labels can distinguish the various MMBMs. This makes control of the feed ban very difficult because analytical differentiation between ruminant and non-ruminant MBM is difficult if not impossible.
Due to the highly specialised production system in the USA, various mammalian MBM streams can be separated. Such a feed ban would therefore be assessed as "reasonably OK", for all regions where this highly specialised system exists. However, several areas in the USA do have mixed farming and mixed feed mills, and in such regions an RMBM ban would not suffice. Additionally, official controls for cattle feeds to control for compliance with the ban started in 2002. Thus, for the whole country, the assessment of the feeding after 1997 remains "not OK", but improving.
Rendering
The rendering industry is operating with processes that are not known to reduce infectivity. It is therefore concluded that rendering was and is "not OK".
SRM-removal
SRM were and are still rendered for feed, as are (parts of) the fallen stock. SRMremoval is therefore regarded as "not OK".
BSE-surveillance
Before 1989, the ability of the system to identify (and eliminate) BSE-cases was limited. Since 1990 this ability is improved, thanks to a specific (passive) BSE surveillance. The initiated introduction of active surveillance in risk populations should improve the system significantly.
Stability of the BSE/cattle system in the USA over time
Stability Reasons
Period Level Feeding Rendering SRM removal BSE surveillance 1980 to 2003
Extremely unstable
Not OK
Not OK
Not OK
Passive but improving with some testing of risk groups
Table 4: Stability resulting from the interaction of the three main stability factors and the BSE surveillance. The stability level is determined according to the SSC-opinion on the GBR of July 2000 (as updated in 2002).
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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On the basis of the available information, it has to be concluded that the country's BSE/cattle system was extremely unstable until today, i.e., it would have recycled and amplified BSE-infectivity very fast, should it have entered the system. The stability of the BSE/cattle system in the USA overtime is as given in table 4.
The present assessment modifies the stability assessment of the previous GBR report in 2000 mainly due to a different perception of the impact of BSE surveillance on stability and of the efficiency of the RMBM feed ban.
4. CONCLUSION ON THE RESULTING RISKS
4.1 Interaction of stability and challenges
In conclusion, the stability of the USA BSE/cattle system in the past and the external challenge the system has coped with, are summarised in table 5 below. From the interaction of the two parameters “stability” and “external challenge” a conclusion is drawn on the level of “internal challenge” that emerged and had to be met by the system, in addition to external challenges that occurred.
Interaction of stability and external challenge in the USA
Period Stability External Challenge Internal challenge
1980 to 1985 1986 to 1990 Moderate Possibly present 1991 to 1995 Very high 1996 to 2000 2001 to 2003
Extremely unstable
Extremely high
Likely to be present and growing
Table 5: Internal challenge resulting from the interaction of the external challenge and stability. The internal challenge level is determined according to guidance given in the SSC-opinion on the GBR of July 2000 (as updated in 2002).
An external challenge resulting from cattle import could only lead to an internal challenge once imported infected cattle were rendered for feed and this contaminated feed reached domestic cattle. Cattle imported for slaughter would normally be slaughtered at an age too young to harbour plenty of BSE infectivity or to show signs, even if infected prior to import. Breeding cattle, however, would normally live much longer and only animals having problems would be slaughtered younger. If being 4-6 years old when slaughtered, they could suffer from early signs of BSE, being approaching the end of the BSE-incubation period. In that case, they would harbour, while being pre-clinical, as much infectivity as a clinical BSE case. Hence cattle imports could have led to an internal challenge about 3 years after the import of Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
- 15 -
breeding cattle (that are normally imported at 20-24 months of age) that could have been infected prior to import.
In the case of the USA a few potentially infected cattle were imported from the UK and more from other BSE-risk countries. Furthermore, large numbers of imported animals came from Canada. This implies that cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early 90s.
On the other hand imports of contaminated MBM would lead to an internal challenge in the year of import, if fed to cattle. The feeding system is of utmost importance in this context. If it could be excluded that imported, potentially contaminated feed stuffs reached cattle, such imports might not lead to an internal challenge at all.
In case of the USA this implies that it was possible that imported MBM reached domestic cattle and lead to an internal challenge in the early 90s.
If Canadian imports would be excluded from this assessment, we find that the USA receives a moderate challenge for all 5-year intervals since 1980, a high challenge between 1985 and 2000 and a low challenge thereafter. If combining these moderate to high challenges due to imports with the extremely unstable system, the conclusion would still be that the occurrence of an internal challenge is possible during the early 80s and likely in the late 80s.
4.2 Risk that BSE infectivity entered processing
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
4.3 Risk that BSE infectivity was recycled and propagated
A risk that BSE-infectivity was recycled and propagated exists since a processing risk first appeared, i.e. in the early 90s. Until today this risk persists and increases fast because of the extremely/very unstable BSE/cattle system in the USA.
5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK
5.1 The current GBR as function of the past stability and challenge
• The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
Note1: It is also worth noting that the current GBR conclusions are not dependent on the large exchange of imports between USA and Canada. External challenge due to exports to the USA from European countries varied from moderate to high. These Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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challenges indicate that it was likely that BSE infectivity was introduced into the North American continent.
Note2: This assessment deviates from the previous assessment (SSC opinion, 2000) because at that time several exporting countries were not considered a potential risk.
5.2 The expected development of the GBR as a function of the past and present stability and challenge
• As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (preclinically or clinically) infected with the BSE-agent persistently increases.
• Since recent improvements in the safety of MBM production in many countries or significant recent reductions in the incidence of BSE are not taken into account for the assessment of the external challenge, the external challenge assessed after 2001 could be overestimated and is the worst case assumption. However all current GBR conclusions are not dependent on these assumptions in any of the countries assessed. For future assessments and when the impact of the production, surveillance and true incidence changes have been fully quantified, these developments should be taken into account.
5.3 Recommendations for influencing the future GBR
• Measures that improve the stability of the system, will, over time, reduce the probability that cattle could get infected with the BSE-agent. Possible actions include
- removal of SRM and/or fallen stock from rendering of animal by-products into feed,
- high pressure standards in rendering processes,
- significant improvement of ban on use of ruminant MBM in cattle feed, supported by regular sampling of feed for the occurrence of such MBM.
• Improved passive and active surveillance, i.e. sampling of animals not showing signs compatible with BSE from “at-risk” cattle populations, such as adult cattle in fallen stock and emergency slaughter, by means of rapid screening, would allow monitoring the efficiency of stability enhancing measures.
Documentation provided to EFSA
• Letter with the ref D (2003) KVD/ip/420722 from the European Commission requesting a geographical risk assessment for the appearance of BSE in a country.
• Country Dossier as prepared by the country in response to the EC and EFSA data collection request.
• Other sources of data information i.e. exports from third countries and Eurostat data.
• SSC, July 2000. Final opinion on the Geographical Risk of Bovine Spongiform Encephalopathy (GBR).
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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• SSC, January 2002. Updated opinion on the Geographical Risk of Bovine Spongiform Encephalopathy (GBR).
Acknowledgment
Members of the EFSA Scientific Expert Working Group on GBR are acknowledged for their valuable contribution to this mandate. The members are: Didier Calavas, Aline De Koeijer, Michael Gravenor, John Griffin, Dagmar Heim, Matthias Kramer, Riitta Maijala, Mo Salman, Vittorio Silano, Emmanuel Vanopdenbosch, and Stig Widell.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 1 - European Food Safety Authority Scientific Expert Working Group on GBR Working Group Report on the Assessment of the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
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Brazil evaluate the implementation of health rules on animal by-products and derived products SRM BSE TSE PRION aka MAD COW DISEASE
Wednesday, December 19, 2012
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Brazil
Friday, December 07, 2012
ATYPICAL BSE BRAZIL 2010 FINALLY CONFIRMED OIE 2012
MONDAY, MAY 29, 2017
Canada CCA optimistic over potential for revisions to OIE criteria for BSE negligible risk
LOL!
Friday, February 20, 2015
A BSE CANADIAN COW MAD COW UPDATE Transcript - Briefing (February 18, 2015)
SATURDAY, FEBRUARY 14, 2015
Canadian Food Inspection Agency Confirms Bovine Spongiform Encephalopathy (BSE) in Alberta
FRIDAY, JANUARY 10, 2014
USDA AUDIT ON CANADA'S MEAT INSPECTION DISTURBING (pot calling kettle black again)
Tuesday, May 21, 2013
Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$
Thursday, January 17, 2013
Canada, U.S. agree on animal-disease measures to protect trade, while reducing human and animal health protection.
Sunday, December 2, 2012
CANADA 19 cases of mad cow disease SCENARIO 4: ‘WE HAD OUR CHANCE AND WE BLEW IT’
Tuesday, October 2, 2012
Canadian veterinarian fined after approving banned BSE high risk cattle for export to U.S.A.
Saturday, January 21, 2012
Quick facts about mad cow disease
Friday, March 4, 2011.
Alberta dairy cow found with mad cow disease.
Thursday, February 10, 2011.
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31.
Wednesday, December 22, 2010.
Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease?
Thursday, August 19, 2010.
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA.
Wednesday, August 11, 2010.
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA.
Increased Atypical Scrapie Detections.
Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.
SUNDAY, JULY 27, 2008
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
CANADA MBM LIVE CATTLE BSE TSE PRION TO USA
Date: Sat, 14 Jun 2003 02:23:12 +0200
OIG REPORT ON IMPORTS FROM CANADA
FRIDAY, MAY 26, 2017
OIE World Assembly of OIE Delegates distributed SCOTLAND, NORTHERN IRELAND, AND POLAND BSE NEGLIGIBLE RISK STATUS
WEDNESDAY, JANUARY 18, 2017
Ireland Department of Agriculture confirmed a case of Atypical BSE 18 year old cow
SUNDAY, JANUARY 15, 2017
US lifts French beef MAD COW BSE import embargo, France says… LOL!
MONDAY, MAY 2, 2016
France Confirms Case of Classical Mad Cow Disease BSE
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
TUESDAY, NOVEMBER 7, 2017
OIE Opens Texas Office Bovine Spongiform Encephalopathy BSE, Scrapie, CWD, TSE Prion
OIE BSE TSE PRION
please understand this is not all the reported BSE cases in the world. the OIE only reports what is reported to them. ...terry
Tracking spongiform encephalopathies in North America
Xavier Bosch
Published: August 2003
Summary;
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”
49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.
To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.
Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.
Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.
"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."
Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.
Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.
CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited".
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
2 January 2000 British Medical Journal U.S.
Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S.
2001 FDA CJD TSE Prion Singeltary Submission
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
SUNDAY, AUGUST 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
TUESDAY, AUGUST 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
THURSDAY, JULY 13, 2017
TEXAS CREUTZFELDT JAKOB DISEASE CJD TSE PRION
SUNDAY, NOVEMBER 23, 2014
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European
National Prion Center could lose all funding just as concern about CWD jumping to humans rises
SATURDAY, JULY 15, 2017
*** National Prion Center could lose all funding just as concern about CWD jumping to humans rises
MONDAY, OCTOBER 02, 2017
Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species
THURSDAY, AUGUST 17, 2017
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
Singeltary et al
FRIDAY, AUGUST 11, 2017
Infectivity in bone marrow from sporadic CJD patients
Bioassays in transgenic mice expressing the human prion protein revealed the presence of unexpectedly high levels of infectivity in the bone marrow from seven out of eight sCJD cases. These findings may explain the presence of blood-borne infectivity in sCJD patients. They also suggest that the distribution of prion infectivity in peripheral tissues in sCJD patients could be wider than currently believed, with potential implications for the iatrogenic transmission risk of this disease.
WEDNESDAY, NOVEMBER 22, 2017
NIH scientists and collaborators find infectious prion protein in skin of CJD patients
http://creutzfeldt-jakob-disease.blogspot.com/2017/11/nih-scientists-and-collaborators-find.html
NIH scientists and collaborators find infectious prion protein in skin of CJD patients
http://creutzfeldt-jakob-disease.blogspot.com/2017/11/nih-scientists-and-collaborators-find.html
WEDNESDAY, NOVEMBER 22, 2017
Prion seeding activity and infectivity in skin samples from patients with sporadic Creutzfeldt-Jakob disease
http://creutzfeldt-jakob-disease.blogspot.com/2017/11/prion-seeding-activity-and-infectivity.html
THURSDAY, AUGUST 10, 2017
Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
MONDAY, NOVEMBER 06, 2017
Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque
''On secondary and tertiary transmissions, however, the proportion of PrPres positive animals gradually increased to almost 100%.
''Recent communications suggest that a similar situation might exist in other models of experimental exposure to prions involving swine32 and cattle33.''
''Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque''
SATURDAY, DECEMBER 02, 2017
Public health risks from subclinical variant CJD
TUESDAY, DECEMBER 12, 2017
Creutzfeldt-Jakob disease: recent developments
Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
snip...see full Singeltary Nature comment here;
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO 4
November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk.
However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed. 1
92/11.4/1.1
BSE101/1 0137 4.
The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion.
The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis
Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00
WEDNESDAY, NOVEMBER 1, 2017
Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies
SATURDAY, DECEMBER 12, 2015
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
*** CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Wednesday, December 14, 2016
Diagnosis of Human Prion Disease Using Real-Time Quaking-Induced Conversion Testing of Olfactory Mucosa and Cerebrospinal Fluid Samples
Diagnosis of Human Prion Disease Using Real-Time Quaking-Induced Conversion Testing of Olfactory Mucosa and Cerebrospinal Fluid Samples
THE BSE INQUIRY
sporadic cjd in farmers and farmers wives with BSE HERDS
TSE Prion and Vaccines
BSE and Baby Foods
Draft Factual Account DFA
*** THE BSE DFA INQUIRY FILES ***
SEAC 91/2
MEDICAL IMPLANTS CONTAINING BOVINE MATERIAL ISSUE
TUESDAY, AUGUST 22, 2017
BSE INQUIRY DFA 16 MID 1995 TO THE FINAL DAYS
TUESDAY, AUGUST 1, 2017
BSE INQUIRY DFA 17 Medicines and medical devices
TUESDAY, AUGUST 1, 2017
Could Insulin be contaminated with and potentially spread, Transmissible Spongiform Encephalopathy TSE Prion, what if?
THURSDAY, AUGUST 3, 2017
BSE INQUIRY DFA 18 COSMETICS FDA OVERSIGHT WARNING The Honorable Frank Pallone, Jr.
SATURDAY, AUGUST 26, 2017
BSE Inquiry
DFA 15 Monitoring and Enforcement of the SBO Specified Bovine Offal Regulations
SATURDAY, AUGUST 26, 2017
BSE Inquiry
DFA 14 Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989-1990
THE BSE INQUIRY
Volume 2: Science
4. The link between BSE and vCJD
Summary
4.29 The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. 1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD. It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people.
4.30 Estimates of the likely scale of a possible epidemic of vCJD are wide-ranging and the subject of much debate. To know the likely number of cases is very important, not least to enable preparations to be made for the care of victims, as well as to be able to draw up guidelines to reduce the risk of transmission from infected but asymptomatic people. Preliminary results of the study examining tonsil and appendix material for signs of infection were not informative in this regard and full results are awaited. A blood test that would allow the widespread screening of the population by a simple method is still being sought.
THE BSE INQUIRY
TUESDAY, DECEMBER 12, 2017
Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017
DECEMBER 14, 2017, 20 YEARS POST DOD MOM HEIDENHAIN VARIANT CREUTZFELDT JAKOB DISEASE HVCJD DECEMBER 14, 1997, JUST MADE A PROMISE TO MOM, AND YOU DON'T BREAK PROMISES WITH YOUR MOM, NEVER FORGET, AND NEVER LET THEM FORGET...TERRY S. SINGELTARY SR.
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