Thursday, April 28, 2016

Persistent residual contamination in endoscope channels; a fluorescence epimicroscopy study

Endoscopy DOI: 10.1055/s-0042-105744 Original article
 
© Georg Thieme Verlag KG Stuttgart · New York
 
Persistent residual contamination in endoscope channels; a fluorescence epimicroscopy study
 
Rodolphe C. Hervé, Charles W. Keevil
 
Environmental Healthcare Unit, Centre of Biological Sciences, University of Southampton, Southampton, UK Further Information Publication History submitted 10 July 2015
 
accepted after revision 23 February 2016
 
Publication Date: 25 April 2016 (eFirst)
 
Abstract
 
Background and study aims: The increasing demand for endoscopic procedures poses new contamination challenges, given developing antimicrobial resistance worldwide and potential viral or prion diseases in populations at risk. We examined working channels from reusable luminal endoscopes used in recent years.
 
Methods: Very sensitive fluorescence epimicroscopy was used to examine working channels from 6 decommissioned and 6 factory-new channels, as received, or following spiking and washing in the laboratory.
 
Results: After a single contamination and wash test cycle, new channels retained approximately 75 pg/mm2 of proteins; through 7 subsequent cycles residual proteins fluctuated between 25 and 75 pg/mm2. Decommissioned channels harbored 1 – 4 µg of proteins each, except in one gastroscope (33 µg), including up to 2 % amyloid proteins except in one gastroscope and one sigmoidoscope (with over 80 %); lumens showed wearing with established abraded biofilms in 3 cases. After spiking with scrapie-infected blood components and washing, residual protein levels in new channels varied following standard (17.23 pg/mm2), duplicated (2.39 pg/mm2) or extended (11.3 pg/mm2) washing; no changes were measured among the long-established contamination in old channels.
 
Conclusions: Our observations suggest that wear effects in endoscope lumens may contribute to the adsorption of proteins, thus facilitating retention and survival of bacteria. As demonstrated by recent outbreaks worldwide despite recommended reprocessing, the development of antimicrobial-resistant bacterial strains, and the estimated prevalence of variant Creutzfeldt-Jakob disease (vCJD) in the UK particularly, combined with increasing demand for endoscopic procedures, call for sustained precautions and improved methods for the reprocessing of nonautoclavable, reusable surgical instruments.
 

>>>Conclusions: Our observations suggest that wear effects in endoscope lumens may contribute to the adsorption of proteins, thus facilitating retention and survival of bacteria. As demonstrated by recent outbreaks worldwide despite recommended reprocessing, the development of antimicrobial-resistant bacterial strains, and the estimated prevalence of variant Creutzfeldt-Jakob disease (vCJD) in the UK particularly, combined with increasing demand for endoscopic procedures, call for sustained precautions and improved methods for the reprocessing of nonautoclavable, reusable surgical instruments.<<<

ALL IATROGENIC CJD IS, IS SPORADIC CJD, UNTIL THE IATROGENIC EVENT IS DOCUMENTED, CONFIRMED, PUT INTO THE ACADEMIC DOMAIN, AND THEN FINALLY PUT INTO THE PUBLIC DOMAIN, which very seldom happens due to incubation period and lack of trace back efforts...tss

 
Monday, August 17, 2015
 
FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
 
I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;
 
 
Wednesday, March 02, 2016
 
Endoscope Maker Olympus Agrees To $646 Million Settlement Over Kickbacks, while still ignoring the elephant in the room, CJD TSE PRIONS
 
 
Saturday, April 16, 2016
 
More infections from dirty scopes than estimated, what about CJD TSE Prion aka mad cow type disease?
 
Report: More infections from dirty scopes than estimated
 
 
2003
 
*** Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al ***
 
Evidence For CJD/TSE Transmission Via Endoscopes
 
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
 
 
Monday, December 26, 2011
 
Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites
 
 
*** PRION CONFERENCE 2016 ***
 
P-101
 
v-CJD prion distribution in the tissues of patients at preclinical and clinical stage of the disease
 
Olivier Andreoletti a, Caroline Lacroux a, Jean Yves Douet a, Severine Lugan a, Naima Aron a, James w Ironside b, Vincent Beringue c
 
"UMR INRA ENVT 1225 - IHAP, France;
 
"National Creutzfeldt-Jakob Disease Surveillance Unit, Centre for Clinical Brain Sciences, University of Edinburgh, Western General Hospital, Edinburgh EH42X U, UK;
 
"UR892 Virologie et lmmunologie Moléculaires Centre de Recherche de Jouy-en—Josas F-78352 Jouy-en-Josas, France
 
Author's e-mail address:
 
o.andreoletti@envt.fr
 
The emergence of variant Creutzfeldt Jakob Disease (VCJD) is considered a likely consequence of human dietary exposure to Bovine Spongiform Encephalopathy (BSE) agent. The prevalence of the disease in the human population remains uncertain but in the United Kingdom secondary vCJD cases were identified in patients transfused with blood products prepared from apparently healthy donors who later developed the disease. In that context the risk of VCJ D iatrogenic transmission is considered as a serious concern by health authorities.
 
In this study, in vitro amplification of vCJD prion by Protein Misfolding Cyclic Assay (PMCA) was used to estimate the relative quantity of agent present in a panel of tissues from patients at clinical (n=4, Met/Met129) and preclinical (n=1, Met/VaI129) stage of the disease. As expected, the vCJD agent was detected in the central nervous system and in various lymphoid organs.
 
Strikingly PMCA also revealed the presence of consistent level of vCJD prion in various other tissues like liver, salivary gland, kidney or bone marrow. Bioassays carried out using certain of these tissues confirmed the presence of vCJD infectivity. These data confirm the possibility of a vCJD transmission risk that could be associated to various medical procedures (surgery, tissue grafts). They also represent an important contribution towards developing adapted prevention measures to mitigate the risk of vCJD iatrogenic transmission.
 
 
*** 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.
 
 
Thursday, August 13, 2015
 
Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years
 
 
Thursday, June 04, 2015
 
Catholic Medical Center v. Civil No. 14-cv-180-JL Opinion No. 2015 DNH 110 Fireman’s Fund Insurance Company Creutzfeldt Jakob Disease TSE Prion tainted medical instruments
 
UNITED STATES DISTRICT COURT DISTRICT OF NEW HAMPSHIRE
 
 
Tuesday, February 11, 2014
 
Novant Health Forsyth Medical Center Information on potential CJD exposure
 
 
Monday, February 10, 2014
 
18 Forsyth Medical Center patients exposed to CJD; apology issued...OOOPS, SORRY, TOO BAD $$$
 
 
Thursday, January 16, 2014
 
The Anspach Effort, Inc. RECALL FDA Blackmax motor had been used in a case where the patient was diagnosed with Creutzfeldt-Jacob Disease (CJD) MARYLAND HOSTPITAL
 
 
Friday, January 10, 2014
 
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
 
 
Thursday, January 23, 2014
 
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) [Docket No. FDA–2013–D–1574]
 
 
Sunday, April 06, 2014
 
SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date
 
 
Thursday, April 17, 2014
 
Novant: Three more may have been exposed to disease CJD
 
 
Wednesday, September 10, 2014
 
Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with updated guidance on decontamination of gastrointestinal endoscopy equipment
 
Research and analysis
 
 
Tuesday, August 26, 2014
 
Blood reference materials from macaques infected with variant Creutzfeldt-Jakob disease agent
 
 
Wednesday, November 27, 2013
 
NHS failed to sterilise surgical instruments contaminated with 'mad cow' disease
 
 
Saturday, November 16, 2013
 
Management of neurosurgical instruments and patients exposed to creutzfeldt-jakob disease 2013 December
 
Infect Control Hosp Epidemiol.
 
 
Tuesday, September 24, 2013
 
NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)
 
Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15
 
 
Thursday, September 05, 2013
 
Possible Patient Exposure to Creutzfeldt-Jakob Disease Announced New Hampshire DHHS
 
Press Release
 
 
Friday, July 19, 2013
 
Beaumont Hospital in Dublin assessing patients for CJD
 
 
Monday, April 15, 2013
 
Dr. Stephen B. Thacker Director Centers for Disease Control and Prevention′s Office of Science, Epidemiology and Laboratory Services (OSELS) dies from Creutzfeldt Jakob Disease CJD
 
 
Thursday, April 12, 2012
 
Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010
 
Eurosurveillance, Volume 17, Issue 15, 12 April 2012
 
Research articles
 
 
Tuesday, July 31, 2012
 
11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital
 
 
Thursday, August 02, 2012
 
CJD case in Saint John prompts letter to patients Canada CJD case in Saint John prompts letter to patients
 
 
Tuesday, July 31, 2012
 
11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital
 
 
Thursday, August 02, 2012
 
CJD case in Saint John prompts letter to patients Canada CJD case in Saint John prompts letter to patients
 
 
Saturday, February 12, 2011
 
Another Pathologists dies from CJD, another potential occupational death ?
 
another happenstance of bad luck, a spontaneous event from nothing, or friendly fire ???
 
 
Wednesday, November 30, 2011
 
First iCJD Death Confirmed in Korea
 
 
Thursday, December 08, 2011
 
A case of Iatrogenic Creutzfeldt Jakob Disease (iCJD) in a patient who had received a German-manufactured human dura mater graft 23 years ago
 
 
Thursday, December 8, 2011
 
S. Korea confirms second case of iatrogenic Creutzfeldt-Jakob disease 48-year-old man
 
2011/12/08 11:08 KST
 
 
Monday, December 12, 2011
 
Second iatrogenic CJD case confirmed Korea
 
 
 
Saturday, February 13, 2016
 
The Risk of Prion Infection through Bovine Grafting Materials in dentistry
 
 
Saturday, January 16, 2016
 
Revised Preventive Measures to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and Blood Products Guidance for Industry
 
 
Tuesday, May 26, 2015
 
Minimise transmission risk of CJD and vCJD in healthcare settings Last updated 15 May 2015
 
 
Friday, October 09, 2015
 
An alarming presentation level II trauma center of Creutzfeldt-Jakob disease following a self-inflicted gunshot wound to the head
 
 
Wednesday, January 06, 2016
 
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE U.K. 23rd ANNUAL REPORT 2014 (published 18th November 2015)
 
 
Saturday, December 12, 2015
 
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
 
 
Thursday, March 17, 2016
 
Preliminary Diagnosis Creutzfeldt-Jakob Disease Confirmed in Patient that had Lumbar Puncture at Washington Regional Medical Center
 
 
all iatrogenic cjd is, is sporadic cjd, until the iatrogenic event is discovered, traced back, documented in the Academic domain, and then put into the public domain and documented as an iatrogenic CJD event. that’s why 85%+ of all human TSE prion disease is still sporadic CJD. problem solved $$$
 
PLEASE REMEMBER, IN 55 YEARS AND OLDER, THE RATE OF DOCUMENTED CJD JUMPS TO ONE IN 9,000.
 
Thursday, September 10, 2015
 
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
 
 
Sunday, January 17, 2016
 
Of Grave Concern Heidenhain Variant Creutzfeldt Jakob Disease
 
 
Saturday, February 13, 2016
 
The Risk of Prion Infection through Bovine Grafting Materials in dentistry
 
 
Monday, February 15, 2016
 
Distinctive properties of plaque-type dura mater graft-associated Creutzfeldt–Jakob disease in cell-protein misfolding cyclic amplification
 
 
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
 
 
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
 
Taylor & Francis
 
Prion 2016 Animal Prion Disease Workshop Abstracts
 
WS-01: Prion diseases in animals and zoonotic potential
 
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
 
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
 
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
 
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
 
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
 
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
 
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Title: Transmission of scrapie prions to primate after an extended silent incubation period
 
Authors
 
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -
 
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573.
 
Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans. Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health.
 
*** 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.
 
 
Suspect symptoms
 
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
 
28 Mar 01 Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
 
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
 
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...
 
2001
 
Suspect symptoms
 
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
 
28 Mar 01
 
Like lambs to the slaughter
 
31 March 2001
 
by Debora MacKenzie Magazine issue 2284.
 
FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
 
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
 
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
 
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
 
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
 
Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
 
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.
 
"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.
 
But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.
 
People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.
 
But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
 
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
 
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
 
 
Then follow up with PNAS studies from which new scientist article written from;
 
Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt- Jakob disease: Implications for human health
 
THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*, Virginie Nouvel*,
 
Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger
 
] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique
 
Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible for French iatrogenic growth hormone-linked CJD taken as a control is very different from vCJD but is similar to that found in one case of sporadic CJD and one sheep scrapie isolate;
 
 
CWD to CJD in humans (why not?), as easy as BSE/Scrapie;
 
The EMBO Journal, Vol. 19, No. 17 pp. 4425-4430, 2000
 
© European Molecular Biology Organization
 
Evidence of a molecular barrier limiting susceptibility of humans, cattle and sheep to chronic wasting disease
 
G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O?Rourke3,
 
L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M.
 
Smits2
 
and B. Caughey1,7
 
1NIAID/NIH Rocky Mountain Laboratories, Hamilton, MT 59840,
 
3USDA/ARS/ADRU, Pullman, WA 99164-7030, 4USDA/ARS/ABADRL,
 
Laramie, WY 82071, 5Colorado Division of Wildlife, Wildlife Research
 
Center, Fort Collins, CO 80526-2097, 6Department of Veterinary Sciences,
 
University of Wyoming, Laramie, WY 82070, USA and 2ID-Lelystad,
 
Institute for Animal Science and Health, Lelystad, The Netherlands
 
7Corresponding author e-mail: bcaughey@nih.gov Received June 7, 2000;
 
revised July 3, 2000; accepted July 5, 2000.
 
Abstract
 
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of deer and elk, and little is known about its transmissibility to other species. An important factor controlling interspecies TSE susceptibility is prion protein (PrP) homology between the source and recipient species/genotypes. Furthermore, the efficiency with which the protease-resistant PrP (PrP-res) of one species induces the in vitro conversion of the normal PrP (PrP-sen) of another species to the protease-resistant state correlates with the cross-species transmissibility of TSE agents. Here we show that the CWD-associated PrP-res (PrPCWD) of cervids readily induces the conversion of recombinant cervid PrP-sen molecules to the protease-resistant state in accordance with the known transmissibility of CWD between cervids. In contrast, PrPCWD-induced conversions of human and bovine PrP-sen were much less efficient, and conversion of ovine PrP-sen was intermediate. These results demonstrate a barrier at the molecular level that should limit the susceptibility of these non-cervid species to CWD.
 
snip...
 
Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs.
 
snip...
 
 
Scrapie to Humans USA?
 
1: Neuroepidemiology. 1985;4(4):240-9. Related Articles,
 
Links
 
Sheep consumption: a possible source of spongiform encephalopathy in humans.
 
Davanipour Z, Alter M, Sobel E, Callahan M.
 
A fatal spongiform encephalopathy of sheep and goats (scrapie) shares many characteristics with Creutzfeldt-Jakob disease (CJD), a similar dementing illness of humans. To investigate the possibility that CJD is acquired by ingestion of contaminated sheep products, we collected information on production, slaughtering practices, and marketing of sheep in Pennsylvania. The study revealed that sheep were usually marketed before central nervous system signs of scrapie are expected to appear; breeds known to be susceptible to the disease were the most common breeds raised in the area; sheep were imported from other states including those with a high frequency of scrapie; use of veterinary services on the sheep farms investigated and, hence, opportunities to detect the disease were limited; sheep producers in the area knew little about scrapie despite the fact that the disease has been reported in the area, and animal organs including sheep organs were sometimes included in processed food. Therefore, it was concluded that in Pennsylvania there are some 'weak links' through which scrapie-infected animals could contaminate human food, and that consumption of these foods could perhaps account for spongiform encephalopathy in humans. The weak links observed are probably not unique to Pennsylvania.
 
PMID: 3915057 [PubMed - indexed for MEDLINE]
 
 
2015
 
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.
 
==============
 
 
Tuesday, December 16, 2014
 
*** Evidence for zoonotic potential of ovine scrapie prions
 
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics
 
Abstract
 
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE.
 
***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans.
 
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
 
Subject terms: Biological sciences• Medical research At a glance
 
 
see more here ;
 
 
***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans.***
 
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.***
 
why do we not want to do TSE transmission studies on chimpanzees $
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
snip...
 
R. BRADLEY
 
 
1: J Infect Dis 1980 Aug;142(2):205-8
 
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
 
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
 
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
 
snip...
 
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
 
PMID: 6997404
 
 
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
 
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
 
snip...
 
76/10.12/4.6
 
 
Nature. 1972 Mar 10;236(5341):73-4.
 
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
 
Gibbs CJ Jr, Gajdusek DC.
 
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
 
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
 
C. J. GIBBS jun. & D. C. GAJDUSEK
 
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
 
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
 
 
 
Saturday, July 6, 2013
 
*** Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy
 
Research Article
 
 
Monday, December 14, 2009
 
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
 
(hmmm, this is getting interesting now...TSS)
 
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits,
 
see also ;
 
All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.
 
 
see full text ;
 
Monday, December 14, 2009
 
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
 
 
*** OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO CONTINUE SPREADING IT AROUND THE GLOBE
 
 
Monday, November 30, 2009
 
*** USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE, DOES NOT SURPRISE ME $
 
 
Confucius confused again, and Ponders, what about those Libyan Jews and sheep scrapie and codon 200 of the prion protein gene of the CJD Victims therefrom?
 
Could it be not that the codon 200 of the prion protein gene made these poor victims of CJD just more susceptible to the sheep scrapie agent?
 
Pondering Confucius...
 
European Journal of Epidemiology
 
September 1991, Volume 7, Issue 5, pp 490-493
 
First online:
 
Creutzfeldt-Jakob disease among libyan jews A. D. Korczyn
 
Abstract
 
The focus of CJD among Jews of Libyan origin has been recognized for two decades, but the reasons underlying it were unknown. Prevailing views suggested transmission from sheep infected with scrapie. However, recent data show that in fact CJD in this ethnic group is a genetically determined disease due to a point mutation on the codon 200 of the prion protein gene. The clinical characteristics of CJD in this group, and particularly the less common periodic activity in the EEG, are reviewed. New findings include peripheral neuropathy of the demyelinating type in two cases, presumably due to involvement of Schwann cells. The pathophysiology of the disease includes, presumably, a focal post-translational modification of the prion protein, (predisposed by the mutation). Later, the disease progresses through cell-to-cell transmission.
 
Key words Creutzfeldt-Jakob diseases – Prion disease – Jews – Libya – Genetics – Pathophysiology
 
 
1: Cent Eur J Public Health 2003 Mar;11(1):19-22
 
Analysis of unusual accumulation of Creutzfeldt-Jakob disease cases in Orava and Liptov regions (northern Slovak focus) 1983-2000.
 
Mad'ar R, Maslenova D, Ranostajova K, Straka S, Baska T.
 
Institute of Epidemiology, Jessenius Faculty of Medicine, Comenius University, Sklabinska 26, Martin, 037 53 Slovakia. MADAR@jfmed.uniba.sk
 
While familial cases of Creutzfeldt-Jakob disease are extremely rare all over the world, 3 familial clusters were observed between 1983-2000 in a relatively small area situated in the North of Slovakia. Prevalence of CJD in this area exceeded the overall prevalence in Slovakia more than 8 times. The majority of CJD patients admitted consuming sheep brain. Most patients lived in small secluded villages with rather common familial intermarriage. CJD affected both sexes equally. All patients were prior to the disease mentally normal individuals. Shortly after the onset of CJD their mental status deteriorated remarkably with an average survival rate of 3.6 months.
 
PMID: 12690798
 
 
------------------------------------------------------------------------
 
1: Eur J Epidemiol 1991 Sep;7(5):520-3
 
"Clusters" of CJD in Slovakia: the first laboratory evidence of scrapie.
 
Mitrova E, Huncaga S, Hocman G, Nyitrayova O, Tatara M.
 
Institute of Preventive and Clinical Medicine, Bratislava.
 
Epidemic-like occurrence of Creutzfeldt-Jakob disease was observed in 1987 in Slovakia (Orava). Search for the cause of CJD focus indicated a coincidence of genetic and environmental risks in clustering patients. Since Spongiform Encephalopathies might be transmitted orally, (Bovine Spongiform Encephalopathy), the possibility of zoonotic source of CJD cases in Orava was also considered. A deficient knowledge about the occurrence of scrapie in Slovakia stimulated an examination of sheep with signs of CNS disorders in two flocks of Valasky breed in Orava. In one flock, neurohistopathological examination revealed in sheep brains lesions characteristic for scrapie. Frozen brain tissue of these animals were used for the detection of scrapie associated fibrils. They were found in 2 animals from the same flock. This is the first laboratory confirmation of scrapie in Czecho-Slovakia. The possible epidemiological and economical implications are emphasized.
 
 
Mutation of the prion protein in Libyan Jews with Creutzfeldt-Jakob disease Article Abstract:
 
Creutzfeldt-Jakob disease (CJD) is a neurodegenerative disease of a class referred to as the spongiform encephalopathies. The disease can be transmitted experimentally and has also been transmitted accidentally. The causative agent in these transmissions is unlike any well characterized infectious agent and is referred to by many as a prion. Creutzfeldt-Jakob disease may occur in families, but is usually sporadic. The incidence of Creutzfeldt-Jakob disease is about one or two cases per million people. However, among Jews from Libya, the incidence is 100 times higher. Many possible explanations have been put forward to account for this unusually high incidence, but none has sustained any scrutiny. One of the more popular notions was that the eating of sheep brains, a popular delicacy in the region, infected people with scrapie, a prion disease of sheep similar to CJD. However, the eating of sheep brain is popular throughout the Mediterranean, and cannot explain the specificity of the increased incidence to Libyan Jews. Mediterranean sheep, if anything, have a lower rate of scrapie than other areas of Europe and North America. A study was undertaken to determine if the increased incidence of CJD among these people might be accounted for by genetic factors. The prion protein genes were analyzed in 11 Libyan Jews with Creutzfeldt-Jakob disease. Investigation of one patient revealed that a mutation had occurred in the 200th codon of the gene, that is, the 200th set of three DNA bases. The net result of this change would be to substitute a lysine for glutamine in the resulting protein. After this mutation was identified, it was confirmed in the other 10 Libyan patients. It is interesting to note that the mutation was not present in a Moroccan Jew with CJD. The results suggest that the increased incidence of Creutzfeldt-Jakob disease in this population is the result of a gene carried by this group. In eight of the present cases, a family history of CJD could be confirmed. Although not all families were cooperative in providing information of the ancestral heritage, all the families for which such information was available could be traced to Djerba, which is an island off the coast of Tunisia. (Consumer Summary produced by Reliance Medical Information, Inc.)
 
author: Scarlato, Guglielmo, Prusiner, Stanley B., Hsiao, Karen, Meiner, Zeev, Kahana, Esther, Cass, Carin, Kahana, Irit, Avrahami, Dana, Abramsky, Oded, Gabizon, Ruth Publisher: Massachusetts Medical Society Publication Name: The New England Journal of Medicine Subject: Health ISSN: 0028-4793 Year: 1991
 
 
Epidemiology of Scrapie in the United States 1977
 
 
 
Monday, March 28, 2016
 
National Scrapie Eradication Program February 2016 Monthly Report
 
 
Comment from Terry Singeltary This is a Comment on the Animal and Plant Health Inspection Service (APHIS) Proposed Rule: Scrapie in Sheep and Goats
 
For related information, Open Docket Folder Docket folder icon
 
--------------------------------------------------------------------------------
 
Show agency attachment(s) AttachmentsView All (0)
 
--------------------------------------------------------------------------------
 
Comment View document:Indeed, much science has changed about the Scrapie TSE prion, including more science linking Scrapie to humans. sadly, politics, industry, and trade, have not changed, and those usually trump sound science, as is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing animals and the OIE. we can look no further at the legal trading of the Scrapie TSE prion both typical and atypical of all strains, and CWD all stains. With as much science of old, and now more new science to back this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE, and all trading partners to take heed to the latest science on the TSE prion disease, all of them, and seriously reconsider the blatant disregards for human and animal health, all in the name of trade, with the continued relaxing of TSE Prion trade regulations through the 'NEGLIGIBLE BSE RISK' PROGRAM, which was set up to fail in the first place. If the world does not go back to the 'BSE RISK ASSESSMENTS', enhance, and or change that assessment process to include all TSE prion disease, i.e. 'TSE RISK ASSESSMENT', if we do not do this and if we continue this farce with OIE and the USDA et al, and the 'NEGLIGIBLE BSE RISK' PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they will continue to mutate and spread among species of human and animal origin, and they will continue to kill. ...
 
please see ;
 
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 longe 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***
 
===============
 
 
***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.
 
***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.
 
 
please see file attachment for full submission and recent science and my deep concerns on the TSE Prion disease... No documents available. AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:
 
 
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...
 
 
*** 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
 
 
 
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
 
 
Comment from Terry S. Singeltary Sr. Return to Docket Folder Summary This is a Comment on the Food and Drug Administration (FDA) Notice: Risk Assessment of Foodborne Illness Associated With Pathogens From Produce Grown in Fields Amended With Untreated Biological Soil Amendments of Animal Origin; Request for Scientific Data, Information, and Comments
 
For related information, Open Docket Folder Docket folder icon
 
--------------------------------------------------------------------------------
 
Show agency attachment(s) AttachmentsView All (0)
 
--------------------------------------------------------------------------------
 
Comment View document:Greetings FDA et al, I kindly would like to make comment submission to ;
 
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated with Pathogens from Produce Grown in Fields Amended with Untreated Biological Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and Information
 
A Notice by the Food and Drug Administration on 03/04/2016
 
MY comment as follows,
 
There has been proven documented risk for Untreated Biological Soil Amendments of Animal Origin and risk of transmitting Transmissible Spongiform Encephalopathy TSE Prion disease aka mad cow type disease such as the typical and atypical Bovine Spongiform Encephalopathy strains, typical and atypical Scrapie strains, typical and atypical Chronic Wasting Disease CWD strains, and even the Transmissible Mink Encephalopathy TME Prion disease.
 
Science has shown that infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces thereby leading to transmission by direct contact and environmental contamination.
 
Ingestion of prion contaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate.
 
Plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves) [please see data from Soto et al Prion2015 Conference below in Science reference data].
 
Also, Detection of protease-resistant cervid prion protein in water from a CWD-endemic area is very concerning.
 
Science has shown that soil plays a role in the spreading and transmission of the CWD and Scrapie TSE prion agent.
 
For these reason and more (see reference materials) I urge the FDA to stop this practice of Untreated Biological Soil Amendments of Animal Origin, including blood, for use on our produce grown in fields, for the following reasons,
 
please see attachments and updated TSE Prion science on these very important matters here (I do not advertise or make money the science is there for educational use for Transmissible Spongiform Encephalopathy TSE Prion disease.
 
just made a promise to mom dod 12/14/97 confirmed Heidenhain Variant Creutzfeldt Jakob Disease, hvCJD. ... AttachmentsView All (1) Comment from Terry S Singeltary Sr View Attachment:
 
 
 
Tuesday, March 15, 2016
 
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated with Pathogens from Produce Grown in Fields Amended with Untreated Biological Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and Information Singeltary Submission
 
 
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
 
 
Friday, April 22, 2016
 
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease Authors
 
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -
 
Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
 
 
 
Thursday, April 07, 2016
 
What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016
 
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008).
 
***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, 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...
 
For the purpose of the qualitative risk assessment developed here it is necessary to estimate the probability that a 30-ml bottle of lure contains urine from an infected deer. This requires an estimate of the proportion of deer herds in the USA which are infected with CWD together with the within herd prevalence.
 
The distribution map of CWD in US shows it is present mainly in central states (Figure 1). However, Virginia in the east of the country has recorded seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take steps to prevent urine being taken from infected animals eg by sourcing from farms where the deer are randomly tested for CWD (Anon 2015a). However, if disease is already present and testing is not carried out regularly, captive populations are not necessarily disease free (Strausser 2014). Urine-based deer lures have been known to be collected from domestic white-tailed deer herds and therefore there is a recognised risk. This is reflected by 6 US States which have
 
14
 
banned the use of natural deer urine for lures, as the deer urine may be sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For example, the US State of Virginia is banning the use of urine-based deer lures on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned urine-based deer lures and acknowledged that there is no way to detect their use (Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it appears that up to 50% of deer herds can be infected with 80-90% of animals infected within some herds.
 
*** It is therefore assumed that probability that a 30-ml bottle of deer urine lure imported from the USA is sources from an infected deer is medium.
 
SNIP...
 
In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. ***For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. ***However, this recommendation is guidance and not a requirement by law.
 
***Animals considered at high risk for CWD include:
 
***1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
 
***2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
 
***Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB cannot be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the very low tonnage of non-fish origin processed animal proteins that were imported from US into GB.
 
*** Overall, therefore, it is considered there is a greater than negligible risk that (non-ruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
 
SNIP...
 
 
Summary and MORE HERE ;
 
What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016
 
 
Saturday, January 31, 2015
 
European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route
 
 
 
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...
 
======
 
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.
 
***However, this recommendation is guidance and not a requirement by law.
 
======
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
31 Jan 2015 at 20:14 GMT
 
see Singeltary comment ;
 
 
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...
 
 
BSE: TIME TO TAKE H.B. PARRY SERIOUSLY
 
If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...
 
 
Thursday, August 20, 2015 Doctor William J. Hadlow
 
William J. Hadlow Dr. Hadlow (Ohio State ’48), 94, Hamilton, Montana, died June 20, 2015.
 
 
Biological Warfare, or another happenstance of bad luck ???
 
The Alfords believe their son's illness was caused by eating sheep's brains while he was serving in Oman. Medical experts say they don't know the cause. snip... "In June of 2003 they told us he wouldn't see his 25th birthday; then in August they were absolutely certain he wouldn't be here at Christmas.
 
"Here we are at his fourth birthday since he was diagnosed. I'm not ready to say anything about having a fourth Christmas with him, but we're headed in that direction."
 
Alford was assigned to the U.S. Army's 5th Special Forces Group. His illness was chronicled in a front-page story in The Tennessean in November 2003.
 
According to the Creutzfeldt-Jakob Foundation, the incidence of CJD in the United States is one case per 9,000 adults age 55 and older; it occurs much less frequently in people 30 and younger.
 
The disease can be contracted by contamination during surgery or inherited at birth, but 85 percent of cases are of the "sporadic" variety, meaning the cause for the disease is unknown, the CJD Foundation reported. That's the case in Alford's situation.
 
Because he was so well traveled as a Special Forces soldier, his family said he may have eaten contaminated beef in England, where more than 125 persons have contracted the disease after eating beef from cows that were fed products rendered from scrapie-infected sheep. Scrapie is a form of a brain disorder found in sheep.
 
The soldier also told his family that in 2001 he ate a sheep's brain while stationed in Oman. However, while the disease is linked to cattle that have eaten sheep-byproducts, there has been no evidence of direct transfer from sheep to humans, according to the CJD Foundation.
 
 
At the time of infection, it is believed that Jamie contracted it from eating sheep's brain with tribesmen in Oman. This was something that he HAD to do in order to win the respect of the Omani tribesmen. Oman is a key territory in the War on Terror.
 
 
 
Saturday, April 23, 2016
 
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
 
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
 
 
Friday, April 22, 2016
 
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
 
 
Thursday, March 31, 2016
 
*** Chronic Wasting Disease CWD TSE Prion Roundup USA 2016 ***
 
 
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
 
 
now think iatrogenic potential from all of the above, not a pleasant thought. ...
 
kindest regards, terry
 
 
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518 flounder9@verizon.net
 

Links to this post:

Create a Link

<< Home