Saturday, January 16, 2016

Revised Preventive Measures to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and Blood Products Guidance for Industry

Revised Preventive Measures to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and Blood Products Guidance for Industry
 
U.S. Department of Health and Human Services Food and Drug Administration Center for Biologics Evaluation and Research May 2010 Updated January 2016
 
i
 
Table of Contents
 
I. INTRODUCTION..............................................................................................................1
 
II. BACKGROUND................................................................................................................3
 
A. CJD and vCJD....................................................................................................... 3
 
B. Evolution of the Global BSE epidemic................................................................ 6
 
C. TSE Agents and Blood.......................................................................................... 7
 
D. FDA Regulatory History .................................................................................... 10
 
E. Rationale for Geographic Donor Deferrals ...................................................... 15
 
III. EXPLANATION OF CURRENT VCJD RECOMMENDATIONS...........................17
 
A. Exposure to British Beef in the U.K.................................................................. 17
 
B. Exposure to British Beef Products Distributed Outside of the U.K............... 17
 
C. Indigenous BSE Exposure Outside the U.K. .................................................... 18
 
D. Potential Infection with vCJD Agent Acquired by Transfusion .................... 21
 
E. Exposure to Bovine Insulin ................................................................................ 21
 
F. Reports of Biological Product Deviations ......................................................... 21
 
G. Definitions............................................................................................................ 22
 
IV. RECOMMENDATIONS FOR DONOR DEFERRAL ................................................24
 
A. Donor Deferral Criteria ..................................................................................... 24
 
B. Questions to Identify Donors at an Increased Risk for CJD .......................... 25
 
C. Donor Reentry after Donor Deferral for Risk of Familial CJD..................... 26
 
D. Questions for Identifying Donors at Risk for Exposure to BSE..................... 26
 
V. POST-DONATION INFORMATION: RECOMMENDATIONS FOR PRODUCT RETRIEVAL AND QUARANTINE, CONSIGNEE NOTIFICATION, AND BIOLOGICAL PRODUCT DEVIATION REPORTING...........................................29
 
A. Whole Blood and Blood Components Intended for Transfusion, Cellular Blood Components Intended for Further Manufacture into Injectable Products, and Source Plasma From Donors with CJD or CJD Risk Factors29
 
B. Whole Blood and Blood Components Intended for Transfusion, Source Leukocytes and Other Cellular Blood Components Intended for Further Manufacture into Injectable Products, from Donors with Geographic Risk Deferrals and/or Exposure to Bovine Insulin Made in the U.K. since 1980.. 30
 
C. Source Plasma and Recovered Plasma from Donors with Geographic Risk Deferrals and/or Exposure to Bovine Insulin Made in the U.K. Since 1980 . 31
 
D. Whole Blood and Blood Components Intended for Transfusion, Recovered Plasma, Source Leukocytes, Other Cellular Blood Components Intended for Manufacturing into Injectable Products, and Source Plasma from Donors with vCJD, suspected vCJD, or CJD and Age Less Than 55 Years............... 31
 
E. Plasma Derivatives.............................................................................................. 32
 
F. Disposal of Retrieved and Quarantined Products ........................................... 33
 
VI. RECOMMENDATIONS FOR RECIPIENT TRACING AND NOTIFICATION...34
 
Contains Nonbinding Recommendations
 
ii VII. LABELING RECOMMENDATIONS...........................................................................34
 
VIII. IMPLEMENTATION OF RECOMMENDATIONS...................................................36
 
IX. THE IMPACT OF GEOGRAPHIC DONOR DEFERRALS THAT ARE MORE STRINGENT THAN THOSE RECOMMENDED BY THIS GUIDANCE...............37
 
X. SOURCES OF ADDITIONAL INFORMATION ........................................................38
 
XI. REFERENCES.................................................................................................................39
 
APPENDIX TABLE 1: DONOR DEFERRAL, PRODUCT DISPOSITION, RECIPIENT NOTIFICATION FOR WHOLE BLOOD, BLOOD COMPONENTS INTENDED FOR TRANSFUSION, SOURCE LEUKOCYTES, AND OTHER CELLULAR BLOOD COMPONENTS INTENDED FOR FURTHER MANUFACTURE...........45
 
APPENDIX TABLE 2: DONOR DEFERRAL, PRODUCT DISPOSTION, AND RECIPIENT NOTIFICATION FOR SOURCE PLASMA (SP), RECOVER PLASMA (RP) AND PLASMA DERIVATIVES (PD) ................................................47
 
Contains Nonbinding Recommendations
 
1
 
Revised Preventive Measures to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and Blood Products
 
Guidance for Industry
 
This guidance represents the current thinking of the Food and Drug Administration (FDA or Agency) on this topic. It does not establish any rights for any person and is not binding on FDA or the public. You can use an alternative approach if it satisfies the requirements of the applicable statutes and regulations. To discuss an alternative approach, contact the FDA staff responsible for this guidance as listed on the title page.
 
I. INTRODUCTION
 
II. BACKGROUND
 
A. CJD and vCJD
 
CJD is a rare but invariably fatal degenerative disease of the central nervous system, one of a group of transmissible diseases called transmissible spongiform encephalopathies (TSEs) or prion diseases. TSEs are associated with a poorly understood transmissible agent (Refs. 1-6), now designated TSE agents or prions (Ref. 7). Cases of sporadic CJD—the most common human TSE—occur at low frequency by an unknown mechanism. CJD may be acquired by an identified exogenous (usually iatrogenic) exposure to infectious material; or it may be familial, associated with one of a number of mutations in the prion-protein-encoding (PRNP) gene. Clinical latency for iatrogenic CJD, following point exposures to contaminated materials, has sometimes exceeded 30 years (Ref. 8); incubation periods of kuru—another human TSE—appear to have sometimes exceeded 50 years (Ref. 9).
 
In 1996, a previously unrecognized variant of CJD, now designated vCJD, was reported in the United Kingdom (U.K.) (Ref. 10). vCJD is distinguished from CJD by differences in clinical presentation, cerebral imaging and neuropathologic changes, summarized in Table 1 (Refs. 10-14).
 
snip...
 
B. Evolution of the Global BSE Epidemic
 
================================
 
LOL, I omitted this part, see real facts on BSE typical and atypical risk factors and the infamous BSE MRR policy, the legal trading of TSE prion disease in links below. ...tss
 
================================
 
D. FDA Regulatory History
 
================================
 
LOL, see links below as well for past regulatory history by the FDA. ...TSS
 
================================
 
2. Evidence that vCJD Has Been Transmitted by Blood Products
 
Soon after the first description in the U.K. of vCJD affecting 10 young patients in 1996 (Ref. 10), vCJD was recognized to be an emerging infectious disease with several unique clinical and pathological characteristics differing from those of previously known forms of CJD. It was uncertain whether human blood might transmit the vCJD agent. FDA therefore recommended in the 1999 guidance a donor deferral policy more stringent for donors at increased risk of vCJD than for those at increased risk of the “classical” forms of the disease (see Section IV below), including a recommendation to withdraw plasma derivatives should a plasma donor later be diagnosed with vCJD (a situation never recognized in the U.S. to date) and a case-by-case review when a plasma donor is suspected of having vCJD (including all donors with onset of CJD before the age of 55 years) instead of a more common form of CJD.
 
In December 2003, U.K. authorities reported a case of vCJD in a recipient of non-leukoreduced red blood cell concentrate obtained from a clinically healthy donor who later developed typical vCJD (Ref. 53). In July 2004, a second recipient of non-leukoreduced red blood cell concentrate from another such donor in the U.K. was reported to have died of other causes without clinical or neuropathological evidence of vCJD, but at autopsy the recipient had abnormal accumulations of prion protein in lymphoid tissues (Ref. 54). This finding is typical of vCJD, although the recipient had a PRNP genotype (heterozygous for the sequences encoding methionine and valine at PRNP codon 129 [129 MV]) not previously found in cases of vCJD (all of which have been 129 MM homozygous). Two additional recipients of non-leukoreduced red blood cell concentrates from a donor incubating vCJD were subsequently reported by U.K. authorities in February 2006 (Refs. 55-56) and January 200726 to have died with confirmed vCJD. These four cases provided convincing epidemiological evidence that vCJD infections have been transmitted by non-leukoreduced red blood cell concentrates. Although no other blood components have been associated with transfusion-transmitted vCJD, experience is still too limited to allow a conclusion that other blood components cannot transmit the infection.
 
24 U.K. Health Protection Agency (HPA), “vCJD abnormal prion protein found in a patient with haemophilia at post mortem,” dated February 17, 2009, and “Variant CJD and plasma products,” dated July 27, 2009 at http://www.hpa.org.uk.
 
25 Transfusion Medicine Epidemiology Review: http://www.cjd.ed.ac.uk/TMER/TMER.htm.
 
26 Transfusion Medicine Epidemiology Review: http://www.cjd.ed.ac.uk/TMER/TMER.htm.
 
Contains Nonbinding Recommendations
 
10
 
In February 2009, the United Kingdom Health Protection Agency announced evidence of vCJD infection in a patient with type-A hemophilia at postmortem.27 The patient had been treated with human plasma-derived Factor VIII clotting factor manufactured using plasma from U.K. donors, including one batch that was manufactured using plasma from a donor who later developed typical vCJD. This is the first report that vCJD abnormal protein has been found in a patient with hemophilia or any patient treated with plasma products. The patient, who was over 70 years old, died of other causes and may have been exposed to other risk factors for vCJD. A risk assessment performed by U.K. health authorities concluded that, assuming that the abnormal prion protein finding was a marker for asymptomatic vCJD infection, the most likely source of such an infection was plasma-derived Factor VIII, rather than dietary exposure, endoscopy procedures, or red blood cell transfusions.
 
At this time, plasma derivatives have not been implicated in vCJD transmission in any country other than the U.K. To date, no U.S.-licensed plasma-derived products have been manufactured from a donor known to have developed vCJD and no cases of vCJD have been reported from use of a U.S.-licensed plasma derivative. In addition, published studies and information submitted to FDA show that certain plasma derivative manufacturing steps can remove TSE infectivity, although such experiments have inherent limitations (Refs. 51, 57). Based on animal studies as well as on FDA risk assessments, the possibility of vCJD transmission by a U.S.-licensed plasma derivative is extremely small.
 
snip...
 
Criteria A.
 
Donor deferral criteria 1-7 apply to all donors. Donor deferral criterion 8 (residence in Europe for 5 years or more between 1980 and the present) applies to all donors with the exception of donors of Source Plasma.
 
1. You should permanently defer donors who have been diagnosed with vCJD or any other form of CJD.66
 
2. You should permanently defer donors at increased risk for CJD (as identified by questions 2 and 3 in Section IV.B. Donors are considered to have an increased risk for CJD if they have received a dura mater transplant or an injection of human cadaveric pituitary-derived growth hormone. Donors with one or more blood relatives diagnosed with CJD (as identified in Section IV.B., Question 1 below) are also considered to be at increased risk of CJD, and should be indefinitely deferred (see Section IV.C. for donor reentry recommendations).
 
3. You should indefinitely defer donors who have spent three months or more cumulatively in the U.K. from the beginning of 1980 through the end of 1996.
 
4. You should indefinitely defer donors who have spent five years or more cumulatively in France from the beginning of 1980 to the present.
 
5. You should indefinitely defer former or current U.S. military personnel, civilian military personnel, and their dependents as follows:
 
a. Individuals who resided at U.S. military bases in Northern Europe (Germany, United Kingdom, Belgium, and the Netherlands) for six months or more from 1980 through 1990, or
 
b. Individuals who resided at U.S. military bases elsewhere in Europe (Greece, Turkey, Spain, Portugal, and Italy) for six months or more from 1980 through 1996.
 
6. You should indefinitely defer donors who have received a transfusion of blood or blood components in the U.K. or in France between the beginning of 1980 and the present.
 
66 For the purposes of this document, FDA considers the less common TSEs, Gerstmann-Sträussler-Scheinker syndrome and fatal insomnia syndromes, to be equivalent in risk to familial and sporadic CJD. The blood establishment need not name these rare syndromes in the questionnaire but might consider them as equivalent in risk to CJD if, in response to a question about CJD, the donor offers information that a family member has been diagnosed with one of them.
 
Contains Nonbinding Recommendations 25
 
7. You should indefinitely defer donors who have injected bovine insulin since 1980, unless you can confirm that the product was not manufactured after 1980 from U.K. cattle.
 
8. You should indefinitely defer donors of Whole Blood, blood components for transfusion, and Source Leukocytes, who have lived cumulatively for five years or more in Europe from the beginning of 1980 until the present. (Note this criterion includes time spent in the U.K. from 1980 through 1996 and time spent in France from 1980 to the present.) Unless otherwise unsuitable (for example, because they lived in the U.K. or France or on U.S. military bases for the periods of time noted previously), these donors remain eligible for Source Plasma donation.
 
NOTE: Donors who are otherwise deferred based upon the above criteria 2-8 may continue to donate if they are participating in a CBER-approved program that allows collection of Source Plasma solely for use in manufacturing of non-injectable products. We recommend special labeling for products obtained from such donors (see Section VII.A).
 
Questions to Identify Donors at an Increased Risk for CJD B.
 
You should question frequent Source Plasma donors at the first donation following implementation of the recommendations in this guidance, and annually thereafter. You should question donors of Whole Blood and blood components, infrequent Source Plasma donors and Source Leukocyte donors at each donation. If the donor is not familiar with the term “Creutzfeldt-Jakob Disease,” you may take that as a negative response. These questions are similar to those in the 1999 and 2002 guidances. We consider donors who answer “Yes” to any of the questions below to have an increased risk for developing CJD.
 
Question 1: Have any of your blood relatives ever had Creutzfeldt-Jakob Disease?67
 
Question 2: Have you ever received growth hormone made from human pituitary glands?
 
NOTE: If the donor is uncertain about his or her treatment, the following question describing human pituitary-derived growth hormone injections may be asked: “Was the hormone treatment given repeatedly by injection?” This question needs to be asked only once, since human cadaveric pituitary growth hormone is no longer available.
 
67 See footnote 66.
 
Contains Nonbinding Recommendations
 
26
 
Question 3: Have you ever received a dura mater (brain covering) graft?
 
NOTE: This question may be preceded by the more general question “Have you ever had brain surgery?” Ask the specific question only if the donor responds “yes” to the general question.
 
Donor Reentry after Donor Deferral for Risk of Familial CJD C.
 
If you defer a donor because of family history of CJD, you may reenter that donor if:
 
1) The diagnosis of CJD in the family member(s) is confidently excluded, or CJD in the family member(s) is iatrogenic, or the family member(s) is (are) not a blood relative(s); or
 
2) Laboratory testing (gene sequencing) shows that the donor does not have a mutation associated with familial CJD. Note that gene sequencing of the donor is not necessary to demonstrate that the donor is not at risk for familial CJD. Sequencing of the family member with CJD or the appropriate parent of the donor, if the CJD-affected family member was a second-degree relative, may be sufficient to demonstrate that the donor does not have a mutation associated with familial CJD.
 
Questions for Identifying Donors at Risk for Exposure to BSE D.
 
1. Method of Donor Questioning
 
Due to the added complexity of screening donors for cumulative periods of potential exposure to BSE, a trained staff member should administer the revised geographic donor deferral criteria by face-to-face interview to each new donor (as defined in your blood establishment’s standard operating procedures (SOP)). Instead of face-to-face interviews, you may use a computerized interactive donor interview program that includes an audio component (audio-CASI) as described in the FDA guidance entitled “Guidance for Industry: Streamlining the Donor Interview Process: Recommendations for Self-Administered Questionnaires,” dated July 2003.68 You should submit changes to your donor interview procedure according to 21 CFR 601.12. For repeat donors, you may use alternative methods for introducing and emphasizing the new questions. Your alternative method should provide the repeat donor with a detailed description of the changes to the donor questionnaire, to highlight any new questions and modifications.
 
 
Contains Nonbinding Recommendations 27
 
2. Donor Questions
 
You should indefinitely defer donors who answer “Yes” to the following questions:
 
To identify donors with geographic risk of BSE exposure.
 
SNIP...
 
LOL...
 
NO NEED TO GO ANY FURTHER, BECAUSE THE GEOGRAPHICAL RISK ASSESSMENT ON BSE EXPOSURE IS BASED ON FALSE INFORMATION AND LIES, thanks to the USDA, FDA, and OIE, in my opinion, see information and links below. ...tss
 
see full text ;
 
 
P197
 
Misfolded prion protein (PrPTSE) can be detected in the blood of squirrel monkeys infected with variant Creutzfeldt-Jakob disease (vCJD)
 
Larisa Cervenakova1, Oksana Yakovleva1, Paula Saá1, David M. Asher2, Thomas R. Kreil3, Susan Gibson4, Christian Abee5, James W. Ironside6, Paul W. Brown7 1Scientific Affairs, American Red Cross, Rockville, MD, USA, 2Office of Blood Research and Review, Center for Biologics Evaluation and Research, FDA, Silver Prion2015 Program Guide
 
36
 
Prion 2015 Fort Collins Spring, MD, USA, 3Global Pathogen Safety, Baxter BioScience, Vienna, Austria, 4University of South Alabama, Mobile, AL (deceased), USA, 5University of Texas, Anderson Cancer Center, Bastrop, TX, USA, 6National CJD Surveillance Unit, Edinburgh, UK, 7NINDS, National Institutes of Health, Bethesda, MD (retired), USA
 
Variant CJD infections have been recognized in 4 recipients of non-leukocyte-depleted red blood cell (RBC) transfusions (and in a hemophilia patient treated with a plasmaderived coagulation factor). In the UK, PrPTSE has been detected in blood of 70% of vCJD patients and in appendices of as many as 1 in 2000 asymptomatic individuals. Reliable tests are needed to detect blood donors infected with vCJD before the appearance of overt illness to protect transfusion recipients. We previously reported the co-localization of PrPTSE with extracellular vesicles (EVs) in plasma of vCJD-infected mice. Here we report detecting PrPTSE in EVs from archived plasma samples of vCJD-infected squirrel monkeys. Blood was collected from infected and uninfected monkeys into anticoagulant every 3 months and separated into RBCs, buffy coat and plasma. EVs were extracted from plasma using ExoQuickTM. PMCA was performed using uninfected TgHu mouse brain homogenate as PrPC substrate. We tested samples of blood from 2 groups of monkeys inoculated intracerebrally with vCJD brain diluted 10-1 (4 monkeys) or 10-3 (3 monkeys) and from 4 control monkeys inoculated with 10-1 normal human brain. PrPTSE was detected in plasma EV of 5 of 7 vCJD-inoculated monkeys (3/4 10-1 and 2/3 10-3). Multiple tests of control plasma EV samples from the 4 control monkeys were all negative. Whole blood collected from 4 monkeys during incubation and clinical stages of vCJD was transfused into individual recipient monkeys. We continue to test archived plasma samples from donor and transfusion-recipient monkeys. Baxter and FABS funded the study.
 
 
prion2013
 
 
ORIGINAL RESEARCH
 
Blood transmission studies of prion infectivity in the squirrel monkey (Saimiri sciureus): the Baxter study
 
Diane L. Ritchie1,*, Susan V. Gibson2,†, Christian R. Abee3, Thomas R. Kreil4, James W. Ironside1 and Paul Brown5
 
Article first published online: 23 NOV 2015
 
DOI: 10.1111/trf.13422
 
© 2015 AABB
 
Issue
 
Cover image for Vol. 55 Issue 11
 
Transfusion
 
Early View (Online Version of Record published before inclusion in an issue)
 
Abstract
 
BACKGROUND
 
Four secondary transmissions of variant Creutzfeldt-Jakob disease (vCJD) infectivity have been associated with the transfusion of nonleukoreduced red blood cells collected from vCJD patients during the asymptomatic phase of the disease. Establishing efficient experimental models for assessing the risk of future transmissions of vCJD infectivity via blood transfusion is of paramount importance in view of a study of archived appendix samples in which the prevalence of asymptomatic vCJD infection in the United Kingdom was estimated at approximately 1 in 2000 of the population. In this study, we investigated transmission of vCJD and sporadic CJD (sCJD) infectivity from blood using the squirrel monkey, which is highly susceptible to experimental challenge with human prion disease.
 
STUDY DESIGN AND METHODS
 
Whole blood collected from vCJD- and sCJD-infected squirrel monkeys was transfused at multiple time points into recipient squirrel monkeys. Blood recipients were euthanized approximately 7 years after their first blood transfusion.
 
RESULTS
 
No clinical or pathologic signs of a prion disease were observed in either the sCJD- or the vCJD-transfused monkeys, and immunohistochemistry and biochemical investigations showed no PrPTSE in central nervous system or lymphoreticular tissues. Similarly, monkeys inoculated intracerebrally (IC) and intravenously (IV) with either buffy coat or plasma from vCJD and sCJD patients failed to develop disease. However, white blood cells from a chimpanzee-passaged strain of human Gerstmann-Sträussler-Scheinker (GSS) disease transmitted autopsy-proven disease to two IC-inoculated monkeys after incubation periods of 34 and 39 months.
 
CONCLUSION
 
Blood transmits GSS but not sCJD or vCJD infectivity to IC- or IV-inoculated squirrel monkeys within a 7-year observation period.
 
 
2015 PRION CONFERENCE
 
*** RE-P.164: Blood transmission of prion infectivity in the squirrel monkey: The Baxter study
 
***suggest that blood donations from cases of GSS (and perhaps other familial forms of TSE) carry more risk than from vCJD cases, and that little or no risk is associated with sCJD. ***
 
P.164: Blood transmission of prion infectivity in the squirrel monkey: The Baxter study
 
Paul Brown1, Diane Ritchie2, James Ironside2, Christian Abee3, Thomas Kreil4, and Susan Gibson5 1NIH (retired); Bethesda, MD USA; 2University of Edinburgh; Edinburgh, UK; 3University of Texas; Bastrop, TX USA; 4Baxter Bioscience; Vienna, Austria; 5University of South Alabama; Mobile, AL USA
 
Five vCJD disease transmissions and an estimated 1 in 2000 ‘silent’ infections in UK residents emphasize the continued need for information about disease risk in humans. A large study of blood component infectivity in a non-human primate model has now been completed and analyzed. Among 1 GSS, 4 sCJD, and 3 vCJD cases, only GSS leukocytes transmitted disease within a 5–6 year surveillance period. A transmission study in recipients of multiple whole blood transfusions during the incubation and clinical stages of sCJD and vCJD in ic-infected donor animals was uniformly negative. These results, together with other laboratory studies in rodents and nonhuman primates and epidemiological observations in humans, suggest that blood donations from cases of GSS (and perhaps other familial forms of TSE) carry more risk than from vCJD cases, and that little or no risk is associated with sCJD. The issue of decades-long incubation periods in ‘silent’ vCJD carriers remains open.
 
 
ran across an old paper from 1984 ;
 
***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent. ***
 
 
Monday, November 23, 2015
 
*** Blood transmission studies of prion infectivity in the squirrel monkey (Saimiri sciureus): the Baxter study
 


Article | Open

Preclinical detection of infectivity and disease-specific PrP in blood throughout the incubation period of prion disease

Elizabeth B. Sawyer , Julie Ann Edgeworth , Claire Thomas , John Collinge
& Graham S. Jackson

Scientific Reports 5, Article number: 17742 (2015) doi:10.1038/srep17742 Download Citation Diagnostic markers | Experimental models of disease | Prion diseases
Received:18 June 2015Accepted:06 November 2015Published online:03 December 2015

Abstract

Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disorder characterised by accumulation of pathological isoforms of the prion protein, PrP. Although cases of clinical vCJD are rare, there is evidence there may be tens of thousands of infectious carriers in the United Kingdom alone. This raises concern about the potential for perpetuation of infection via medical procedures, in particular transfusion of contaminated blood products. Accurate biochemical detection of prion infection is crucial to mitigate risk and we have previously reported a blood assay for vCJD. This assay is sensitive for abnormal PrP conformers at the earliest stages of preclinical prion disease in mice and precedes the maximum infectious titre in blood. Not only does this support the possibility of screening asymptomatic individuals, it will also facilitate the elucidation of the complex relationship that exists between the ensemble of abnormal PrP conformers present in blood and the relationship to infectivity.

Discussion

The ability to accurately diagnose prion infection using biochemical methods is crucial to protect public health from iatrogenic transmissions, particularly arising from the transfusion of contaminated blood and blood products10,11,12,33. In the United Kingdom (UK) measures taken to prevent secondary infections of vCJD have included leucodepletion of donor blood, sourcing of plasma from non-UK sources, exclusion of transfusion recipients from donation, use of recombinant clotting factors for patients with bleeding disorders and ceasing the use of UK plasma for fractionation and export34. We have previously reported the development19 and validation20,35 of a blood test for vCJD based upon the detection of abnormal disease-specific isoforms of PrP, which is now in clinical use for the diagnosis of prion disease. The wider application of this test, or indeed other emerging assays36,37, for screening asymptomatic individuals for potential infection is confounded by an inability to confirm that an assay detection limit is sufficient for the detection of preclinical infections. This problem arises as there are currently no samples available from individuals confirmed as sub-clinical carriers of vCJD with which to assess either the prevalence of prionaemia in BSE prion-exposed populations or the sensitivity of any potential blood tests. A definitive answer will require prolonged longitudinal study of individuals testing positive to determine what proportion of patients with vCJD prionaemia go on to develop clinical vCJD and how many are chronic carriers38.

It has been suggested that carriers would have lower concentrations of abnormal PrP compared to individuals with clinical CJD13, and this seems likely. Despite potentially lower levels, animal models indicate clear preclinical blood involvement23,24,39,40 and very efficient transmission of prion infection has been demonstrated from blood taken from sheep in early preclinical stages of scrapie9. The use of the RML-prion strain allows rapid and precise estimates of low prion titre using cell-based assays41,42. Previous attempts to detect infectivity in low titre sources have required either the use of large numbers of recipient animals or the transfusion or large volumes of infected analyte in large animals. By using the SSBA18 we have not only verified but accurately quantified the presence of infectivity in blood even at the earliest stages of preclinical prion disease. A comparison of RML-infected brain diluted into either FVB/N-Prnp0/0 brain homogenate or blood showed that although the presence of whole blood impacted on the overall detection limit of the assay, it remained capable of detecting RML prions at concentrations of less than 1 LD50 units/ml. Infectivity was found to rise by approximately 10–20-fold throughout the incubation period (Fig. 4) as might be anticipated from historical estimates derived from conventional large scale rodent bioassays26, albeit with significant fluctuations approaching the clinical end-point of disease. The significant increase in infectious titre in the last few days of the incubation period are unexpected with the change in titre identifiable only as a result of the high precision of SSBA and related cell-culture assays which are providing unique insights into the replication of prion isoforms during pathogenesis43,44. Levels of MMP-9 in serum provide an indication of BBB integrity and although complicated by age-related decline45, sudden elevation towards the clinical end point for prion disease (Fig. 5) may indicate a sudden perturbation leading to exchange of prion material between the CNS and circulating blood and fluctuations in the concentration of prion disease-related PrP isoforms in blood.

Surprisingly, analysis of the same samples using our DDA assay revealed relatively consistent positive signals throughout the RML incubation period (Fig. 3). Positive detection was achieved from the earliest time point sampled and could not be ascribed to the detection of residual inoculum as similar signals were not observed in the blood of FVB/N-Prnp0/0 mice unable to replicate prions (data not shown), and the half-life of prion-infected inocula has previously been shown to be short: 36 hours in rodent brain tissue46 and less in cell-culture47. The lack of correlation between DDA reactivity and infectivity seen by SSBA indicates DDA is capable of detecting a wider ensemble of abnormal PrP conformers associated with prion infection44,48 of which infectivity may only constitute a minority component. Such observations are not without precedent and there is increasing evidence to suggest that abnormal PrP conformers may be as much as 106-fold more abundant than assayable infectivity49. The ability to detect the plethora of abnormal PrP increases the analytical sensitivity of assays and in the case of DDA an analytical sensitivity equivalent to a 109-fold dilution of prion-infected brain is sufficient for clinical sensitivity at the earliest stages of preclinical prion disease.

http://www.nature.com/articles/srep17742

 
 Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Title: Transmission of scrapie prions to primate after an extended silent incubation period
 
Authors
 
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -
 
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573.
 
Interpretive Summary:
 
The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.
 
Technical Abstract:
 
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
 
***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
 
 
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***
 
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
 
SUMMARY: We are reopening the comment period for our proposed rule that would revise completely the scrapie regulations, which concern the risk groups and categories established for individual animals and for flocks, the use of genetic testing as a means of assigning risk levels to animals, movement restrictions for animals found to be genetically less susceptible or resistant to scrapie, and recordkeeping requirements. This action will allow interested persons additional time to prepare and submit comments.
 
DATES: The comment period for the proposed rule published on September 10, 2015 (80 FR 54660-54692) is reopened. We will consider all comments that we receive on or before December 9, 2015. ...
 
 
 
 
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
 
WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I kindly submit the following ;
 
>>>The last major revision of the scrapie regulations occurred on August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket No. 97-093-5) a final rule amending part 79 by imposing additional restrictions on the interstate movement of sheep and goats.<<<
 
Indeed, much science has changed about the Scrapie TSE prion, including more science linking Scrapie to humans. sadly, politics, industry, and trade, have not changed, and those usually trump sound science, as is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing animals and the OIE. we can look no further at the legal trading of the Scrapie TSE prion both typical and atypical of all strains, and CWD all stains. With as much science of old, and now more new science to back this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE, and all trading partners to take heed to the latest science on the TSE prion disease, all of them, and seriously reconsider the blatant disregards for human and animal health, all in the name of trade, with the continued relaxing of TSE Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set up to fail in the first place. If the world does not go back to the ‘BSE RISK ASSESSMENTS’, enhance, and or change that assessment process to include all TSE prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’ PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they will continue to mutate and spread among species of human and animal origin, and they will continue to kill. ...
 
please see ;
 
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
 
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
 
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
 
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
 
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
 
***is the third potentially zoonotic PD (with BSE and L-type BSE),
 
***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
 
===============
 
***thus questioning the origin of human sporadic cases***
 
===============
 
 
snip...see ;
 
Monday, November 16, 2015
 
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***
 
 
 
==========================================
 
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
 
==========================================
 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
Zoonotic Potential of CWD Prions
 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
 
*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.
 
==================
 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
 
==================
 
P.105: RT-QuIC models trans-species prion transmission
 
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
 
Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.
 
================
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
 
================
 
 
 
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
 
 
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
 
 
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
 
From: TSS (216-119-163-189.ipset45.wt.net)
 
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
 
Date: September 30, 2002 at 7:06 am PST
 
From: "Belay, Ermias"
 
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
 
Sent: Monday, September 30, 2002 9:22 AM
 
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Dear Sir/Madam,
 
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
 
Ermias Belay, M.D. Centers for Disease Control and Prevention
 
-----Original Message-----
 
From: Sent: Sunday, September 29, 2002 10:15 AM
 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
 
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
 
Thursday, April 03, 2008
 
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
 
snip...
 
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
 
snip... full text ;
 
 
CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.
 
Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.
 
 
I urge everyone to watch this video closely...terry
 
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
 
 
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
 
 
Creutzfeldt-Jakob Disease, Prion Protein Gene Codon 129VV, and a Novel PrPSc Type in a Young British Woman
 
Simon Mead, PhD, MRCP; Susan Joiner, MSc; Melanie Desbruslais, BSc; et al Arch Neurol. 2007;64(12):1780 doi:10.1001/archneur.64.12.1780
 
Observation | December 2007 Creutzfeldt-Jakob Disease, Prion Protein Gene Codon 129VV, and a Novel PrPSc Type in a Young British Woman Simon Mead, PhD, MRCP; Susan Joiner, MSc; Melanie Desbruslais, BSc; Jonathan A. Beck, BSc; Michael O’Donoghue, PhD; Peter Lantos, FRCP; Jonathan D. F. Wadsworth, PhD; John Collinge, FRS [+-] Author Affiliations Author Affiliations: MRC [Medical Research Council] Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, London, England (Drs Mead, Wadsworth, and Collinge; Mss Joiner and Desbruslais; and Mr Beck); and Institute of Psychiatry, King's College London (Dr Lantos). Dr O’Donoghue is now with the Department of Clinical Neurology, Nottingham University Hospitals NHS [National Health Service] Trust, Nottingham, England.
 
Arch Neurol. 2007;64(12):1780-1784. doi:10.1001/archneur.64.12.1780.
 
ABSTRACT Background Variant Creutzfeldt-Jakob disease (vCJD) is an acquired prion disease causally related to bovine spongiform encephalopathy that has occurred predominantly in young adults. All clinical cases studied have been methionine homozygotes at codon 129 of the prion protein gene (PRNP) with distinctive neuropathological findings and molecular strain type (PrPSc type 4). Modeling studies in transgenic mice suggest that other PRNP genotypes will also be susceptible to infection with bovine spongiform encephalopathy prions but may develop distinctive phenotypes.
 
Objective To describe the histopathologic and molecular investigation in a young British woman with atypical sporadic CJD and valine homozygosity at PRNP codon 129.
 
Design Case report, autopsy, and molecular analysis.
 
Setting Specialist neurology referral center, together with the laboratory services of the MRC [Medical Research Council] Prion Unit.
 
Subject Single hospitalized patient.
 
Main Outcome Measures Autopsy findings and molecular investigation results.
 
Results Autopsy findings were atypical of sporadic CJD, with marked gray and white matter degeneration and widespread prion protein (PrP) deposition. Lymphoreticular tissue was not available for analysis. Molecular analysis of PrPSc (the scrapie isoform of PrP) from cerebellar tissue demonstrated a novel PrPSc type similar to that seen in vCJD (PrPSc type 4). However, this could be distinguished from the typical vCJD pattern by an altered protease cleavage site in the presence of the metal ion chelator EDTA.
 
Conclusions Further studies will be required to characterize the prion strain seen in this patient and to investigate its etiologic relationship with bovine spongiform encephalopathy. This case illustrates the importance of molecular analysis of prion disease, including the use of EDTA to investigate the metal dependence of protease cleavage patterns of PrPSc.
 
 
COMMENT Does the PrPSc typing suggest a BSE-related cause, or can our findings be accommodated by the spectrum seen in sporadic CJD cases worldwide?
 
The molecular strain typing of the patient's brain material demonstrated a novel PrPSc type when compared with our archived cases.21 There is as yet no internationally agreed-on classification of PrPSc type. Parchi and colleagues23 identified 2 PrPSc types in sporadic CJD. However, Hill et al21 described 3 PrPSc types associated with sporadic and iatrogenic CJD (types 1-3) and PrPSc type 4 associated with vCJD. The PrPSc type 5 has, to our knowledge, been observed only in mice expressing human PrP 129V inoculated with vCJD.3,12 Hill et al21 recently described a novel PrPSc type 6 in sporadic CJD.
 
The PrPSc type from our case has features similar to PrPSc type 4 (vCJD) in the predominance of the diglycosylated band; however, it is distinct from PrPSc type 4 in the dependence of the protease cleavage pattern of PrPSc on metal ions, suggesting a distinct PrPSc conformation. Unfortunately, only cerebellum was available for Western blotting in this case, although in vCJD cases from which whole brain was available we have not found evidence of any regional variation in PrPSc type. Others have reported coexistence of Gambetti PrPSc type 1 in the brain from patients with vCJD as a minority component.24 It would also have been interesting to look for peripheral lymphoreticular PrP deposition because this is prominent in vCJD, but that tissue was not available for analysis. Transmission of BSE isolates to transgenic mice expressing human PrP 129 valine results in clinical prion disease with undetectable PrPSc; however, transmission of vCJD isolates to the same mice produces PrPSc type 5 that shares the same predominance of diglycosylated PrPSc to that of PrPSc type 4, and these data suggest that the molecular signature of BSE may be preserved after BSE transmission to PRNP codon 129 VV humans.3,12 Transmission studies of the current case in transgenic mice are now being undertaken to investigate transmission characteristics.
 
We have described a novel PrPSc type that would be designated type 7 by our classification. A firm connection between novel PrPSc types and BSE cannot be made on the basis of a single case, and it will be important to see whether other similar cases occur in the United Kingdom and other BSE-exposed countries but not elsewhere and to perform detailed transmission studies of prions from this patient into transgenic and conventional mice to compare with BSE-derived isolates from cattle and other species. Two other cases of prion disease with valine homozygosity and atypical features have been reported in the United Kingdom and the Netherlands. One of these cases was atypical because of very young onset and a protracted psychiatric history25; the other was notable because certain clinical and molecular features of the case overlapped with those of vCJD, including Western blot analysis of autopsied brain showing a predominance of a diglycosylated PrPSc isoform.26
 
We recommend keeping an open mind about the etiology of such cases during the ensuing years. These cases emphasize the importance both of continued surveillance of prion disease and the further development and refinement of molecular classification of prion diseases of humans and animals. It will also be important to assess lymphoreticular involvement in subsequent cases either at diagnostic tonsil biopsy or at autopsy.
 
 
2015
 
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...
 
======
 
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.
 
***However, this recommendation is guidance and not a requirement by law.
 
======
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
31 Jan 2015 at 20:14 GMT
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.
 
 
it is clear that the designing scientists must have also shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.
 
 
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
 
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
 
snip...
 
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
 
 
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
 
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
 
 
 
10 years post mad cow feed ban August 1997
 
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
 
Date: March 21, 2007 at 2:27 pm PST
 
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
 
PRODUCT
 
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
 
CODE
 
Cattle feed delivered between 01/12/2007 and 01/26/2007
 
RECALLING FIRM/MANUFACTURER
 
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
 
Firm initiated recall is ongoing.
 
REASON
 
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
 
VOLUME OF PRODUCT IN COMMERCE
 
42,090 lbs.
 
DISTRIBUTION
 
WI
 
___________________________________
 
PRODUCT
 
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
 
CODE
 
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
 
RECALLING FIRM/MANUFACTURER
 
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
 
REASON
 
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
 
VOLUME OF PRODUCT IN COMMERCE
 
9,997,976 lbs.
 
DISTRIBUTION
 
ID and NV
 
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
 
 
16 years post mad cow feed ban August 1997
 
2013
 
Sunday, December 15, 2013
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
 
 
17 years post mad cow feed ban August 1997
 
Tuesday, December 23, 2014
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
 
 
Sunday, June 14, 2015
 
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion
 
 
*** Monday, October 26, 2015 ***
 
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
 
 
the OIE BSE TSE Prion policy now, the BSE MRR, legalized the free trading of the TSE Prion disease, humans and animals have now become expendable. ...
 
‘’AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.’’
 
IN A NUT SHELL ;
 
(Adopted by the International Committee of the OIE on 23 May 2006)
 
11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,
 
 
snip...see ;
 
*** Thursday, January 14, 2016
 
*** EMERGING ANIMAL DISEASES Actions Needed to Better Position USDA to Address Future Risks Report to the Chairman, Committee on Energy and Commerce, House of Representatives December 2015 GAO-16-132
 
*** GAO
 
 
Sunday, October 18, 2015
 
World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research
 
 
Thursday, December 17, 2015
 
Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738 10 December 2015
 
 
Friday, January 1, 2016
 
South Korea Lifts Ban on Beef, Veal Imports From Canada
 
 
US CONGRESS, another failed entity...tss
 
Tuesday, December 29, 2015
 
*** Congress repeals country-of-origin labeling rule for beef and pork
 
 
December 28, 2015 at 2:21am
 
*** Australian government assessing risk of importing beef from US, Japan and the Netherlands
 
 
Thursday, December 24, 2015
 
Infectious disease spread is fueled by international trade
 
 
*** you can find some history of the BSE cases in Canada and Klein’s BSE SSS policy comment here ;
 
 
Tuesday, August 12, 2014
 
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST 2014
 
 
Saturday, December 12, 2015
 
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
 
 
Thursday, October 22, 2015
 
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened
 
 
*** Needless conflict ***
 
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
 
Published online 16 May 2012
 
Terry S. Singeltary Sr. said:
 
I kindly wish to submit the following please ;
 
 
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 19–28 February 2013
 
In response to a Member Country’s detailed justification for listing of chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2., the Code Commission recommended this disease be reconsidered for listing.
 
 
OIE CWD TSE PRION TO HUMANS RISK FACTORS STILL IGNORED
 
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 17–26 September 2013
 
Item 5 Criteria for listing diseases (Chapter 1.2.)
 
Comments were received from Australia, EU, Japan, New Zealand, Switzerland, Thailand and AU-IBAR The Code Commission noted a Member Country’s comment suggesting that greater clarity was needed for the term ‘significant morbidity and mortality’. As noted in the February 2013 report, the Code Commission considered that the structured process of listing diseases, first by an expert group whose conclusions are documented and circulated for Member Countries’ review and comment, then consideration by the World Assembly of Delegates before final adoption, is sufficiently rigorous and transparent.
 
 
link updated ;
 
Monday, May 05, 2014
 
Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing
 
 
*** Singeltary submission ;
 
*** Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
 
*** DOCUMENT ID: APHIS-2006-0118-0411 ***
 
see attachments PDF @ bottom of submission...tss
 
 
 
SCRAPIE TO HUMANS RISK FACTORS STILL IGNORED
 
***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.
 
***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
 
 
Monday, November 16, 2015
 
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***
 
 
98 | Veterinary Record | January 24, 2015
 
EDITORIAL
 
Scrapie: a particularly persistent pathogen
 
Cristina Acín
 
Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’
 
From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).
 
Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.
 
Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.
 
The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).
 
In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.
 
Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).
 
In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.
 
The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).
 
Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).
 
So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?
 
What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.
 
References
 
snip...
 
98 | Veterinary Record | January 24, 2015
 
 
*** These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils.
 
*** These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
 
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
 
The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.
 
 
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
 
Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.
 
 
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
 
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.
 
 
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
 
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
 
In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
PL1
 
Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
 
Claudio Soto
 
Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
 
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
 
=========================
 
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
 
========================
 
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
 
 
Wednesday, December 16, 2015
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
 
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
 
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
 
snip...
 
Discussion
 
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
 
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
 
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
 
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
 
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
 
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
 
 
Wednesday, December 16, 2015
 
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
 
Tuesday, December 16, 2014
 
Evidence for zoonotic potential of ovine scrapie prions
 
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics
 
Abstract
 
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
 
Subject terms: Biological sciences• Medical research At a glance
 
 
why do we not want to do TSE transmission studies on chimpanzees $
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
snip...
 
R. BRADLEY
 
 
Monday, January 4, 2016
 
Long live the OIE, or time to close the doors on a failed entity?
 
 
Saturday, December 12, 2015
 
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
 
 
TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL DON'T GET IT $
 
Chronic Wasting Unease
 
The emergence of a deadly disease has wildlife officials and deer breeders eyeing each other suspiciously.
 
 
Subject: Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data
 
To date, we are unaware of a study that documents a decrease in CWD prevalence over time in mule deer, white-tailed deer or elk. We briefly consider three plausible explanations for our findings: a) that natural oscillations occur in CWD outbreaks; b) that the outbreak has peaked and is declining to a lower endemic level; or c) that previous management actions were more successful at suppressing the outbreak than originally believed.
 
Sharp & Pastor [41] illustrated that CWD outbreaks may play out as a series of reoccurring epidemics characterized by either stable limit cycles or oscillations that may dampen or amplify as a function of deer density. If this is the case, we would expect today’s declining deer population to feedback on conditions–lowering transmission rates leading to reduced CWD effects and a growing population. Increasing abundance would support higher transmission rates, deer decline, and oscillations of CWD prevalence and deer. Alternatively, Almberg et al. [21] (see also [22–24,41,42]) suggested that CWD outbreaks could reach endemic equilibrium characterized by coexistence of a smaller deer population and CWD. Under these scenarios, population prevalence would reach a lower, constant level after a period of high prevalence and deer decline.
 
Although neither of the foregoing scenarios can be dismissed completely, invoking them ignores the extensive management of this deer population that occurred in the years between the two time points we chose as the basis for our analyses. Management aimed to reduce CWD transmission between 2000 and 2005, which included a combination of (crude and unpopular) focal culling and a broader increase in female harvest, decreased overall deer abundance by about 25%. Analyses carried out shortly after suggested that reductions in deer density had made little impact on CWD prevalence [10]. However, our current findings suggest that these management actions may indeed have attenuated the outbreak. Observed dynamics over the last decade closely approximate those predicted from models by Wild et al. [42] that included a substantial amount of selective predation on CWD-infected individuals. That harvest could be a source of selective mortality is supported by an early notion that CWD-infected deer might be more vulnerable to harvest [43], just as infected deer also appear to be more vulnerable to vehicle collisions and predation [20,33,44]. This offers the possibility that hunting could be used as a more tightly controlled substitute for predation in studies of system responses with CWD and perhaps other similar diseases.
 
The protracted time-scale of the CWD outbreak is much longer than the timespan of our research, which limits our ability to identify the true explanation of our findings. Nonetheless, our research suggests that, at least for the foreseeable future (e.g., decades), mule deer populations sharing the overall survival and infection probabilities estimated from our analyses may persist but likely will not thrive where CWD becomes established as an endemic infectious disease.
 
 
‘’Nonetheless, our research suggests that, at least for the foreseeable future (e.g., decades), mule deer populations sharing the overall survival and infection probabilities estimated from our analyses may persist but likely will not thrive where CWD becomes established as an endemic infectious disease. ‘’
 
*** Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data
 
‘’Mountain lions prey selectively on CWD infected deer [33] and CWD could result in an abundance of vulnerable prey, thereby enhancing mountain lion survival and reproduction [20].’’
 
please see ;
 
‘’preliminary results suggesting that bobcats (Lynx rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting disease agent.’’
 
references on Feline Spongiform Encephalopathy FSE toward the bottom, see ;
 
Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In Vitro Prion Protein Conversion Assay
 
Friday, January 01, 2016
 
Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data
 
 
Saturday, December 12, 2015
 
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
 
 
Wednesday, December 30, 2015
 
Michigan Deer suspected positive for CWD found in Watertown Township; Jan. 12 public meeting set
 
 
TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL DON'T GET IT $
 
Chronic Wasting Unease
 
The emergence of a deadly disease has wildlife officials and deer breeders eyeing each other suspiciously.
 
 
Wednesday, December 16, 2015
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
 
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
 
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
 
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
 
 
Sunday, November 22, 2015
 
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis ***
 
 
Friday, December 04, 2015
 
Iatrogenic and sporadic Creutzfeldt-Jakob disease in two sisters without mutation in the prion protein gene
 
 
*** Friday, January 10, 2014
 
*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
 
 
Thursday, September 10, 2015
 
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
 
 
Thursday, August 13, 2015
 
Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years
 
 
 
INSULIN
 
Do we know what bovine materials are used in which
products, both as the active ingredient and in production? Bovine active
ingredients in human products include insulin, vasopressin, bone, immune
globulins, fibrin, dermal collagen, albumin. Bovine serum albumin and
fetal calf serum must be used in preparation of very many products. For
each of these products would any “BSE agent” be destroyed or eliminated
in processing? If not, and the product is administered parenterally or
topically into an open wound, might there be a risk? [For oral
products, there would only be a trivially increased load on top of that
taken in food in omnivores/carnivores including man. But for some
herbivores, this might allow the agent to be introduced into yet another
species].
 
--------------------------
 
Medicines and medical devises;
 
 
 
 please see why as follows ;
 
 "The fact that certain medicinal products could be injected directly into the body (most commonly intramuscularly) meant that in theory they would pose a greater risk than beef products in food."
 
 Infectivity of bovine materials used in medicinal products and the importance of inoculation route
 
 3.221 The risk from infectivity present in medicinal products was considered by the Southwood Working Party. They noted that ‘the greatest risk . . . would be from the parenteral injection of material derived from bovine brain or lymphoid tissue’.538 (As described previously, it was generally accepted that the oral route was considerably less efficient than the parenteral route.539)
 
 3.222 In reality, different routes exist within the parenteral category – intracerebral, intraperitoneal, intramuscular, intravenous, intraspinal and subcutaneous. Experiments in 1978 looking at several of these routes found the efficiency between them to vary. Intracerebral and intraspinal were generally the most efficient, followed by intravenous, intraperitoneal and then subcutaneous.540 The fact that certain medicinal products could be injected directly into the body (most commonly intramuscularly) meant that in theory they would pose a greater risk than beef products in food.
 
 3.223 Various cattle tissues were of relevance to medicinal products, including insulin, heparin, surgical catgut sutures and serum. The consideration given to these materials prior to March 1996 is addressed in vol. 7: Medicines and Cosmetics.
 
 533 SEAC 22/5 534 Wells, G. (1998) Preliminary Observations on the Pathogenesis of Experimental Bovine Spongiform Encephalopathy (BSE): An Update, Veterinary Record, 142, 103 535 Wells, G., Hawkins, S., Green, P., Spencer, Y., Dexter, I. and Dawson, D. (1999) Limited Detection of Sternal Bone Marrow Infectivity in the Clinical Phase of Experimental Bovine Spongiform Encephalopathy (BSE), Veterinary Record, 144, 292–4 536 Scott, M.R., Will, R., Ironside, J., Nguyen, H.-O., Tremblay, P., DeArmond, S.J. and Prusiner, S.B. (1999) Compelling Transgenetic Evidence for Transmission of Bovine Spongiform Encephalopathy Prions to Humans, Proceedings of the National Academy of Sciences of the USA, 96, 15137–42 537 Scott, M.R., Safar, J., Telling, G., Nguyen, H.-O., Groth, D., Torchia, M., Kochler, R., Tremblay, P., Walther, D., Cohen, F., DeArmond, S. and Prusiner, S. (1997) Identification of a Prion Protein Epitope Modulating Transmission of Bovine Spongiform Encephalopathy Prions to Transgenic Mice, Proceedings of the National Academy of Sciences of the United States of America, 94, 14279–84 538 IBD1 tab 2 para. 5.3.3 539 Kimberlin, R. and Walker, C. (1989) Pathogenesis of Scrapie in Mice after Intragastric Infection, Virus Research, 12, 213–20; Diringer, H., Beekes, M. and Oberdieck, U. (1994) The Nature of the Scrapie Agent: The Virus Theory, Annals of The New York Academy of Science, 724, 246–58; Prusiner, S., Cochran, S. and Alpers, S. (1985) Transmission of Scrapie in Hamsters, Journal of Infectious Diseases, 152, 971–8 540 Kimberlin, R.H. and Walker, C.A. (1978) Pathogenesis of Mouse Scrapie: Effect of Route of Inoculation on Infectivity Titres and Dose-Response Curves, Journal of Comparative Pathology, 88, 39–47
 
 
 
 
 
 COMMERCIAL IN CONFIDENCE
 
 NOT FOR PUBLICATION
 
 COMMITTEE ON SAFETY OF MEDICINES
 
 WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY
 
 3. Products for injection using bovine tissue
 
 This category includes tissue derived products, other than from brain or lymphoid tissue and excludes bovine blood.
 
 3.1 Bovine Pancreas
 
 3.1.1 Insulin
 
 The following companies hold licences for bovine insulin.
 
 Source Country
 
 Denmark
 
 USA
 
 USA
 
 Denmark, Sweden, USA, Italy, Canada, Portugal, Netherlands
 
 In 1988 a sample consignment from UK was used. UK source material is no longer used.
 
 Comment
 
 There are no bovine insulins manufctured from UK sourced material.
 
 Bovine insulin is not widely prescribed, but has a niche in the market for diabetics unable to tolerate other products.
 
 3.1.2 Glucagon
 
 bovine pancreas from USA.
 
 as for insulin - Scandinavia, USA, Italy, Canada, Portugal and Netherlands.
 
 3.1.3
 
 Miscellaneous products containing Bovine Pancreas
 
 3.1.3.1 Zonulysin (Chymotrypsin) - sourced from Canada
 
 3.1.3.2 Streptokinase - culture medium, containing bovine muscle and pancreas are used in process - all sourced from Germany
 
 3.1.3.3 Fibrinogen + Desoxyribonuclease - bovine pancreas sourced from Canada and S Africa.
 
 3.2. Vaccines using Bovine Products in process
 
 snip...see full text ;
 
 
USDA allows diseased animals into human food supply
 
 Mon, 14 Aug 2000. Information provided by Terry S. Singeltary Sr. Farm Sanctuary web site
 
 In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - Report of a visit to the USA - April-May 1989 - G A H Wells [head of England's main veterinary lab -- webmaster]
 
 2. Meeting with USDA, BSE Task Force
 
 
 
 MAD COW DISEASE BSE CJD CHILDREN VACCINES
 
 Sunday, May 18, 2008
 
 MAD COW DISEASE BSE CJD CHILDREN VACCINES
 
 TIP740203/l 0424 CONFIDENTIAL
 
 
Subject: Louping-ill vaccine documents from November 23rd, 1946
 
 Date: Sat, 9 Sep 2000 17:44:57 -0700
 
 From: "Terry S. Singeltary Sr."
 
 Reply-To: Bovine Spongiform Encephalopathy
 
 To: BSE-L@uni-karlsruhe.de
 
 ######### Bovine Spongiform Encephalopathy #########
 
 THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946
 
 NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND
 
 ANNUAL CONGRESS, 1946
 
 snip...
 
 As a result of this experience a large-scale transmision experiment involving the ue of 788 sheep was commenced in 1938 on a farm specially taken for the purpose by the Animal Diseases Research Association with funds provided by the Agricultural Research Council. The experiment was designed to determine the nature of the infective agent and the pathogenesis of the disease. It is only possible here to give a summary of the result which showed that (1) saline suspensions of brain and spinal cord tissue of sheep affected with scrapie were infective to normal sheep when inoculatted intracerebrally or subcutaneously; (2) the incubation period after intracerebral inoculation was seven months and upwards and only 60 percent of the inoculated sheep developed scrapie during a period of four and a half years; (3) the incubation period after subcutaneous inoculation was 15 months and upwards and only about 30 percent of the inoculated sheep developed the disease during the four and a half years: (4) the infective agent was of small size and probably a filtrable virus.
 
 The prolonged incubative period of the disease and the remarkable resistance of the causal agent to formalin are features of distinct interest. It still remains to determine if a biological test can be devised to detect infected animals so that they can be killed for food before they develop clinical symptoms and to explore the possibilities of producing an immunity to the disease.
 
 ==================================================================
 
 Greetings List Members,
 
 pretty disturbing document. now, what would stop this from happening with the vaccineCJD in children???
 
 kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
 
 
Subject: Re: VACCINES/CHILDREN/TSE'S -- 'CONFIDENTIAL'
 
 From: tom
 
 Reply-To: Bovine Spongiform Encephalopathy
 
 Date: Wed, 6 Sep 2000 18:20:09 -0800
 
 Content-Type: text/plain
 
 Parts/Attachments: text/plain (110 lines)
 
 Reply
 
 ######### Bovine Spongiform Encephalopathy #########
 
 Just when I was thinking the Internet had reached a terminal condition of shallow pages and broken links, some young people come along and invent a really effective Internet search engine: http://www.google.com/ This works quite well to search the entire http://www.mad-cow.org site (or find 393 web sites such as GenBank that link to it, or 936 sites that cite it in text) back to 1996 as well as the BSE Inquiry http://www.bse.org.uk/
 
 Thus for louping ill (unnecessary cites suppressed):
 
 http://www.bse.org.uk/witness/htm/stat537.htm Witness Statements 537 - Coulthard
 
 29.Pituitary FSH from pigs has been used in the USA prior to its use in the UK and much more extensively there and Canada.... 30.Thousands of embryos were exported from this country to the USA prior to the ban being imposed... 42. No cow pituitaries were used in the preparation of FSH [follicular stimulating hormone] products compared with the case of louping ill vaccine for scrapie.
 
 
 In the 1930's: 18,000 UK sheep were inoculated against louping ill, a brain inflammatory illness spread by ticks. Despite formalin-treatment of the inoculated agent, the procedure gave rise to 1,500 cases of scrapie. Louping is a Scottish word for fleeing or leaping, related to loping. In humans, louping ill is called Russian spring-summer encephalitis, a meningo-encephalitis with muscular tremors and spasms followed by varying degrees of paralysis.... [John Lanchester 2 Dec 96 New Yorker]
 
 
 In what the story calls a grand historical irony, this landmark series of experiments was being confirmed at the same time in England as a result of an outbreak of scrapie in several hundred sheep that had been immunized against louping ill with a vaccine prepared from tissue from the brain, spinal cord, and spleen of sheep that were belatedly discovered to have been exposed to natural scrapie infection.[6.Gordon WS. Advances in veterinary research. Vet Rec 1946; 58: 516-520] The transmissible nature of the scrapie agent was thus established beyond any doubt. [P Brown, 1755 and All That: A Historical Primer of TSE.
 
 We need to look at the full text of the article and its cites to see how they actually made the vaccine, whether they exported vaccine-infected sheep to Canada and the US, and what became of the vaccinated flocks. Perhaps there is still sample available, Moredun Institute is still around.
 
 Gordon WS. Advances in veterinary research. Vet Rec 1946; 58: 516-520 (not covered by Medline) Gordon, Bronlee and Wilson 1939 [full cite is available only in a letter we don't have)
 
 Terry was reading Draft Factual Account 17 http://www.bse.org.uk/dfa/dfa17.htm
 
 236. Mrs Alderman replied on 3 June 1988, listing products containing bovine insulin and noting there were two rabies vaccines listed but the species used in manufacture was not shown.[282] 237. On 6 June 1988 Mr Lawrence wrote to Sir Richard Southwood and enclosed some brief answers to the questions that had been tabled at the meeting on 19 May.[283] In relation to Q6, which asked ŒWhat is meat and other material from scrapie infected sheep used for - does it include pet food and material for biological products?¹ Part of the answer stated: ...
 
 There has been one instance of inadvertant [sic] transmission of the scrapie agent to sheep through louping ill vaccine (Gordon, Bronlee and Wilson 1939). One of the three batches of vaccine made in 1935 at the Moredun Institute contained the scrapie agent resulting in 7% of the recipients of the 18, 000 doses in the batch developing scrapie. This vaccine was made from formalin-inactivated sheep brain, and brought to the attention of research workers that formalin, at a concentration of 0.35% for at least 3 months, which inactivated conventional viruses, did not totally inactivate the scrapie agent. ---------------------------- 4. Questions we might want to have answered are: the highest risk would be from parenterals prepared from brain (eg rabies vaccine). Any species in which transmissible spongiform encephalopathies have been described would be suspect (“natural” infections in sheep, goats, cattle, deer, mink, but can be transmitted to hamster, mouse, guinea-pig etc). Are sterilisation processes adequate for the most resistant strain of scrapie agent or for CJD agent? Should companies be asked to include investigation for inclusion of scrapie agent (eg mouse innoculation [sic]) in at least some batches? If BSE behaves like scrapie, then we might expect other nervous tissue, spleen, lymph nodes and placenta to be contaminated. Infection has been described in other tissues too, eg gut wall, and we can not [sic] be sure blood is free. Do we know what bovine materials are used in which products, both as the active ingredient and in production? Bovine active ingredients in human products include insulin, vasopressin, bone, immune globulins, fibrin, dermal collagen, albumin. Bovine serum albumin and fetal calf serum must be used in preparation of very many products. For each of these products would any “BSE agent” be destroyed or eliminated in processing? If not, and the product is administered parenterally or topically into an open wound, might there be a risk? [For oral products, there would only be a trivially increased load on top of that taken in food in omnivores/carnivores including man. But for some herbivores, this might allow the agent to be introduced into yet another species]. -------------------------- Medicines and medical devises;
 
 
 Friday, March 25, 2011
 
 Detection of Prion Protein in Urine-Derived Injectable Fertility Products by a Targeted Proteomic Approach
 
 
 
SNIP...PLEASE SEE MORE HERE ;
 
Wednesday, January 28, 2015
 
BOVINE HEPARIN POSITION STATEMENT ON THE REINTRODUCTION and POTENTIAL BSE TSE PRION RISK FACTORS THEREFROM
 
 
Tuesday, December 30, 2014
 
TSEAC USA Reason For Recalls Blood products, collected from a donors considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were distributed END OF YEAR REPORT 2014
 
 
Tuesday, April 21, 2015
 
Transmissible Spongiform Encephalopathy Advisory Committee TSEAC MEETING SCHEDULED FOR June 1, 2015
 
 
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE MEETING
 
Thursday, June 2, 1999
 
CHAIRMAN BROWN: My name is Dr. Paul Brown.
 
Welcome to the FDA traveling road show. We are asked yet once more by the FDA to consider a question of theoretical risk in the absence of sufficient knowledge on which to base any firm conclusion. The issue before us today is that of excluding categories of American blood donors who have either visited or resided for longer periods of time in Great Britain. The issue is sufficiently delicate, as you see that we have been moved outside the Beltway. (Laughter.)
 
snip...
 
see all here ;
 
 
Saturday, April 18, 2015
 
*** vCJD TEXAS CDC Emerging Infectious Diseases May 2015 Baylor College of Medicine Neuroscience 2014 case of human form of “mad cow disease” highlights need for continued surveillance
 
 
>>> Variant CJD and blood transfusion: are there additional cases?
 
TSE Prion and blood transfusion: will there be additional cases? this should be the concern. ...TSS
 
Thursday, March 26, 2015
 
Variant CJD and blood transfusion: are there additional cases?
 
Vox Sanguinis (2014) 107, 220–225 ORIGINAL PAPER © 2014 International Society of Blood Transfusion DOI: 10.1111/vox.12161
 
 
Tuesday, December 30, 2014
 
TSEAC USA Reason For Recalls Blood products, collected from a donors considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were distributed END OF YEAR REPORT 2014
 
 
Sunday, March 09, 2014
 
A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease
 
FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES
 
 
Sunday, June 9, 2013
 
TSEAC March 14, 2013: Transmissible Spongiform Encephalopathies Advisory Committee Meeting Webcast
 
 
Wednesday, June 29, 2011
 
TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood and blood products
 
 
Wednesday, June 29, 2011 TSEAC JUNE 2, 1999 Welcome to the FDA traveling road show From: TSS
 
Subject: TSEAC JUNE 2, 1999 Welcome to the FDA traveling road show
 
Date: October 15, 2007 at 3:18 pm PST
 
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE MEETING Thursday, June 2, 1999
 
 
Wednesday, March 2, 2011
 
Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011 Posted: 3/2/2011
 
October 28, 2010
 
Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011
 
 
Monday, February 7, 2011
 
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
 
 
October 29, 2010
 
Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011
 
 
Monday, October 18, 2010
 
TSEAC Transmissible Spongiform Encephalopathies Advisory Committee Draft Agenda and Meeting Materials,
 
Posted: 10/18/2010
 
Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Center Date Time Location
 
 
Tuesday, September 14, 2010
 
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
 
 
Saturday, September 5, 2009
 
TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS
 
 
Sunday, May 10, 2009
 
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
 
TO : william.freas@fda.hhs.gov
 
May 8, 2009
 
Greetings again Dr. Freas, TSEAC et al,
 
I would kindly, once again, wish to comment at this meeting about the urgent actions that need to be taken asap, to the Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009. Due to my disability from my neck injury, I will not be attending this meeting either, however I hope for my submission to be read and submitted. ...
 
IN reply to ;
 
 
snip...see full text ;
 
Sunday, May 10, 2009
 
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
 
TO : william.freas@fda.hhs.gov
 
 
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 INTRODUCTION The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website:
 
 
Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary. This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
 
 
From: Terry S. Singeltary Sr.
 
To: FREAS@CBER.FDA.GOV
 
Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
 
Sent: Friday, December 01, 2006 2:59 PM
 
Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION
 
snip...
 
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)
 
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 blood 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. ...
 
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
 
snip... 48 pages...
 
 
Wednesday, October 17, 2007
 
TSEAC MEETINGS
 
----- Original Message -----
 
From: Terry S. Singeltary Sr.
 
To: FREAS@CBER.FDA.GOV
 
Cc: 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-derivedantihemophilic factor (FVIII) productsmanufactured from U.S. plasma donors and related communication material ;
 
 
i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;
 
 
however, i seem to disagree. from my primitive ciphering, i see it another way. 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, wha tabout 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 industry fed crap. i pray that my assessment is the one that is wrong. but it is THEY who roll the dice with your life. it is THEY who refuse to regulate an industry that has run amok. just from are call aspect of potentially tainted blood, and these are just recent recalls ;
 
PRODUCT
 
Source Plasma, Recall # B-0054-7CODEUnits: 03MMNC5465, 03MMNC6361, 03MMNC6801, 03MMNC7510, 03MMNC7891,03MMNC8252, 03MMNC8801, 03MMNC9144, 03MMND1122, 03MMND1478, 03MMND1969,03MMND2350, 03MMND2825, 03MMND3211, 03MMND3708, 03MMND4072, 03MMND4588,03MMND4831, 03MMND5320, 03MMND5719, 03MMND6268, 03MMND6683, 03MMND7228,03MMND7656, 03MMND8211, 03MMND8652, 03MMND9195, 03MMND9618, 03MMNE0628,03MMNE0884, 03MMNE1597, 03MMNE1979, 03MMNE2644, 03MMNE3064, 03MMNE3707,03MMNE4122, 03MMNE4750, 03MMNE5080, 03MMNE5876, 03MMNE6218, 03MMNE7189,03MMNE7587, 03MMNE8027, 03MMNE8645, 03MMNE9029, 03MMNE9641, 03MMNE9979,03MMNF0491, 03MMNF0685, 03MMNF0937, 03MMNF1260, 04MMNA0351, 04MMNA0707,04MMNA1241, 04MMNA1650, 04MMNA2291, 04MMNA2646, 04MMNA3340, 04MMNA3719,04MMNA4312, 04MMNA4683, 04MMNA5298, 04MMNA5750, 04MMNA6407, 04MMNA6816,04MMNA7482, 04MMNA7915, 04MMNA8632, 04MMNA9076, 04MMNA9723, 04MMNB0063,04MMNB0696, 04MMNB1100, 04MMNB1845, 04MMNB2285, 04MMNB3035, 04MMNB3485,04MMNB4213, 04MMNB4672, 04MMNB5841, 04MMNB6652, 04MMNB7162, 04MMNB7930,04MMNB8453, 04MMNB9239, 04MMNB9747, 04MMNC0456, 04MMNC0931, 04MMNC1578
 
RECALLING FIRM/MANUFACTURER
 
BioLife Plasma Services, L.P., Mankato, MN, by facsimile on June 4, 2004.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
89 units
 
DISTRIBUTION
 
CA and Austria
 
END OF ENFORCEMENT REPORT FOR October 25, 2006
 
###
 
 
USA FDA MAD COW BLOOD HUMANS RECALL (these are dime a dozen)RECALLS AND FIELD CORRECTIONS: BIOLOGICS -- CLASS II
 
______________________________
 
PRODUCTSource Plasma, Recall # B-1708-6CODEUnits: MI180733, MI180927, MI181625, MI181780, MI182337, MI182519, MI183140,MI183311, MI183955, MI185006, MI185278, MI185822, MI186081, MI186855,MI187183, MI187903, MI188273, MI188695, MI189257, MI189553, MI190136,MI190473, MI191073, MI191395, MI191972, MI192303, MI193473, MI194343,04MINA0377, 04MINA0801, 05MINA7147, 05MINA7451, 05MINA8094, 05MINA8504,05MINA9548, 05MINA9883, 05MINB0489, 05MINB0875, 05MINB1469, 05MINB1874,05MINB3116, 05MINB7192, 05MINB7529, 05MINB8246, 05MINB8612, 05MINB9236,05MINB9366, 05MINB9475, 05MINB9641, 05MINC0031, 05MINC0237, 05MINC0336,05MINC0894, 05MINC0964, 05MINC1138, 05MINC1619, 05MINC1750, 05MINC1907,05MINC1977, 05MINC2375, 05MINC2774, 05MINC3113, 05MINC3484, 05MINC4277,05MINC4623, 05MINC5623, 05MINC5914, 05MINC7545, 05MINC7870, 05MINC8355,05MINC8689, 05MINC9437, 05MINC9775, 05MIND0067, 05MIND0393, 05MIND0892,05MIND0951, 05MIND1836, 05MIND2183 and 05MIND2962
 
RECALLING FIRM/MANUFACTURER
 
BioLife Plasma Services L.P., Muncie, IN, by facsimile on November 22, 2005.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, collected from unsuitable donors based on risk factors for Creutzfeldt-Jakob Disease (CJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
80 units
 
DISTRIBUTION CA, NC, and MD
 
______________________________
 
PRODUCT
 
a) Red Blood Cells, Leukocytes Reduced, Recall # B-1714-6;b) Fresh Frozen Plasma, Recall # B-1715-6;c) Platelets, Recall # B-1716-6CODEa),
 
b), and c) Unit: 2443732RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by letters dated November 11, 2003 and December 18, 2003. Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
TX and WI
 
END OF ENFORCEMENT REPORT FOR SEPTEMBER 13, 2006
 
###
 
 
PRODUCT
 
Fresh Frozen Plasma, Recall # B-1751-6
 
CODE
 
Unit: 4936623
 
RECALLING FIRM/MANUFACTURER
 
Gulf Coast Regional Blood Center, Houston, TX, by facsimile dated September 16, 2005.
 
Firm initiated recall is complete.
 
REASON
 
Blood product, which was collected from an unsuitable donor based on risk factors for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
1 unit
 
DISTRIBUTION
 
TX
 
END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006
 
###
 
 
Mon Aug 7, 2006 10:2471.248.132.189
 
PRODUCT
 
a) Red Blood Cells, Recall # B-1587-6;b) Cryoprecipitated AHF, Recall # B-1588-6;c) Recovered Plasma, Recal # B-1589-6
 
CODE
 
a), b) and c)
 
Unit: 2016719
 
RECALLING FIRM/MANUFACTURER
 
Walter Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile on March 13, 2003.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
GA and Germany
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1590-6;b) Fresh Frozen Plasma, Recall # B-1591-6
 
CODE
 
a) and b)
 
Unit: 2443595
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on June30, 2004.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1592-6;b) Fresh Frozen Plasma, Recall # B-1593-6
 
CODEa) and b)
 
Unit: 2545596
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on December 14, 2004 and January 3, 2005.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX
 
______________________________
 
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1550-6;b) Fresh Frozen Plasma, Recall # B-1551-6
 
CODEa) and b)
 
Unit 2395371
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by fax on August 20,2003.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1552-6;b) Platelets, Recall # B-1553-6;c) Fresh Frozen Plasma, Recall # B-1554-6
 
CODE
 
a), b) and c)
 
Unit 2438702
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by fax on May 29,2003.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increasedrisk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
TX
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1555-6;b) Fresh Frozen Plasma, Recall # B-1556-6
 
CODEa) and b)
 
Unit 2454970
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by fax on July 23 and December 11. 2003.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX
 
______________________________
 
PRODUCT
 
a) Red Blood Cells, Recall # B-1494-6b) Cryoprecipitated AHF, Recall # B-1495-6
 
CODEa) and b)
 
Unit 5013100
 
RECALLING FIRM/MANUFACTURER
 
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on May17, 2005. Firm initiated recall is complete.REASONBlood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
GA
 
______________________________
 
PRODUCT
 
Source Plasma, Recall # B-1450-6
 
CODE
 
Unit numbers ST0824313 and ST0824764
 
RECALLING FIRM/MANUFACTURER
 
Stillwater Plasma Center LLC, Stillwater, OK, by fax on November 21, 2003.
 
Firm initiated recall is complete.REASON
 
Blood products, which were collected from a donor whose suitability pertaining to risk factors for Creutzfeldt-Jakob Disease (vCJD) was not adequately determined, were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
UK
 
______________________________
 
PRODUCT
 
Plasma Frozen, Recall # B-1422-6;Recovered Plasma, Recall # B-1423-6
 
CODE
 
a) Unit 03E42218;
 
b) Unit 03E38153
 
RECALLING FIRM/MANUFACTURER
 
American Red Cross Blood Services, Atlanta, GA, by telephone, e-mail orletter on February 20 or 21, 2004. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
GA and Switzerland
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1374-6;
 
b) Recovered Plasma, Recall # B-1375-6CODEa) and b) unit 2453906
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by fax on October 31 and November 5, 2003. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX and Austria
 
______________________________
 
PRODUCT
 
Source Plasma.
 
Recall # B-1295-6
 
CODE
 
Units: NG0046551, NG0045950
 
RECALLING FIRM/MANUFACTURERD
 
CI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax onDecember 20, 2002, Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor who did not answer the questions on the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire appropriately, were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
KY
 
______________________________
 
PRODUCT
 
Source Plasma. Recall # B-1296-6
 
CODE
 
Unit: NG 0044520RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax onDecember 12, 2002. Firm initiated recall is complete.
 
REASON
 
Blood product, collected from a donor who did not answer the questions on the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire, was distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
1 unit
 
DISTRIBUTION
 
KY
 
______________________________
 
PRODUCT
 
Source Plasma. Recall # B-1297-6
 
CODE
 
Units: NG0042874, NG0043139, NG0043312, NG0043618, NG0043797, NG0044020,NG0044209, NG0044507, NG0044718, NG0044977, NG0045161, NG0045412, NG0045555RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax onDecember 20, 2002. Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
13 units
 
DISTRIBUTION
 
KY
 
______________________________
 
PRODUCT
 
Source Plasma, Recall # B-1298-6
 
CODE
 
Units: NG 0046823, NG 0046671, NG 0045205, NG 0044635, NG 0043095, NG0042525, NG 0042341RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax onDecember 20, 2002. Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor who answered questions on the variant Creutzfeldt-Jacob disease (vCJD) questionnaire inappropriately, were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
7 units
 
DISTRIBUTION
 
KY
 
______________________________
 
PRODUCT
 
Recovered Plasma, Recall # B-1299-6CODEUnit: 4357117
 
RECALLING FIRM/MANUFACTURER
 
Department of the Navy, Naval Medical Center, San Diego, CA, by fax and letter on September 25, 2003. Firm initiated recall is complete.
 
REASON
 
Blood product, collected from a donor considered to be at risk of exposure to Creutzfeldt-Jacob Disease (CJD), was distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
1 unit
 
DISTRIBUTION
 
Germany
 
END OF ENFORCEMENT REPORT FOR July 12, 2006
 
###
 
 
CJD WATCH MESSAGE BOARD
 
TSS
 
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY Fri Jul 7, 2006 09:3770.110.83.160
 
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1379-6;
 
b) Platelets, Recall # B-1380-6;
 
c) Fresh Frozen Plasma, Recall # 1381-6;
 
d) Recovered Plasma, Recall # B-1382-6
 
CODE
 
a) Unit numbers: 2343106, 2377779, and 2403533;
 
b) and c) Unit numbers: 2377779;
 
d) Unit numbers: 2343106 and 2403533
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on June12, 2003. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
7 units
 
DISTRIBUTIONTX and Austria
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1467-6;
 
b) Recovered Plasma, Recall # B-1468-6
 
CODE
 
a) and b)
 
Unit numbers: 2329380
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on May 8,2003. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTIONTX and Switzerland
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1479-6;
 
b) Cryoprecipitated AHF, Recall # B-1480-6;
 
c) Recovered Plasma, Recall # B-1481-6
 
CODE
 
a), b), and c)
 
Unit numbers: 2383280
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on July23 and 29, 2004. Firm initiated recall is complete.
 
REASONBlood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
TX and Switzerland
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1482-6;
 
b) Fresh Frozen Plasma, Recall # B-1483-6
 
CODE
 
a) and b)
 
Unit number: 2501452
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile onOctober 5, 2004. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX and NY
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1484-6;
 
b) Plasma Cryoprecipitated Reduced, Recall # B-1485-6;
 
c) Recovered Plasma, Recall # B-1486-6
 
CODE
 
a) and c)
 
Unit number: 2554077;
 
b) Unit number: 2415708
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on August13, 2004. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
TX and Austria
 
_____________________________________
 
END OF ENFORCEMENT REPORT FOR July 5, 2006
 
###
 
 
Greetings again Dr. Freas et al at FDA,
 
WITH new atypical TSE in the bovine, in the sheep, goat, and humans, and the fact that the new BASE TSE in cattle being very very similar to sporadic CJD, rather than the nvCJD, the fact that now science showing the TSE agent of the atypical cattle in Japan showing infectivity other than CNS tissue, the fact that the latest Texas mad cow and the recent Alabama mad cow both being of the atypical strain, it would seem prudent to include all human TSE in the blood ban, in my opinion. with sporadic CJD, you have many strains and or phenotypes, some of which are 'UNKNOWN', so we do not know how this will transmit, what tissues are infectious and or if blood transmits. that's the bottomline, however it has been reported that the BASE is more virulent to humans.With this, and the fact that sporadic CJD has tripled in the past few years or so, i see itas being prudent to take serious and immediate action ;
 
snip...see full text ;
 
Wednesday, October 17, 2007 TSEAC MEETINGS ----- Original Message -----
 
From: Terry S. Singeltary Sr.
 
To: FREAS@CBER.FDA.GOV
 
Cc: 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-derivedantihemophilic factor (FVIII) productsmanufactured from U.S. plasma donors and related communication material ;
 
 
i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;
 
 
however, i seem to disagree. from my primitive ciphering, i see it another way. 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, wha tabout 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 industry fed crap. i pray that my assessment is the one that is wrong. but it is THEY who roll the dice with your life. it is THEY who refuse to regulate an industry that has run amok. just from are call aspect of potentially tainted blood, and these are just recent recalls ;
 
PRODUCT
 
Source Plasma, Recall # B-0054-7CODEUnits: 03MMNC5465, 03MMNC6361, 03MMNC6801, 03MMNC7510, 03MMNC7891,03MMNC8252, 03MMNC8801, 03MMNC9144, 03MMND1122, 03MMND1478, 03MMND1969,03MMND2350, 03MMND2825, 03MMND3211, 03MMND3708, 03MMND4072, 03MMND4588,03MMND4831, 03MMND5320, 03MMND5719, 03MMND6268, 03MMND6683, 03MMND7228,03MMND7656, 03MMND8211, 03MMND8652, 03MMND9195, 03MMND9618, 03MMNE0628,03MMNE0884, 03MMNE1597, 03MMNE1979, 03MMNE2644, 03MMNE3064, 03MMNE3707,03MMNE4122, 03MMNE4750, 03MMNE5080, 03MMNE5876, 03MMNE6218, 03MMNE7189,03MMNE7587, 03MMNE8027, 03MMNE8645, 03MMNE9029, 03MMNE9641, 03MMNE9979,03MMNF0491, 03MMNF0685, 03MMNF0937, 03MMNF1260, 04MMNA0351, 04MMNA0707,04MMNA1241, 04MMNA1650, 04MMNA2291, 04MMNA2646, 04MMNA3340, 04MMNA3719,04MMNA4312, 04MMNA4683, 04MMNA5298, 04MMNA5750, 04MMNA6407, 04MMNA6816,04MMNA7482, 04MMNA7915, 04MMNA8632, 04MMNA9076, 04MMNA9723, 04MMNB0063,04MMNB0696, 04MMNB1100, 04MMNB1845, 04MMNB2285, 04MMNB3035, 04MMNB3485,04MMNB4213, 04MMNB4672, 04MMNB5841, 04MMNB6652, 04MMNB7162, 04MMNB7930,04MMNB8453, 04MMNB9239, 04MMNB9747, 04MMNC0456, 04MMNC0931, 04MMNC1578
 
RECALLING FIRM/MANUFACTURER
 
BioLife Plasma Services, L.P., Mankato, MN, by facsimile on June 4, 2004.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
89 units
 
DISTRIBUTION
 
CA and Austria
 
END OF ENFORCEMENT REPORT FOR October 25, 2006
 
###
 
 
USA FDA MAD COW BLOOD HUMANS RECALL (these are dime a dozen)RECALLS AND FIELD CORRECTIONS: BIOLOGICS -- CLASS II
 
______________________________
 
PRODUCTSource Plasma, Recall # B-1708-6CODEUnits: MI180733, MI180927, MI181625, MI181780, MI182337, MI182519, MI183140,MI183311, MI183955, MI185006, MI185278, MI185822, MI186081, MI186855,MI187183, MI187903, MI188273, MI188695, MI189257, MI189553, MI190136,MI190473, MI191073, MI191395, MI191972, MI192303, MI193473, MI194343,04MINA0377, 04MINA0801, 05MINA7147, 05MINA7451, 05MINA8094, 05MINA8504,05MINA9548, 05MINA9883, 05MINB0489, 05MINB0875, 05MINB1469, 05MINB1874,05MINB3116, 05MINB7192, 05MINB7529, 05MINB8246, 05MINB8612, 05MINB9236,05MINB9366, 05MINB9475, 05MINB9641, 05MINC0031, 05MINC0237, 05MINC0336,05MINC0894, 05MINC0964, 05MINC1138, 05MINC1619, 05MINC1750, 05MINC1907,05MINC1977, 05MINC2375, 05MINC2774, 05MINC3113, 05MINC3484, 05MINC4277,05MINC4623, 05MINC5623, 05MINC5914, 05MINC7545, 05MINC7870, 05MINC8355,05MINC8689, 05MINC9437, 05MINC9775, 05MIND0067, 05MIND0393, 05MIND0892,05MIND0951, 05MIND1836, 05MIND2183 and 05MIND2962
 
RECALLING FIRM/MANUFACTURER
 
BioLife Plasma Services L.P., Muncie, IN, by facsimile on November 22, 2005.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, collected from unsuitable donors based on risk factors for Creutzfeldt-Jakob Disease (CJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
80 units
 
DISTRIBUTION CA, NC, and MD
 
______________________________
 
PRODUCT
 
a) Red Blood Cells, Leukocytes Reduced, Recall # B-1714-6;b) Fresh Frozen Plasma, Recall # B-1715-6;c) Platelets, Recall # B-1716-6CODEa),
 
b), and c) Unit: 2443732RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by letters dated November 11, 2003 and December 18, 2003. Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
TX and WI
 
END OF ENFORCEMENT REPORT FOR SEPTEMBER 13, 2006
 
###
 
 
PRODUCT
 
Fresh Frozen Plasma, Recall # B-1751-6
 
CODE
 
Unit: 4936623
 
RECALLING FIRM/MANUFACTURER
 
Gulf Coast Regional Blood Center, Houston, TX, by facsimile dated September 16, 2005.
 
Firm initiated recall is complete.
 
REASON
 
Blood product, which was collected from an unsuitable donor based on risk factors for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
1 unit
 
DISTRIBUTION
 
TX
 
END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006
 
###
 
 
Mon Aug 7, 2006 10:2471.248.132.189
 
PRODUCT
 
a) Red Blood Cells, Recall # B-1587-6;b) Cryoprecipitated AHF, Recall # B-1588-6;c) Recovered Plasma, Recal # B-1589-6
 
CODE
 
a), b) and c)
 
Unit: 2016719
 
RECALLING FIRM/MANUFACTURER
 
Walter Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile on March 13, 2003.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
GA and Germany
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1590-6;b) Fresh Frozen Plasma, Recall # B-1591-6
 
CODE
 
a) and b)
 
Unit: 2443595
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on June30, 2004.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1592-6;b) Fresh Frozen Plasma, Recall # B-1593-6
 
CODEa) and b)
 
Unit: 2545596
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on December 14, 2004 and January 3, 2005.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX
 
______________________________
 
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1550-6;b) Fresh Frozen Plasma, Recall # B-1551-6
 
CODEa) and b)
 
Unit 2395371
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by fax on August 20,2003.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1552-6;b) Platelets, Recall # B-1553-6;c) Fresh Frozen Plasma, Recall # B-1554-6
 
CODE
 
a), b) and c)
 
Unit 2438702
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by fax on May 29,2003.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increasedrisk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
TX
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1555-6;b) Fresh Frozen Plasma, Recall # B-1556-6
 
CODEa) and b)
 
Unit 2454970
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by fax on July 23 and December 11. 2003.
 
Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX
 
______________________________
 
PRODUCT
 
a) Red Blood Cells, Recall # B-1494-6b) Cryoprecipitated AHF, Recall # B-1495-6
 
CODEa) and b)
 
Unit 5013100
 
RECALLING FIRM/MANUFACTURER
 
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on May17, 2005. Firm initiated recall is complete.REASONBlood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
GA
 
______________________________
 
PRODUCT
 
Source Plasma, Recall # B-1450-6
 
CODE
 
Unit numbers ST0824313 and ST0824764
 
RECALLING FIRM/MANUFACTURER
 
Stillwater Plasma Center LLC, Stillwater, OK, by fax on November 21, 2003.
 
Firm initiated recall is complete.REASON
 
Blood products, which were collected from a donor whose suitability pertaining to risk factors for Creutzfeldt-Jakob Disease (vCJD) was not adequately determined, were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
UK
 
______________________________
 
PRODUCT
 
Plasma Frozen, Recall # B-1422-6;Recovered Plasma, Recall # B-1423-6
 
CODE
 
a) Unit 03E42218;
 
b) Unit 03E38153
 
RECALLING FIRM/MANUFACTURER
 
American Red Cross Blood Services, Atlanta, GA, by telephone, e-mail orletter on February 20 or 21, 2004. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
GA and Switzerland
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1374-6;
 
b) Recovered Plasma, Recall # B-1375-6CODEa) and b) unit 2453906
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by fax on October 31 and November 5, 2003. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX and Austria
 
______________________________
 
PRODUCT
 
Source Plasma.
 
Recall # B-1295-6
 
CODE
 
Units: NG0046551, NG0045950
 
RECALLING FIRM/MANUFACTURERD
 
CI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax onDecember 20, 2002, Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor who did not answer the questions on the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire appropriately, were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
KY
 
______________________________
 
PRODUCT
 
Source Plasma. Recall # B-1296-6
 
CODE
 
Unit: NG 0044520RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax onDecember 12, 2002. Firm initiated recall is complete.
 
REASON
 
Blood product, collected from a donor who did not answer the questions on the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire, was distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
1 unit
 
DISTRIBUTION
 
KY
 
______________________________
 
PRODUCT
 
Source Plasma. Recall # B-1297-6
 
CODE
 
Units: NG0042874, NG0043139, NG0043312, NG0043618, NG0043797, NG0044020,NG0044209, NG0044507, NG0044718, NG0044977, NG0045161, NG0045412, NG0045555RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax onDecember 20, 2002. Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
13 units
 
DISTRIBUTION
 
KY
 
______________________________
 
PRODUCT
 
Source Plasma, Recall # B-1298-6
 
CODE
 
Units: NG 0046823, NG 0046671, NG 0045205, NG 0044635, NG 0043095, NG0042525, NG 0042341RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax onDecember 20, 2002. Firm initiated recall is complete.
 
REASON
 
Blood products, collected from a donor who answered questions on the variant Creutzfeldt-Jacob disease (vCJD) questionnaire inappropriately, were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
7 units
 
DISTRIBUTION
 
KY
 
______________________________
 
PRODUCT
 
Recovered Plasma, Recall # B-1299-6CODEUnit: 4357117
 
RECALLING FIRM/MANUFACTURER
 
Department of the Navy, Naval Medical Center, San Diego, CA, by fax and letter on September 25, 2003. Firm initiated recall is complete.
 
REASON
 
Blood product, collected from a donor considered to be at risk of exposure to Creutzfeldt-Jacob Disease (CJD), was distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
1 unit
 
DISTRIBUTION
 
Germany
 
END OF ENFORCEMENT REPORT FOR July 12, 2006
 
###
 
 
CJD WATCH MESSAGE BOARD
 
TSS
 
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY Fri Jul 7, 2006 09:3770.110.83.160
 
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1379-6;
 
b) Platelets, Recall # B-1380-6;
 
c) Fresh Frozen Plasma, Recall # 1381-6;
 
d) Recovered Plasma, Recall # B-1382-6
 
CODE
 
a) Unit numbers: 2343106, 2377779, and 2403533;
 
b) and c) Unit numbers: 2377779;
 
d) Unit numbers: 2343106 and 2403533
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on June12, 2003. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
7 units
 
DISTRIBUTIONTX and Austria
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1467-6;
 
b) Recovered Plasma, Recall # B-1468-6
 
CODE
 
a) and b)
 
Unit numbers: 2329380
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on May 8,2003. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTIONTX and Switzerland
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1479-6;
 
b) Cryoprecipitated AHF, Recall # B-1480-6;
 
c) Recovered Plasma, Recall # B-1481-6
 
CODE
 
a), b), and c)
 
Unit numbers: 2383280
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on July23 and 29, 2004. Firm initiated recall is complete.
 
REASONBlood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
TX and Switzerland
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1482-6;
 
b) Fresh Frozen Plasma, Recall # B-1483-6
 
CODE
 
a) and b)
 
Unit number: 2501452
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile onOctober 5, 2004. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
2 units
 
DISTRIBUTION
 
TX and NY
 
______________________________
 
PRODUCT
 
a) Red Blood Cells Leukocytes Reduced, Recall # B-1484-6;
 
b) Plasma Cryoprecipitated Reduced, Recall # B-1485-6;
 
c) Recovered Plasma, Recall # B-1486-6
 
CODE
 
a) and c)
 
Unit number: 2554077;
 
b) Unit number: 2415708
 
RECALLING FIRM/MANUFACTURER
 
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on August13, 2004. Firm initiated recall is complete.
 
REASON
 
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
 
VOLUME OF PRODUCT IN COMMERCE
 
3 units
 
DISTRIBUTION
 
TX and Austria
 
_____________________________________
 
END OF ENFORCEMENT REPORT FOR July 5, 2006
 
###
 
 
Greetings again Dr. Freas et al at FDA,
 
WITH new atypical TSE in the bovine, in the sheep, goat, and humans, and the fact that the new BASE TSE in cattle being very very similar to sporadic CJD, rather than the nvCJD, the fact that now science showing the TSE agent of the atypical cattle in Japan showing infectivity other than CNS tissue, the fact that the latest Texas mad cow and the recent Alabama mad cow both being of the atypical strain, it would seem prudent to include all human TSE in the blood ban, in my opinion. with sporadic CJD, you have many strains and or phenotypes, some of which are 'UNKNOWN', so we do not know how this will transmit, what tissues are infectious and or if blood transmits. that's the bottomline, however it has been reported that the BASE is more virulent to humans.With this, and the fact that sporadic CJD has tripled in the past few years or so, i see itas being prudent to take serious and immediate action ;
 
 
2001 Singeltary Submission to FDA on blood related risk factors from TSE prion aka mad cow type disease
 
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 08,2001 3:03 PM freas ...
 
 
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
 
 
Transmissible Spongiform Encephalopthy TSE Prion Disease
 
*** Kuru Video
 
Kuru: The Science and The Sorcery
 
 
*** Scrapie Video
 
 
*** Human Mad Cow Video
 
 
*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video
 
 
2014
 
***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
 
***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent.
 
*** Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15].
 
snip...
 
 
Monday, October 10, 2011
 
EFSA Journal 2011 The European Response to BSE: A Success Story
 
snip...
 
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far
 
*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded.
 
*** Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
 
snip...
 
 
 
Thursday, August 12, 2010
 
Seven main threats for the future linked to prions
 
First threat
 
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
 
*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.
 
*** These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
 
Second threat
 
snip...
 
 
*** Creutzfeldt-Jakob Disease Public Health Crisis VIDEO
 
 
 
 
 
Tuesday, May 26, 2015
 
*** Minimise transmission risk of CJD and vCJD in healthcare settings ***
 
Last updated 15 May 2015
 
 
 
Monday, November 23, 2015
 
1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
 
 
>>> The only tenable public line will be that "more research is required’’ <<<
 
>>> possibility on a transmissible prion remains open<<<
 
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
 
Sunday, August 09, 2009
 
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
 
 
Tuesday, August 18, 2009
 
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009
 
 
Friday, October 23, 2015
 
CJD FOUNDATION CREUTZFELDT JAKOB DISEASE TSE PRION QUESTIONNAIRE UPDATE OCTOBER 2015
 
 
Saturday, December 12, 2015
 
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
 
 
Thursday, September 10, 2015
 
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
 
 
Friday, November 13, 2015
 
No evidence of asymptomatic variant CJD infection in immunodeficiency patients treated with UK-sourced immunoglobulin ?
 
 
P.85: Improving Creutzfeldt-Jakob disease incidence estimates by incorporating results of neuropathological analyses, United States, 2003–2011
 
Ryan Maddox1, Marissa Person1, Arialdi Minino2, Janis Blevins3, Lawrence Schonberger1, and Ermias Belay1
 
1National Center for Emerging and Zoonotic Infectious Diseases; Centers for Disease Control and Prevention, Atlanta GA USA; 2National Center for Health Statistics; Centers for Disease Control and Prevention; Hyattsville, MD USA; 3National Prion Disease Pathology Surveillance Center; Case Western Reserve University; Cleveland, OH USA
 
Introduction. The incidence of invariably fatal prion diseases such as Creutzfeldt-Jakob disease (CJD) can be estimated by analyzing death certificate data, but there are limitations.
 
Methods. Prion disease decedents were identified from the US national multiple cause-ofdeath data and the National Prion Disease Pathology Surveillance Center (NPDPSC) database for 2003–2011. Due to limited personal identifying information, an algorithm was constructed to determine likely decedent matches between the 2 databases. NPDPSC decedents with a positive prion disease autopsy or biopsy result or genetic mutation for whom no match was found in the multiple cause-of-death data were added as cases for incidence calculations; those with negative neuropathology results but Prion 2015 Poster Abstracts S55 with a death certificate indicating prion disease were removed. The resulting average annual age-adjusted incidence was then calculated.
 
Results. A total of 2986 decedents were identified as having prion disease indicated as a cause of death in the multiple cause-of-death data; 469 additional NPDPSC decedents were identified with positive neuropathology and/or genetic findings, while 140 decedents with death certificates indicating prion disease had negative neuropathology results. Incorporating the matched data, the average annual ageadjusted incidence of CJD in the United States was 1.2 per million.
 
Conclusion. Analysis of multiple cause-of death data is an efficient means of conducting CJD surveillance. However, not all decedents are captured as the death certificate may not list the diagnosis; conversely, a CJD diagnosis on the certificate may be contradicted by neuropathology results. Incorporating findings from NPDPSC neuropathological and genetic analyses produces an estimate closer to the true incidence of the disease.
 
 
spontaneous atypical BSE ???
 
don’t let anyone fool you. spontaneous TSE prion disease is a hoax in natural cases, never proven.
 
all one has to do is look at France. France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow disease in numbers they could find any with, after those atypical BSE cases started showing up. shut down the testing to numbers set up by OIE that are so low, you could only by accident find a case of BSE aka mad cow disease. and this brilliant idea by the WHO et al, to change the name of mad cow disease, thinking that might change things is preposterous. it’s all about money now folks, when the OIE, USDA and everyone else went along and made the TSE prion disease aka mad cow type disease a legal trading commodity by the BSE MRR policy, I would say everyone bit off more then they can chew, and they will just have to digest those TSE Prions coming from North America, and like it, and just prey you don’t get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE prion disease in the decades to come, and or pass it to some other poor soul via the iatrogenic medical surgical tissue friendly fire mode of transmission i.e. second hand transmission. it’s real folks, just not documented much, due to lack of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the iatrogenic event is tracked down and documented, and put into the academic and public domain, which very seldom happens. ...
 
As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France.
 
 
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many spontaneous events of mad cow disease $$$
 
so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS
 
Sunday, October 5, 2014
 
France stops BSE testing for Mad Cow Disease
 
 
19 May 2010 at 21:21 GMT
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
snip...see link ;
 
Saturday, May 09, 2015
 
Expression of genes involved in the T cell signalling pathway in circulating immune cells of cattle 24 months following oral challenge with Bovine Amyloidotic Spongiform Encephalopathy (BASE)
 
 
Saturday, January 9, 2016
 
***Transmission of sheep-bovine spongiform encephalopathy to pigs Research article
 
 
IN CONFIDENCE
 
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY 1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs.
 
...see full text ;
 
 
IN CONFIDENCE
 
So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...
 
 
snip...
 
CONFIDENTIAL EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
 
PLEASE NOTE, these old BSE Inquiry links take a while to open with the wayback machine, so be patient. ...tss Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility.
 
snip...
 
IN CONFIDENCE EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY 1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought pigs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;
 
 
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
 
 
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
 
 
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
 
 
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
 
 
***Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
 
 
snip...
 
It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.
 
 
4.303 The minutes of the meeting record that: It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17
 
 
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;
 
1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles, Links Click here to read
 
The neuropathology of experimental bovine spongiform encephalopathy in the pig.
 
Ryder SJ, Hawkins SA, Dawson M, Wells GA. Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
 
In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals. PMID: 10684682 [PubMed - indexed for MEDLINE]
 
 
Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie.
 
Emerg Infect Dis. 2009 Aug; [Epub ahead of print]
 
 
Wednesday, July 06, 2011
 
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation snip... In the US, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine, mink and poultry still occurs. Although unlikely, the potential for swine to have access to TSE-contaminated feedstuffs exists.
 
snip...
 
 
Wednesday, July 06, 2011
 
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation (see tonnage of mad cow feed in commerce USA...tss)
 
 
In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy.
 
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract


Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report
 
In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility. snip... snip... In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility.
 
see full text and more transmission studies here ;
 
 
snip... see full text ;
 
Thursday, November 10, 2011
 
National Meat Association v. Harris Docket No., 10-224 DEADSTOCK DOWNER PIGS AND PORCINE SPONGIFORM ENCEPHALOPATHY PSE Court Likely to Overturn Calif. Law on Livestock
 
 
Friday, April 20, 2012
 
Ultrastructural findings in pigs experimentally infected with bovine spongiform encephalopathy agent
 
 
Wednesday, July 29, 2015
 
Porcine Prion Protein Amyloid or mad pig disease PSE
 
 
The Pathological Protein:
 
Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases
 
Philip Yam
 
''Answering critics like Terry Singeltary, who feels that the US undercounts CJD, Schonberger _conceded_ that the current surveillance system has errors but stated that most of the errors will be confined to the older population''....end
 
 
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
 
Terry S. Singeltary, Sr Bacliff, Tex
 
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
 
 
2 January 2000
 
British Medical Journal
 
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
 
 
15 November 1999
 
British Medical Journal
 
vCJD in the USA * BSE in U.S.
 
 
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
 
Tracking spongiform encephalopathies in North America
 
Original
 
Xavier Bosch
 
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...
 
 
Suspect symptoms
 
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
 
28 Mar 01
 
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
 
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...
 
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
 
Terry S. Singeltary, Sr Bacliff, Tex
 
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
 
 
26 March 2003
 
Terry S. Singeltary, retired (medically) CJD WATCH
 
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
 
 
Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
 
 
07 02:27 AM
 
Terry S. Singeltary Sr. said:
 
re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy
 
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
 
 
I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.
 
***snip...see full text ;
 
 
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
 
BSE101/1 0136
 
IN CONFIDENCE
 
CMO
 
From: . Dr J S Metiers DCMO
 
4 November 1992
 
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
 
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
 
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.
 
what are the implications for public health?
 
3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
 
1
 
92/11.4/1.1
 
BSE101/1 0137
 
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
 
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2
 
 
>>> The only tenable public line will be that "more research is required’’ <<<
 
>>> possibility on a transmissible prion remains open<<<
 
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
 
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
 
Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014
 
 
*** Singeltary comment PLoS ***
 
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
 
Posted by flounder on 05 Nov 2014 at 21:27 GMT
 
 
Wednesday, January 13, 2016
 
ALS-Causing Mutations Significantly Perturb the Self-Assembly and Interaction with Nucleic Acid of the Intrinsically Disordered Prion-Like Domain of TDP-43
 
Research Article
 
 
Wednesday, January 13, 2016
 
An efficient procedure for removal and inactivation of alpha-synuclein assemblies from laboratory materials
 
***>>>An efficient procedure for removal and inactivation of alpha-synuclein assemblies from laboratory materials<<<***
 
***>>> This retrospective study, however, does not definitively exclude the possibility that a-synucleinopathy can transmit between humans. <<<***
 
An efficient procedure for removal and inactivation of alpha-synuclein assemblies from laboratory materials ???
 
 
Thursday, January 14, 2016
 
*** Preventable Tragedies: Superbugs and How Ineffective Monitoring of Medical Device Safety Fails Patients REPORT
 
*** how can it be, HOW CAN IT BE $$$ not a word about CJD GSS FFI VPSPR TSE Prions that I saw...absolutely crazy, WE ARE MISSING THE BIGGER PICTURE!
 
*** how many victims that will never be reported ???
 
 
BSE INQUIRY DFAs
 
 
Sunday, May 18, 2008
 
BSE Inquiry DRAFT FACTUAL ACCOUNT DFA
 
BSE Inquiry DRAFT FACTUAL ACCOUNTS DFA's
 
 
Sunday, May 18, 2008
 
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
 
 
Sunday, May 18, 2008
 
MAD COW DISEASE BSE CJD CHILDREN VACCINES
 
 
 
 
 Terry S. Singeltary Sr.

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