2010 10 August 2010 -A report of SEAC’s 17 June discussion about a risk assessment on Drayton farm, Warwickshire is available.
Spongiform Encephalopathy Advisory Committee
JOINT MEETING OF UK TSE COMMITTEES, 17th JUNE 2010. SUMMARY
Horizon scanning
The Committee Chairs identified the main issues they would be dealing with as follows:
ACDP TSE Working Group
• Infection control guidance is under constant review.
• Much progress has been made in making endoscopy safer through development of less invasive approaches and techniques to reduce risk of potential contamination, but more remains to be done.
• Work is beginning with surgeons on risk reduction in relation to other invasive procedures where instruments are difficult to decontaminate. Advisory Committee on Decontamination Science & Technology
• Quality assurance for decontamination procedures.
• Ways of keeping used surgical instruments wet/damp to maximise removal of protein.
• Introduction of anti-prion agents into validated decontamination cycles. Manufacturers need to know what is required and Trusts need to recognise vCJD transmission risks from conventionally decontaminated surgical instruments.
• Ways of minimising the number of discarded endoscopes and other instruments. Advisory Committee on the Safety of Blood Tissues and Organs
• Risk assessment and risk management of a wide spectrum of issues from blood to liver transplantation.
• Achieving a more consistent approach to consent for blood transfusion across the UK following the recent public consultation. Spongiform Encephalopathy Advisory Committee
• Obtaining more data on vCJD prevalence.
• Preventing new TSE epidemics.
• Ensuring that cost saving measures do not result in prevention of TSE transmission being compromised. CJD Incidents Panel
• Applying new prevalence data when available.
• Engagement of people who need to change practice on the ground.
• Coping with changes caused by cost pressures.
Conclusions
It was agreed that the presentations/discussions had achieved an interesting and useful day for participants. Whilst the purpose of the meeting was not necessarily to reach conclusions or provide advice for Government, there was consensus on the following:
• The TSE committees work well together.
• Advice should continue to be based on the available scientific evidence.
• Infection control and decontamination practice had improved widely as a result of the work on prevention of TSE
http://www.seac.gov.uk/summaries/tse-meeting-summary.pdf
10 August 2010 - A report of the 17th June 2010 Joint Meeting of the UK Committees (the Advisory Committee on Dangerous Pathogens TSE Working Group, the Advisory Committee on Decontamination Science and Technology, the Advisory Committee on the Safety of Blood Tissues and Organs, the CJD Incidents Panel and SEAC) that advise Government on TSEs is available.
2010
RESIDUAL TSE RISK AT DRAYTON FARM
Drayton farm (in Warwickshire) has been a site of research projects involving experimentally infected TSE animals. Due to the long incubation periods and on site farm bio-security, the animals were kept such that they had access to pasture for most of the year. Infected animals were allowed to graze on pasture and pasture contamination from infected grazing animals contributes to the potential TSE risk of infection for the farm.
The experiments at Drayton have now ended and Defra asked the Veterinary Laboratories Agency to perform a quantitative risk assessment on the residual risks associated with the land where infected animals grazed, or were subject to composted manure or the release of wastewater. This work is of wider interest than just Drayton farm as there are several farms in the UK where such experimentally infected animals were kept.
Defra and the Devolved Administrations asked the advice of SEAC on the risk assessment.
SEAC considered this on 17 June 2010 in London.
Further background material on this subject can be found at:
http://randd.defra.gov.uk/Default.aspx?Menu=Menu&Module=More&Location=None&ProjectID=16637&FromSearch=Y&Publisher=1&SearchText=SE0256&SortString=ProjectCode&SortOrder=Asc&Paging=10#Description
http://www.seac.gov.uk/papers/drayton-background.pdf
Spongiform Encephalopathy Advisory Committee
17 JUNE 2010.
Drayton Farm Risk Assessment
The Committee was presented with a Risk Assessment prepared by the Veterinary Laboratories Agency, which assesses the residual TSE risk at Drayton Farm due to the presence of experimental animals and field cases on the site, and the land spreading of composted manure and wastewater. SEAC last considered this issue at its 53rd Meeting on 21-22 September 1998.
Several Members commented that the methodology of the Risk Assessment was sound. However, concerns were raised that some of the specific input values to the risk assessment are problematic because of the large number of assumptions on which these are based.
A Member suggested that the outputs of the Risk Assessment needed to be checked against the available data to ascertain whether these were consistent. For example, there are data from Iceland and the Ripley flock which clearly show that there is a risk from re-introducing livestock onto land which has previously held a scrapie infected flock. This should have raised questions in the minds of the authors about why the model comes out with a very low risk.
Additionally, a Member suggested that more consideration should be given to whether the theoretical assumptions based on regulations, actually correlate with the real life activity on the farm.
A Member noted that the Risk Assessment adds little to SEAC’s previous advice on this issue provided in 1998, and the Chair stated that because there are no additional data available, it is difficult for SEAC to update its previous advice on this issue.
The Committee agreed that:
• The methodology of the Risk Assessment is sound; however:
• there are serious problems with the input assumption to the model, given the lack of data;
• The outputs of the model are therefore uncertain; and
• There is no need to revise SEAC’s advice of 21-22 September 1998. Extract from Minutes of SEAC 53, 21/22 September 1998.
Item 9 - Disposal of excreta from cattle experimentally infected with BSE (paper SEAC 53/6)
42. The Committee had previously considered options for disposal of waste from cattle exposed to BSE in January 1998. Members had before them paper SEAC 53/6 providing details of possible disposal options for excreta from two long term experiments which were starting at Drayton Experimental Husbandry Farm. Alternative measures to incineration had been examined due to the practical and cost problems of pursuing this option for such a long period. Further information about the farm and methods of disposal which would comply with Good Agricultural Practice were provided. The key change was the proposal to utilise crops from the farm and the Committee were asked to note the concerns of a neighbouring farmer with a watercourse on his property which ran through the experimental farm about possible run off.
43. The Committee noted that the animals were being held in brand new buildings and that there were arrangements for separation of solid and liquid waste. The housing arrangements and husbandry procedures would ensure rigorous separation of the different groups of animals. It was reported that the Committee’s views would be applied to disposal arrangements for excreta from the sheep experimentally exposed to BSE at the Institute for Animal Health.
44. The Committee confirmed their previous advice that the waste from challenged animals should be incinerated for the first 28 days (which represented an extended “safe” clearance time from cattle intestines) and that, thereafter, the excreta should be composted for one year. They agreed that there was no scientific basis why composted material should not be spread on land as fertiliser prior to planting crops which could then be used for human consumption or animal feed, although coppicing may present the most desirable option from the point of view of public perception. However, the Committee felt it would be prudent not to spread the material on pasture which would be grazed by cattle, and that the experimental animals which were part of the cattle bioassay experiment should not be given the food from the farm. This was in order to prevent any future challenge of a positive result that contaminated food may have been a route of exposure which might lead to a consequent claim that the tissue being assayed was not really positive.
http://www.seac.gov.uk/papers/drayton-report.pdf
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
T.A. Nichols,1,2 Bruce Pulford,1 A. Christy Wyckoff,1,2 Crystal Meyerett,1 Brady Michel,1 Kevin Gertig,3 Edward A. Hoover,1 Jean E. Jewell,4 Glenn C. Telling5 and Mark D. Zabel1,*
1Department of Microbiology, Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort Collins, CO USA; 2National Wildlife Research Center; Wildlife Services; United States Department of Agriculture; Fort Collins, CO USA; 3Fort Collins Utilities; Fort Collins; CO USA; 4Department of Veterinary Sciences; Wyoming State Veterinary Laboratory; University of Wyoming; Laramie, WY USA; 5Department of Microbiology, Immunology, Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky; Lexington, KY USA Key words: prions, chronic wasting disease, water, environment, serial protein misfolding cyclic amplification Abbreviations: CWD, chronic wasting disease; sPMCA, serial protein misfolding cyclic amplification; PrPC, cellular prion protein; PrPSc, disease-related, misfolded murine PrP; PrPCWD, disease-related, misfolded cervid PrP; PrPRES, protease-resistant PrP; FCWTF, Fort Collins water treatment facility
Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Although the exact mode of natural transmission remains unknown, substantial evidence suggests that prions can persist in the environment, implicating components thereof as potential prion reservoirs and transmission vehicles.1-4 CWD-positive animals may contribute to environmental prion load via decomposing carcasses and biological materials including saliva, blood, urine and feces.5-7 Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in soil and water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify a 1.3 x 10-7 dilution of CWD-infected brain homogenate spiked into water samples, equivalent to approximately 5 x 107 protease resistant cervid prion protein (PrPCWD) monomers. We also detected PrPCWD in one of two environmental water samples from a CWD endemic area collected at a time of increased water runoff from melting winter snow pack, as well as in water samples obtained concurrently from the flocculation stage of water processing by the municipal water treatment facility. Bioassays indicated that the PrPCWD detected was below infectious levels. These data demonstrate detection of very low levels of PrPCWD in the environment by sPMCA and suggest persistence and accumulation of prions in the environment that may promote CWD transmission.
snip...
CWD has been endemic in the area for forty years, and it remains unclear how long prions can persist in the environment. If persistent for at least several years, CWD prions deposited into the environment from thousands of infected carcasses may accumulate on soil and vegetation such that it can be washed into surface water draining the basin during snowmelt or rainstorms. Symptomatic and asymptomatic positive animals can also contribute to environmental CWD load via biological materials such as saliva, blood, urine and feces.5-7,32,36,38 Deer and elk defecate approximately 900,000 kg of feces and urinate approximately 14 million liters of urine in the area immediately surrounding the Cache la Poudre river per year.39-42 Although urine and feces likely contain much lower prion loads than blood or saliva, the sheer amount of excreta may contribute significantly to overall environmental prion contamination. The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.
see full text ;
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf
Wednesday, October 14, 2009
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html
Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
The L-type BSE prion is much more virulent in primates and in humanized mice than is the classical BSE prion, which suggests the possibility of zoonotic risk associated with the L-type BSE prion. These findings emphasize the critical importance of understanding tissue distribution of L-type BSE prions in cattle because, among the current administrative measures for BSE controls, the specified risk materials removal policy plays a crucial role in consumer protection.
In Japan, atypical BSE was detected in an aged Japanese Black cow (BSE/JP24) (8). We recently reported the successful transmission of BSE/JP24 prions to cattle and showed that the characteristics of these prions closely resemble those of L-type BSE prions found in Italy (9). In this study, we report the peripheral distribution of L-type BSE prions in experimentally challenged cattle.
http://www.cdc.gov/EID/content/16/7/1151.htm
Thursday, August 12, 2010
Seven main threats for the future linked to prions
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
Showing posts with label BSE. Show all posts
Showing posts with label BSE. Show all posts
Thursday, August 12, 2010
Thursday, February 4, 2010
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft Minutes of the 103rd Meeting held on 24th November 2009
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft Minutes of the 103rd Meeting held on 24th November 2009
snip...
ITEM 4 – UPDATE ON CJD EPIDEMIOLOGY
11. Professor Richard Knight (National CJD Surveillance Unit) provided the Committee with the latest figures for the number of clinical vCJD and sporadic CJD (sCJD) cases. To date there had been 170 definite or probable clinical cases of vCJD in the UK - 167 from probable dietary infection with BSE and three from probable vCJD infection via transfusion of blood from donors who later developed vCJD. Of the 150 cases tested all were codon 129MM. Four cases are still alive. The number of deaths from vCJD peaked at 28 in 2000 and had since declined with two known deaths so far in 2009. The median age of death is 30 years of age.
12. Professor Knight explained that elsewhere in the world 47 clinical vCJD cases have been reported with 25 in France, five in Spain, four in the Republic of Ireland, three in both the USA and the Netherlands, two in Portugal and Italy and single cases in Canada, Saudi Arabia and Japan. Infection was presumed to have occurred in the UK in respect of two Irish and two USA cases, one French case, one Japanese case and one Canadian case.
13. Professor Knight explained that one MV genotype case had been classified as possible vCJD as clinical features were consistent with the disease. However, it had not been possible to undertake neuropathological examination post mortem so the diagnosis could not be confirmed. The clinical profile of this MV case was consistent with that observed for MM cases.
14. Professor Knight summarised data on sCJD cases stating that from May 1990 to September 2009, 1080 cases of sCJD had been identified in the UK with a mean age at death of 67 years and genotype distribution of 63% MM, 19% MV and 18% VV at codon 129 of the prion protein gene.
15. Professor Knight also provided a brief report on the novel human disease known as Protease-Sensitive Prionopathy (PSPr). The initial eleven cases described by Gambetti2 exhibited a mean age of onset of 62 years and mean disease duration of 20 months. Eight out of ten had a family history of dementia and were codon 129VV. Cases had minimal spongiform change and minimal immunohistochemical stained PrP deposits with distinct patterns in the cortex and cerebellum. Western Blot (WB) also shows a minimal amount of PrPres present. Further studies by Gambetti have now identified codon 129MV and MM cases which have a
longer disease duration and exhibit some PK resistance. The cases did not have clinical profiles typical for sCJD. A UK case and a Dutch case have also been identified, with characteristics not inconsistent with the Gambetti studies.
16. Professor Knight added that due to the unique clinical presentation of the disease it was likely that at least some cases of disease would not be identified for referral, making it hard to obtain complete data on this disease. However, it was likely that a case would be identified as a prion disease at autopsy and the WB currently used would be able to identify the unique profile which categorises this disease. A retrospective review of the NCJDSU brain bank is underway to look for more cases.
17. A Member asked whether the recent review of neuropathology archives in the UK would have identified PSPr. Professor Knight responded that it would be dependent on the type of WB used at the time which is currently not known. The use of appropriate WB methodology would be an issue in accurately identifying the relevant characteristics.
18. One Member was not convinced by the characterisation of this disease, adding that clinical cases classified as Alzheimer’s Disease have shown similar laddering profiles in WB, protease resistant fragments and the presence of abnormal PrP. The disease has, to date, not been shown to be transmissible which means it should not yet be categorised a prion disease under the current terminology.
19. Summing up, the Chair noted that it was clear that more information was required to fully characterise and fill knowledge gaps regarding this disease. It was important that its unique pathology be more widely recognised to enable future diagnosis and enable tissue collection during autopsy procedures. SEAC will keep a watching brief on emerging data which may characterise the disease further.
http://www.seac.gov.uk/minutes/draftminutes103.pdf
>>>12. Professor Knight explained that elsewhere in the world 47 clinical vCJD cases have been reported with 25 in France, five in Spain, four in the Republic of Ireland, three in both the USA and the Netherlands, two in Portugal and Italy and single cases in Canada, Saudi Arabia and Japan. Infection was presumed to have occurred in the UK in respect of two Irish and two USA cases, one French case, one Japanese case and one Canadian case.<<<
>>>Two of the three U.S. cases, two of the four cases from Ireland and the single cases from Canada and Japan were likely exposed to the BSE agent while residing in the United Kingdom. One of the 25 French cases may also have been infected in the United Kingdom.<<<
>>>There has never been a case of vCJD that did not have a history of exposure within a country where the cattle disease, BSE, was occurring.<<<
>>>vCJD Cases Reported in the US Three cases of vCJD have been reported from the United States. By convention, variant CJD cases are ascribed to the country of initial symptom onset, regardless of where the exposure occurred. There is strong evidence that suggests that two of the three cases were exposed to the BSE agent in the United Kingdom and that the third was exposed while living in Saudi Arabia.<<<
http://www.cdc.gov/ncidod/dvrd/vcjd/factsheet_nvcjd.htm
Heaven forbid any human mad cow disease coming from the U.S.A. ???
hmmm, i don't recall any madcows in Saudi Arabia ???
Eurosurveillance, Volume 11, Issue 49, 07 December 2006 Articles Editorial team1
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Citation style for this article: Editorial team. Third case of vCJD reported in the United States. Euro Surveill. 2006;11(49):pii=3091. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3091 Date of submission:
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Third case of vCJD reported in the United States
Editorial Team (eurosurveillance.weekly@hpa.org.uk), Eurosurveillance editorial office
A clinical diagnosis of variant Creutzfeldt Jakob Disease (vCJD) was confirmed after brain biopsy investigations in a United States (US) resident and reported in November [1]. The patient is a young man who grew up in Saudi Arabia and lived in the US since late 2005. Before that he visited the US once in 1989 and several times after 2001. He has never visited any country in Europe or received a blood transfusion nor has he undergone any neurosurgical procedure. This vCJD case is the third in a US resident. The previous two patients both grew up in the United Kingdom (UK), and this is where they were believed to have been infected [2].
In Saudi Arabia, the first and only previous case of vCJD was reported in 2005. This was suspected to be related to consumption of meat contaminated with the prion agent which causes bovine spongiform encephalitis in cattle (BSE). The European Food Safety Authority (http://www.efsa.org) has not published a geographical BSE risk assessment for Saudi Arabia [3] and there have been no cases of BSE in cattle reported by Saudi Arabia to the World Organisation for Animal Health (http://www.oie.int). Although the UK is not the only potential beef exporter to have had a BSE epidemic, it remains plausible, subject to Saudi Arabia's import policy, that contaminated beef was inadvertently imported from the UK to Saudi Arabia in the period before 1996 (when the EU banned the export of UK beef and cattle).
Based on this patient's history, the occurrence of a previously reported case of vCJD in Saudi Arabia, and the expected length of the incubation period for food-related vCJD, the most likely source of infection is thought to be contaminated meat products the patient consumed as a child when living in Saudi Arabia. The patient has no known history of donating blood, and investigations have identified no risk of onwards transmission within the US.
Variant Creutzfeldt-Jakob disease was first identified in the United Kingdom in the mid-1990s. As of November 2006, worldwide there have been 200 vCJD cases: 164 patients in the United Kingdom, 21 in France, four in Ireland, three in the US (including the present case), two in the Netherlands and one each in Canada, Italy, Japan, Portugal, Saudi Arabia and Spain [4]. All patients, except 10 (including the present case) had lived either in the United Kingdom (170 cases) or in France (20 cases). Evidence so far indicates that the most probable source of infection in most cases was consumption of meat products contaminated with the prion agent causing BSE.
References: 1.Centers for Disease Control and Prevention. Confirmed Case of Variant Creutzfeldt Jakob Disease (vCJD) in the United States in a Patient from the Middle East. (http://www.cdc.gov/ncidod/dvrd/vcjd/other/vCJD_112906.htm) 2.Belay ED, Sejvar JJ, Shieh W-J, Wiersma ST, Zou W-Q, Gambetti P, Hunter S, Maddox RA, Crockett L, Zaki SR, Schonberger LB. Variant Creutzfeldt-Jakob disease death, United States. Emerg Infect Dis 2005, 11 (9):1351-1354. 3.European Food Safety Authority . Geographical BSE Risk (GBR) assessments covering 2000-2006. List of countries and their GBR level of risk as assessed by the Scientific Steering Committee and the (EFSA). 1 August 2006. (http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/summary_list_countries.Par.0001.File.dat/GBR_assessments_table_Overview_assessed_countries_2002-2006.pdf) 4.Variant Creuzfeldt-Jakob disease. Current data – December 2006. (http://www.cjd.ed.ac.uk/vcjdworld.htm)
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3091
18.173 page 189
Experimental Challenge of Cattle with H-type and L-type Atypical BSE
A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada
Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.
Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.
Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.
http://www.isid.org/14th_icid/
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
http://www.isid.org/publications/ICID_Archive.shtml
From: xxxx
To: Terry Singeltary
Sent: Saturday, December 05, 2009 9:09 AM
Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'
Your preliminary abstract number: 670
Dear Mr. Singeltary,
On behalf of the Scientific Committee, I am pleased to inform you that your abstract
'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'
WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.
Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.
Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Author: T. Singeltary; Bacliff, TX/US
Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange
This abstract has been ACCEPTED.
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Authors: T. Singeltary; Bacliff, TX/US
Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Body: Background
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and feed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods
12 years independent research of available data
Results
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.
I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion
http://www.isid.org/14th_icid/
http://www.isid.org/publications/ICID_Archive.shtml
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
snip...
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.
Thanks for your interest.''
Best regards,
Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
END...TSS
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
for those interested, please see full text ;
Friday, January 29, 2010 14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)
http://bse-atypical.blogspot.com/2010/01/14th-international-congress-on.html
Monday, February 01, 2010
Import Alert 17-04 BSE CJD HIGH RISK TISSUES, Nutritional Supplements and Cosmetics
http://creutzfeldt-jakob-disease.blogspot.com/2010/02/import-alert-17-04-bse-cjd-high-risk.html
Monday, February 01, 2010
Import Alert 57-20 and 84-03 Human Dura Mater and risk factors there from due to Creutzfeldt Jakob Disease (CJD)
http://creutzfeldt-jakob-disease.blogspot.com/2010/02/import-alert-57-20-and-84-03-human-dura.html
Wednesday, February 3, 2010
Import Alert 62-07 Sygen Injectable (Bovine-Extracted GMI Monosialoganglioside) manufactured from bovine brain starting material
http://bseusa.blogspot.com/2010/02/import-alert-62-07-sygen-injectable.html
Wednesday, February 3, 2010
Import Alert 71-02 Detention Without Physical Examination Of Animal Feeds And Feed Ingredients That May Contain Ingredients Of Animal Origin Import Alert 71-02
http://madcowfeed.blogspot.com/2010/02/import-alert-71-02-detention-without.html
Wednesday, February 3, 2010
Import Alert 99-25 Detention Without Physical Examination of Animal Feed...BSE...and Not the Subject of a Valid USDA Import Permit Import Alert 99-25
http://madcowfeed.blogspot.com/2010/02/import-alert-99-25-detention-without.html
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed
USA sporadic CJD cases rising ;
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
2008
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
CJD USA RISING, with UNKNOWN PHENOTYPE ;
5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
CJD RISING SWITZERLAND
CJD is a predominantly sporadic disorder but can also occur as a dominantly inherited or infective condition. Only one of the 26 most recent confirmed cases was identified as carrying a disease related mutation of the PRNP gene, none had identifiable iatrogenic exposure, and none resembled variant CJD. Thus 25 of the 26 cases appear to be sporadic cases. Sporadic CJD is distributed worldwide with a reported incidence of about one in a million per year. Raised awareness of the disease in recent years could account for an increase in reported cases of CJD, although neither an increase in the average age of patients nor more frequent recognition of CJD amongst residents of nursing homes (where dementing illness is prevalent and misdiagnosis might be expected) were seen in the Swiss cases. Moreover, improved ascertainment as an explanation for the observed increase would imply levels of under-reporting in countries other than Switzerland, which appear implausible. The authors of the Lancet report suggest that the rise in cases might be due to some form of unidentified iatrogenic transmission or to exposure to a zoonotic source of infection, though cases do not resemble variant Creutzfeldt-Jakob disease (vCJD). The ongoing surveillance of CJD in Switzerland and the rest of Europe is essential to monitor the situation to see if this rise is sustained in Switzerland, and if a similar rise occurs in other countries (see http://www.eurocjd.ed.ac.uk).
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=1921
Prion data suggest BSE link to sporadic CJD Declan Butler
Predicting the number of cases of Creutzfeldt–Jakob disease (CJD) in people as a result of transmission of bovine spongiform encephalopathy (BSE) has just got more difficult.Whereas it was thought that BSE only caused a new form of the disease called variant CJD (vCJD), a study in mice from a team led by John Collinge at University College London suggests that it may also cause a disease indistinguishable from the commonest form of classical, or 'sporadic', CJD (E.
http://www.nature.com/nature/journal/v420/n6915/full/420450a.html
IF we look at sporadic incidence of CJD in UK from 1993 to 2003, the incidence rose from 37 in 1993 to 77 in 2003. THIS seems to show an increase to me? I do not understand the statement ;
However, in the period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of U.K. sporadic CJD deaths (52).
IF we go further and look at some of the other documented BSE countries, you will the increase of sporadic CJD there as well ;
Canada from 2 to 25
France from 35 to 108
Germany 21+ to 96
Italy 27 to 76
http://www.eurocjd.ed.ac.uk/sporadic.htm
Switzerland sporadic CJD ;
Swiss rise in CJD raises concerns over possible BSE link [LONDON] THE LANCET
Plaque attack: Swiss patients have spongiform patterns in the brain typical of sporadic CJD. The number of people dying from Creutzfeldt-Jakob disease (CJD) has risen sharply in Switzerland -- sparking fears of a possible link with bovine spongiform encephalopathy (BSE).
BSE is thought to be the cause of a distinctive form of the brain-wasting disease known as variant CJD. The Swiss cases, in contrast, are standard 'sporadic' CJD. Each year between 1997 and 2000, no more than 11 Swiss people developed CJD. But 19 cases were reported in 2001, and seven were recorded in the first quarter of this year. This is some four times higher than the incidence elsewhere, reports a team led by Adriano Aguzzi of the University Hospital Zurich (M. Glatzel et al. Lancet 360, 139-141; 2002).
The increase could be a mere statistical blip, or it may be due to increased awareness of the disease leading to more diagnoses. More disturbing is the possibility that the cases are linked to the consumption of BSE-infected meat products -- which would mean that the BSE agent can cause two distinct forms of CJD.
Possible links between the Swiss CJD cases and BSE will now be explored by strain-typing experiments in which the disease is transmitted to mice. These tests will take at least a year to complete. "It's the best way to establish or exclude any suspected link," says Moira Bruce of the UK Institute for Animal Health's Neuropathogenesis Unit in Edinburgh.
======================================
Experiences in England and Switzerland -- two countries that discovered mad cow disease in their cattle -- have heightened concerns about the possibility some cases of sporadic CJD are due to consuming mad-cow-tainted beef. Both countries have reported increases in sporadic CJD since mad cow was first detected in British herds in 1986.
Switzerland discovered last year its CJD rate was twice that of any other country in the world. Switzerland had been seeing about eight to 11 cases per year from 1997 to 2000. Then the incidence more than doubled, to 19 cases in 2001 and 18 cases in 2002.
http://www.upi.com/view.cfm?StoryID=20030721-102924-4786r
Mouse model sheds new light on human prion disease
snip...
Professor John Collinge said We are not saying that all or even most cases of sporadic CJD are as a result of BSE exposure, but some more recent cases may be the incidence of sporadic CJD has shown an upward trend in the UK over the last decade. While most of this apparent increase may be because doctors are now more aware of CJD and better at diagnosing it, serious consideration should be given to a proportion of this rise being BSE-related. Switzerland, which has had a substantial BSE epidemic, has noted a sharp recent increase in sporadic CJD.
snip...
http://www.mrc.ac.uk/txt/index/public-interest/public-news-4/public-news_archive/public-news-archive_nov_dec_02/public-bse_and_sporadic_cjd.htm
Monday, May 19, 2008
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
http://bseinquiry.blogspot.com/
Sunday, August 10, 2008
A New Prionopathy OR more of the same old BSe and sporadic CJD
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html
Saturday, December 12, 2009
103RD MEETING OF THE SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE
http://seac992007.blogspot.com/2009/12/103rd-meeting-of-spongiform.html
Thursday, January 31, 2008
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 99th meeting held on 14th December 2007
snip...
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION
40. The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base
13 © SEAC 2007
cases in Texas and Alabama, with both scrapie and chronic wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?”
41. A member considered that this question ............
http://www.seac.gov.uk/minutes/99.pdf
http://seac992007.blogspot.com/2008/01/spongiform-encephalopathy-advisory.html
Wednesday, November 18, 2009
R-CALF: 40 Groups Disagree With USDA's Latest BSE Court Submission
http://bse-atypical.blogspot.com/2009/11/r-calf-40-groups-disagree-with-usdas.html
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
Sunday, September 6, 2009
MAD COW USA 1997 SECRET VIDEO
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? see video at bottom
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN see video
http://maddeer.org/video/embedded/prusinerclip.html
Sunday, January 17, 2010
BSE USA feed inspection violations 01/01/2009 to 01/17/2010 FDA BSE/Ruminant Feed Inspections Firms Inventory Report
http://madcowfeed.blogspot.com/2010/01/bse-usa-feed-inspection-violations.html
Tuesday, January 19, 2010
CVM's OR Develops New PCR-Based Method for Testing Animal Feed
http://madcowfeed.blogspot.com/2010/01/cvms-or-develops-new-pcr-based-method.html
Thursday, January 07, 2010
Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008
http://scrapie-usa.blogspot.com/2010/01/scrapie-and-nor-98-scrapie-november.html
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html
TSS
snip...
ITEM 4 – UPDATE ON CJD EPIDEMIOLOGY
11. Professor Richard Knight (National CJD Surveillance Unit) provided the Committee with the latest figures for the number of clinical vCJD and sporadic CJD (sCJD) cases. To date there had been 170 definite or probable clinical cases of vCJD in the UK - 167 from probable dietary infection with BSE and three from probable vCJD infection via transfusion of blood from donors who later developed vCJD. Of the 150 cases tested all were codon 129MM. Four cases are still alive. The number of deaths from vCJD peaked at 28 in 2000 and had since declined with two known deaths so far in 2009. The median age of death is 30 years of age.
12. Professor Knight explained that elsewhere in the world 47 clinical vCJD cases have been reported with 25 in France, five in Spain, four in the Republic of Ireland, three in both the USA and the Netherlands, two in Portugal and Italy and single cases in Canada, Saudi Arabia and Japan. Infection was presumed to have occurred in the UK in respect of two Irish and two USA cases, one French case, one Japanese case and one Canadian case.
13. Professor Knight explained that one MV genotype case had been classified as possible vCJD as clinical features were consistent with the disease. However, it had not been possible to undertake neuropathological examination post mortem so the diagnosis could not be confirmed. The clinical profile of this MV case was consistent with that observed for MM cases.
14. Professor Knight summarised data on sCJD cases stating that from May 1990 to September 2009, 1080 cases of sCJD had been identified in the UK with a mean age at death of 67 years and genotype distribution of 63% MM, 19% MV and 18% VV at codon 129 of the prion protein gene.
15. Professor Knight also provided a brief report on the novel human disease known as Protease-Sensitive Prionopathy (PSPr). The initial eleven cases described by Gambetti2 exhibited a mean age of onset of 62 years and mean disease duration of 20 months. Eight out of ten had a family history of dementia and were codon 129VV. Cases had minimal spongiform change and minimal immunohistochemical stained PrP deposits with distinct patterns in the cortex and cerebellum. Western Blot (WB) also shows a minimal amount of PrPres present. Further studies by Gambetti have now identified codon 129MV and MM cases which have a
longer disease duration and exhibit some PK resistance. The cases did not have clinical profiles typical for sCJD. A UK case and a Dutch case have also been identified, with characteristics not inconsistent with the Gambetti studies.
16. Professor Knight added that due to the unique clinical presentation of the disease it was likely that at least some cases of disease would not be identified for referral, making it hard to obtain complete data on this disease. However, it was likely that a case would be identified as a prion disease at autopsy and the WB currently used would be able to identify the unique profile which categorises this disease. A retrospective review of the NCJDSU brain bank is underway to look for more cases.
17. A Member asked whether the recent review of neuropathology archives in the UK would have identified PSPr. Professor Knight responded that it would be dependent on the type of WB used at the time which is currently not known. The use of appropriate WB methodology would be an issue in accurately identifying the relevant characteristics.
18. One Member was not convinced by the characterisation of this disease, adding that clinical cases classified as Alzheimer’s Disease have shown similar laddering profiles in WB, protease resistant fragments and the presence of abnormal PrP. The disease has, to date, not been shown to be transmissible which means it should not yet be categorised a prion disease under the current terminology.
19. Summing up, the Chair noted that it was clear that more information was required to fully characterise and fill knowledge gaps regarding this disease. It was important that its unique pathology be more widely recognised to enable future diagnosis and enable tissue collection during autopsy procedures. SEAC will keep a watching brief on emerging data which may characterise the disease further.
http://www.seac.gov.uk/minutes/draftminutes103.pdf
>>>12. Professor Knight explained that elsewhere in the world 47 clinical vCJD cases have been reported with 25 in France, five in Spain, four in the Republic of Ireland, three in both the USA and the Netherlands, two in Portugal and Italy and single cases in Canada, Saudi Arabia and Japan. Infection was presumed to have occurred in the UK in respect of two Irish and two USA cases, one French case, one Japanese case and one Canadian case.<<<
>>>Two of the three U.S. cases, two of the four cases from Ireland and the single cases from Canada and Japan were likely exposed to the BSE agent while residing in the United Kingdom. One of the 25 French cases may also have been infected in the United Kingdom.<<<
>>>There has never been a case of vCJD that did not have a history of exposure within a country where the cattle disease, BSE, was occurring.<<<
>>>vCJD Cases Reported in the US Three cases of vCJD have been reported from the United States. By convention, variant CJD cases are ascribed to the country of initial symptom onset, regardless of where the exposure occurred. There is strong evidence that suggests that two of the three cases were exposed to the BSE agent in the United Kingdom and that the third was exposed while living in Saudi Arabia.<<<
http://www.cdc.gov/ncidod/dvrd/vcjd/factsheet_nvcjd.htm
Heaven forbid any human mad cow disease coming from the U.S.A. ???
hmmm, i don't recall any madcows in Saudi Arabia ???
Eurosurveillance, Volume 11, Issue 49, 07 December 2006 Articles Editorial team1
--------------------------------------------------------------------------------
Citation style for this article: Editorial team. Third case of vCJD reported in the United States. Euro Surveill. 2006;11(49):pii=3091. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3091 Date of submission:
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
Third case of vCJD reported in the United States
Editorial Team (eurosurveillance.weekly@hpa.org.uk), Eurosurveillance editorial office
A clinical diagnosis of variant Creutzfeldt Jakob Disease (vCJD) was confirmed after brain biopsy investigations in a United States (US) resident and reported in November [1]. The patient is a young man who grew up in Saudi Arabia and lived in the US since late 2005. Before that he visited the US once in 1989 and several times after 2001. He has never visited any country in Europe or received a blood transfusion nor has he undergone any neurosurgical procedure. This vCJD case is the third in a US resident. The previous two patients both grew up in the United Kingdom (UK), and this is where they were believed to have been infected [2].
In Saudi Arabia, the first and only previous case of vCJD was reported in 2005. This was suspected to be related to consumption of meat contaminated with the prion agent which causes bovine spongiform encephalitis in cattle (BSE). The European Food Safety Authority (http://www.efsa.org) has not published a geographical BSE risk assessment for Saudi Arabia [3] and there have been no cases of BSE in cattle reported by Saudi Arabia to the World Organisation for Animal Health (http://www.oie.int). Although the UK is not the only potential beef exporter to have had a BSE epidemic, it remains plausible, subject to Saudi Arabia's import policy, that contaminated beef was inadvertently imported from the UK to Saudi Arabia in the period before 1996 (when the EU banned the export of UK beef and cattle).
Based on this patient's history, the occurrence of a previously reported case of vCJD in Saudi Arabia, and the expected length of the incubation period for food-related vCJD, the most likely source of infection is thought to be contaminated meat products the patient consumed as a child when living in Saudi Arabia. The patient has no known history of donating blood, and investigations have identified no risk of onwards transmission within the US.
Variant Creutzfeldt-Jakob disease was first identified in the United Kingdom in the mid-1990s. As of November 2006, worldwide there have been 200 vCJD cases: 164 patients in the United Kingdom, 21 in France, four in Ireland, three in the US (including the present case), two in the Netherlands and one each in Canada, Italy, Japan, Portugal, Saudi Arabia and Spain [4]. All patients, except 10 (including the present case) had lived either in the United Kingdom (170 cases) or in France (20 cases). Evidence so far indicates that the most probable source of infection in most cases was consumption of meat products contaminated with the prion agent causing BSE.
References: 1.Centers for Disease Control and Prevention. Confirmed Case of Variant Creutzfeldt Jakob Disease (vCJD) in the United States in a Patient from the Middle East. (http://www.cdc.gov/ncidod/dvrd/vcjd/other/vCJD_112906.htm) 2.Belay ED, Sejvar JJ, Shieh W-J, Wiersma ST, Zou W-Q, Gambetti P, Hunter S, Maddox RA, Crockett L, Zaki SR, Schonberger LB. Variant Creutzfeldt-Jakob disease death, United States. Emerg Infect Dis 2005, 11 (9):1351-1354. 3.European Food Safety Authority . Geographical BSE Risk (GBR) assessments covering 2000-2006. List of countries and their GBR level of risk as assessed by the Scientific Steering Committee and the (EFSA). 1 August 2006. (http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/summary_list_countries.Par.0001.File.dat/GBR_assessments_table_Overview_assessed_countries_2002-2006.pdf) 4.Variant Creuzfeldt-Jakob disease. Current data – December 2006. (http://www.cjd.ed.ac.uk/vcjdworld.htm)
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3091
18.173 page 189
Experimental Challenge of Cattle with H-type and L-type Atypical BSE
A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada
Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.
Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.
Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.
http://www.isid.org/14th_icid/
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
http://www.isid.org/publications/ICID_Archive.shtml
From: xxxx
To: Terry Singeltary
Sent: Saturday, December 05, 2009 9:09 AM
Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'
Your preliminary abstract number: 670
Dear Mr. Singeltary,
On behalf of the Scientific Committee, I am pleased to inform you that your abstract
'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'
WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.
Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.
Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Author: T. Singeltary; Bacliff, TX/US
Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange
This abstract has been ACCEPTED.
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Authors: T. Singeltary; Bacliff, TX/US
Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Body: Background
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and feed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods
12 years independent research of available data
Results
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.
I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion
http://www.isid.org/14th_icid/
http://www.isid.org/publications/ICID_Archive.shtml
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
snip...
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.
Thanks for your interest.''
Best regards,
Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
END...TSS
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
for those interested, please see full text ;
Friday, January 29, 2010 14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)
http://bse-atypical.blogspot.com/2010/01/14th-international-congress-on.html
Monday, February 01, 2010
Import Alert 17-04 BSE CJD HIGH RISK TISSUES, Nutritional Supplements and Cosmetics
http://creutzfeldt-jakob-disease.blogspot.com/2010/02/import-alert-17-04-bse-cjd-high-risk.html
Monday, February 01, 2010
Import Alert 57-20 and 84-03 Human Dura Mater and risk factors there from due to Creutzfeldt Jakob Disease (CJD)
http://creutzfeldt-jakob-disease.blogspot.com/2010/02/import-alert-57-20-and-84-03-human-dura.html
Wednesday, February 3, 2010
Import Alert 62-07 Sygen Injectable (Bovine-Extracted GMI Monosialoganglioside) manufactured from bovine brain starting material
http://bseusa.blogspot.com/2010/02/import-alert-62-07-sygen-injectable.html
Wednesday, February 3, 2010
Import Alert 71-02 Detention Without Physical Examination Of Animal Feeds And Feed Ingredients That May Contain Ingredients Of Animal Origin Import Alert 71-02
http://madcowfeed.blogspot.com/2010/02/import-alert-71-02-detention-without.html
Wednesday, February 3, 2010
Import Alert 99-25 Detention Without Physical Examination of Animal Feed...BSE...and Not the Subject of a Valid USDA Import Permit Import Alert 99-25
http://madcowfeed.blogspot.com/2010/02/import-alert-99-25-detention-without.html
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed
USA sporadic CJD cases rising ;
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
2008
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
CJD USA RISING, with UNKNOWN PHENOTYPE ;
5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
CJD RISING SWITZERLAND
CJD is a predominantly sporadic disorder but can also occur as a dominantly inherited or infective condition. Only one of the 26 most recent confirmed cases was identified as carrying a disease related mutation of the PRNP gene, none had identifiable iatrogenic exposure, and none resembled variant CJD. Thus 25 of the 26 cases appear to be sporadic cases. Sporadic CJD is distributed worldwide with a reported incidence of about one in a million per year. Raised awareness of the disease in recent years could account for an increase in reported cases of CJD, although neither an increase in the average age of patients nor more frequent recognition of CJD amongst residents of nursing homes (where dementing illness is prevalent and misdiagnosis might be expected) were seen in the Swiss cases. Moreover, improved ascertainment as an explanation for the observed increase would imply levels of under-reporting in countries other than Switzerland, which appear implausible. The authors of the Lancet report suggest that the rise in cases might be due to some form of unidentified iatrogenic transmission or to exposure to a zoonotic source of infection, though cases do not resemble variant Creutzfeldt-Jakob disease (vCJD). The ongoing surveillance of CJD in Switzerland and the rest of Europe is essential to monitor the situation to see if this rise is sustained in Switzerland, and if a similar rise occurs in other countries (see http://www.eurocjd.ed.ac.uk).
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=1921
Prion data suggest BSE link to sporadic CJD Declan Butler
Predicting the number of cases of Creutzfeldt–Jakob disease (CJD) in people as a result of transmission of bovine spongiform encephalopathy (BSE) has just got more difficult.Whereas it was thought that BSE only caused a new form of the disease called variant CJD (vCJD), a study in mice from a team led by John Collinge at University College London suggests that it may also cause a disease indistinguishable from the commonest form of classical, or 'sporadic', CJD (E.
http://www.nature.com/nature/journal/v420/n6915/full/420450a.html
IF we look at sporadic incidence of CJD in UK from 1993 to 2003, the incidence rose from 37 in 1993 to 77 in 2003. THIS seems to show an increase to me? I do not understand the statement ;
However, in the period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of U.K. sporadic CJD deaths (52).
IF we go further and look at some of the other documented BSE countries, you will the increase of sporadic CJD there as well ;
Canada from 2 to 25
France from 35 to 108
Germany 21+ to 96
Italy 27 to 76
http://www.eurocjd.ed.ac.uk/sporadic.htm
Switzerland sporadic CJD ;
Swiss rise in CJD raises concerns over possible BSE link [LONDON] THE LANCET
Plaque attack: Swiss patients have spongiform patterns in the brain typical of sporadic CJD. The number of people dying from Creutzfeldt-Jakob disease (CJD) has risen sharply in Switzerland -- sparking fears of a possible link with bovine spongiform encephalopathy (BSE).
BSE is thought to be the cause of a distinctive form of the brain-wasting disease known as variant CJD. The Swiss cases, in contrast, are standard 'sporadic' CJD. Each year between 1997 and 2000, no more than 11 Swiss people developed CJD. But 19 cases were reported in 2001, and seven were recorded in the first quarter of this year. This is some four times higher than the incidence elsewhere, reports a team led by Adriano Aguzzi of the University Hospital Zurich (M. Glatzel et al. Lancet 360, 139-141; 2002).
The increase could be a mere statistical blip, or it may be due to increased awareness of the disease leading to more diagnoses. More disturbing is the possibility that the cases are linked to the consumption of BSE-infected meat products -- which would mean that the BSE agent can cause two distinct forms of CJD.
Possible links between the Swiss CJD cases and BSE will now be explored by strain-typing experiments in which the disease is transmitted to mice. These tests will take at least a year to complete. "It's the best way to establish or exclude any suspected link," says Moira Bruce of the UK Institute for Animal Health's Neuropathogenesis Unit in Edinburgh.
======================================
Experiences in England and Switzerland -- two countries that discovered mad cow disease in their cattle -- have heightened concerns about the possibility some cases of sporadic CJD are due to consuming mad-cow-tainted beef. Both countries have reported increases in sporadic CJD since mad cow was first detected in British herds in 1986.
Switzerland discovered last year its CJD rate was twice that of any other country in the world. Switzerland had been seeing about eight to 11 cases per year from 1997 to 2000. Then the incidence more than doubled, to 19 cases in 2001 and 18 cases in 2002.
http://www.upi.com/view.cfm?StoryID=20030721-102924-4786r
Mouse model sheds new light on human prion disease
snip...
Professor John Collinge said We are not saying that all or even most cases of sporadic CJD are as a result of BSE exposure, but some more recent cases may be the incidence of sporadic CJD has shown an upward trend in the UK over the last decade. While most of this apparent increase may be because doctors are now more aware of CJD and better at diagnosing it, serious consideration should be given to a proportion of this rise being BSE-related. Switzerland, which has had a substantial BSE epidemic, has noted a sharp recent increase in sporadic CJD.
snip...
http://www.mrc.ac.uk/txt/index/public-interest/public-news-4/public-news_archive/public-news-archive_nov_dec_02/public-bse_and_sporadic_cjd.htm
Monday, May 19, 2008
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
http://bseinquiry.blogspot.com/
Sunday, August 10, 2008
A New Prionopathy OR more of the same old BSe and sporadic CJD
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html
Saturday, December 12, 2009
103RD MEETING OF THE SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE
http://seac992007.blogspot.com/2009/12/103rd-meeting-of-spongiform.html
Thursday, January 31, 2008
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 99th meeting held on 14th December 2007
snip...
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION
40. The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base
13 © SEAC 2007
cases in Texas and Alabama, with both scrapie and chronic wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?”
41. A member considered that this question ............
http://www.seac.gov.uk/minutes/99.pdf
http://seac992007.blogspot.com/2008/01/spongiform-encephalopathy-advisory.html
Wednesday, November 18, 2009
R-CALF: 40 Groups Disagree With USDA's Latest BSE Court Submission
http://bse-atypical.blogspot.com/2009/11/r-calf-40-groups-disagree-with-usdas.html
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
Sunday, September 6, 2009
MAD COW USA 1997 SECRET VIDEO
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? see video at bottom
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN see video
http://maddeer.org/video/embedded/prusinerclip.html
Sunday, January 17, 2010
BSE USA feed inspection violations 01/01/2009 to 01/17/2010 FDA BSE/Ruminant Feed Inspections Firms Inventory Report
http://madcowfeed.blogspot.com/2010/01/bse-usa-feed-inspection-violations.html
Tuesday, January 19, 2010
CVM's OR Develops New PCR-Based Method for Testing Animal Feed
http://madcowfeed.blogspot.com/2010/01/cvms-or-develops-new-pcr-based-method.html
Thursday, January 07, 2010
Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008
http://scrapie-usa.blogspot.com/2010/01/scrapie-and-nor-98-scrapie-november.html
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html
TSS
Saturday, October 24, 2009
SaBTO Advisory Committee on the Safety of Blood, Tissues and Organs 2nd Public Meeting 27 October 2009
SaBTO
Advisory Committee on the Safety of Blood, Tissues and Organs
2nd Public Meeting
“Blood Donation – Selection, Deferral and Exclusion”
27 October 2009
Royal Horticultural Halls, London SW1P
At their inaugural meeting in January 2008, members of SaBTO decided that a public meeting should be held every year, focusing on a particular issue within the committee’s remit. The 2009 Public Meeting will focus on the issue of donor selection. Selection of donors is key to the delivery of a safe blood supply. Many prospective donors may be turned down for a variety of reasons, including age, sexual history and medical concerns. As a scientific advisory committee, SaBTO is concerned that exclusion or deferral of prospective blood donors is done for justifiable reasons and in the best interests of blood recipients.
The format of the afternoon will include an introduction to SaBTO and donor selection, and an open forum with the opportunity for the audience to comment and ask questions.
The committee hopes that the audience will reflect a wide range of stakeholders and interest groups. Should the event be oversubscribed, there will be a limit of one delegate per organisation. If you are interested in attending. please e-mail SaBTO@dh.gsi.gov.uk or telephone 020 7972 4750 by 13 October 2009 (this deadline has been extended). Please note that this event is free of charge for all delegates.
The Advisory Committee on the Safety of Blood, Tissues, and Organs (SaBTO) is a Non-Departmental Public Body, with an independent Chair and members selected by the Appointments Commission for their specific areas of expertise. SaBTO provides independent advice to the UK Government and the Devolved Administrations on the most appropriate ways to ensure the safety of blood, cells, tissues, and organs for transfusion/transplantation. SaBTO also provides advice on the microbiological safety of gametes and stem cells, and considers both risk assessment and risk management options for Ministers and UK Health Departments to consider.
Further detailed information about SaBTO and its remit can be found at
http://www.dh.gov.uk/ab/SaBTO/index.htm
http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@dh/@ab/documents/digitalasset/dh_104789.pdf
see other SaBTO meetings minutes here ;
2009 Download summary of seventh meeting, 14-15 July 2009 (PDF, 65K)
Download minutes of sixth meeting, 28 April 2009 (PDF, 104K)
Download summary of sixth meeting, 28 April 2009 (PDF, 64K)
Download minutes of fifth meeting, 20 January 2009 (PDF, 102K)
Download agenda for the fifth meeting, 20 January 2009 (PDF, 15K)
2008
snip...end
http://www.dh.gov.uk/ab/SaBTO/DH_089412
Tuesday, November 11, 2008 SaBTO Summary of 1st Public Meeting – variant CJD and blood Tuesday 21st October 2008, 2pm-4pm
http://vcjdblood.blogspot.com/2008/11/sabto-summary-of-1st-public-meeting.html
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007
snip...
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION 40.
The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base cases in Texas and Alabama, with both scrapie and chronic 14 © SEAC 2007 wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?” 41.
A member considered that this question appeared to be primarily related to possible links between animal and human TSEs in the USA.
There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA. Current evidence does not suggest that CWD is a significant risk to human health. There are unpublished data from a case of human TSE in the USA that are suggestive of an apparently novel form of prion disease with distinct molecular characteristics. However, it is unclear whether the case had been further characterised, if it could be linked to animal TSEs or if other similar cases had been found in the USA or elsewhere. In relation to the possible public health implications of atypical scrapie, H-type BSE and CWD, research was being conducted to investigate possible links and surveillance was in place to detect any changes in human TSEs. Although possible links between these diseases and human TSEs are of concern and require research, there is no evidence to suggest immediate public health action is warranted. The possible human health risks from classical scrapie had been discussed earlier in the meeting. Members noted that there are effective channels of discussion and collaboration on research between USA and European groups. Members agreed it is important to keep a watching brief on new developments on TSEs.
snip...
http://www.seac.gov.uk/minutes/99.pdf
http://seac992007.blogspot.com/2008/07/seac-draft-minutes-of-100th-meeting.html
http://seac992007.blogspot.com/
>>>There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA.<<<
10 people killed by new CJD-like disease
Public release date: 9-Jul-2008 [ Print Article E-mail Article Close Window ]
Contact: Claire Bowles mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000076/!x-usc:mailto:claire.bowles@rbi.co.uk 44-207-611-1210 New Scientist
10 people killed by new CJD-like disease A NEW form of fatal dementia has been discovered in 16 Americans, 10 of whom have already died of the condition. It resembles Creutzfeldt-Jakob disease - with patients gradually losing their ability to think, speak and move - but has features that make it distinct from known forms of CJD.
No one yet knows how the disease originates, or under what conditions it might spread. Nor is it clear how many people have the condition. "I believe the disease has been around for many years, unnoticed," says Pierluigi Gambetti, director of the US National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, Ohio. Cases may previously have been mistaken for other forms of dementia.
Since Gambetti's team wrote a paper describing an initial 11 cases referred to his centre between 2002 and 2006 (Annals of Neurology, vol 63, p 697), another five have come to light. "So it is possible that it could be just the tip of the iceberg," Gambetti says.
snip... see full text ;
http://www.eurekalert.org/pub_releases/2008-07/ns-tpk070908.php
Thursday, July 10, 2008
A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html
Thursday, July 10, 2008
A New Prionopathy update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html
Communicated by: Terry S. Singeltary Sr. <:flounder9@verizon.net>
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html
http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
2008
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
Friday, October 23, 2009
Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008
http://cjdtexas.blogspot.com/2009/10/creutzfeldt-jakob-disease-surveillance.html
O.2.2
vCJD infection in an asymptomatic UK haemophilic patient
Alexander Peden1, Graham Fairfoul1, Suzanne Lowrie1, Linda McCardle1, Mark Head1, Seth Love2, Hester Ward1, Simon Cousens3, David Keeling4, Carolyn Millar5, FGH Hill6, James Ironside1 1University of Edinburgh, UK; 2Frenchay Hospital, Bristol, UK; 3London School of Hygiene and Tropical Medicine, UK; 4Churchill Hospital, Oxford, UK; 5Imperial College London, UK; 6Birmingham Children’s Hospital, Birmingham, UK
We describe a study of 17 UK patients with haemophilia considered to be at increased risk of vCJD through exposure to UK plasma products. 10 autopsy cases and 7 biopsy cases were analysed for disease- associated, protease-resistant prion protein (PrPres). The tissues available from each case were variable, ranging from a single biopsy sample to a wide range of autopsy tissues. A single specimen from the spleen of one autopsy case gave a strong positive result on repeated testing for PrPres by Western blot analysis. This tissue came from a 73 year-old male with no history of neurological disease, who was heterozygous (methionine/valine) at codon 129 in the prion protein gene. He had received over 9,000 units of Factor VIII concentrate prepared from plasma pools known to include donations from a vCJD-infected donor, and some 400,000 units not known to include donations from vCJD-infected donors. He had also received 14 units of red blood cells and had undergone several surgical and invasive endoscopic procedures. Estimates of the relative risks of exposure though diet, surgery, endoscopy, blood transfusion and receipt of UK plasma products suggest that by far the most likely route of infection was receipt of UK plasma products.
O.2.3
Detection of prion particles in body fluids of humans and animals
Detlev Riesner Institut fur Physikalische Biologie, Heinrich-Heine- Universitat Dusseldorf, Germany
A major structural difference between the cellular isoform of the prion protein PrPC and the pathogenic isoform PrPSc is the much higher state of molecular aggregation of PrPSc. PK-resistance as normally used for PrPSc-characterization is not reliably valid for all species, strains and sources of prions. The method of suface-FIDA (fluorescence-intensity distribution analysis) was developed avoiding PK-digestion and detecting specifically disease related PrP-aggregates (Birkmann et al 2007, J. Vet. Microbiol 123, 294-304). After partial purification PrP-aggregates are bound to a chip covered with the captureantibody SAF32, labeled with two types of antibodies against two different epitopes and carrying two different fluorescent dyes. A dual-color laser beam is scanning the chip surface, and the fluorescence signals are evaluated in respect to local coincidence, intensities and particle size. The method was applied to brain homogenate of sCJD-victims (post mortem), to CSF-samples of BSE-afflicted cattle (ante mortem) and blood plasma of scrapie sheep (ante mortem). Particles of PrP-aggregates could be detected in all samples, exhibiting a diameter range of 300 nm (optical resolution) to 1ƒÊm. PrP-aggregates were detected with 100% sensitivity in the sCJD-brain homogenate samples; studies on CSF are ongoing. PrP-aggregates were detected in CSF of BSE-cattle, but the number of samples was too little to evaluate the sensitivity. Only one antibody was available to detect scrapie-PrP-aggregates from blood plasma; the sensitivity of 60% will be improved in the ongoing experiments with a second antibody. PrP-aggregates can be used as seeds for fibril formation with recombinant PrP as template (Stohr et al., 2008, PNAS 105, 2409-14). This system will be used as amplification of the particle detection method.
O.2.4
Detection of prions in blood leucocytes
Linda A. Terry, Laurence Howells, Jeremy Hawthorn, Sally Everest, Sarah Jo Moore, Jane C. Edwards Veterinary Laboratories Agency, UK
Background: Infected human blood has been implicated in the iatrogenic transmission of vCJD in four reported cases. Experimental transmission studies have demonstrated that blood from scrapie and BSE infected sheep also contains infectivity. Rodent models of prion disease implicated both cellular and plasma fractions. However, direct detection of PrPsc from blood in the absence of in vitro amplification or bioassay has proved difficult. Methods for the direct detection of PrPsc in blood would be advantageous for the study of the pathogenesis of TSEs and as a basis for a blood test. Objectives: To develop a method for the direct detection of PrPsc in blood cells from scrapie and BSE infected sheep; to study the temporal distribution of PrPsc in blood and to determine the identity of the cells bearing prions in blood. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from sheep naturally infected with scrapie or experimentally infected with BSE at the clinical stage of disease and from scrapie infected sheep from 3 months of age through to clinical end-point. PBMCs were tested for PrPsc content by a direct immunoassay based on the IDEXX CWD HerdChek kit. Different subsets of PBMCs were isolated by subset specific cell surface markers and magnetic bead separation and analysed for PrPsc content. Results: PrPSc was detected in 54% of sheep with clinical scrapie and 71% of sheep with clinical BSE. A longitudinal study of the temporal distribution of blood PBMC associated PrPsc showed that the detection rate increases during the course of disease and is more likely to be observed during the second half of the incubation period. Additionally detection is more likely in scrapie infected sheep if they carry the PRNP genotype of VRQ/VRQ. Cell separation studies showed that the PrPsc is associated with a specific cell subset implicating a subset of B lymphocytes. Discussion. This is the first report of the direct detection of PrPsc in cells isolated from sheep blood in the absence of in vitro amplification or bioassay. Since PrPsc can be detected from as early as 3 months of age in sheep naturally infected with scrapie, correlating with initial replication in the gut-associated lymphoid tissue, the assay could be the basis of a preclinical test. The identification of the cell subset carrying PrPsc progresses our understanding of the pathogenesis of the disease. However, it remains unclear whether this cell subset is responsible for the dissemination of prions or in clearance of circulating PrPsc. Funded by defra, UK and IDEXX.
O.2.6
Human urine and PrP
Silvio Notari1*, Liuting Qing1*, Ayuna Dagdanova1*, Sergei Ilchenko1, Mark E. Obrenovich1, Wen-Quan Zou1, Maurizio Pocchiari2, Pierluigi Gambetti1, Qingzhong Kong1, Shu G. Chen1 1Case Western Reserve University, USA; 2Istituto Superiore di Sanità, Italy
Background: The presence and the characteristics of prion protein (PrP) in human urine under normal conditions are controversial. Similarly, there are no definite data on the presence of infectivity in urine in the course of naturally occurring human prion diseases. Objectives: 1) To definitely determine the presence and characteristics of PrPC in normal urine. 2) To evaluate the prion infectivity in human urine in sporadic Creutzfeldt-Jakob disease (sCJD), we have carried out a set of bioassays in humanized transgenic mouse with urine samples collected from sCJD subjects. Methods: 1) Advanced mass spectrometry and experimental treatments have been used to demonstrate the presence, primary structure and posttranslational modifications of purified urinary PrPC (uPrP). 2) Bioassays were performed by intracerebral inoculation of 100 times concentrated and dialyzed urine, collected from three sCJD-MM1 cases to humanized transgenic mice and from appropriate controls. Results: We found that human urine contains significant amount of PrP (approximately 10 ng/ml) that is truncated with the major N-terminus at residue 112 as the PrPC fragment identified as C1, and it carries an anchor, which is soluble because likely lacks the phosholipid component. None of the humanized transgenic mice inoculated with sCJD concentrated urine had evidence of prion disease during a period of over 700 days (their normal life expectancy) leading to the conclusion that prion infectivity in sCJD urine, if present, must be less than 6 infectious units/100ml. Discussion: The issues raised in the discussion will include: 1) The origin of the truncated uPrP; 2) How the present data compare with the experimental studies published to date that indicate presence of infectivity; 3) The practical implications of our findings. *
These authors contributed equally
O.4.6
All separated components, prepared from BSE-infected sheep blood, are infectious upon transfusion
Sandra McCutcheon1, Anthony Richard Alejo Blanco1, Christopher de Wolf1, Boon Chin Tan1, Nora Hunter1, Valerie Hornsey2, Christopher Prowse2, Marc Turner2, Martin H Groschup3, Dietmar Becher4, Fiona Houston5, Jean C Manson1 1The Roslin Institute and R (D) SVS, University of Edinburgh, UK; 2Scottish National Blood Transfusion Service, UK; 3FLIFederal Research Institute for Animal Health, Germany; 4Micromun, Germany; 5University of Glasgow, UK
Background: The possibility that vCJD may be transmitted by blood transfusion is serious public health issue, of which 4 probable (3 clinical) cases have been attributed. Recently a case of asymptomatic vCJD infection was identified in a haemophiliac; following treatment with clotting factors from UK plasma pools. Sheep orally infected with BSE provide a suitable model, to assess vCJD infection in humans & risk reduction methods, as the distribution of PrPSc & infectivity in lymphoid tissues resembles that of vCJD patients.
Objectives: To determine qualitative and quantitative data on the changes in infectivity in blood and its clinically relevant components with time, to assess the effect of leucodepletion of such products and the potential for secondary transmission by blood transfusion.
Methods: We orally infected sheep with bovine BSE brain homogenate and collected two full-sized donations of whole blood, before the onset of clinical signs. The following components were transfused into naive recipients: whole blood, buffy coat and leucoreduced and non leucoreduced plasma, platelets and red cells. A sub sample of all components was inoculated into TgShpXI mice for determination of infectivity titers. A unit of whole blood from selected primary recipients was transfused into secondary recipients. We are creating a blood archive throughout this study.
Results: 33% of the infected donors have been confirmed as having BSE. We have 4 transmissions of BSE-infectivity following the transfusion of whole blood, buffy coat and plasma. Short incubation times were recorded in these recipients (468, 513, 567 and 594 days) & were similar to those seen in their respective donors (534, 628, 614 and 614 days). The donor of buffy coat also donated both leucodepleted and non leucodepleted blood components to other recipients.
Discussion: Our study will provide invaluable data on the safety of blood products, in relation to TSE infection, used in human medicine (DoH 007/0162)
O.8.1
Variant CJD and plasma products
Robert G. Will National CJD Surveillance Unit, Edinburgh, UK
Evidence from the Transfusion Medicine Epidemiology Review (TMER) project indicates that variant CJD is transmissible through transfusion of labile blood components. The question as to whether plasma products sourced from vCJD contaminated plasma pools has been addressed by a number of risk assessments, with conflicting conclusions. Recently a case of possible vCJD infection in an individual with haemophilia has been described and analysis has suggested that infection may have been related to prior treatment with vCJD implicated Factor VIII. The details of this case will be described together with an analysis of plasma product exposures in UK clinical cases of vCJD.
O.8.2
Blood safety: from screening tests to prion removal
Marc Turner Scottish National Blood Transfusion Service and Department of Haematology, Royal Infirmary, Edinburgh, UK
Although the number of clinical cases of variant CJD continues to fall, concern remains within UK and Western European Blood Services in relation to the risk of transmission of variant CJD due to the estimated prevalence of sub-clinical infection in the general population and the clinical cases of transmission of variant CJD prions by blood components and plasma products. The UK Advisory Committee on the Safety of Blood, Tissues and Organs (SaBTO) has considered a number of further precautionary measures including reducing exposure to blood transfusion, importation of blood components, implementation of prion assays and prion reduction for red cell concentrates. The latter two technologies are currently under independent evaluation and it is expected that contingent on the outcome of these an initial decision on whether or not to recommend implementation of these technologies will be made by SaBTO in Autumn 2009.
O.9.3
Updated risk assessment of variant Creutzfeldt-Jakob disease (vCJD) risks for recipients of plasma-derived blood clotting products in the U.S.
Hong Yang, Richard Forshee, Mark Walderhaug, Steven Anderson US Food and Drug Administration, USA
Background: A recent announcement by UK health authorities of a case of vCJD infection in a >70 year old person with hemophilia has prompted the US Food & Drug Administration (FDA) to re-evaluate vCJD risks in the U.S. via plasma-derived Factor VIII (pdFVIII) and to update its 2006 risk assessment. As of May 2009, confirmed vCJD deaths have occurred in persons who are homozygous methionine (MM) at codon 129 of the PRP gene. Several reports in the last few years have indicated signs of vCJD infection in persons of methionine-valine (MV) and homozygous valine (VV) genotypes. FDA updated risk assessment by assuming all genotypes are susceptible to vCJD and modeling the incubation periods for all three genotypes.
Objectives: To evaluate the vCJD risk for pdFVIII recipients with severe hemophilia and vonWillebrand diseases.
Methods: The model assumed equal susceptibility of three genotypes, a median incubation period of 12 years for the MM and 32 years for MV and VV genotypes, and vCJD infectivity was present in the blood of infected donors during the last 50% to 90% of incubation period. Model used statistical distributions for inputs including susceptibility to the disease, donation rates, frequency and duration of travel to the UK, France and other countries in Europe since 1980, the effectiveness of donor deferral policies and infectivity clearance during manufacturing processes.
Results: For severe hemophilia patients at the highest risk (prophylaxis, with inhibitor, with immune tolerance) the model estimated annual mean exposure to be ~7 x 10-8 iv ID50 or ~1 in 270,000 with the lower prevalence (4 per million) assumption, and ~1 x 10-4 iv ID50 or ~1 in 12,000 with the higher prevalence (1 per 4,225) assumption. Donor deferral policies reduce the risk by >92%.
Discussion: Due to limited data and knowledge of vCJD, the model estimates are uncertain. However, it suggests the risk is small, and donor deferral and manufacturing processes greatly reduce the risk.
P.10.7
Serial passage of sCJD in humanised transgenic mice indicates two major transmission strains associated with PrPSc of either type 1 or 2
Matthew Bishop, Robert Will, Enrico Cancellotti, Jean Manson University of Edinburgh, UK
Background: Questions remain about the aetiology of sporadic CJD and whether phenotypic variation is solely controlled by factors such as codon 129 genotype and biochemistry of PrPC. Variation in infective strain has not been clearly demonstrated in sCJD.
Objectives: By serial passage of sCJD in transgenic mice expressing human prion protein with MM, MV, and VV codon 129 genotypes we aimed to understand strain transmission characteristics for the three most commonly observed phenotypes of sCJD.
Methods: We performed intracerebral inoculation of humanised transgenic mice with brain homogenates derived from similar mice previously inoculated with frontal cortex from sCJD patients of subgroups MM1, MV2, and VV2. These mice were assessed for clinical TSE signs, for TSE vacuolation, and deposition of PrPSc.
Results: sCJD(MM1) passage via all mice showed transmission profiles similar to primary inoculation. sCJD(MV2) passage via HuMM and HuVV mice showed a transmission profile similar to primary inoculation. Passage via a HuMV mouse showed transmission properties similar to not only the primary inoculum but also sCJD(MM1). sCJD(VV2) passage via HuMV and HuVV mice showed transmission profiles similar to the primary inoculation. Passage via a HuMM mouse showed transmission properties similar to not only the sCJD(VV2) primary inoculum but also sCJD(MM1). Cluster analysis of the lesion profile data showed that three clusters seen after primary inoculation were reduced to two following second passage, identified by the biochemical type of PrPSc (1 or 2) found in the host mice.
Discussion: Serial passage of sCJD subgroups MM1, MV2, and VV2 shows that PrPSc type and mouse codon 129 genotype determine the secondary transmission profile, independently of the originating inoculum strain. There are associations between type 1 PrPSc and C129-Met, and type 2 PrPSc and C129-Val. This should allow us to investigate further the relationship between PrPSc, genotype, infection, and pathology.
P.5.1
Detection of cellular prion protein (PrPc) in plasma from healthy cynomolgus monkeys (Macaca fascicularis) and changes observed after BSE infection
Barbara Yutzy, Edgar Holznagel, Johannes Löwer Paul-Ehrlich-Institut, Germany
Background: Orally BSE-dosed cynomolgus monkeys represent a valuable model to examine the kinetic of blood infectivity and to assess the risk of blood-borne transmission of variant Creutzfeldt-Jacob disease (vCJD).
Methods: Blood samples were collected monthly from BSE-infected (n = 18) and non-infected female cynomolgus monkeys (n = 8) over a period of up to 9 years. PrPc concentrations were retrospectively analyzed in plasma samples by a dot blot assay and by a sandwich ELISA using a highly sensitive dissociation- enhanced lanthanide fluoro-immunoassay (DELFIA) for detection. Different blood preparation protocols were evaluated to obtain plasma.
Objective: To detect changes in the levels of soluble plasmaderived PrPc. Results: Different blood preparation protocols had a significant effect on the measured plasma PrPc concentrations. In non-infected macaques, concentrations of soluble, plasmaderived PrPc were at least 10-fold lower compared to plasma concentrations in healthy humans. Levels of plasma PrPc increased 6 – 12 months after experimental BSE infection, remained high during the asymptomatic phase, and dropped towards the clinical phase. Soluble, plasma-derived PrPc molecules were PK-sensitive in BSE-infected macaques.
Discussion: There is a species-specific difference in the PrPc concentrations between human and macaque. At least a part of the plasma-derived PrPc fraction originates from blood cells. Andfinally, BSE infection caused an increase in plasma PrPc levels during the asymptomatic phase of infection. Blood transfusion studies have been initiated to examine whether these PK-sensitive PrP molecules carry infectivity.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html
Friday, October 23, 2009
Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008
http://cjdtexas.blogspot.com/2009/10/creutzfeldt-jakob-disease-surveillance.html
Sunday, May 17, 2009
WHO WILL WATCH THE CHILDREN ? SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
http://downercattle.blogspot.com/2009/05/who-will-watch-children.html
http://downercattle.blogspot.com/
Sunday, September 6, 2009
MAD COW USA 1997 SECRET VIDEO
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? see video at bottom
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN see video
http://maddeer.org/video/embedded/prusinerclip.html
Saturday, August 22, 2009
FREE Kim Min-sun, she is correct about mad cow fears from USDA BEEF
http://usdavskorea.blogspot.com/2009/08/free-kim-min-sun-she-is-correct-about.html
Office of Inspector General Semiannual Report to Congress FY 2007 - 2nd Half
Two Texas Companies Sentenced and Fined for Misbranding Meat Products In April 2007, two closely held and related Texas companies pled guilty in Federal court and were sentenced to 12 months of probation and ordered to pay $10,250 in fines for misbranding meat products. One of the companies sold adulterated meat products to a retail store in New Mexico. Additionally, portions of the invoices failed to properly and consistently identify the meat products as being from cattle more than 30 months old at time of slaughter. This information is required to be disclosed because of bovine spongiform encephalopathy (BSE, or "mad cow disease") concerns. No adulterated meat reached consumers.
http://www.usda.gov/oig/webdocs/sarc071212.pdf
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html
THIS recall is not confusing ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009
http://madcowfeed.blogspot.com/2009/10/wisconsin-firm-recalls-beef-tongues.html
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009
http://madcowfeed.blogspot.com/2009/10/nebraska-firm-recalls-beef-tongues-that.html
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html
Sunday, December 28, 2008
MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy
http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ? August 20, 2008
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Monday, May 11, 2009
Rare BSE mutation raises concerns over risks to public health
http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Advisory Committee on the Safety of Blood, Tissues and Organs
2nd Public Meeting
“Blood Donation – Selection, Deferral and Exclusion”
27 October 2009
Royal Horticultural Halls, London SW1P
At their inaugural meeting in January 2008, members of SaBTO decided that a public meeting should be held every year, focusing on a particular issue within the committee’s remit. The 2009 Public Meeting will focus on the issue of donor selection. Selection of donors is key to the delivery of a safe blood supply. Many prospective donors may be turned down for a variety of reasons, including age, sexual history and medical concerns. As a scientific advisory committee, SaBTO is concerned that exclusion or deferral of prospective blood donors is done for justifiable reasons and in the best interests of blood recipients.
The format of the afternoon will include an introduction to SaBTO and donor selection, and an open forum with the opportunity for the audience to comment and ask questions.
The committee hopes that the audience will reflect a wide range of stakeholders and interest groups. Should the event be oversubscribed, there will be a limit of one delegate per organisation. If you are interested in attending. please e-mail SaBTO@dh.gsi.gov.uk or telephone 020 7972 4750 by 13 October 2009 (this deadline has been extended). Please note that this event is free of charge for all delegates.
The Advisory Committee on the Safety of Blood, Tissues, and Organs (SaBTO) is a Non-Departmental Public Body, with an independent Chair and members selected by the Appointments Commission for their specific areas of expertise. SaBTO provides independent advice to the UK Government and the Devolved Administrations on the most appropriate ways to ensure the safety of blood, cells, tissues, and organs for transfusion/transplantation. SaBTO also provides advice on the microbiological safety of gametes and stem cells, and considers both risk assessment and risk management options for Ministers and UK Health Departments to consider.
Further detailed information about SaBTO and its remit can be found at
http://www.dh.gov.uk/ab/SaBTO/index.htm
http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@dh/@ab/documents/digitalasset/dh_104789.pdf
see other SaBTO meetings minutes here ;
2009 Download summary of seventh meeting, 14-15 July 2009 (PDF, 65K)
Download minutes of sixth meeting, 28 April 2009 (PDF, 104K)
Download summary of sixth meeting, 28 April 2009 (PDF, 64K)
Download minutes of fifth meeting, 20 January 2009 (PDF, 102K)
Download agenda for the fifth meeting, 20 January 2009 (PDF, 15K)
2008
snip...end
http://www.dh.gov.uk/ab/SaBTO/DH_089412
Tuesday, November 11, 2008 SaBTO Summary of 1st Public Meeting – variant CJD and blood Tuesday 21st October 2008, 2pm-4pm
http://vcjdblood.blogspot.com/2008/11/sabto-summary-of-1st-public-meeting.html
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007
snip...
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION 40.
The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base cases in Texas and Alabama, with both scrapie and chronic 14 © SEAC 2007 wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?” 41.
A member considered that this question appeared to be primarily related to possible links between animal and human TSEs in the USA.
There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA. Current evidence does not suggest that CWD is a significant risk to human health. There are unpublished data from a case of human TSE in the USA that are suggestive of an apparently novel form of prion disease with distinct molecular characteristics. However, it is unclear whether the case had been further characterised, if it could be linked to animal TSEs or if other similar cases had been found in the USA or elsewhere. In relation to the possible public health implications of atypical scrapie, H-type BSE and CWD, research was being conducted to investigate possible links and surveillance was in place to detect any changes in human TSEs. Although possible links between these diseases and human TSEs are of concern and require research, there is no evidence to suggest immediate public health action is warranted. The possible human health risks from classical scrapie had been discussed earlier in the meeting. Members noted that there are effective channels of discussion and collaboration on research between USA and European groups. Members agreed it is important to keep a watching brief on new developments on TSEs.
snip...
http://www.seac.gov.uk/minutes/99.pdf
http://seac992007.blogspot.com/2008/07/seac-draft-minutes-of-100th-meeting.html
http://seac992007.blogspot.com/
>>>There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA.<<<
10 people killed by new CJD-like disease
Public release date: 9-Jul-2008 [ Print Article E-mail Article Close Window ]
Contact: Claire Bowles mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000076/!x-usc:mailto:claire.bowles@rbi.co.uk 44-207-611-1210 New Scientist
10 people killed by new CJD-like disease A NEW form of fatal dementia has been discovered in 16 Americans, 10 of whom have already died of the condition. It resembles Creutzfeldt-Jakob disease - with patients gradually losing their ability to think, speak and move - but has features that make it distinct from known forms of CJD.
No one yet knows how the disease originates, or under what conditions it might spread. Nor is it clear how many people have the condition. "I believe the disease has been around for many years, unnoticed," says Pierluigi Gambetti, director of the US National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, Ohio. Cases may previously have been mistaken for other forms of dementia.
Since Gambetti's team wrote a paper describing an initial 11 cases referred to his centre between 2002 and 2006 (Annals of Neurology, vol 63, p 697), another five have come to light. "So it is possible that it could be just the tip of the iceberg," Gambetti says.
snip... see full text ;
http://www.eurekalert.org/pub_releases/2008-07/ns-tpk070908.php
Thursday, July 10, 2008
A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html
Thursday, July 10, 2008
A New Prionopathy update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html
Communicated by: Terry S. Singeltary Sr. <:flounder9@verizon.net>
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html
http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
2008
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
Friday, October 23, 2009
Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008
http://cjdtexas.blogspot.com/2009/10/creutzfeldt-jakob-disease-surveillance.html
O.2.2
vCJD infection in an asymptomatic UK haemophilic patient
Alexander Peden1, Graham Fairfoul1, Suzanne Lowrie1, Linda McCardle1, Mark Head1, Seth Love2, Hester Ward1, Simon Cousens3, David Keeling4, Carolyn Millar5, FGH Hill6, James Ironside1 1University of Edinburgh, UK; 2Frenchay Hospital, Bristol, UK; 3London School of Hygiene and Tropical Medicine, UK; 4Churchill Hospital, Oxford, UK; 5Imperial College London, UK; 6Birmingham Children’s Hospital, Birmingham, UK
We describe a study of 17 UK patients with haemophilia considered to be at increased risk of vCJD through exposure to UK plasma products. 10 autopsy cases and 7 biopsy cases were analysed for disease- associated, protease-resistant prion protein (PrPres). The tissues available from each case were variable, ranging from a single biopsy sample to a wide range of autopsy tissues. A single specimen from the spleen of one autopsy case gave a strong positive result on repeated testing for PrPres by Western blot analysis. This tissue came from a 73 year-old male with no history of neurological disease, who was heterozygous (methionine/valine) at codon 129 in the prion protein gene. He had received over 9,000 units of Factor VIII concentrate prepared from plasma pools known to include donations from a vCJD-infected donor, and some 400,000 units not known to include donations from vCJD-infected donors. He had also received 14 units of red blood cells and had undergone several surgical and invasive endoscopic procedures. Estimates of the relative risks of exposure though diet, surgery, endoscopy, blood transfusion and receipt of UK plasma products suggest that by far the most likely route of infection was receipt of UK plasma products.
O.2.3
Detection of prion particles in body fluids of humans and animals
Detlev Riesner Institut fur Physikalische Biologie, Heinrich-Heine- Universitat Dusseldorf, Germany
A major structural difference between the cellular isoform of the prion protein PrPC and the pathogenic isoform PrPSc is the much higher state of molecular aggregation of PrPSc. PK-resistance as normally used for PrPSc-characterization is not reliably valid for all species, strains and sources of prions. The method of suface-FIDA (fluorescence-intensity distribution analysis) was developed avoiding PK-digestion and detecting specifically disease related PrP-aggregates (Birkmann et al 2007, J. Vet. Microbiol 123, 294-304). After partial purification PrP-aggregates are bound to a chip covered with the captureantibody SAF32, labeled with two types of antibodies against two different epitopes and carrying two different fluorescent dyes. A dual-color laser beam is scanning the chip surface, and the fluorescence signals are evaluated in respect to local coincidence, intensities and particle size. The method was applied to brain homogenate of sCJD-victims (post mortem), to CSF-samples of BSE-afflicted cattle (ante mortem) and blood plasma of scrapie sheep (ante mortem). Particles of PrP-aggregates could be detected in all samples, exhibiting a diameter range of 300 nm (optical resolution) to 1ƒÊm. PrP-aggregates were detected with 100% sensitivity in the sCJD-brain homogenate samples; studies on CSF are ongoing. PrP-aggregates were detected in CSF of BSE-cattle, but the number of samples was too little to evaluate the sensitivity. Only one antibody was available to detect scrapie-PrP-aggregates from blood plasma; the sensitivity of 60% will be improved in the ongoing experiments with a second antibody. PrP-aggregates can be used as seeds for fibril formation with recombinant PrP as template (Stohr et al., 2008, PNAS 105, 2409-14). This system will be used as amplification of the particle detection method.
O.2.4
Detection of prions in blood leucocytes
Linda A. Terry, Laurence Howells, Jeremy Hawthorn, Sally Everest, Sarah Jo Moore, Jane C. Edwards Veterinary Laboratories Agency, UK
Background: Infected human blood has been implicated in the iatrogenic transmission of vCJD in four reported cases. Experimental transmission studies have demonstrated that blood from scrapie and BSE infected sheep also contains infectivity. Rodent models of prion disease implicated both cellular and plasma fractions. However, direct detection of PrPsc from blood in the absence of in vitro amplification or bioassay has proved difficult. Methods for the direct detection of PrPsc in blood would be advantageous for the study of the pathogenesis of TSEs and as a basis for a blood test. Objectives: To develop a method for the direct detection of PrPsc in blood cells from scrapie and BSE infected sheep; to study the temporal distribution of PrPsc in blood and to determine the identity of the cells bearing prions in blood. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from sheep naturally infected with scrapie or experimentally infected with BSE at the clinical stage of disease and from scrapie infected sheep from 3 months of age through to clinical end-point. PBMCs were tested for PrPsc content by a direct immunoassay based on the IDEXX CWD HerdChek kit. Different subsets of PBMCs were isolated by subset specific cell surface markers and magnetic bead separation and analysed for PrPsc content. Results: PrPSc was detected in 54% of sheep with clinical scrapie and 71% of sheep with clinical BSE. A longitudinal study of the temporal distribution of blood PBMC associated PrPsc showed that the detection rate increases during the course of disease and is more likely to be observed during the second half of the incubation period. Additionally detection is more likely in scrapie infected sheep if they carry the PRNP genotype of VRQ/VRQ. Cell separation studies showed that the PrPsc is associated with a specific cell subset implicating a subset of B lymphocytes. Discussion. This is the first report of the direct detection of PrPsc in cells isolated from sheep blood in the absence of in vitro amplification or bioassay. Since PrPsc can be detected from as early as 3 months of age in sheep naturally infected with scrapie, correlating with initial replication in the gut-associated lymphoid tissue, the assay could be the basis of a preclinical test. The identification of the cell subset carrying PrPsc progresses our understanding of the pathogenesis of the disease. However, it remains unclear whether this cell subset is responsible for the dissemination of prions or in clearance of circulating PrPsc. Funded by defra, UK and IDEXX.
O.2.6
Human urine and PrP
Silvio Notari1*, Liuting Qing1*, Ayuna Dagdanova1*, Sergei Ilchenko1, Mark E. Obrenovich1, Wen-Quan Zou1, Maurizio Pocchiari2, Pierluigi Gambetti1, Qingzhong Kong1, Shu G. Chen1 1Case Western Reserve University, USA; 2Istituto Superiore di Sanità, Italy
Background: The presence and the characteristics of prion protein (PrP) in human urine under normal conditions are controversial. Similarly, there are no definite data on the presence of infectivity in urine in the course of naturally occurring human prion diseases. Objectives: 1) To definitely determine the presence and characteristics of PrPC in normal urine. 2) To evaluate the prion infectivity in human urine in sporadic Creutzfeldt-Jakob disease (sCJD), we have carried out a set of bioassays in humanized transgenic mouse with urine samples collected from sCJD subjects. Methods: 1) Advanced mass spectrometry and experimental treatments have been used to demonstrate the presence, primary structure and posttranslational modifications of purified urinary PrPC (uPrP). 2) Bioassays were performed by intracerebral inoculation of 100 times concentrated and dialyzed urine, collected from three sCJD-MM1 cases to humanized transgenic mice and from appropriate controls. Results: We found that human urine contains significant amount of PrP (approximately 10 ng/ml) that is truncated with the major N-terminus at residue 112 as the PrPC fragment identified as C1, and it carries an anchor, which is soluble because likely lacks the phosholipid component. None of the humanized transgenic mice inoculated with sCJD concentrated urine had evidence of prion disease during a period of over 700 days (their normal life expectancy) leading to the conclusion that prion infectivity in sCJD urine, if present, must be less than 6 infectious units/100ml. Discussion: The issues raised in the discussion will include: 1) The origin of the truncated uPrP; 2) How the present data compare with the experimental studies published to date that indicate presence of infectivity; 3) The practical implications of our findings. *
These authors contributed equally
O.4.6
All separated components, prepared from BSE-infected sheep blood, are infectious upon transfusion
Sandra McCutcheon1, Anthony Richard Alejo Blanco1, Christopher de Wolf1, Boon Chin Tan1, Nora Hunter1, Valerie Hornsey2, Christopher Prowse2, Marc Turner2, Martin H Groschup3, Dietmar Becher4, Fiona Houston5, Jean C Manson1 1The Roslin Institute and R (D) SVS, University of Edinburgh, UK; 2Scottish National Blood Transfusion Service, UK; 3FLIFederal Research Institute for Animal Health, Germany; 4Micromun, Germany; 5University of Glasgow, UK
Background: The possibility that vCJD may be transmitted by blood transfusion is serious public health issue, of which 4 probable (3 clinical) cases have been attributed. Recently a case of asymptomatic vCJD infection was identified in a haemophiliac; following treatment with clotting factors from UK plasma pools. Sheep orally infected with BSE provide a suitable model, to assess vCJD infection in humans & risk reduction methods, as the distribution of PrPSc & infectivity in lymphoid tissues resembles that of vCJD patients.
Objectives: To determine qualitative and quantitative data on the changes in infectivity in blood and its clinically relevant components with time, to assess the effect of leucodepletion of such products and the potential for secondary transmission by blood transfusion.
Methods: We orally infected sheep with bovine BSE brain homogenate and collected two full-sized donations of whole blood, before the onset of clinical signs. The following components were transfused into naive recipients: whole blood, buffy coat and leucoreduced and non leucoreduced plasma, platelets and red cells. A sub sample of all components was inoculated into TgShpXI mice for determination of infectivity titers. A unit of whole blood from selected primary recipients was transfused into secondary recipients. We are creating a blood archive throughout this study.
Results: 33% of the infected donors have been confirmed as having BSE. We have 4 transmissions of BSE-infectivity following the transfusion of whole blood, buffy coat and plasma. Short incubation times were recorded in these recipients (468, 513, 567 and 594 days) & were similar to those seen in their respective donors (534, 628, 614 and 614 days). The donor of buffy coat also donated both leucodepleted and non leucodepleted blood components to other recipients.
Discussion: Our study will provide invaluable data on the safety of blood products, in relation to TSE infection, used in human medicine (DoH 007/0162)
O.8.1
Variant CJD and plasma products
Robert G. Will National CJD Surveillance Unit, Edinburgh, UK
Evidence from the Transfusion Medicine Epidemiology Review (TMER) project indicates that variant CJD is transmissible through transfusion of labile blood components. The question as to whether plasma products sourced from vCJD contaminated plasma pools has been addressed by a number of risk assessments, with conflicting conclusions. Recently a case of possible vCJD infection in an individual with haemophilia has been described and analysis has suggested that infection may have been related to prior treatment with vCJD implicated Factor VIII. The details of this case will be described together with an analysis of plasma product exposures in UK clinical cases of vCJD.
O.8.2
Blood safety: from screening tests to prion removal
Marc Turner Scottish National Blood Transfusion Service and Department of Haematology, Royal Infirmary, Edinburgh, UK
Although the number of clinical cases of variant CJD continues to fall, concern remains within UK and Western European Blood Services in relation to the risk of transmission of variant CJD due to the estimated prevalence of sub-clinical infection in the general population and the clinical cases of transmission of variant CJD prions by blood components and plasma products. The UK Advisory Committee on the Safety of Blood, Tissues and Organs (SaBTO) has considered a number of further precautionary measures including reducing exposure to blood transfusion, importation of blood components, implementation of prion assays and prion reduction for red cell concentrates. The latter two technologies are currently under independent evaluation and it is expected that contingent on the outcome of these an initial decision on whether or not to recommend implementation of these technologies will be made by SaBTO in Autumn 2009.
O.9.3
Updated risk assessment of variant Creutzfeldt-Jakob disease (vCJD) risks for recipients of plasma-derived blood clotting products in the U.S.
Hong Yang, Richard Forshee, Mark Walderhaug, Steven Anderson US Food and Drug Administration, USA
Background: A recent announcement by UK health authorities of a case of vCJD infection in a >70 year old person with hemophilia has prompted the US Food & Drug Administration (FDA) to re-evaluate vCJD risks in the U.S. via plasma-derived Factor VIII (pdFVIII) and to update its 2006 risk assessment. As of May 2009, confirmed vCJD deaths have occurred in persons who are homozygous methionine (MM) at codon 129 of the PRP gene. Several reports in the last few years have indicated signs of vCJD infection in persons of methionine-valine (MV) and homozygous valine (VV) genotypes. FDA updated risk assessment by assuming all genotypes are susceptible to vCJD and modeling the incubation periods for all three genotypes.
Objectives: To evaluate the vCJD risk for pdFVIII recipients with severe hemophilia and vonWillebrand diseases.
Methods: The model assumed equal susceptibility of three genotypes, a median incubation period of 12 years for the MM and 32 years for MV and VV genotypes, and vCJD infectivity was present in the blood of infected donors during the last 50% to 90% of incubation period. Model used statistical distributions for inputs including susceptibility to the disease, donation rates, frequency and duration of travel to the UK, France and other countries in Europe since 1980, the effectiveness of donor deferral policies and infectivity clearance during manufacturing processes.
Results: For severe hemophilia patients at the highest risk (prophylaxis, with inhibitor, with immune tolerance) the model estimated annual mean exposure to be ~7 x 10-8 iv ID50 or ~1 in 270,000 with the lower prevalence (4 per million) assumption, and ~1 x 10-4 iv ID50 or ~1 in 12,000 with the higher prevalence (1 per 4,225) assumption. Donor deferral policies reduce the risk by >92%.
Discussion: Due to limited data and knowledge of vCJD, the model estimates are uncertain. However, it suggests the risk is small, and donor deferral and manufacturing processes greatly reduce the risk.
P.10.7
Serial passage of sCJD in humanised transgenic mice indicates two major transmission strains associated with PrPSc of either type 1 or 2
Matthew Bishop, Robert Will, Enrico Cancellotti, Jean Manson University of Edinburgh, UK
Background: Questions remain about the aetiology of sporadic CJD and whether phenotypic variation is solely controlled by factors such as codon 129 genotype and biochemistry of PrPC. Variation in infective strain has not been clearly demonstrated in sCJD.
Objectives: By serial passage of sCJD in transgenic mice expressing human prion protein with MM, MV, and VV codon 129 genotypes we aimed to understand strain transmission characteristics for the three most commonly observed phenotypes of sCJD.
Methods: We performed intracerebral inoculation of humanised transgenic mice with brain homogenates derived from similar mice previously inoculated with frontal cortex from sCJD patients of subgroups MM1, MV2, and VV2. These mice were assessed for clinical TSE signs, for TSE vacuolation, and deposition of PrPSc.
Results: sCJD(MM1) passage via all mice showed transmission profiles similar to primary inoculation. sCJD(MV2) passage via HuMM and HuVV mice showed a transmission profile similar to primary inoculation. Passage via a HuMV mouse showed transmission properties similar to not only the primary inoculum but also sCJD(MM1). sCJD(VV2) passage via HuMV and HuVV mice showed transmission profiles similar to the primary inoculation. Passage via a HuMM mouse showed transmission properties similar to not only the sCJD(VV2) primary inoculum but also sCJD(MM1). Cluster analysis of the lesion profile data showed that three clusters seen after primary inoculation were reduced to two following second passage, identified by the biochemical type of PrPSc (1 or 2) found in the host mice.
Discussion: Serial passage of sCJD subgroups MM1, MV2, and VV2 shows that PrPSc type and mouse codon 129 genotype determine the secondary transmission profile, independently of the originating inoculum strain. There are associations between type 1 PrPSc and C129-Met, and type 2 PrPSc and C129-Val. This should allow us to investigate further the relationship between PrPSc, genotype, infection, and pathology.
P.5.1
Detection of cellular prion protein (PrPc) in plasma from healthy cynomolgus monkeys (Macaca fascicularis) and changes observed after BSE infection
Barbara Yutzy, Edgar Holznagel, Johannes Löwer Paul-Ehrlich-Institut, Germany
Background: Orally BSE-dosed cynomolgus monkeys represent a valuable model to examine the kinetic of blood infectivity and to assess the risk of blood-borne transmission of variant Creutzfeldt-Jacob disease (vCJD).
Methods: Blood samples were collected monthly from BSE-infected (n = 18) and non-infected female cynomolgus monkeys (n = 8) over a period of up to 9 years. PrPc concentrations were retrospectively analyzed in plasma samples by a dot blot assay and by a sandwich ELISA using a highly sensitive dissociation- enhanced lanthanide fluoro-immunoassay (DELFIA) for detection. Different blood preparation protocols were evaluated to obtain plasma.
Objective: To detect changes in the levels of soluble plasmaderived PrPc. Results: Different blood preparation protocols had a significant effect on the measured plasma PrPc concentrations. In non-infected macaques, concentrations of soluble, plasmaderived PrPc were at least 10-fold lower compared to plasma concentrations in healthy humans. Levels of plasma PrPc increased 6 – 12 months after experimental BSE infection, remained high during the asymptomatic phase, and dropped towards the clinical phase. Soluble, plasma-derived PrPc molecules were PK-sensitive in BSE-infected macaques.
Discussion: There is a species-specific difference in the PrPc concentrations between human and macaque. At least a part of the plasma-derived PrPc fraction originates from blood cells. Andfinally, BSE infection caused an increase in plasma PrPc levels during the asymptomatic phase of infection. Blood transfusion studies have been initiated to examine whether these PK-sensitive PrP molecules carry infectivity.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html
Friday, October 23, 2009
Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008
http://cjdtexas.blogspot.com/2009/10/creutzfeldt-jakob-disease-surveillance.html
Sunday, May 17, 2009
WHO WILL WATCH THE CHILDREN ? SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
http://downercattle.blogspot.com/2009/05/who-will-watch-children.html
http://downercattle.blogspot.com/
Sunday, September 6, 2009
MAD COW USA 1997 SECRET VIDEO
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? see video at bottom
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN see video
http://maddeer.org/video/embedded/prusinerclip.html
Saturday, August 22, 2009
FREE Kim Min-sun, she is correct about mad cow fears from USDA BEEF
http://usdavskorea.blogspot.com/2009/08/free-kim-min-sun-she-is-correct-about.html
Office of Inspector General Semiannual Report to Congress FY 2007 - 2nd Half
Two Texas Companies Sentenced and Fined for Misbranding Meat Products In April 2007, two closely held and related Texas companies pled guilty in Federal court and were sentenced to 12 months of probation and ordered to pay $10,250 in fines for misbranding meat products. One of the companies sold adulterated meat products to a retail store in New Mexico. Additionally, portions of the invoices failed to properly and consistently identify the meat products as being from cattle more than 30 months old at time of slaughter. This information is required to be disclosed because of bovine spongiform encephalopathy (BSE, or "mad cow disease") concerns. No adulterated meat reached consumers.
http://www.usda.gov/oig/webdocs/sarc071212.pdf
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html
THIS recall is not confusing ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009
http://madcowfeed.blogspot.com/2009/10/wisconsin-firm-recalls-beef-tongues.html
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009
http://madcowfeed.blogspot.com/2009/10/nebraska-firm-recalls-beef-tongues-that.html
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html
Sunday, December 28, 2008
MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy
http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ? August 20, 2008
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Monday, May 11, 2009
Rare BSE mutation raises concerns over risks to public health
http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Wednesday, December 12, 2007
SEAC 99th meeting on Friday 14th December 2007
SEAC 99th meeting on Friday 14th December 2007
1 09.30 Introduction SEAC Chair
Approval of draft minutes from SEAC 98
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE
Draft open minutes of the 98th meeting held on 29th July 2007
23. The Chair summarised the discussion noting that SEAC agreed: • there are no substantive new data to allow a reassessment of the infectivity of plasma derivatives from fractionation of contaminated plasma. • only research that measures the clearance of endogenous infectivity in blood would support a reassessment of the infectivity of plasma derivatives. • the National Haemophiliac Database could provide important data to assess the risks of transmission of vCJD via plasma derivatives.
snip...
32. A member noted that from a public and consumer perspective SEAC has always been seen as an exemplar of good practice for example by holding its meetings in public and communicating its statements and decisions using clear language. It was noted that the House of Commons report is not in favour of consumer or lay representatives on all scientific committees as a matter of course and it advises that their roles are re-evaluated. The member noted that lay members are in fact important in ensuring that information produced by committees can be understood by non-experts. However, it is important to make clear that a single consumer representative cannot represent the thoughts of all consumers. Periodic review of scientific advisory committees, such as is
3 http://www.dti.gov.uk/files/file39981.pdf
4 http://www.publications.parliament.uk/pa/cm200506/cmselect/cmsctech/900/900-i.pdf
undertaken with SEAC, is important as a quality assurance mechanism.
see full text 14 pages ;
http://www.seac.gov.uk/papers/99-1.pdf
USE OF PREVIOUS SEAC OPINIONS ISSUE
1. Given the evolving nature of scientific understanding of transmissible spongiform encephalopathies (TSEs), it is suggested that an agreed procedure be in place setting out a time limit for the use of SDEAC advice by a Government Department without referral back to the committee. It is suggested this is needed because new data could have appeared since the advice was given that would cause the committee to alter that advice.
CONSIDERATION
see full text page ;
http://www.seac.gov.uk/papers/99-6.pdf
REPORT FROM THE SEAC SHEEP SUBGROUP
31. Given the low prevalence of classical scrapie and assuming that BSE in sheep would occur independently from that of classical scrapie, if BSE is or was present in the national sheep flock, it would have been expected to arise more frequently as a single infection rather than mixed with classical scrapie. However, since BSE as a single infection in sheep has never been found, it is highly unlikely that an appreciable number of mixed infections of classical scrapie and BSE are present currently in sheep unless BSE and classical scrapie are more efficiently transmitted together between sheep compared with BSE in isolation but there are no data to suggest this may or may not be the case. However, unpublished results from inoculations into mice of a mixed inoculum compared with individual inocula indicate an increased attack rate suggesting higher transmission efficiencies of mixed strains is a possibility12.
Summary 33. The data from the strain typing study, while intriguing and not fully explained, provide no evidence for the presence of BSE in sheep as a single infection. Whilst these data may indicate the presence of mixed BSE and classical scrapie infections, this is one of several possible interpretations. These data should not give rise to concern that there is an appreciable number of mixed BSE-12 classical scrapie infections that would significantly influence estimates of the prevalence of BSE in the UK sheep flock.
Unpublished Roslin Institute studies.
13 SEAC Sheep Subgroup statement (2006)
http://www.seac.gov.uk/statements/sheepsubgrp-statement131006.pdf
14 Opinion on the quantitative risk assessment on the residual BSE risk in sheep meat and meat products. The EFSA Journal. (2007) 442, 1-44.
http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej442_qra_sheep_en,3.pdf
Maternal transfer of classical scrapie prion protein via sheep milk Background 34. The mechanisms for transmission of classical scrapie between sheep are not fully understood, however there is evidence to suggest that the risk of transmission is high during the neonatal period15. A study by VLA is examining whether milk may be a significant route of transmission by bottle feeding milk collected from ewes genetically susceptible to, and infected with classical scrapie, to genetically susceptible TSE-free lambs. Data 35. Early unpublished findings from the study suggest that milk may be a route of transmission. Post mortem examination of three lambs that were bottle-fed milk from classical scrapie infected ewes which died early in the study from intercurrent disease revealed the presence of PrPSc in gut lymphoid tissue in two lambs. The milk fed to these two lambs was from two ewes that developed clinical signs of classical scrapie during lactation. The milk fed to the third lamb was from a ewe with clinical signs of classical scrapie at the beginning of lactation from which only a relatively small volume of milk was produced. Somatic cell counts were high in at least a proportion of the milk collected from the ewes. PrPSc was not found in a control lamb, which also died from intercurrent disease, that was fed milk from an uninfected ewe. Implications 36. These data suggest that PrPSc may be transmitted from ewe to lamb via milk or colostrum. As a full lactation was fed to the lambs it is not possible to determine whether transmission occurred via colostrum and/or the subsequent milk. The study is at too early a stage to assess whether classical scrapie develops as a result of this exposure, although this should be considered likely.
snip...see full text 15 pages ;
http://www.seac.gov.uk/papers/99-2.pdf
SCIENTIFIC BASIS FOR CLASSICAL SCRAPIE CONTROLS
Scientific basis for relaxation of classical scrapie controls
AFSSA OPINION 13. The AFSSA opinion (Annex 1) describes three areas of scientific uncertainty that have led to the conclusion that the proposed changes to controls may significantly increase the risk to human health from the slaughter of sheep from classical scrapie affected flocks for human consumption. In summary, AFSSA considered that: • the tests to detect and discriminate between BSE and classical and atypical scrapie are limited as (i) their sensitivity has not been accurately determined, (ii) they may not detect BSE in animals that are also infected with classical scrapie and (iii) the conduct of the discriminatory test on the index case would not guarantee the absence of BSE in the flock. Furthermore, as only brain tissue is tested, the rapid tests cannot detect TSE infections during the incubation period prior to accumulation of abnormal prion protein in the brain. • although there are no epidemiological data to suggest a link between classical scrapie strains and human TSEs, in view of the diversity of classical scrapie strains and the lack of a robust prospective study to examine potential links between these TSE strains and human TSEs, a link cannot be ruled out. • the incidence of classical scrapie infections in classical scrapie affected sheep flocks can be relatively high, particularly in those animals of susceptible genotypes5 suggesting classical scrapie infection may be widespread in affected flocks. 14. In view of these considerations, AFSSA concluded that allowing animals from classical scrapie affected flocks to be slaughtered for human consumption, particularly without any restriction on genotype, would increase the human health risk as: (i) the presence of BSE in a sheep cannot be ruled out by the application of discriminatory tests as the sensitivity of the tests is not known precisely and detection may be compromised when classical scrapie is also present. (ii) classical scrapie infections can be widespread in sheep flocks and as rapid TSE tests cannot identify infected animals in the early part of the incubation period, it is possible that an appreciable number of classical scrapie infected animals could enter the human food chain. (iii) the transmission to humans of TSE strains other than BSE cannot be ruled out.
5 Corbiere et al. (2007) Advanced survival models for risk-factor analysis in scrapie. J. Gen Virol. 88, 696-705.
EFSA OPINION 15.
The EFSA Scientific Panel on Biological Hazards considered the AFSSA opinion and in particular the evidence for possible links between classical or atypical scrapie and human TSEs and the performance characteristics of discriminatory tests for sheep TSEs (Annex 2). The Panel concluded that: • there is no evidence for an epidemiological or molecular link between classical and/or atypical scrapie and TSEs in humans. The BSE agent is the only agent identified as zoonotic. However, in view of their diversity it is currently not possible to exclude transmissibility to humans of other animal TSE agents. • current discriminatory tests appear, up to now, to be reliable for the differentiation of BSE from classical and atypical scrapie. However, at the current stage of scientific knowledge, neither their diagnostic sensitivity nor their specificity can be assumed to be perfect. KOM AG TSE OPINION 16. KOM AG TSE considered the changes to classical scrapie controls (Annex 4) and noted that recently published research by Reckzeh et al. (2007)6 (Annex 4) showed that some sheep of susceptible genotypes that had tested negative for TSE infection when brain samples were tested, were in fact positive for TSE infection when peripheral tissues were tested. Thus, the committee concluded that the current strategy of testing brain tissue cannot exclude the presence of TSE infections at the stage of the incubation period prior to involvement of the brain. Thus, the changes to classical scrapie controls could allow classical scrapie infectivity into the human food chain. 17. In addition, the committee noted that, although the EFSA Biohazard Panel concluded that there are no indications of the existence of zoonotic link between classical scrapie and human TSEs, as classical scrapie strains are not uniform and are poorly defined, a zoonotic potential cannot be ruled out. In view of this, the committee considered that consumer exposure to classical scrapie should be avoided and was not in favour of the changes to the classical scrapie controls that would allow this to occur.
6 Reckzeh et al. (2007) Rapid testing leads to the underestimation of the scrapie prevalence in an affected sheep and goat flock. Vet. Microbiol. 123, 320-327.
PREVIOUS SEAC OPINIONS
snip...
Opinion of the French Food Safety Agency (AFSSA) on changes to the control measures for sheep and goat herds in which a case of classical or atypical scrapie has been detected
http://www.afssa.fr/Documents/ESST2006sa0343EN.pdf
Opinion of the Scientific Panel on Biological Hazards on certain aspects related to the risk of transmissible spongiform encephalopathies (TSEs) in ovine and caprine animals
snip...
5- Conclusions and opinion
On the following grounds:
- the discriminatory tests do not enable the presence of BSE to be ruled out either in the tested animal or by extension in the flock to which it belongs;
- the transmission to humans of TSE strains other than BSE cannot be ruled out;
- the knowledge acquired of the genetic susceptibility of sheep to scrapie and BSE should be used, insofar as this is possible, to limit the risk of consumer exposure,
The Committee is making the following recommendations:
Recommendations common to both types of control measure:
- permanent individual identification of all small ruminants belonging to the herds concerned.
- for sheep, genotyping for the four cordons (136, 141, 154 and 171) of all animals in an infected flock.
- all tests carried out on animals slaughtered or culled as part of the control measures must be effected with one of the rapid tests with the best sensitivity for the detection of atypical scrapie (currently Idexx, Biorad).
- conduct of a discriminatory test on all secondary cases identified.
- destruction of all positive animals.
snip...please see full text 9 pages ;
http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej466_tse_ovine_caprine_en.pdf
Opinion of the KOM AG TSE Evaluation of the catalogue of measures after detecting a TSE case Reckzeh et al. (2007) Rapid testing leads to the underestimation of the scrapie prevalence in an affected sheep and goat flock. Vet. Microbiol. 123, 320-327.
snip see full text 21 pages ;
http://www.seac.gov.uk/papers/99-3.pdf
Consideration of various options relating to relaxation of the total feed ban
ISSUE
1. The Department for Environment, Food and Rural Affairs (Defra) the devolved Rural Affairs Departments and the Food Standards Agency (FSA) have asked SEAC to consider, in qualitative terms, the potential for further transmissible spongiform encephalopathy (TSE) infections and epidemics to arise as a result of possible implementation of various future options for relaxing the TSE-related feed controls. This paper, prepared by Defra, provides an overview of European Union (EU) proposals and relevant science.
BACKGROUND
snip...
Work Programme8 on TSEs in November 2006. In relation to the feed ban, the document proposed discussions on:
i. Permitting a tolerance of “insignificant amounts” of animal protein, including fish meal in feed, arising as a result of “adventitious” (e.g. rodent/avian) or “technically unavoidable” (e.g. fish meal) contamination.
ii. The use of fish meal in feed for young ruminants on the basis of a scientific assessment of their dietary needs and following an assessment of the control aspects.
iii. Permitting a general tolerance level with regard to the “small presence” of mammalian MBM in feed for farmed animals.
Currently it is not possible to expand on the terms “insignificant amount” or “small presence”. Any future tolerance level would be determined to a large extent by the sensitivity and specificity of the quantitative tests available. Quantitative risk assessments (e.g. EFSA quantitative risk assessment of animal BSE risk posed by mammalian MBM 2005) may also be taken into account. Also it is not clear exactly what is envisaged under (iii) but the UK Government’s current understanding is that it is a variation on (i) in that an accepted “tolerance” level would be agreed below which the Member State would not be obliged to investigate and assess the individual risk.
9. In January 2007, the TSE Regulation was amended by co-decision. This provided a legal basis for the future options of (i) feeding fishmeal to young ruminants only – a political compromise between the European Commission which wanted the option of permitting the feeding of fish meal to ruminants and the European Parliament which opposed the feeding of such animal protein to herbivores on “ethical” grounds, but conceded to allowing the option of feeding fish meal to young ruminants based on a scientific assessment of their dietary needs – and (ii) the introduction of a risk-based tolerance level for the presence of “insignificant” amounts of animal protein in feed “caused through adventitious and technically unavoidable contamination”. Apart from the circumstances outlined above (and existing exemptions), the ban on feeding animal protein to ruminants remained. The TSE Regulation required that rules for the prevention of cross contamination and methods of sampling and analysis to check compliance, should be based upon a European Commission report covering the sourcing, processing, control and traceability of feedingstuffs of animal origin. The recitals of the TSE Regulation were also amended to propose that “the feeding to non-ruminants of certain PAP originating from non-ruminants should be allowed taking into account the prohibition on intra-species recycling…
8 http://ec.europa.eu/food/food/biosafety/bse/work_prog_tse_en.pdf
and the control aspects in particular linked to differentiation of PAP specific to certain species”: this proposal could be agreed by the European Commission and EU Member States. 10. At SEAC 98 (July 2007) following the media coverage referred to in paragraph 7, SEAC “considered it important that Defra should seek the views of SEAC should such a policy [of feeding non-ruminant MBM to non-ruminants] be proposed as part of the TSE Roadmap”. 11. In July 2007, the European Parliament adopted a report9, which called on the European Commission and the European Council to “lift the ban on feeding fish meal and fish oil to ruminants” (although there is no ban on feeding fish oil to ruminants). The report stressed that "there is no scientific evidence to support a total ban on fish meal on the grounds that it may transmit BSE or other TSEs". 12. In September 2007, the European Commission tabled a proposal (SANCO/2017/2007) to permit the use of fish meal in milk replacers for feeding to young ruminants before weaning, while maintaining strict controls on the feeding of fish meal to adult ruminants, in line with the requirements of the TSE Regulation. In November 2007, the European Commission discussed an amended proposal (SANCO/2017/2007rev.1) to permit the use of fish meal in milk replacers for feeding to young ruminants, with Member States. The amended proposal indicated that it applied to milk replacers administered in either dry or liquid form, provided to young ruminants as a supplement or milk substitute before the completion of weaning. The Commission explained that the European Food Safety Authority had advised that a scientific assessment of the dietary needs of young ruminants was outside its remit. Consequently, the Commission was considering establishing a group of animal nutrition experts to carry out this task. The European Commission indicated following additional training, the qualitative performance of National Reference Laboratories had improved beyond the position reported from the 2006 inter-laboratory trial. However, no further progress could be made on tolerance proposals (e.g. an agreed tolerance level for the presence of fish meal in adult ruminant feed) until there had been a significant improvement in the performance of quantitative tests and this could take at least a year. The European Commission undertook to make data relating to the assessment of dietary needs (EFSA) and the assessment of control aspects (further report from Community Reference Laboratory for Animal Proteins) available to Member States in due course.
9 European Parliament (2007) European Parliament resolution of 10 July 2007 on industrial fisheries and the production of fishmeal and fish oil. P6_TA-PROV(2007)0327
http://www.europarl.europa.eu/news/expert/infopress_page/033-9006-190-07-28-904-20070709IPR08984-09-07-2007-2007-false/default_en.htm
http://www.europarl.europa.eu/sides/getDoc.do?pubRef=-//EP//TEXT+TA+P6-TA-2007-0327+0+DOC+XML+V0//EN&language=EN
snip...see full text 29 pages ;
http://www.seac.gov.uk/papers/99-4.pdf
Horizon scanning
ISSUE
1. To consider emerging scientific issues in relation to transmissible spongiform encephalopathies (TSEs) and to raise awareness of issues SEAC may consider in the future.
snip...
SEAC 99/5 ANNEX 1 DEFRA
To advise SEAC of possible animal-health related TSE developments in 2008.
BACKGROUND 1.
World Organisation for Animal Health (OIE)
The World Organisation for Animal Health is considering current trade guidelines on scrapie and BSE in relation to the emergence of atypical forms of the diseases. While it is unlikely that changes are required to guidelines for BSE, significant revision will be required to take into account the implications of atypical scrapie.
The OIE is expected to endorse the provisional recognition of the UK as “controlled risk” for BSE, at its General Session in May 2008 .
2. European Union Many of the short term goals of the EU’s 2005 TSE Roadmap have been achieved. Those outstanding include:
i) Revision of the BSE Monitoring Programme in Cattle The European Commission is currently discussing a revision of the BSE monitoring programme in cattle, with Member States, to achieve better targeting of the surveillance activity and a reduction in the number of tests. We anticipate that there will be an increase in the testing age limit for fallen stock and date/age based changes to the testing age limit for cattle slaughtered for human consumption. We envisage that SEAC will be consulted on significant changes to the BSE monitoring programme in relation to cattle slaughtered for human consumption.
ii) EU Feed Controls The European Commission is currently discussing the feeding of fish meal to young ruminants, with Member States. The European Commission intends to establish an expert group to examine the nutritional aspects of the proposal. The Community Reference laboratory for animal proteins in feed is working to improve the quantitative method and a further inter-laboratory study is expected. The outcome of this work could pave the way for the introduction of tolerances from 2008. Other research on feed tests could support the feeding of non-ruminant PAP to non-ruminants in the longer term. It may be necessary to consult SEAC again on specific developments.
iii) EU Scrapie Controls
In April 2007, the EU’s Standing Committee on the food chain and animal health adopted more proportionate control measures for scrapie. Following a subsequent legal challenge from France, the European Court of First Instance suspended the new measures relating to classical scrapie pending the hearing of the main case. For sheep flocks in which classical scrapie has been detected the remaining options are whole-flock cull and genotyping and culling. For goats the only remaining option is whole-flock cull. The legal case centred on scientific opinions from the French Food Safety Agency (AFSSA) and the European Food Safety Authority (EFSA) and the application of the precautionary principle. It highlights the importance of close liaison between national risk assessment bodies and EFSA. The Commission is planning to appeal against the judgement and seek acceleration of the main case.
snip...
3. TSEs in Cattle
We predict a continued decline in cases of BSE in the EU and estimate fewer than 75 cases in UK by the end of 2007 (compared to 114 in 2006). The majority of cases are still being detected in cattle born before the 1996 feed ban. The Older Cattle Disposal Scheme closes at the end of 2008 and we are working with industry to maximise the uptake. The prevalence in successive BARB birth cohorts is extremely low and appears to be decreasing. However, as the pre-1996 cattle population declines, BARBs will form an increasing percentage of the total number of cases.
The overall prevalence of atypical BSE appears low. Two cases of atypical BSE have been detected in UK to date in older cattle. Oral challenge studies are being planned in Europe and Japan which will provide further information on the pathogenesis. While the aetiology of atypical BSE remains unknown the long term consequences for the maintenance of key BSE controls remains uncertain.
snip...full text 10 pages ;
http://www.seac.gov.uk/papers/99-5.pdf
8 12.15 Public Q&A SEAC Chair
9 13.20 Update on vCJD and sCJD epidemiology Dr R Knight (NCJDSU)
10 13.40 Update on NATA and other vCJD prevalence studies Professor N Gill (HPA) Dr J Clewley (HPA)
11 14.30 Re-assessment of the potential risk of vCJD transmission via dentistry Dr P Bennett (DH) Dr P Grove (DH)
A RE-ASSESSMENT OF THE POTENTIAL RISK OF VCJD TRANSMISSION VIA DENTISTRY ISSUE
1. The Department of Health (DH) has asked SEAC to consider an interim assessment of the potential risk of vCJD transmission via dental procedures. This work builds on previous risk assessments on possible dental transmission considered by SEAC.
BACKGROUND
Previous SEAC considerations of vCJD transmission via dentistry
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The New DH Risk Assessment
8. The research on infectivity just noted forms one strand of a wider programme at the HPA, which is also intended to quantify protein residues found on dental instruments and the effectiveness of sterilisation in reducing infectivity. Following SEAC 97 (May 2007), DH commissioned a comprehensive re-assessment of the potential risks of vCJD transmission associated with dentistry to take account of research at the HPA and elsewhere. The assessment aims to clarify the range of plausible scenarios for vCJD transmission via dental instruments that could occur, given what is currently known, and to identify the most important factors affecting this risk. The assessment will be used to identify the most important areas of further work to address the uncertainties and any robust ways of cost effectively reducing risks further.
9. This new interim risk assessment has been produced by DH analysts (annex 3) in collaboration with a Scientific Reference Group of independent experts (Chaired by Professor Graham Medley). Members of the Group have expertise in dentistry, instrument decontamination, human and animal prion diseases, anatomy, public health, risk assessment modelling and epidemiology. This group met three times to review and refine the modelling framework and agree the risk assessment. The group provided advice on the inputs and assumptions incorporated into the risk assessment, particularly where expert judgement was required due to a lack of hard data. Under circumstances where key data are absent, precautionary assumptions were agreed. As a number of large uncertainties that strongly influence the quantification of risk remain, the risk assessment is considered as interim and will be updated in the future when new scientific evidence becomes available.
10. The assessment examines the risk that vCJD may be transmitted via dental procedures by establishing plausible ranges for key parameters, including (see sections 2 and 3 of the risk assessment):
• the vCJD infectivity of tissues of the oral cavity of infected patients
• the deposition of that material onto different types of dental instruments and the effectiveness of standard cleaning and sterilisation processes used in dental practice
• the mechanisms and efficiency of transfer of vCJD infectivity from contaminated instruments used on subsequent patients
• the probability of transmission based on assessments of the number and types of dental procedure conducted and the number of people who might be carrying an asymptomatic vCJD infection.
Findings 11.
As there is lack of substantial data with which to accurately quantify many of these parameters, plausible ranges for these parameters have been established to take account of the often large uncertainties in the data. The large uncertainties in many of these parameters strongly influence the quantification of the risk.
12. Plausible scenarios built up using ranges for each of these factors include many in which dental transmission would have no detectable effect on the course of the vCJD outbreak (see section 4 of the risk assessment). However, there are some which include a combination of pessimistic assumptions as regards the infectivity of dental / oral tissues and the effects of instrument decontamination which suggest that:
• there could be some hundreds of vCJD transmissions per annum via dentistry - albeit against a background of several thousand existing vCJD infections (not clinical cases of vCJD), or where
• dental transmission could generate a self-sustaining reservoir of vCJD infection within the population.
13. The distinction between vCJD infections and clinical cases of vCJD is important. If a large proportion of secondary transmissions result in subclinical infections (either never developing into clinical disease or doing so over an extended time-scale) and those infected are infectious, the likelihood of a self-sustaining epidemic increases. The proportion of individuals who might enter such a subclinical “carrier state” is unknown. Key Assumptions and areas of uncertainty
14. Work on the risk assessment is on-going and new data should enable some of the inputs and assumptions underpinning these scenarios to be revised. Key areas of uncertainty are:
• Infectivity in relevant tissues. Of all the unknowns, that of overriding importance is whether dental/oral tissues in patients incubating vCJD would be infective, and if so at what level.
There are as yet no results of studies using human gingival and dental pulp tissues, and these studies may extend into 2009 and 2010 respectively. This is examined in section 2.3 of the risk assessment.
• Protein Residues on dental instruments. This is examined in section 2.2 of the risk assessment.
• Efficacy of Autoclaving. This is examined in section 2.3 of the risk assessment.
• Current prevalence of vCJD infection. This is examined in section 3.3 of the risk assessment.
• Epidemiology of vCJD. This is examined in section 4 of the risk assessment.
15. Suggested areas of further work to reduce the uncertainty in these key areas are described in section 5 of the risk assessment together with a preliminary analysis of possible interventions and risk reduction measures.
ADVICE SOUGHT FROM THE COMMITTEE
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POSITION STATEMENT vCJD AND ENDODONTIC DENTISTRY
snip...
Endodontic instruments
5. Evidence suggests that the files and reamers used in endodontic procedures are reused and are difficult to reliably decontaminate4. Appreciable quantities of residual material remain adherent to the surface after normal cleaning and sterilisation5. Thus, there is potential for transfer of dental pulp between patients undergoing endodontic procedures.
vCJD infectivity in dental tissues
6. There are no data on vCJD infectivity in dental pulp. Although no abnormal prions were found in a study of dental tissues, including dental pulp, from vCJD cases6, dental pulp includes blood and peripheral nerve tissue known to carry vCJD infectivity7,8. In addition, appreciable infectivity has been found in the dental pulp of hamsters with hamster scrapie9. Although it is possible that the peripheral nerve may only become infective close to, or after, the onset of clinical vCJD, inflammation may promote the propagation of prions10. Thus, although the data are limited and indirect, it is reasonable to assume that the dental pulp of individuals subclinically-infected with vCJD may be infectious although the level of infectivity is unknown. Studies underway will provide direct data on the infectivity in dental tissues from vCJD cases. level of infectivity is unknown.
4 Letters et al. (2005) A study of visual and blood contamination on reprocessed endodontic files from general dental practice. Br. Dent. J. 199, 522-525. 5 Smith et al. (2005) Residual protein levels on reprocessed dental instruments. J. Hosp. Infect. 61, 237-241. 6 Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343. 7 SEAC 91 minutes paragraph 9.
www.seac.gov.uk/papers/papers.htm 8
Department of Health (2005) Assessing the risk of vCJD transmission via surgery: an interim view. Unpublished. 9 Ingrosso et al. (1999) Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80, 3043-3047. 10 Heikenwalder et al. (2005) Chronic lymphocytic inflammation specifies the organ tropism of prions. Science. 307, 1107-1110.
Subclinical carrier state
7. A study of humanised mice showed that vCJD infections may not always progress to clinical disease within the normal lifespan of the animals11. Another study suggested that prion infections in mice that remain at a subclinical level can be transmitted to other mice, resulting in clinical disease12. Thus, there is evidence to suggest that individuals infected with the BSE / vCJD agent may remain in a subclinical infection carrier state instead of developing vCJD. A discrepancy between prevalence estimates based on a survey of abnormal prion protein in appendix and tonsil tissue and data on vCJD cases supports this hypothesis13. As no diagnostic test exists to identify such individuals, they could over the course of their lives be potential sources of numerous secondary infections arising from invasive medical or dental procedures.
8. The prevalence of subclinical infection in the UK population is uncertain. A recent estimate suggests the number of subclinical carriers may be of the order of several thousand14. SEAC has strongly recommended that further studies to ascertain better the prevalence of vCJD infection be urgently considered15.
Transmission risks
9. The new DH analysis suggests that, on the basis that residual dental pulp on endodontic files and reamers is transferred relatively efficiently to patients on reuse, dental pulp is as infective as peripheral nerve tissue and a subclinical carrier population for vCJD exists, a self-sustaining vCJD epidemic arising from endodontic surgery is plausible. There are uncertainties about the efficiency of vCJD transmission via endodontic procedures, the vCJD infectivity of dental pulp and the existence of a subclinical infection carrier state. However, even if a self-sustaining epidemic were not possible, clusters of vCJD infections could arise from the use of instruments contaminated with the vCJD agent from endodontic procedures on infected patients. Interactions between this and other routes of secondary transmission, such as blood transfusion and hospital surgery, would make a self-sustaining epidemic more likely.
Potential risk reduction measures
10. Endodontic files and reamers have a limited lifespan, restricting the number of possible secondary transmissions. Improving the effectiveness of procedures used to decontaminate dental instruments would reduce the risk of transmission. Restricting endodontic files and reamers to single use would prevent potential secondary transmission via these instruments. Conclusions
11. A preliminary risk assessment produced by DH suggests that vCJD transmission via endodontic dentistry may, under certain hypothetical but plausible scenarios, be sufficient to sustain a secondary vCJD epidemic. However, there are uncertainties around the data and assumptions underpinning the assessment. Research underway will address some of these uncertainties and allow the risk assessment to be refined. Once the research is complete and / or other data become available, the risks should be reassessed. A watching brief should be maintained.
12. It is unclear whether or not vCJD infectivity can be transmitted via endodontic files and reamers. However, given the plausibility of such a scenario and the large number of procedures undertaken annually, it would be prudent to consider restricting these instruments to single use as a precautionary measure. Since sufficiently rigorous decontamination of these instruments is difficult, single use of these instruments would eliminate this risk, should it exist.
SEAC May 2006
© SEAC 2007
New research
4. Preliminary, unpublished results of research from the Health Protection Agency, aimed at addressing some of the uncertainties in the risk assessments, were reviewed by SEAC (SEAC 97, May 2007). The prion agent used in these studies is closely related to the vCJD agent. This research, using a mouse model, shows that following inoculation of mouse-adapted bovine spongiform encephalopathy (BSE) directly into the gut, infectivity subsequently becomes widespread in tissues of the oral cavity, including dental pulp, salivary glands and gingiva, during the preclinical as well as clinical stage of disease.
5. It is not known how closely the level and distribution of infectivity in the oral cavity of infected mice reflects those of humans infected with vCJD, as there are no comparable data from oral tissues, in particular dental pulp and gingiva, from human subclinical or clinical vCJD cases. Although no abnormal prion protein was found in a study of human dental tissues, including dental pulp, salivary glands and gingiva from vCJD cases22, the relationship between levels of infectivity and abnormal prion protein is unclear23. Infectivity studies underway using the mouse model and oral tissues that are presently available from human vCJD cases will provide some comparable data. On the basis of what is currently known, there is no reason to suppose that the mouse is not a good model for humans in respect to the distribution of infectivity in oral tissues. Furthermore, the new data are consistent with published results from experiments using a hamster scrapie model24.
6. A second set of experiments using the same mouse model showed that non-invasive and transient contact between gingival tissue and fine dental files contaminated with mouse-adapted BSE brain homogenate transmits infection very efficiently. It is not known how efficient gingival transmission would be if dental files were contaminated with infectious oral tissues and then subsequently cleaned and sterilised, a situation which would more closely model human dental practice. Further studies using the mouse model that would be more representative of the human situation, comparing oral tissues with a range of doses of infectivity, cleaned and sterilised files and the kind of tissue contact with instruments that occurs during dentistry, should be considered.
7. SEAC considered that the experiments appear well designed and the conclusions justified and reliable, while recognising that the research is incomplete and confirmatory experiments have yet to be completed. It is recommended that the research be completed, submitted for peer-review and widely disseminated as soon as possible so others can consider the implications. Nevertheless, these preliminary data increase the possibility that some oral tissues of humans infected with vCJD may potentially become infective during the preclinical stage of the disease. In addition, they increase the possibility that infection could potentially be transmitted not only via accidental abrasion of the lingual tonsil or endodontic procedures but a variety of routine dental procedures.
20 Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished. 21 SEAC (2006) Position statement on vCJD and endodontic dentistry.
http://www.seac.gov.uk/statements/statement0506.htm
22 Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343. 23 SEAC 90 reserved business minutes.
Implications for transmission risks
snip...
11. The new research also suggests that dental procedures involving contact with other oral tissues, including gingiva, may also be capable of transmitting vCJD. In the absence of a detailed risk assessment examining the potential for transmission via all dental procedures, it is not possible to come to firm conclusions about the implications of these findings for transmission of vCJD. However, given the potential for transmission by this route serious consideration should be given to assessing the options for reducing transmission risks such as improving decontamination procedures and practice or the implementation of single use instruments.
12. The size of the potential risk from interactions between the dental and other routes of secondary transmission, such as blood transfusion and hospital surgery, to increase the likelihood of a self-sustaining epidemic is unclear.
13. It is likely to be difficult to distinguish clinical vCJD cases arising from dietary exposure to BSE from secondary transmissions via dental procedures, should they arise, as a large proportion of the population is likely both to have consumed contaminated meat and undergone dentistry. However, an analysis of dental procedures by patient age may provide an indication of the age group in which infections, if they occur, would be most likely to be observed. Should the incidence of clinical vCJD cases in this age group increase significantly, this may provide an indication that secondary transmission via dentistry is occurring. Investigation of the dental work for these cases may provide supporting data. There is no clear evidence, to date, based on surveillance or investigations of clinical vCJD cases, that any vCJD cases have been caused by dental procedures but this possibility cannot be excluded.
Conclusions
14. Preliminary research findings suggest that the potential risk of transmission of vCJD via dental procedures may be greater than previously anticipated. Although this research is incomplete, uses an animal model exposed to relatively high doses of infectivity, and there are no data from infectivity studies on human oral tissues, these findings suggest an increased possibility that vCJD may be relatively efficiently transmitted via a range of dental procedures. Ongoing infectivity studies using human oral tissues and the other studies suggested here will enable more precise assessment of the risks of vCJD transmission through dental procedures.
15. Guidance was issued to dentists earlier this year recommending that endodontic files and reamers be treated as single use which, provided it is adhered to, will remove any risk of a self-sustaining epidemic arising from re-use of these instruments. To minimise risk it is critical that appropriate management and audit is in place, both for NHS and private dentistry.
16. It is also critical that a detailed and comprehensive assessment of the risks of all dental procedures be conducted as a matter of urgency. While taking into account the continuing scientific uncertainties, this will allow a more thorough consideration of the possible public health implications of vCJD transmission via dentistry and the identification of possible additional precautionary risk reduction measures. The assessment will require continued updating as more evidence becomes available on the transmissibility of vCJD by dental routes, and on the prevalence of infection within the population. A DH proposal to convene an expert group that includes dental professionals to expedite such an assessment is welcomed. Given the potential for transmission via dentistry, consideration should be given to the urgent assessment of new decontamination technologies which, if proved robust and effective, could significantly reduce transmission risks.
SEAC June 2007
27 SEAC Epidemiology Subgroup (2006) position statement of the vCJD epidemic.
http://www.seac.gov.uk/statements/state260106subgroup.htm
28 DH (2007) Precautionary advice given to dentists on re-use of instruments
http://www.gnn.gov.uk/environment/fullDetail.asp?ReleaseID=279256&NewsAreaID=2&NavigatedFromDepartment=False
see full text 17 pages ;
http://www.seac.gov.uk/papers/99-7.pdf
SEAC 99th meeting on Friday 14th December 2007
DECEMBER 14, 2007, 10 year Anniversary of my Moms death 'confirmed' from Heidenhain Variant Creutzfeldt Jakob Disease
Greetings,
AS one of them _lay_ folks, one must only ponder ;
"WITH the Nor-98 now documented in five different states so far in the USA in 2007, and with the TWO atypical BSE H-BASE cases in Texas and Alabama, with both scrapie and CWD running rampant in the USA, IS there any concern from SEAC with the rise of sporadic CJD in the USA from ''UNKNOWN PHENOTYPE'', and what concerns if any, in relations to blood donations, surgery, optical, and dental, do you have with these unknown atypical phenotypes in both humans and animals in the USA ???"
"Does it concern SEAC, or is it of no concern to SEAC?"
"Should it concern USA animal and human health officials?"
snip...
----- Original Message -----
From: xxxxxxxxxx
To: flounder9@verizon.net
Sent: Thursday, November 22, 2007 5:39 AM
Subject: QUESTION FOR SEAC
Mr Terry S Singeltary Sr., Bacliff, Texas 77518 USA.
Dear Mr Singeltary,
"Thank you for your e-mail of yesterday with the question for SEAC. I can confirm that this will be asked at the meeting on your behalf and the question and answer will appear in the minutes of the meeting which will be published on the SEAC Internet site."
snip...end...TSS
Archive Number 20071105.3602 Published Date 05-NOV-2007 Subject PRO/AH/EDR> Prion disease update 2007 (07)
PRION DISEASE UPDATE 2007 (07) ****************************** A ProMED-mail post
snip...
[2] USA: National Prion Disease Pathology Surveillance Center Date: June 2007 Source: National Prion Disease Pathology Surveillance Center (USA) [edited]
CJD Cases examined ---------------------- Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD
1996 / 42 / 32 / 26 / 4 / 0 / 0 1997 / 115 / 68 / 57 / 9 / 0 / 0 1998 / 93 / 53 / 45 / 7 / 1 / 0 1999 / 114 / 69 / 61 / 8 / 0 / 0 2000 / 151 / 103 / 89 / 14 / 0 / 0 2001 / 208 / 116 / 106 / 9 / 0 / 0 2002 / 255 / 143 / 118 / 23 / 2 / 0 2003 / 272 / 174 / 132 / 41 / 0 / 0 2004 / 334 / 183 / 157 / 21 / 0 / 1* 2005 / 352 / 195 / 152 / 37 / 1 / 0 2006 / 372 / 186 / 143 / 30 / 0 / 1** 2007 / 120 / 68 / 35 / 7 / 0 / 0 TOTAL / 2428*** / 1390**** / 1121 / 210 / 4 / 2
*Acquired in UK ** Acquired in Saudi Arabia *** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007. **** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, 26 from 2007).
Notes:
-- Cases are listed based on the year of death when available. If the year of death is not available, the year of sample receipt is used.
-- Referrals: Cases with possible or probable prion disease from which brain tissue or blood in the case of familial disease were submitted.
-- Inconclusive: Cases in which the samples were not sufficient to make a diagnosis.
-- Non-vCJD type unknown are cases in which the tissue submitted was adequate to establish the presence but not the type; in all cases, vCJD could be excluded.
-- Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
flounder@wt.net
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?
http://www.neurology.org/cgi/eletters/60/2/176#535
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
Available online 29 July 2003. Volume 3, Issue 8, August 2003, Page 463
“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." ...
http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fulltext
http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734.
http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535
Like lambs to the slaughter
31 March 2001 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. ...
http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html
DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehörden sind lax. Link auf diesen Artikel im Archiv:
http://service.spiegel.de/digas/find?DID=18578755
"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...
http://service.spiegel.de/digas/servlet/find/DID=18578755
Thu Dec 6, 2007 11:38
FDA IN CRISIS MODE, AMERICAN LIVES AT RISK
http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html
FDA SCIENCE AND MISSION AT RISK
http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
http://cjdusa.blogspot.com/
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/
SCRAPIE USA
http://scrapie-usa.blogspot.com/
NOR-98 ATYPICAL SCRAPIE CASES USA
http://nor-98.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA
http://cjdmadcowbaseoct2007.blogspot.com/
Transmissible Mink Encephalopathy TME
http://transmissible-mink-encephalopathy.blogspot.com/
CHRONIC WASTING DISEASE
http://chronic-wasting-disease.blogspot.com/
TSEAC MEETING
----- Original Message -----
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOVCc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Wednesday, November 29, 2006 1:24 PM
Subject: TSE advisory committee for the meeting December 15, 2006 [TSSSUBMISSION] November 29, 2006
Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,
a kind and warm Holiday Greetings to you all. i kindly wish to submit the following to the TSE advisory committee for the meeting December 15, 2006, about the assessment for potential exposure to vCJD in human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related communication material ;
http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm
i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;
http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines
however, i seem to disagree. from my primitive ciphering, i see it anotherway. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million. also, what about the mixed genotypes/mixed susceptibility? what about the silent carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN strain or phenotype? this risk assessment is just more BSe to me. just another in a long line of ...
Greetings again Dr. Freas et al at FDA,
THIS was like closing the barn door after the mad cows got loose. not only the red cross, but the FDA has failed the public in protecting them from the TSE aka madcow agent. TSE agent i.e. bse, base, cwd, scrapie, tme, and any sub strains thereof. we do not know if these strains will or have transmitted to humans as subclinical TSE or clinical disease, and we do not know if they have or will transmit second, third, forth passage via friendly fire i.e. multiple potential routes via medical, surgical, pharmaceutical etc. IF you remember correctly Dr. Freas et al, i called this long ago, almost 6 years ago ;
PDF]Freas, William TSS SUBMISSION
Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08, 200l 3:03 PM freas ...Freas, William From: Terry S. Singeltary Sr. [flounder@wt.net] Sent: Monday, January 08,200l 3:03 PM
To: freas@CBS5055530.CBER.FDA.GOV
Subject: CJD/BSE (aka madcow) Human/Animal TSE?s--U.S.--Submission
To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products.
snip...
I am beginning to think that the endless attempt to track down and ban, potential victims from known BSE Countries from giving blood will be futile. You would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT SWIFTLY to find blood test for TSE's, whether it be blood test, urine test, eyelid test, anything at whatever cost, we need a test FAST. DO NOT let the incubation time period of these TSEs fool you. To think of Scrapie as the prime agent to compare CJD, but yet overlook the Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by scrapie from a vaccine made of scrapie infected sheep brains, would be foolish. I acquired this full text version of the event which was recorded in the Annual Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. From the BVA and the URL is posted in my (long version). ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
see full text ;
http://tseac.blogspot.com/
vCJD case study highlights blood transfusion risk
http://vcjdblood.blogspot.com/
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle
9/13/2005
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed
Subject: Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION Date: August 24, 2005 at 2:47 pm PST August 24, 2005
Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION
Greetings APHIS ET AL,
My name is Terry S. Singeltary Sr.
I would kindly like to comment on [Docket No. 05-004-1] RIN 0579-AB93 ;
snip...
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.
MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???
go figure. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Comment Submitted Comment Receipt
Thank you. Your comment on Document ID: APHIS-2006-0041-0001 has been sent. Comment Tracking Number: APHIS-2006-0041-DRAFT-0028
Attachments: C:\My Music\My Documents\APHIS-2006-0041_January 28.doc
If you wish to retain a copy of the receipt, use the following link to print a copy for your files. Print
http://www.regulations.gov/fdmspublic/component/main
THE only difference between the UK poisoning the globe, and the USA, it is now legal with GWs and OIEs BSE MRR policy ;
IT's O.K. to poison 3rd world countries ;
http://www.bseinquiry.gov.uk/files/yb/1994/05/20002001.pdf
On 20 February 1990, Dr Pickles wrote to Ms Verity (APS/CMO). Dr Pickles minute included the following: 1. Mr Meldrum is arguing that MAFF have already taken all the necessary and responsible steps to warn importing countries of the BSE dangers in UK meat and bone meal. Yet the action taken so far overseas suggest the message has not got through, or where it has this has been late. The first nation that woke up to the danger did so a year after our own feed ban. It seems even now several EC countries neither ban our imports or the general feeding of ruminant protein. It also seems the OIE and CVO have yet to inform the rest of the world. 2. I do not see how this can be claimed to be responsible. We do not need an expert group of the Scientific Veterinary Committee to tell us British meat and bone meal is unsafe for ruminants. I fail to understand why this cannot be tackled from the British end which seems to be the only sure way of doing it, preferably by banning exports. As CMO says in his letter of 3 January surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries. [79]
http://www.bse.org.uk/dfa/dfa25.htm
http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh
OLD DOCKET SUBMISSION TSS
Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)
https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
PART 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
Asante/Collinge et al, 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;
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7
http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm
[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1 File Format: PDF/Adobe Acrobat - View as HTML Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of those who provided comments in response to Docket No. ... Meager 8/18/01 Terry S. Singeltary Sr ...
www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)
Docket Management
Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm
Dockets Entered On October 2, 2003 Table of Contents, Docket #, Title, 1978N-0301,
OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr. Vol #: 1, ...
www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm
Daily Dockets Entered on 02/05/03
DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2. ... Vol#: 1.
03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...
www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm
Docket Management
Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater
Comment Number: EC -1
Accepted - Volume 1
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html
Daily Dockets - 04/10/03
... 00D-1662 Use of Xenotransplantation Products in Humans. EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...
www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm
- 05-20-2003 - Cached
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #:1
http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm
http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm
01N-0423 Substances Prohibited from use in animal food/Feed Ruminant
EMC 1 Terry S. Singeltary Sr. Vol#: 3
http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm
TSS
1 09.30 Introduction SEAC Chair
Approval of draft minutes from SEAC 98
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE
Draft open minutes of the 98th meeting held on 29th July 2007
23. The Chair summarised the discussion noting that SEAC agreed: • there are no substantive new data to allow a reassessment of the infectivity of plasma derivatives from fractionation of contaminated plasma. • only research that measures the clearance of endogenous infectivity in blood would support a reassessment of the infectivity of plasma derivatives. • the National Haemophiliac Database could provide important data to assess the risks of transmission of vCJD via plasma derivatives.
snip...
32. A member noted that from a public and consumer perspective SEAC has always been seen as an exemplar of good practice for example by holding its meetings in public and communicating its statements and decisions using clear language. It was noted that the House of Commons report is not in favour of consumer or lay representatives on all scientific committees as a matter of course and it advises that their roles are re-evaluated. The member noted that lay members are in fact important in ensuring that information produced by committees can be understood by non-experts. However, it is important to make clear that a single consumer representative cannot represent the thoughts of all consumers. Periodic review of scientific advisory committees, such as is
3 http://www.dti.gov.uk/files/file39981.pdf
4 http://www.publications.parliament.uk/pa/cm200506/cmselect/cmsctech/900/900-i.pdf
undertaken with SEAC, is important as a quality assurance mechanism.
see full text 14 pages ;
http://www.seac.gov.uk/papers/99-1.pdf
USE OF PREVIOUS SEAC OPINIONS ISSUE
1. Given the evolving nature of scientific understanding of transmissible spongiform encephalopathies (TSEs), it is suggested that an agreed procedure be in place setting out a time limit for the use of SDEAC advice by a Government Department without referral back to the committee. It is suggested this is needed because new data could have appeared since the advice was given that would cause the committee to alter that advice.
CONSIDERATION
see full text page ;
http://www.seac.gov.uk/papers/99-6.pdf
REPORT FROM THE SEAC SHEEP SUBGROUP
31. Given the low prevalence of classical scrapie and assuming that BSE in sheep would occur independently from that of classical scrapie, if BSE is or was present in the national sheep flock, it would have been expected to arise more frequently as a single infection rather than mixed with classical scrapie. However, since BSE as a single infection in sheep has never been found, it is highly unlikely that an appreciable number of mixed infections of classical scrapie and BSE are present currently in sheep unless BSE and classical scrapie are more efficiently transmitted together between sheep compared with BSE in isolation but there are no data to suggest this may or may not be the case. However, unpublished results from inoculations into mice of a mixed inoculum compared with individual inocula indicate an increased attack rate suggesting higher transmission efficiencies of mixed strains is a possibility12.
Summary 33. The data from the strain typing study, while intriguing and not fully explained, provide no evidence for the presence of BSE in sheep as a single infection. Whilst these data may indicate the presence of mixed BSE and classical scrapie infections, this is one of several possible interpretations. These data should not give rise to concern that there is an appreciable number of mixed BSE-12 classical scrapie infections that would significantly influence estimates of the prevalence of BSE in the UK sheep flock.
Unpublished Roslin Institute studies.
13 SEAC Sheep Subgroup statement (2006)
http://www.seac.gov.uk/statements/sheepsubgrp-statement131006.pdf
14 Opinion on the quantitative risk assessment on the residual BSE risk in sheep meat and meat products. The EFSA Journal. (2007) 442, 1-44.
http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej442_qra_sheep_en,3.pdf
Maternal transfer of classical scrapie prion protein via sheep milk Background 34. The mechanisms for transmission of classical scrapie between sheep are not fully understood, however there is evidence to suggest that the risk of transmission is high during the neonatal period15. A study by VLA is examining whether milk may be a significant route of transmission by bottle feeding milk collected from ewes genetically susceptible to, and infected with classical scrapie, to genetically susceptible TSE-free lambs. Data 35. Early unpublished findings from the study suggest that milk may be a route of transmission. Post mortem examination of three lambs that were bottle-fed milk from classical scrapie infected ewes which died early in the study from intercurrent disease revealed the presence of PrPSc in gut lymphoid tissue in two lambs. The milk fed to these two lambs was from two ewes that developed clinical signs of classical scrapie during lactation. The milk fed to the third lamb was from a ewe with clinical signs of classical scrapie at the beginning of lactation from which only a relatively small volume of milk was produced. Somatic cell counts were high in at least a proportion of the milk collected from the ewes. PrPSc was not found in a control lamb, which also died from intercurrent disease, that was fed milk from an uninfected ewe. Implications 36. These data suggest that PrPSc may be transmitted from ewe to lamb via milk or colostrum. As a full lactation was fed to the lambs it is not possible to determine whether transmission occurred via colostrum and/or the subsequent milk. The study is at too early a stage to assess whether classical scrapie develops as a result of this exposure, although this should be considered likely.
snip...see full text 15 pages ;
http://www.seac.gov.uk/papers/99-2.pdf
SCIENTIFIC BASIS FOR CLASSICAL SCRAPIE CONTROLS
Scientific basis for relaxation of classical scrapie controls
AFSSA OPINION 13. The AFSSA opinion (Annex 1) describes three areas of scientific uncertainty that have led to the conclusion that the proposed changes to controls may significantly increase the risk to human health from the slaughter of sheep from classical scrapie affected flocks for human consumption. In summary, AFSSA considered that: • the tests to detect and discriminate between BSE and classical and atypical scrapie are limited as (i) their sensitivity has not been accurately determined, (ii) they may not detect BSE in animals that are also infected with classical scrapie and (iii) the conduct of the discriminatory test on the index case would not guarantee the absence of BSE in the flock. Furthermore, as only brain tissue is tested, the rapid tests cannot detect TSE infections during the incubation period prior to accumulation of abnormal prion protein in the brain. • although there are no epidemiological data to suggest a link between classical scrapie strains and human TSEs, in view of the diversity of classical scrapie strains and the lack of a robust prospective study to examine potential links between these TSE strains and human TSEs, a link cannot be ruled out. • the incidence of classical scrapie infections in classical scrapie affected sheep flocks can be relatively high, particularly in those animals of susceptible genotypes5 suggesting classical scrapie infection may be widespread in affected flocks. 14. In view of these considerations, AFSSA concluded that allowing animals from classical scrapie affected flocks to be slaughtered for human consumption, particularly without any restriction on genotype, would increase the human health risk as: (i) the presence of BSE in a sheep cannot be ruled out by the application of discriminatory tests as the sensitivity of the tests is not known precisely and detection may be compromised when classical scrapie is also present. (ii) classical scrapie infections can be widespread in sheep flocks and as rapid TSE tests cannot identify infected animals in the early part of the incubation period, it is possible that an appreciable number of classical scrapie infected animals could enter the human food chain. (iii) the transmission to humans of TSE strains other than BSE cannot be ruled out.
5 Corbiere et al. (2007) Advanced survival models for risk-factor analysis in scrapie. J. Gen Virol. 88, 696-705.
EFSA OPINION 15.
The EFSA Scientific Panel on Biological Hazards considered the AFSSA opinion and in particular the evidence for possible links between classical or atypical scrapie and human TSEs and the performance characteristics of discriminatory tests for sheep TSEs (Annex 2). The Panel concluded that: • there is no evidence for an epidemiological or molecular link between classical and/or atypical scrapie and TSEs in humans. The BSE agent is the only agent identified as zoonotic. However, in view of their diversity it is currently not possible to exclude transmissibility to humans of other animal TSE agents. • current discriminatory tests appear, up to now, to be reliable for the differentiation of BSE from classical and atypical scrapie. However, at the current stage of scientific knowledge, neither their diagnostic sensitivity nor their specificity can be assumed to be perfect. KOM AG TSE OPINION 16. KOM AG TSE considered the changes to classical scrapie controls (Annex 4) and noted that recently published research by Reckzeh et al. (2007)6 (Annex 4) showed that some sheep of susceptible genotypes that had tested negative for TSE infection when brain samples were tested, were in fact positive for TSE infection when peripheral tissues were tested. Thus, the committee concluded that the current strategy of testing brain tissue cannot exclude the presence of TSE infections at the stage of the incubation period prior to involvement of the brain. Thus, the changes to classical scrapie controls could allow classical scrapie infectivity into the human food chain. 17. In addition, the committee noted that, although the EFSA Biohazard Panel concluded that there are no indications of the existence of zoonotic link between classical scrapie and human TSEs, as classical scrapie strains are not uniform and are poorly defined, a zoonotic potential cannot be ruled out. In view of this, the committee considered that consumer exposure to classical scrapie should be avoided and was not in favour of the changes to the classical scrapie controls that would allow this to occur.
6 Reckzeh et al. (2007) Rapid testing leads to the underestimation of the scrapie prevalence in an affected sheep and goat flock. Vet. Microbiol. 123, 320-327.
PREVIOUS SEAC OPINIONS
snip...
Opinion of the French Food Safety Agency (AFSSA) on changes to the control measures for sheep and goat herds in which a case of classical or atypical scrapie has been detected
http://www.afssa.fr/Documents/ESST2006sa0343EN.pdf
Opinion of the Scientific Panel on Biological Hazards on certain aspects related to the risk of transmissible spongiform encephalopathies (TSEs) in ovine and caprine animals
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5- Conclusions and opinion
On the following grounds:
- the discriminatory tests do not enable the presence of BSE to be ruled out either in the tested animal or by extension in the flock to which it belongs;
- the transmission to humans of TSE strains other than BSE cannot be ruled out;
- the knowledge acquired of the genetic susceptibility of sheep to scrapie and BSE should be used, insofar as this is possible, to limit the risk of consumer exposure,
The Committee is making the following recommendations:
Recommendations common to both types of control measure:
- permanent individual identification of all small ruminants belonging to the herds concerned.
- for sheep, genotyping for the four cordons (136, 141, 154 and 171) of all animals in an infected flock.
- all tests carried out on animals slaughtered or culled as part of the control measures must be effected with one of the rapid tests with the best sensitivity for the detection of atypical scrapie (currently Idexx, Biorad).
- conduct of a discriminatory test on all secondary cases identified.
- destruction of all positive animals.
snip...please see full text 9 pages ;
http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej466_tse_ovine_caprine_en.pdf
Opinion of the KOM AG TSE Evaluation of the catalogue of measures after detecting a TSE case Reckzeh et al. (2007) Rapid testing leads to the underestimation of the scrapie prevalence in an affected sheep and goat flock. Vet. Microbiol. 123, 320-327.
snip see full text 21 pages ;
http://www.seac.gov.uk/papers/99-3.pdf
Consideration of various options relating to relaxation of the total feed ban
ISSUE
1. The Department for Environment, Food and Rural Affairs (Defra) the devolved Rural Affairs Departments and the Food Standards Agency (FSA) have asked SEAC to consider, in qualitative terms, the potential for further transmissible spongiform encephalopathy (TSE) infections and epidemics to arise as a result of possible implementation of various future options for relaxing the TSE-related feed controls. This paper, prepared by Defra, provides an overview of European Union (EU) proposals and relevant science.
BACKGROUND
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Work Programme8 on TSEs in November 2006. In relation to the feed ban, the document proposed discussions on:
i. Permitting a tolerance of “insignificant amounts” of animal protein, including fish meal in feed, arising as a result of “adventitious” (e.g. rodent/avian) or “technically unavoidable” (e.g. fish meal) contamination.
ii. The use of fish meal in feed for young ruminants on the basis of a scientific assessment of their dietary needs and following an assessment of the control aspects.
iii. Permitting a general tolerance level with regard to the “small presence” of mammalian MBM in feed for farmed animals.
Currently it is not possible to expand on the terms “insignificant amount” or “small presence”. Any future tolerance level would be determined to a large extent by the sensitivity and specificity of the quantitative tests available. Quantitative risk assessments (e.g. EFSA quantitative risk assessment of animal BSE risk posed by mammalian MBM 2005) may also be taken into account. Also it is not clear exactly what is envisaged under (iii) but the UK Government’s current understanding is that it is a variation on (i) in that an accepted “tolerance” level would be agreed below which the Member State would not be obliged to investigate and assess the individual risk.
9. In January 2007, the TSE Regulation was amended by co-decision. This provided a legal basis for the future options of (i) feeding fishmeal to young ruminants only – a political compromise between the European Commission which wanted the option of permitting the feeding of fish meal to ruminants and the European Parliament which opposed the feeding of such animal protein to herbivores on “ethical” grounds, but conceded to allowing the option of feeding fish meal to young ruminants based on a scientific assessment of their dietary needs – and (ii) the introduction of a risk-based tolerance level for the presence of “insignificant” amounts of animal protein in feed “caused through adventitious and technically unavoidable contamination”. Apart from the circumstances outlined above (and existing exemptions), the ban on feeding animal protein to ruminants remained. The TSE Regulation required that rules for the prevention of cross contamination and methods of sampling and analysis to check compliance, should be based upon a European Commission report covering the sourcing, processing, control and traceability of feedingstuffs of animal origin. The recitals of the TSE Regulation were also amended to propose that “the feeding to non-ruminants of certain PAP originating from non-ruminants should be allowed taking into account the prohibition on intra-species recycling…
8 http://ec.europa.eu/food/food/biosafety/bse/work_prog_tse_en.pdf
and the control aspects in particular linked to differentiation of PAP specific to certain species”: this proposal could be agreed by the European Commission and EU Member States. 10. At SEAC 98 (July 2007) following the media coverage referred to in paragraph 7, SEAC “considered it important that Defra should seek the views of SEAC should such a policy [of feeding non-ruminant MBM to non-ruminants] be proposed as part of the TSE Roadmap”. 11. In July 2007, the European Parliament adopted a report9, which called on the European Commission and the European Council to “lift the ban on feeding fish meal and fish oil to ruminants” (although there is no ban on feeding fish oil to ruminants). The report stressed that "there is no scientific evidence to support a total ban on fish meal on the grounds that it may transmit BSE or other TSEs". 12. In September 2007, the European Commission tabled a proposal (SANCO/2017/2007) to permit the use of fish meal in milk replacers for feeding to young ruminants before weaning, while maintaining strict controls on the feeding of fish meal to adult ruminants, in line with the requirements of the TSE Regulation. In November 2007, the European Commission discussed an amended proposal (SANCO/2017/2007rev.1) to permit the use of fish meal in milk replacers for feeding to young ruminants, with Member States. The amended proposal indicated that it applied to milk replacers administered in either dry or liquid form, provided to young ruminants as a supplement or milk substitute before the completion of weaning. The Commission explained that the European Food Safety Authority had advised that a scientific assessment of the dietary needs of young ruminants was outside its remit. Consequently, the Commission was considering establishing a group of animal nutrition experts to carry out this task. The European Commission indicated following additional training, the qualitative performance of National Reference Laboratories had improved beyond the position reported from the 2006 inter-laboratory trial. However, no further progress could be made on tolerance proposals (e.g. an agreed tolerance level for the presence of fish meal in adult ruminant feed) until there had been a significant improvement in the performance of quantitative tests and this could take at least a year. The European Commission undertook to make data relating to the assessment of dietary needs (EFSA) and the assessment of control aspects (further report from Community Reference Laboratory for Animal Proteins) available to Member States in due course.
9 European Parliament (2007) European Parliament resolution of 10 July 2007 on industrial fisheries and the production of fishmeal and fish oil. P6_TA-PROV(2007)0327
http://www.europarl.europa.eu/news/expert/infopress_page/033-9006-190-07-28-904-20070709IPR08984-09-07-2007-2007-false/default_en.htm
http://www.europarl.europa.eu/sides/getDoc.do?pubRef=-//EP//TEXT+TA+P6-TA-2007-0327+0+DOC+XML+V0//EN&language=EN
snip...see full text 29 pages ;
http://www.seac.gov.uk/papers/99-4.pdf
Horizon scanning
ISSUE
1. To consider emerging scientific issues in relation to transmissible spongiform encephalopathies (TSEs) and to raise awareness of issues SEAC may consider in the future.
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SEAC 99/5 ANNEX 1 DEFRA
To advise SEAC of possible animal-health related TSE developments in 2008.
BACKGROUND 1.
World Organisation for Animal Health (OIE)
The World Organisation for Animal Health is considering current trade guidelines on scrapie and BSE in relation to the emergence of atypical forms of the diseases. While it is unlikely that changes are required to guidelines for BSE, significant revision will be required to take into account the implications of atypical scrapie.
The OIE is expected to endorse the provisional recognition of the UK as “controlled risk” for BSE, at its General Session in May 2008 .
2. European Union Many of the short term goals of the EU’s 2005 TSE Roadmap have been achieved. Those outstanding include:
i) Revision of the BSE Monitoring Programme in Cattle The European Commission is currently discussing a revision of the BSE monitoring programme in cattle, with Member States, to achieve better targeting of the surveillance activity and a reduction in the number of tests. We anticipate that there will be an increase in the testing age limit for fallen stock and date/age based changes to the testing age limit for cattle slaughtered for human consumption. We envisage that SEAC will be consulted on significant changes to the BSE monitoring programme in relation to cattle slaughtered for human consumption.
ii) EU Feed Controls The European Commission is currently discussing the feeding of fish meal to young ruminants, with Member States. The European Commission intends to establish an expert group to examine the nutritional aspects of the proposal. The Community Reference laboratory for animal proteins in feed is working to improve the quantitative method and a further inter-laboratory study is expected. The outcome of this work could pave the way for the introduction of tolerances from 2008. Other research on feed tests could support the feeding of non-ruminant PAP to non-ruminants in the longer term. It may be necessary to consult SEAC again on specific developments.
iii) EU Scrapie Controls
In April 2007, the EU’s Standing Committee on the food chain and animal health adopted more proportionate control measures for scrapie. Following a subsequent legal challenge from France, the European Court of First Instance suspended the new measures relating to classical scrapie pending the hearing of the main case. For sheep flocks in which classical scrapie has been detected the remaining options are whole-flock cull and genotyping and culling. For goats the only remaining option is whole-flock cull. The legal case centred on scientific opinions from the French Food Safety Agency (AFSSA) and the European Food Safety Authority (EFSA) and the application of the precautionary principle. It highlights the importance of close liaison between national risk assessment bodies and EFSA. The Commission is planning to appeal against the judgement and seek acceleration of the main case.
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3. TSEs in Cattle
We predict a continued decline in cases of BSE in the EU and estimate fewer than 75 cases in UK by the end of 2007 (compared to 114 in 2006). The majority of cases are still being detected in cattle born before the 1996 feed ban. The Older Cattle Disposal Scheme closes at the end of 2008 and we are working with industry to maximise the uptake. The prevalence in successive BARB birth cohorts is extremely low and appears to be decreasing. However, as the pre-1996 cattle population declines, BARBs will form an increasing percentage of the total number of cases.
The overall prevalence of atypical BSE appears low. Two cases of atypical BSE have been detected in UK to date in older cattle. Oral challenge studies are being planned in Europe and Japan which will provide further information on the pathogenesis. While the aetiology of atypical BSE remains unknown the long term consequences for the maintenance of key BSE controls remains uncertain.
snip...full text 10 pages ;
http://www.seac.gov.uk/papers/99-5.pdf
8 12.15 Public Q&A SEAC Chair
9 13.20 Update on vCJD and sCJD epidemiology Dr R Knight (NCJDSU)
10 13.40 Update on NATA and other vCJD prevalence studies Professor N Gill (HPA) Dr J Clewley (HPA)
11 14.30 Re-assessment of the potential risk of vCJD transmission via dentistry Dr P Bennett (DH) Dr P Grove (DH)
A RE-ASSESSMENT OF THE POTENTIAL RISK OF VCJD TRANSMISSION VIA DENTISTRY ISSUE
1. The Department of Health (DH) has asked SEAC to consider an interim assessment of the potential risk of vCJD transmission via dental procedures. This work builds on previous risk assessments on possible dental transmission considered by SEAC.
BACKGROUND
Previous SEAC considerations of vCJD transmission via dentistry
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The New DH Risk Assessment
8. The research on infectivity just noted forms one strand of a wider programme at the HPA, which is also intended to quantify protein residues found on dental instruments and the effectiveness of sterilisation in reducing infectivity. Following SEAC 97 (May 2007), DH commissioned a comprehensive re-assessment of the potential risks of vCJD transmission associated with dentistry to take account of research at the HPA and elsewhere. The assessment aims to clarify the range of plausible scenarios for vCJD transmission via dental instruments that could occur, given what is currently known, and to identify the most important factors affecting this risk. The assessment will be used to identify the most important areas of further work to address the uncertainties and any robust ways of cost effectively reducing risks further.
9. This new interim risk assessment has been produced by DH analysts (annex 3) in collaboration with a Scientific Reference Group of independent experts (Chaired by Professor Graham Medley). Members of the Group have expertise in dentistry, instrument decontamination, human and animal prion diseases, anatomy, public health, risk assessment modelling and epidemiology. This group met three times to review and refine the modelling framework and agree the risk assessment. The group provided advice on the inputs and assumptions incorporated into the risk assessment, particularly where expert judgement was required due to a lack of hard data. Under circumstances where key data are absent, precautionary assumptions were agreed. As a number of large uncertainties that strongly influence the quantification of risk remain, the risk assessment is considered as interim and will be updated in the future when new scientific evidence becomes available.
10. The assessment examines the risk that vCJD may be transmitted via dental procedures by establishing plausible ranges for key parameters, including (see sections 2 and 3 of the risk assessment):
• the vCJD infectivity of tissues of the oral cavity of infected patients
• the deposition of that material onto different types of dental instruments and the effectiveness of standard cleaning and sterilisation processes used in dental practice
• the mechanisms and efficiency of transfer of vCJD infectivity from contaminated instruments used on subsequent patients
• the probability of transmission based on assessments of the number and types of dental procedure conducted and the number of people who might be carrying an asymptomatic vCJD infection.
Findings 11.
As there is lack of substantial data with which to accurately quantify many of these parameters, plausible ranges for these parameters have been established to take account of the often large uncertainties in the data. The large uncertainties in many of these parameters strongly influence the quantification of the risk.
12. Plausible scenarios built up using ranges for each of these factors include many in which dental transmission would have no detectable effect on the course of the vCJD outbreak (see section 4 of the risk assessment). However, there are some which include a combination of pessimistic assumptions as regards the infectivity of dental / oral tissues and the effects of instrument decontamination which suggest that:
• there could be some hundreds of vCJD transmissions per annum via dentistry - albeit against a background of several thousand existing vCJD infections (not clinical cases of vCJD), or where
• dental transmission could generate a self-sustaining reservoir of vCJD infection within the population.
13. The distinction between vCJD infections and clinical cases of vCJD is important. If a large proportion of secondary transmissions result in subclinical infections (either never developing into clinical disease or doing so over an extended time-scale) and those infected are infectious, the likelihood of a self-sustaining epidemic increases. The proportion of individuals who might enter such a subclinical “carrier state” is unknown. Key Assumptions and areas of uncertainty
14. Work on the risk assessment is on-going and new data should enable some of the inputs and assumptions underpinning these scenarios to be revised. Key areas of uncertainty are:
• Infectivity in relevant tissues. Of all the unknowns, that of overriding importance is whether dental/oral tissues in patients incubating vCJD would be infective, and if so at what level.
There are as yet no results of studies using human gingival and dental pulp tissues, and these studies may extend into 2009 and 2010 respectively. This is examined in section 2.3 of the risk assessment.
• Protein Residues on dental instruments. This is examined in section 2.2 of the risk assessment.
• Efficacy of Autoclaving. This is examined in section 2.3 of the risk assessment.
• Current prevalence of vCJD infection. This is examined in section 3.3 of the risk assessment.
• Epidemiology of vCJD. This is examined in section 4 of the risk assessment.
15. Suggested areas of further work to reduce the uncertainty in these key areas are described in section 5 of the risk assessment together with a preliminary analysis of possible interventions and risk reduction measures.
ADVICE SOUGHT FROM THE COMMITTEE
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POSITION STATEMENT vCJD AND ENDODONTIC DENTISTRY
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Endodontic instruments
5. Evidence suggests that the files and reamers used in endodontic procedures are reused and are difficult to reliably decontaminate4. Appreciable quantities of residual material remain adherent to the surface after normal cleaning and sterilisation5. Thus, there is potential for transfer of dental pulp between patients undergoing endodontic procedures.
vCJD infectivity in dental tissues
6. There are no data on vCJD infectivity in dental pulp. Although no abnormal prions were found in a study of dental tissues, including dental pulp, from vCJD cases6, dental pulp includes blood and peripheral nerve tissue known to carry vCJD infectivity7,8. In addition, appreciable infectivity has been found in the dental pulp of hamsters with hamster scrapie9. Although it is possible that the peripheral nerve may only become infective close to, or after, the onset of clinical vCJD, inflammation may promote the propagation of prions10. Thus, although the data are limited and indirect, it is reasonable to assume that the dental pulp of individuals subclinically-infected with vCJD may be infectious although the level of infectivity is unknown. Studies underway will provide direct data on the infectivity in dental tissues from vCJD cases. level of infectivity is unknown.
4 Letters et al. (2005) A study of visual and blood contamination on reprocessed endodontic files from general dental practice. Br. Dent. J. 199, 522-525. 5 Smith et al. (2005) Residual protein levels on reprocessed dental instruments. J. Hosp. Infect. 61, 237-241. 6 Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343. 7 SEAC 91 minutes paragraph 9.
www.seac.gov.uk/papers/papers.htm 8
Department of Health (2005) Assessing the risk of vCJD transmission via surgery: an interim view. Unpublished. 9 Ingrosso et al. (1999) Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80, 3043-3047. 10 Heikenwalder et al. (2005) Chronic lymphocytic inflammation specifies the organ tropism of prions. Science. 307, 1107-1110.
Subclinical carrier state
7. A study of humanised mice showed that vCJD infections may not always progress to clinical disease within the normal lifespan of the animals11. Another study suggested that prion infections in mice that remain at a subclinical level can be transmitted to other mice, resulting in clinical disease12. Thus, there is evidence to suggest that individuals infected with the BSE / vCJD agent may remain in a subclinical infection carrier state instead of developing vCJD. A discrepancy between prevalence estimates based on a survey of abnormal prion protein in appendix and tonsil tissue and data on vCJD cases supports this hypothesis13. As no diagnostic test exists to identify such individuals, they could over the course of their lives be potential sources of numerous secondary infections arising from invasive medical or dental procedures.
8. The prevalence of subclinical infection in the UK population is uncertain. A recent estimate suggests the number of subclinical carriers may be of the order of several thousand14. SEAC has strongly recommended that further studies to ascertain better the prevalence of vCJD infection be urgently considered15.
Transmission risks
9. The new DH analysis suggests that, on the basis that residual dental pulp on endodontic files and reamers is transferred relatively efficiently to patients on reuse, dental pulp is as infective as peripheral nerve tissue and a subclinical carrier population for vCJD exists, a self-sustaining vCJD epidemic arising from endodontic surgery is plausible. There are uncertainties about the efficiency of vCJD transmission via endodontic procedures, the vCJD infectivity of dental pulp and the existence of a subclinical infection carrier state. However, even if a self-sustaining epidemic were not possible, clusters of vCJD infections could arise from the use of instruments contaminated with the vCJD agent from endodontic procedures on infected patients. Interactions between this and other routes of secondary transmission, such as blood transfusion and hospital surgery, would make a self-sustaining epidemic more likely.
Potential risk reduction measures
10. Endodontic files and reamers have a limited lifespan, restricting the number of possible secondary transmissions. Improving the effectiveness of procedures used to decontaminate dental instruments would reduce the risk of transmission. Restricting endodontic files and reamers to single use would prevent potential secondary transmission via these instruments. Conclusions
11. A preliminary risk assessment produced by DH suggests that vCJD transmission via endodontic dentistry may, under certain hypothetical but plausible scenarios, be sufficient to sustain a secondary vCJD epidemic. However, there are uncertainties around the data and assumptions underpinning the assessment. Research underway will address some of these uncertainties and allow the risk assessment to be refined. Once the research is complete and / or other data become available, the risks should be reassessed. A watching brief should be maintained.
12. It is unclear whether or not vCJD infectivity can be transmitted via endodontic files and reamers. However, given the plausibility of such a scenario and the large number of procedures undertaken annually, it would be prudent to consider restricting these instruments to single use as a precautionary measure. Since sufficiently rigorous decontamination of these instruments is difficult, single use of these instruments would eliminate this risk, should it exist.
SEAC May 2006
© SEAC 2007
New research
4. Preliminary, unpublished results of research from the Health Protection Agency, aimed at addressing some of the uncertainties in the risk assessments, were reviewed by SEAC (SEAC 97, May 2007). The prion agent used in these studies is closely related to the vCJD agent. This research, using a mouse model, shows that following inoculation of mouse-adapted bovine spongiform encephalopathy (BSE) directly into the gut, infectivity subsequently becomes widespread in tissues of the oral cavity, including dental pulp, salivary glands and gingiva, during the preclinical as well as clinical stage of disease.
5. It is not known how closely the level and distribution of infectivity in the oral cavity of infected mice reflects those of humans infected with vCJD, as there are no comparable data from oral tissues, in particular dental pulp and gingiva, from human subclinical or clinical vCJD cases. Although no abnormal prion protein was found in a study of human dental tissues, including dental pulp, salivary glands and gingiva from vCJD cases22, the relationship between levels of infectivity and abnormal prion protein is unclear23. Infectivity studies underway using the mouse model and oral tissues that are presently available from human vCJD cases will provide some comparable data. On the basis of what is currently known, there is no reason to suppose that the mouse is not a good model for humans in respect to the distribution of infectivity in oral tissues. Furthermore, the new data are consistent with published results from experiments using a hamster scrapie model24.
6. A second set of experiments using the same mouse model showed that non-invasive and transient contact between gingival tissue and fine dental files contaminated with mouse-adapted BSE brain homogenate transmits infection very efficiently. It is not known how efficient gingival transmission would be if dental files were contaminated with infectious oral tissues and then subsequently cleaned and sterilised, a situation which would more closely model human dental practice. Further studies using the mouse model that would be more representative of the human situation, comparing oral tissues with a range of doses of infectivity, cleaned and sterilised files and the kind of tissue contact with instruments that occurs during dentistry, should be considered.
7. SEAC considered that the experiments appear well designed and the conclusions justified and reliable, while recognising that the research is incomplete and confirmatory experiments have yet to be completed. It is recommended that the research be completed, submitted for peer-review and widely disseminated as soon as possible so others can consider the implications. Nevertheless, these preliminary data increase the possibility that some oral tissues of humans infected with vCJD may potentially become infective during the preclinical stage of the disease. In addition, they increase the possibility that infection could potentially be transmitted not only via accidental abrasion of the lingual tonsil or endodontic procedures but a variety of routine dental procedures.
20 Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished. 21 SEAC (2006) Position statement on vCJD and endodontic dentistry.
http://www.seac.gov.uk/statements/statement0506.htm
22 Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343. 23 SEAC 90 reserved business minutes.
Implications for transmission risks
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11. The new research also suggests that dental procedures involving contact with other oral tissues, including gingiva, may also be capable of transmitting vCJD. In the absence of a detailed risk assessment examining the potential for transmission via all dental procedures, it is not possible to come to firm conclusions about the implications of these findings for transmission of vCJD. However, given the potential for transmission by this route serious consideration should be given to assessing the options for reducing transmission risks such as improving decontamination procedures and practice or the implementation of single use instruments.
12. The size of the potential risk from interactions between the dental and other routes of secondary transmission, such as blood transfusion and hospital surgery, to increase the likelihood of a self-sustaining epidemic is unclear.
13. It is likely to be difficult to distinguish clinical vCJD cases arising from dietary exposure to BSE from secondary transmissions via dental procedures, should they arise, as a large proportion of the population is likely both to have consumed contaminated meat and undergone dentistry. However, an analysis of dental procedures by patient age may provide an indication of the age group in which infections, if they occur, would be most likely to be observed. Should the incidence of clinical vCJD cases in this age group increase significantly, this may provide an indication that secondary transmission via dentistry is occurring. Investigation of the dental work for these cases may provide supporting data. There is no clear evidence, to date, based on surveillance or investigations of clinical vCJD cases, that any vCJD cases have been caused by dental procedures but this possibility cannot be excluded.
Conclusions
14. Preliminary research findings suggest that the potential risk of transmission of vCJD via dental procedures may be greater than previously anticipated. Although this research is incomplete, uses an animal model exposed to relatively high doses of infectivity, and there are no data from infectivity studies on human oral tissues, these findings suggest an increased possibility that vCJD may be relatively efficiently transmitted via a range of dental procedures. Ongoing infectivity studies using human oral tissues and the other studies suggested here will enable more precise assessment of the risks of vCJD transmission through dental procedures.
15. Guidance was issued to dentists earlier this year recommending that endodontic files and reamers be treated as single use which, provided it is adhered to, will remove any risk of a self-sustaining epidemic arising from re-use of these instruments. To minimise risk it is critical that appropriate management and audit is in place, both for NHS and private dentistry.
16. It is also critical that a detailed and comprehensive assessment of the risks of all dental procedures be conducted as a matter of urgency. While taking into account the continuing scientific uncertainties, this will allow a more thorough consideration of the possible public health implications of vCJD transmission via dentistry and the identification of possible additional precautionary risk reduction measures. The assessment will require continued updating as more evidence becomes available on the transmissibility of vCJD by dental routes, and on the prevalence of infection within the population. A DH proposal to convene an expert group that includes dental professionals to expedite such an assessment is welcomed. Given the potential for transmission via dentistry, consideration should be given to the urgent assessment of new decontamination technologies which, if proved robust and effective, could significantly reduce transmission risks.
SEAC June 2007
27 SEAC Epidemiology Subgroup (2006) position statement of the vCJD epidemic.
http://www.seac.gov.uk/statements/state260106subgroup.htm
28 DH (2007) Precautionary advice given to dentists on re-use of instruments
http://www.gnn.gov.uk/environment/fullDetail.asp?ReleaseID=279256&NewsAreaID=2&NavigatedFromDepartment=False
see full text 17 pages ;
http://www.seac.gov.uk/papers/99-7.pdf
SEAC 99th meeting on Friday 14th December 2007
DECEMBER 14, 2007, 10 year Anniversary of my Moms death 'confirmed' from Heidenhain Variant Creutzfeldt Jakob Disease
Greetings,
AS one of them _lay_ folks, one must only ponder ;
"WITH the Nor-98 now documented in five different states so far in the USA in 2007, and with the TWO atypical BSE H-BASE cases in Texas and Alabama, with both scrapie and CWD running rampant in the USA, IS there any concern from SEAC with the rise of sporadic CJD in the USA from ''UNKNOWN PHENOTYPE'', and what concerns if any, in relations to blood donations, surgery, optical, and dental, do you have with these unknown atypical phenotypes in both humans and animals in the USA ???"
"Does it concern SEAC, or is it of no concern to SEAC?"
"Should it concern USA animal and human health officials?"
snip...
----- Original Message -----
From: xxxxxxxxxx
To: flounder9@verizon.net
Sent: Thursday, November 22, 2007 5:39 AM
Subject: QUESTION FOR SEAC
Mr Terry S Singeltary Sr., Bacliff, Texas 77518 USA.
Dear Mr Singeltary,
"Thank you for your e-mail of yesterday with the question for SEAC. I can confirm that this will be asked at the meeting on your behalf and the question and answer will appear in the minutes of the meeting which will be published on the SEAC Internet site."
snip...end...TSS
Archive Number 20071105.3602 Published Date 05-NOV-2007 Subject PRO/AH/EDR> Prion disease update 2007 (07)
PRION DISEASE UPDATE 2007 (07) ****************************** A ProMED-mail post
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[2] USA: National Prion Disease Pathology Surveillance Center Date: June 2007 Source: National Prion Disease Pathology Surveillance Center (USA) [edited]
CJD Cases examined ---------------------- Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD
1996 / 42 / 32 / 26 / 4 / 0 / 0 1997 / 115 / 68 / 57 / 9 / 0 / 0 1998 / 93 / 53 / 45 / 7 / 1 / 0 1999 / 114 / 69 / 61 / 8 / 0 / 0 2000 / 151 / 103 / 89 / 14 / 0 / 0 2001 / 208 / 116 / 106 / 9 / 0 / 0 2002 / 255 / 143 / 118 / 23 / 2 / 0 2003 / 272 / 174 / 132 / 41 / 0 / 0 2004 / 334 / 183 / 157 / 21 / 0 / 1* 2005 / 352 / 195 / 152 / 37 / 1 / 0 2006 / 372 / 186 / 143 / 30 / 0 / 1** 2007 / 120 / 68 / 35 / 7 / 0 / 0 TOTAL / 2428*** / 1390**** / 1121 / 210 / 4 / 2
*Acquired in UK ** Acquired in Saudi Arabia *** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007. **** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, 26 from 2007).
Notes:
-- Cases are listed based on the year of death when available. If the year of death is not available, the year of sample receipt is used.
-- Referrals: Cases with possible or probable prion disease from which brain tissue or blood in the case of familial disease were submitted.
-- Inconclusive: Cases in which the samples were not sufficient to make a diagnosis.
-- Non-vCJD type unknown are cases in which the tissue submitted was adequate to establish the presence but not the type; in all cases, vCJD could be excluded.
-- Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
flounder@wt.net
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?
http://www.neurology.org/cgi/eletters/60/2/176#535
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
Available online 29 July 2003. Volume 3, Issue 8, August 2003, Page 463
“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." ...
http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fulltext
http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734.
http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535
Like lambs to the slaughter
31 March 2001 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. ...
http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html
DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehörden sind lax. Link auf diesen Artikel im Archiv:
http://service.spiegel.de/digas/find?DID=18578755
"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...
http://service.spiegel.de/digas/servlet/find/DID=18578755
Thu Dec 6, 2007 11:38
FDA IN CRISIS MODE, AMERICAN LIVES AT RISK
http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html
FDA SCIENCE AND MISSION AT RISK
http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
http://cjdusa.blogspot.com/
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/
SCRAPIE USA
http://scrapie-usa.blogspot.com/
NOR-98 ATYPICAL SCRAPIE CASES USA
http://nor-98.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA
http://cjdmadcowbaseoct2007.blogspot.com/
Transmissible Mink Encephalopathy TME
http://transmissible-mink-encephalopathy.blogspot.com/
CHRONIC WASTING DISEASE
http://chronic-wasting-disease.blogspot.com/
TSEAC MEETING
----- Original Message -----
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOVCc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Wednesday, November 29, 2006 1:24 PM
Subject: TSE advisory committee for the meeting December 15, 2006 [TSSSUBMISSION] November 29, 2006
Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,
a kind and warm Holiday Greetings to you all. i kindly wish to submit the following to the TSE advisory committee for the meeting December 15, 2006, about the assessment for potential exposure to vCJD in human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related communication material ;
http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm
i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;
http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines
however, i seem to disagree. from my primitive ciphering, i see it anotherway. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million. also, what about the mixed genotypes/mixed susceptibility? what about the silent carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN strain or phenotype? this risk assessment is just more BSe to me. just another in a long line of ...
Greetings again Dr. Freas et al at FDA,
THIS was like closing the barn door after the mad cows got loose. not only the red cross, but the FDA has failed the public in protecting them from the TSE aka madcow agent. TSE agent i.e. bse, base, cwd, scrapie, tme, and any sub strains thereof. we do not know if these strains will or have transmitted to humans as subclinical TSE or clinical disease, and we do not know if they have or will transmit second, third, forth passage via friendly fire i.e. multiple potential routes via medical, surgical, pharmaceutical etc. IF you remember correctly Dr. Freas et al, i called this long ago, almost 6 years ago ;
PDF]Freas, William TSS SUBMISSION
Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08, 200l 3:03 PM freas ...Freas, William From: Terry S. Singeltary Sr. [flounder@wt.net] Sent: Monday, January 08,200l 3:03 PM
To: freas@CBS5055530.CBER.FDA.GOV
Subject: CJD/BSE (aka madcow) Human/Animal TSE?s--U.S.--Submission
To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products.
snip...
I am beginning to think that the endless attempt to track down and ban, potential victims from known BSE Countries from giving blood will be futile. You would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT SWIFTLY to find blood test for TSE's, whether it be blood test, urine test, eyelid test, anything at whatever cost, we need a test FAST. DO NOT let the incubation time period of these TSEs fool you. To think of Scrapie as the prime agent to compare CJD, but yet overlook the Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by scrapie from a vaccine made of scrapie infected sheep brains, would be foolish. I acquired this full text version of the event which was recorded in the Annual Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. From the BVA and the URL is posted in my (long version). ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
see full text ;
http://tseac.blogspot.com/
vCJD case study highlights blood transfusion risk
http://vcjdblood.blogspot.com/
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle
9/13/2005
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed
Subject: Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION Date: August 24, 2005 at 2:47 pm PST August 24, 2005
Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION
Greetings APHIS ET AL,
My name is Terry S. Singeltary Sr.
I would kindly like to comment on [Docket No. 05-004-1] RIN 0579-AB93 ;
snip...
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.
MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???
go figure. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Comment Submitted Comment Receipt
Thank you. Your comment on Document ID: APHIS-2006-0041-0001 has been sent. Comment Tracking Number: APHIS-2006-0041-DRAFT-0028
Attachments: C:\My Music\My Documents\APHIS-2006-0041_January 28.doc
If you wish to retain a copy of the receipt, use the following link to print a copy for your files. Print
http://www.regulations.gov/fdmspublic/component/main
THE only difference between the UK poisoning the globe, and the USA, it is now legal with GWs and OIEs BSE MRR policy ;
IT's O.K. to poison 3rd world countries ;
http://www.bseinquiry.gov.uk/files/yb/1994/05/20002001.pdf
On 20 February 1990, Dr Pickles wrote to Ms Verity (APS/CMO). Dr Pickles minute included the following: 1. Mr Meldrum is arguing that MAFF have already taken all the necessary and responsible steps to warn importing countries of the BSE dangers in UK meat and bone meal. Yet the action taken so far overseas suggest the message has not got through, or where it has this has been late. The first nation that woke up to the danger did so a year after our own feed ban. It seems even now several EC countries neither ban our imports or the general feeding of ruminant protein. It also seems the OIE and CVO have yet to inform the rest of the world. 2. I do not see how this can be claimed to be responsible. We do not need an expert group of the Scientific Veterinary Committee to tell us British meat and bone meal is unsafe for ruminants. I fail to understand why this cannot be tackled from the British end which seems to be the only sure way of doing it, preferably by banning exports. As CMO says in his letter of 3 January surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries. [79]
http://www.bse.org.uk/dfa/dfa25.htm
http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh
OLD DOCKET SUBMISSION TSS
Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)
https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
PART 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
Asante/Collinge et al, 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;
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7
http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm
[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1 File Format: PDF/Adobe Acrobat - View as HTML Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of those who provided comments in response to Docket No. ... Meager 8/18/01 Terry S. Singeltary Sr ...
www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)
Docket Management
Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm
Dockets Entered On October 2, 2003 Table of Contents, Docket #, Title, 1978N-0301,
OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr. Vol #: 1, ...
www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm
Daily Dockets Entered on 02/05/03
DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2. ... Vol#: 1.
03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...
www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm
Docket Management
Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater
Comment Number: EC -1
Accepted - Volume 1
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html
Daily Dockets - 04/10/03
... 00D-1662 Use of Xenotransplantation Products in Humans. EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...
www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm
- 05-20-2003 - Cached
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #:1
http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm
http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm
01N-0423 Substances Prohibited from use in animal food/Feed Ruminant
EMC 1 Terry S. Singeltary Sr. Vol#: 3
http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm
TSS
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