10 years later, an internet post haunts actress : Despite a decade and a name change, she says people still ask her, ‘aren’t you dead yet?’
Sept 30,2017 이미지뷰
Kim Gyu-ri appeared on the Sept. 23 episode of “We want to know the truth” on SBS, discussing her life after 2008, when she was allegedly put on Lee Myung-bak administration’s cultural blacklist. The subtitles read, “Aren’t you dead yet? Huh? Aren’t you dead yet?” [SCREEN CAPTURE] It’s common for actors and actresses to have nicknames, but such monikers are usually favorable, unlike actress Kim Gyu-ri’s nickname, “potassium cyanide,” which she earned after a post she uploaded in 2008 on her social media account.
Kim was alledgedly on former President Lee Myung-bak’s blacklist of cultural figures and celebrities critical of the government since 2008. The defamed actress, along with other celebrities who claim to have been put on the former president’s list, appeared on SBS channel’s “We want to know the truth” on Sept. 23.
The blacklist controversy is blowing up at the moment, and the latest episode of “We want to know the truth” delved into the existence of the Lee administration’s cultural blacklist, which “had specific plans to oust celebrities and cultural figures critical to the government,” according to the program.
The so-called “MB Blacklist” apparently features 82 people, including celebrities such as Kim Mi-hwa, Moon Sung-geun and Kim Gyu-ri.
“No program would call me and I even got kicked out of the programs I was supposed to be shooting,” said Kim Mi-hwa. “We’ve all been presuming what happened. We all assumed that something was happening somewhere. A lot of strange things have been happening for the past nine years.”
Kim Gyu-ri is one such actress who has suffered from the government’s intentions to hamper her entertainment career. Kim, who went by her birth name Kim Min-sun back then, debuted as a model in 1997, and appeared in her first movie in 1999, “Whispering Corridors 2: Memento Mori.”
She led the life of a top celebrity afterwards, with her name cast in numerous movies, TV shows and her face gracing the cover of magazines. That was, until 2008.
On April 18, 2008, shortly after taking office in February, Lee announced negotiations with the United States to import U.S. beef, which had been banned in 2003 after a cow in the United States was found to have bovine spongiform encephalopathy (BSE), or mad cow disease. A total of one million citizens took to the streets over the course of three months, holding candlelight protests in central Seoul’s Gwanghwamun Square, demanding the government’s decision be reversed.
It was during one of those days on May 1, 2008, that Kim wrote on her social media account: “Soon, we will have U.S. beef even as the whole world shuns it … even the bones. This is just ridiculous … This couldn’t happen even in L.A. Importing beef and bones smothered with mad cow disease … I would rather fill my mouth with potassium cyanide.”
While Kim’s words were welcomed by those who opposed U.S. beef imports, she was harshly criticized by conservatives and even centrists. She was berated even by her fans when a footage of her eating a beef burger in the United States in March 2008 was revealed. Wherever she went, she was called “potassium cyanide,” and internet comments were always asking, “haven’t you filled your mouth with potassium cyanide yet?”
“The comments were always asking me, ‘aren’t you dead yet?’ and telling me to die,” said Kim. “So I tried to die. I went to the charnel house to see my mom the other day, and people were swearing at me there. But all I did was go and see my mom.” After the show, Kim admitted that what she wrote 10 years ago was something she did when she “was young and didn’t know well,” on a post she uploaded on Instagram on Sept. 24. The actress pleaded that she had been suffering for 10 years and that it’s time for people to stop.
Kim changed her name from Min-sun to Gyu-ri on November 2009, and said the reason she did so was because she “had always been called by the two names at home, and it was confusing.”
Nevertheless, the public saw the gesture as a way to escape her past as Kim Min-sun, “potassium cyanide,” and the name still followed afterwards.
Another factor that angered people was that there was already a “Kim Gyu-ri” in the entertainment field, who appeared first on the “Whispering Corridors” series in 1998.
이미지뷰 From the top: two pictures of the original Kim Gyu-ri, portals showing the new Kim Gyu-ri, the original Kim Gyu-ri’s Twitter, Kim’s “potassium cyanide” post in 2008 and a photograph of the original Kim Gyu-ri when she was younger. [INTERNET CAPTURE] Even though the original Kim Gyu-ri debuted first and was much more popular in the early 2000s, she suddenly became forgotten as another Kim Gyu-ri took over. Now, when people look for Kim Gyu-ri on the internet, all they get is the news of the person who used to be called Kim Min-sun.
“A girl who looks like a camel came out of nowhere and took everything,” wrote the original Kim Gyu-ri on her Twitter account on Sept. 23 after the episode of the “We want to know the truth” was aired. “My name and even my good reputation as an actress… Now I don’t even exist on the portal anymore…”
BY YOON SO-YEON [yoon.soyeon@joongang.co.kr]
Greetings again South Korea,
Kim Min-sun now Kim Gyu-ri was in fact a hero to her Nation. She should have been honored for what she did, and what she tried to tell her people. sadly, the Government of South Korea played politics with deadly mad cow disease, and today, in fact, Kim Min-sun now Kim Gyu-ri was correct with all her fears about USA beef, and other livestock in North America. Corporate America i.e. USDA inc., and the OIE, have sold their souls, and yours, to the devil, and made it legal to trade the Transmissible Spongiform Encephalopathy TSE Prion Mad Cow type disease via the BSE Minimal Risk Region i.e. BSE MRR policy. Oprah Winfrey spoke out, and you see what happened to her.
So, in my opinion, Kim Min-sun now Kim Gyu-ri should be treated as a South Korean Hero by her Country.
Today, mad cow disease BSE, and atypical BSE, typical and atypical Scrapie, and Chronic Wasting Disease CWD TSE Prion, have all now been linked to sporadic CJD, it's in hospitals all around the globe, and you can thank the USDA and the OIE for that imo. ...with kindest regards, terry
BSE, Scrapie, and CWD, Zoonosis, Zoonotic Disease
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***
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***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.
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
Transmission of scrapie prions to primate after an extended silent incubation period
Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys
Scientific Reports 5, Article number: 11573 (2015) doi:10.1038/srep11573
Download Citation EpidemiologyNeurological manifestationsPrion diseases Received: 16 February 2015 Accepted: 28 May 2015 Published online: 30 June 2015
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.
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Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. 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.
The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.
We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.
Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.
The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.
Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.
Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.
Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.
Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.
In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
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
TUESDAY, SEPTEMBER 19, 2017
*** USDA APHIS Notice: Animal Disease Traceability (ADT) Summary of Feedback on the ADT Program
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
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
Needless Conflict...
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
THURSDAY, JULY 13, 2017
*** EFSA BSE Sixty cases of mad cow disease since 2001 breached feed ban likely the cause
Scientists investigate origin of isolated BSE cases
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
*** 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, 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
***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.***
MONDAY, JULY 17, 2017
National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017
TUESDAY, JULY 18, 2017
MINK FARMING USA TRANSMISSIBLE MINK ENCEPHALOPATHY TSE PRION DISEASE SURVEILLANCE AND TESTING
IN the USA, the failed ruminant mad cow feed ban is even much worse then the UK and EU.
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
WEDNESDAY, APRIL 05, 2017
*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***
Chronic wasting disease continues to spread Disease of cervids causing local population declines
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016 Monthly Report Prion 2016 Tokyo Update
Wednesday, December 21, 2016
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH
Thursday, December 08, 2016
USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie
Tuesday, August 9, 2016
Concurrence with OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2015-0055]
BILLING CODE: 3410-34-P DEPARTMENT OF AGRICULTURE Animal and Plant Health Inspection Service
snip...see more ;
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
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Sunday, September 27, 2015
TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
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, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as at June 5, 2013
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Wednesday, December 4, 2013
*** Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December 4, 2013
Saturday, November 2, 2013
*** APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe
Monday, November 4, 2013
*** R-CALF Bullard new BSE rule represents the abrogation of USDA’s responsibility to protect U.S. consumers and the U.S. cattle herd from the introduction of foreign animal disease ***
Wednesday, October 30, 2013
SPECIFIED RISK MATERIAL (SRM) CONTROL VERIFICATION TASK FSIS NOTICE 70-13 10/30/13
Terry S. Singeltary Sr. 6/12/08
Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities APHIS-2006-0041
MONDAY, MAY 29, 2017
Canada CCA optimistic over potential for revisions to OIE criteria for BSE negligible risk
SUNDAY, NOVEMBER 13, 2016
Canada Transmissible Spongiform Encephalopathy TSE Prion Report Update
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
CFIA, USDA, AND OIE SHOOT, SHOVEL, AND SHUT THE HELL UP SSS BSE TSE PRION MAD COW TYPE POLICY $$$, and the media is buying it hook, line, and sinker $$$
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.
http://www.edmontonjournal.com/news/Kleinisms+former+Alberta+premier+Ralph+Klein+sound+bite/8171110/story.html
CANADA MBM LIVE CATTLE BSE TSE PRION TO USA
Date: Sat, 14 Jun 2003 02:23:12 +0200
OIG REPORT ON IMPORTS FROM CANADA
Thursday, July 24, 2014
Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA
Subject: Prion 2017 Conference Abstracts CWD
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
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)
Diseases & welfare
Korea urged to stop US beef imports
Posted : 2017-07-28 12:36 Updated : 2017-07-28 18:29
By Park Jae-hyuk
The Korean government should suspend the import of U.S. beef by amending terms of trade, a group of experts said Wednesday.
Amid growing concern on the safety of U.S. beef after an outbreak of mad cow disease, or bovine spongiform encephalopathy (BSE), in Alabama, the experts refuted the government's argument, presenting scientific evidence at a press conference in Seoul.
"The Korean government groundlessly claims, without any epidemiological survey by the U.S. government, that an atypical case of BSE is not dangerous to humans," said Prof. Woo Hee-jong of the Seoul National University College of Veterinary Science. "The terms of trade are unfair as well."
The professor urged the Moon Jae-in administration to confidently request a renegotiation of the deal with the U.S. government if it really respects the will of the candlelit protestors who played a big role in ousting the scandal-laden former President Park Geun-hye.
"An atypical case of BSE may be more dangerous to people, as it also contaminates a cow's lean meat, not only its brain or spinal cord," said Woo Seoc-kyun, vice representative of the Center for Health and Social Change.
"Under the U.S. inspection system, the infected 11-year-old cow might have been sold to consumers, if it had not died before slaughter."
He also noted that although Taiwan added more parts of beef to its list of import bans without any agreement with the U.S. government, it did not face any challenges through the World Trade Organization.
Veterinarian Hong Ha-il said the U.S. government still allows farmers to feed cows with feed containing parts of animals if the feed does not contain specified risk materials (SRM).
Hong also doubted the U.S. government's arguments about the infected cow's age.
"The U.S. government merely estimated its age with abrasion loss of the cow's teeth," he said. "I think it wants to emphasize the cow was born before 2008, when the U.S. government began to ban animal feed made with SRM."
The veterinarian said Washington, not Seoul, should prove the safety of its cows.
Although Song Ki-ho of the Lawyers for a Democratic Society admitted that other countries have yet to prohibit U.S. beef after the latest outbreak of BSE, the experts emphasized that most of those countries are exporters of their beef, unlike Korea.
"BSE occurred in Japan, Canada and Europe as well. Such countries may find it difficult to carry out import bans on U.S. beef," said Cho Neung-hee, a director for MBC's PD Notebook, who spotlighted the issue in 2008.
"Such countries as Australia, Taiwan and China confidently exercised their rights to suspend the import of suspicious U.S. beef during previous BSE outbreaks."
Website opens on mad cow disease after Moon's order The Ministry of Agriculture, Food and Rural Affairs has established a special website on mad cow disease, following President Moon Jae-in’s order to give people details about it. T...
"The Korean government groundlessly claims, without any epidemiological survey by the U.S. government, that an atypical case of BSE is not dangerous to humans," said Prof. Woo Hee-jong of the Seoul National University College of Veterinary Science. "The terms of trade are unfair as well."
"An atypical case of BSE may be more dangerous to people, as it also contaminates a cow's lean meat, not only its brain or spinal cord," said Woo Seoc-kyun, vice representative of the Center for Health and Social Change.
"Under the U.S. inspection system, the infected 11-year-old cow might have been sold to consumers, if it had not died before slaughter."
He also noted that although Taiwan added more parts of beef to its list of import bans without any agreement with the U.S. government, it did not face any challenges through the World Trade Organization.
Veterinarian Hong Ha-il said the U.S. government still allows farmers to feed cows with feed containing parts of animals if the feed does not contain specified risk materials (SRM).
Hong also doubted the U.S. government's arguments about the infected cow's age.
"The U.S. government merely estimated its age with abrasion loss of the cow's teeth," he said. "I think it wants to emphasize the cow was born before 2008, when the U.S. government began to ban animal feed made with SRM."
The veterinarian said Washington, not Seoul, should prove the safety of its cows.
"Under the U.S. inspection system, the infected 11-year-old cow might have been sold to consumers, if it had not died before slaughter."
He also noted that although Taiwan added more parts of beef to its list of import bans without any agreement with the U.S. government, it did not face any challenges through the World Trade Organization.
Veterinarian Hong Ha-il said the U.S. government still allows farmers to feed cows with feed containing parts of animals if the feed does not contain specified risk materials (SRM).
Hong also doubted the U.S. government's arguments about the infected cow's age.
"The U.S. government merely estimated its age with abrasion loss of the cow's teeth," he said. "I think it wants to emphasize the cow was born before 2008, when the U.S. government began to ban animal feed made with SRM."
The veterinarian said Washington, not Seoul, should prove the safety of its cows.
snip...end
YES SIR!
OUTSTANDING DEDUCTION SIR!
everything you stated is the truth, and science shows this.
I have documented it all for you below.
plus, see the HISTORY at the bottom of a letter sent to me back in 2007 from Korea, asking me to come and speak about this very important on TSE Prion disease;
Date: Jan 26, 2007
Dear Terry S. Singeltary Sr.
My name in Seoungwon Lee and I work for National Assemblywoman (MP) Sang-Jeong Sim, in South Korea. Below is a message from Mr. Kwon. Please get back to us regarding the letter. Thank you. Seoungwon Lee Legislative Assistant National Assembly Republic of Korea
Dear Terry S. Singeltary Sr....snip...end...see history at bottom.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
PRION 2017 CONFERENCE VIDEO
Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?
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
URINE
SUNDAY, JULY 16, 2017
*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***
WEDNESDAY, JULY 26, 2017
Chronic wasting disease continues to spread Disease of cervids causing local population declines
CWD state by state
KOREA BANS CANADIAN ELK IMPORTS: According to the Calgary Sun, Korea has moved to ban imports of Canadian deer and elk products (antlers and antler velvet) due to the outbreak of Chronic Wasting Disease (CWD) in Saskatchewan elk herds. Late last year, the Canadian Food Inspection Agency (CFIA) ordered the slaughter of 1,700 domesticated elk at six Saskatchewan farms in attempt to stop the spread of CWD (see CA 0206). The disease has not been detected in any other province. Canada's elk population is estimated at 53,000 head and is raised primarily for antler velvet. Canada is the fourth-largest antler velvet producer in the world, behind New Zealand, China and Russia. Most of Canadian antler velvet is exported to Asia where it is sold for medicinal purposes and as an aphrodisiac.
http://apps.fas.usda.gov/gainfiles/200108/125681717.pdf
spreading CWD around, or Trucking CWD or shipping CWD i.e. interstate movement of CWD by transportation of cervid or cervid materials
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.
***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.
On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.
Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.
Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.
Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.
In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.
http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/c792d0e56e0cb3ee3a6517e754729cac
THURSDAY, JULY 13, 2017
TEXAS CREUTZFELDT JAKOB DISEASE CJD TSE PRION
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
SATURDAY, JULY 22, 2017
Why the U.S. Needs to Continue Prion Disease Surveillance, instead of reducing funding to zero
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
2001 FDA CJD TSE Prion Singeltary Submission
HISTORY
USDA VS KOREA typical or atypical BSe
FRIDAY, MAY 9, 2008
USDA VS KOREA typical or atypical BSe
Honorable people of Korea,
a kind and warm greetings from Texas.
i cannot sit here and allow my government to lie to the korean people. i have been following the issue of Transmissible Spongiform Encephalopathy for over a decade, since the death of my mother to the Heidenhain Variant of Creutzfeldt Jakob Disease, confirmed. i have followed this on a daily basis since 12-14-97. there is so much i want to tell you, that the USDA and the FDA are not telling you.
i almost got to see your beautiful country, but in the last minute, my trip was cancelled. i was asked to come speak a year or so ago ;
Name: Terry S. Singeltary Sr.
Date: Jan 26, 2007
Dear Terry S. Singeltary Sr.
My name in Seoungwon Lee and I work for National Assemblywoman (MP) Sang-Jeong Sim, in South Korea. Below is a message from Mr. Kwon. Please get back to us regarding the letter. Thank you. Seoungwon Lee Legislative Assistant National Assembly Republic of Korea
Dear Terry S. Singeltary Sr.
Greetings from Korea.
I have learned about what you and your family have been through a internet. Being the father of a small family, I can only imagine the sense of loss that you and your family still must feel regarding your mother.
Through the internet, many people here in Korea have learnt about the story of your family and it has created a great deal of concern. Your experience had particular relevance for the citizens here, for the Korean government, in connection to the free trade agreement it is negotiating with the United States, is about to restart the sale of the unsafe American beef to the general public.
The Korean government has already imported the first load American beef and is currently going through the inspection period. There has been a great deal of controversy regarding the safety of these products, and a precipitous increase in public interest regarding the causes and symptoms of vCJD.
It is in this context that we are preparing a session together with National Assembly members and relevant NGOs to hear from those who have had direct experience with the human variant of BSE. We are very interested in hearing about the symptoms that your mother showed, your views on the response from the US government to the many deaths that resulted from this disease, the reaction from the general public, and any other area that you would wish to speak about. There would also be experts and academics in the area to speak at the session as well. We believe that it would greatly contribute to raising awareness about the issue, as well as help politicians and civic activists to consider the repercussions of the beef import issue.
We would like to request your help in this regard. We are planning for the session to be held in Seoul on the 23rd of this November. We would very much like to have you present in order to help prevent such tragic incidents from happening in Korea. We would, of course, pay for the trip and accommodations for the duration of your stay. If you were to participate, we could also meet with members from the agricultural committee of the National Assembly and from other related organizations to urge more interest to the issue.
Please do not hesitate to offer suggestions or ask us any questions that you might have. We look forward to a positive response and to meeting you in Seoul.
Thank you. Sincerely, Sim Sang-Jeong Head of the Democratic Labor Party Parliamentary Committee on the Korea-US FTA Member of the National Assembly Republic of Korea
02-09-2010 19:38
Anti-US Beef Actress Prevails in Court
By Park Si-soo Staff Reporter
Actress Kim Min-sun won a legal battle Tuesday, started by an American beef importer for an article she wrote two years ago on her private blog that allegedly exaggerated the risk of mad cow disease associated with U.S. beef.
In May 2008, when the country was trapped in heated debate over the resumption of U.S. beef imports and its association with mad cow disease, the actress said in the article, “I would gulp a cup of potassium cyanide rather than eat a piece of American beef infected with the disease.”
As the comment drew media attention, an American beef importer in Seoul, A-Meat, filed a suit against the actress and five staff members of an investigative TV journal, PD Notebook, for interrupting its business by spreading what it called “groundless” information about the imported beef. The importer also claimed its bottom line was hit hard by her defamatory article.
But the Seoul Southern District Court Tuesday ruled the actress and the TV program were not liable for any damages to the importer.
Judge Kim Sung-gon said in the ruling, “Her article revealed no specific information associated with the plaintiff. So it cannot be seen that her article interrupted its business.” The judge also acquitted the five TV producers, saying the program was wholly based on data they compiled in the belief that they were all scientifically grounded.
“Also, the program was to criticize the government for a deal with Washington allegedly endorsed in a cursory manner, not a specific company,” the judge said.
Two years have passed since the social unrest, provoked by the resumption of U.S. beef imports without thorough restrictions to keep risky parts of American beef at bay, ended.
To quell enraged citizens, who took to major streets for three months, President Lee Myung-bak solicited for the U.S. government to modify the terms of the contract signed between the two parties, made public apologies and reshuffled the Cabinet.
But society is still divided and shows no immediate sign of mending the rift. Rather, what is left over from the unrest is still plaguing the administration by providing a ground for ideological showdowns between those in favor of the conservative administration and its opponents, levying a heavy political burden on President Lee, who is in the midst of his five-year presidency.
The latest controversy, associated with the beef scandal two years ago, resurfaced after a court ruling early this month that exonerated the five TV producers from defamation charges.
On Jan. 20, the Seoul Central District Court cleared them on defamation charges for allegedly wrongly portraying the actions of two senior state trade negotiators during the Seoul-Washington talks to resume U.S. beef imports in 2008.
The ruling provoked immediate condemnation from conservative activists and politicians, pressuring the head of the judiciary to step down, calling the verdict a decision based on ideological bias. Some overzealous activists even staged rallies in front of the home of the judge in charge of the case, calling for his resignation.
Liberal activists and politicians condemned their moves, describing a series of acts by their counterparts as politically motivated moves to sway the judiciary, whose independent operation is guaranteed under the Constitution.
Galvanized by the ruling, the ruling Grand National Party is now pushing a package of bills to tighten its grip on the judiciary, while opposition parties are trying to strike down the attempt.
pss@koreatimes.co.kr
flounder Del (71.248.137.150) 02-10-2010 07:39
To Honorable Ms. Kim Min-Sun and Korea,
The Truth will set us free.
Thank You Ma’am ! You are very courageous ! Your Country-man and Country-Woman should be proud. …TSS
PLEASE SEE FULL TEXT ;
Why Americans, As Well as Koreans, Should Be Worried About Mad Cow Tainted USA Beef By Terry S. Singeltary Sr. May 15, 2008 Straight to the Source
Tuesday, May 13, 2008
Concerned Americans against Mad Cow Disease STATEMENT OF SOLIDARITY with Koreans May 13, 2008
Wednesday, February 10, 2010
The Honorable Ms. Kim Min-sun Anti-US Beef Actress Prevails in Court
SATURDAY, AUGUST 22, 2009
FREE Kim Min-sun, she is correct about mad cow fears from USDA BEEF
Friday, January 20, 2012
South Korea Lifts Canadian Beef Ban
once exposed to the cwd tse prion agent, once exposed, then there is a risk of friendly fire, second hand transmission via the iatrogenic, medical, surgical, dental, blood, tissue mode of transmission.
see;
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
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.
PMID: 8006664 [PubMed - indexed for MEDLINE]
THURSDAY, AUGUST 17, 2017
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017 ***
THURSDAY, AUGUST 10, 2017
Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017
BSE TSE PRION USDA OIE NEEDLESS CONFLICT
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.
BSE TSE PRION USDA OIE NEEDLESS CONFLICT
2001 FDA CJD TSE Prion Singeltary Submission
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
2017
THURSDAY, AUGUST 17, 2017
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
kindest regards,
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
