Sunday, September 6, 2026

Risk of transmission of amyloid β pathology via transfused blood products, Singeltary Review

 Risk of transmission of amyloid β pathology via transfused blood products, Singeltary Review


a review of TSE PrP iatrogenic risk factors, blood, tissue, amyloid β pathology, iatrogenic cerebral amyloid angiopathy (iCAA), Tau, and potential blood products, a review of the new science to date, with nvCJD risk factors from the old days, TSE, risk factors, testimonies from the BSE Inquiry, cwd blood risk factors from blood,  concerns for medical by-products from pigs, the old days, compared to scientific facts today. might be interesting…terry

Risk of transmission of amyloid β pathology via transfused blood products

Gargi Banerjee, PhDa ∙ Gustaf Edgren, PhDb ∙ Jingcheng Zhao, MDb ∙ Prof Neil M Ferguson, DPhilc ∙ Prof Heli Harvala, PhDd ∙ James Hope, PhDe ∙ Graham S Jackson, PhDa ∙ Prof Philip J Lowry, DScf ∙ Prof Simon Mead, PhDa ∙ Silvia A Purro, PhDa ∙ Prof Jonathan M Schott, FMedScig,h ∙ Prof Marc L Turner, PhDi ∙ Prof David J Werring, FMedScij ∙ Prof Henrik Zetterberg, PhDg,h,k,l,m,n,o ∙ Prof John Collinge, FRSa Send email to j.collinge@ucl.ac.uk

Summary

Seeded protein misfolding and aggregation are relevant to many neurodegenerative diseases. The archetype are prions: protein-only infectious agents that cause fatal neurodegenerative diseases including Creutzfeldt–Jakob disease (CJD). The recent recognition of iatrogenic amyloid β cerebral amyloid angiopathy (CAA) and Alzheimer's disease, caused by inadvertent seeding of amyloid β pathology following historical medical procedures, raises concerns that these conditions might also be transmitted via blood components and products, as was the case in rare instances for variant CJD. Recent epidemiological data showing the apparent transmission of haemorrhage risk between blood donors and recipients raise the possibility of blood-based CAA transmission. In this Viewpoint, we review the evidence for amyloid β transmission, provide an overview of relevant prion biology, and consider the circumstances under which bloodborne prion transmission has previously occurred. We discuss the implications for blood transfusion services, particularly in light of the UK Infected Blood Inquiry, and the key questions that need to be addressed to better quantify transfusion-related risk.


Risk of transmission of amyloid β pathology via transfused blood products

Gargi Banerjee PhD a , Gustaf Edgren PhD b , Jingcheng Zhao MD b , Prof Neil M Ferguson DPhil c , Prof Heli Harvala PhD d , James Hope PhD e , Graham S Jackson PhD a , Prof Philip J Lowry DSc f , Prof Simon Mead PhD a , Silvia A Purro PhD a , Prof Jonathan M Schott FMedSci g h , Prof Marc L Turner PhD i , Prof David J Werring FMedSci j , Prof Henrik Zetterberg PhD g h k l m n o , Prof John Collinge FRS a

Cite https://doi.org/10.1016/S0140-6736(26)00767-1Get rights and content Summary

Seeded protein misfolding and aggregation are relevant to many neurodegenerative diseases. The archetype are prions: protein-only infectious agents that cause fatal neurodegenerative diseases including Creutzfeldt–Jakob disease (CJD). The recent recognition of iatrogenic amyloid β cerebral amyloid angiopathy (CAA) and Alzheimer's disease, caused by inadvertent seeding of amyloid β pathology following historical medical procedures, raises concerns that these conditions might also be transmitted via blood components and products, as was the case in rare instances for variant CJD. Recent epidemiological data showing the apparent transmission of haemorrhage risk between blood donors and recipients raise the possibility of blood-based CAA transmission. In this Viewpoint, we review the evidence for amyloid β transmission, provide an overview of relevant prion biology, and consider the circumstances under which bloodborne prion transmission has previously occurred. We discuss the implications for blood transfusion services, particularly in light of the UK Infected Blood Inquiry, and the key questions that need to be addressed to better quantify transfusion-related risk. Introduction

Blood transfusion is key to medical and surgical practice.1 Transfused products include blood components (eg, red cells, platelets, and clinical plasma) and plasma-derived medicinal products (eg, coagulation factors, immunoglobulins, and albumin).2Transfusion-transmitted infections are rare but potentially catastrophic,3 and even low risks of infection can undermine public confidence. In some cases, concerns that are relevant to blood transfusion can also extend to other allogeneic substances of human origin (eg, transplanted tissues, cells, and organs). In this Viewpoint, we discuss the bloodborne transmission of protein-only pathogens, or prions, given the recent recognition of iatrogenic forms of Alzheimer's disease4, 5 and iatrogenic amyloid β cerebral amyloid angiopathy (CAA).6 Section snippets

Prions and human disease

Prions are protein-only infectious agents composed of assemblies of misfolded host-encoded cellular prion protein (PrPC), which form amyloid fibrils.7 Prions propagate via a process of seeded amyloidosis, where the host PrPC is recruited by an elongating fibril that undergoes fission, producing more seeds in an autocatalytic process.7 As protein-only agents, prions are highly durable, resistant to inactivation via conventional sterilisation methods,8 and have a high binding affinity for steel Acquired amyloid β diseases: iatrogenic Alzheimer's disease and cerebral amyloid angiopathy

The amyloid β protein is traditionally associated with two diseases. The first is Alzheimer's disease, a dementia that is histopathologically characterised by parenchymal and vascular amyloid β deposition alongside aggregates of tau protein. The second is CAA, which causes intracranial haemorrhage—particularly lobar intracerebral haemorrhages—and in which amyloid β deposits are predominantly vascular.18Intracerebral haemorrhage due to CAA has a high risk of recurrence compared with Prion transmission via infected blood products

Variant CJD is a human prion disease first reported in the UK in 1996.42 Unlike other forms of CJD, there is prominent involvement of lymphoreticular tissues, raising early concerns that bloodborne prion transmission might occur via recirculating lymphocytes.43 These fears were realised, with three symptomatic cases of transfusion-associated (secondary) variant CJD following red cell transfusions; two additional people who died of other causes had variant CJD infection confirmed at autopsy in Evidence for bloodborne transmission of amyloid β

Amyloid β is detectable in blood, which plays a role in brain amyloid β clearance,51, 52 is produced by platelets,53 adheres to the surface of red blood cells,54, 55 and is a biomarker for Alzheimer's disease.56 Amyloid β has been detected in human cervical lymph nodes,57 which is an important destination for the meningeal lymphatics, glymphatic system, and other perivascular drainage pathways.58 This finding is particularly relevant, as the presence of variant CJD prions in lymphoreticular Determining amyloid β infectivity

There are no established methods for quantifying amyloid β seed titre in body fluids. Prion research has traditionally used rodent bioassays to measure infectivity, with endpoint titrations used to compare test material with serial dilutions of material with known titre. Through this method, researchers have been able to establish detection thresholds and dynamic range.69 However, unlike models of prion transmission, rodent amyloid β models do not have a clinical endpoint, and histopathological Implications for blood transfusion services

The maintenance of adequate stocks of blood components to meet highly dynamic clinical demand is essential for patient care, and anything that disrupts the balance of supply and demand has the potential to cause more harm than good. Donor numbers have fallen in the UK and internationally and their average age has increased, with blood component shortages becoming more common. The 2024 UK Infected Blood Inquiry83 investigated what has been called “the worst treatment disaster in the history of Conclusion

The transmission of amyloid β pathology via transfused blood and blood products is a justifiable concern. We need to acknowledge that we do not have sufficient information to quantify the extent of the problem or the technologies that are needed to address key questions. Further research is essential for informing both this and future discussions and, therefore, is of strategic national and global importance. Immediate priorities should include an epidemiological replication of the Scandinavian

Declaration of interests

GB has received honoraria for teaching at Universität Bern; has received travel support from the National Institute for Health and Care Research (NIHR), UK Stroke Forum, International Cerebral Amyloid Angiopathy Association, European Stroke Organisation, and European Academy of Neurology; is an unpaid Board Member of the International Cerebral Amyloid Angiopathy Association; is funded by an MRC Clinician Scientist Fellowship; held a previous position as an NIHR Clinical Lecturer; and has

Acknowledgments

In April, 2024, the MRC Prion Unit at UCL convened a workshop to address the question of bloodborne amyloid β transmission, bringing together expert clinicians, scientists, epidemiologists, government officials, and other stakeholders to review and discuss the evidence to date and its implications. This Viewpoint is derived from presented data and roundtable discussions from this workshop. We thank all attendees for their contributions to the workshop and its discussions. The MRC Prion Unit is…


Res Pract. 2025 Sep 3;7(1):63. doi: 10.1186/s42466-025-00423-x

Iatrogenic cerebral amyloid angiopathy: two new cases and systematic review of case reports with neuropathological data

Ana Sofia Costa 1,2,#, João Pinho 1,✉,#, Arno Reich 1, Omid Nikoubashman 3, Kay Nolte 4, Joachim Weis 4, Christian Boy5, Felix M Mottaghy 5, Jörg B Schulz 1,2, Kathrin Reetz 1,2

Copyright and License information PMCID: PMC12409930 PMID: 40903767

Abstract

Awareness concerning iatrogenic cerebral amyloid angiopathy (iCAA) is increasing but its pathophysiology remains unclear. We discuss the implications of the clinical, imaging and neuropathological findings in two previously unpublished cases of probable iCAA: a 55-year-old female presenting with rapidly progressive cognitive impairment, showing imaging and histological evidence of CAA and having undergone neurosurgical treatment at the age of 6; and a 56-year-old male with a four-year history of recurring intracerebral hemorrhages (ICH) and neurosurgical intervention at the age of 5. In the first case, a brain biopsy was performed.

Additionally, a systematic review of iCAA cases with neuropathological data suggests that most of the patients have concomitant amyloid parenchymal deposition and none or minimal tau pathology. The pathophysiological role of tau pathology in iCAA remains unclear. iCAA patients presenting with cognitive impairment without symptomatic ICH may be underdiagnosed.

Introduction Cerebral amyloid angiopathy (CAA) manifesting decades after neurosurgical procedures involving the utilization of cadaveric material, such as dura mater, is gaining increasing awareness [1], and diagnostic criteria for iatrogenic CAA (iCAA) were recently proposed [2] (Additional File 1). Current understanding of the pathophysiology of iCAA suggests a prion-like transmission of amyloid-β seeds from cadaveric material or neurosurgical instruments to the brain. Many patients with iCAA had had traumatic brain injury in the past, and its potential causal role is difficult to disentangle [1–4]. We report two previously unpublished cases of iCAA, perform a systematic review of iCAA cases with neuropathological data and discuss the implications of the findings.

snip..

In conclusion, we report detailed clinical, imaging and pathological characteristics of two patients with iCAA who developed symptoms five decades after neurosurgical procedures. Future detailed study of neuropathological data may help to understand pathophysiology of iCAA.


Singeltary wayback;

“There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread.”

Self-Propagative Replication of Aβ Oligomers Suggests Potential Transmissibility in Alzheimer Disease

Amit Kumar, Kayla M. Pate, Melissa A. Moss, Dexter N. Dean, Vijayaraghavan Rangachari Published: November 3, 2014

https://doi.org/10.1371/journal.pone.0111492

Abstract

The aggregation of amyloid-β (Aβ) peptide and its deposition in parts of the brain form the central processes in the etiology of Alzheimer disease (AD). The low-molecular weight oligomers of Aβ aggregates (2 to 30 mers) are known to be the primary neurotoxic agents whose mechanisms of cellular toxicity and synaptic dysfunction have received substantial attention in the recent years. However, how these toxic agents proliferate and induce widespread amyloid deposition throughout the brain, and what mechanism is involved in the amplification and propagation of toxic oligomer species, are far from clear. Emerging evidence based on transgenic mice models indicates a transmissible nature of Aβ aggregates and implicates a prion-like mechanism of oligomer propagation, which manifests as the dissemination and proliferation of Aβ toxicity. Despite accumulating evidence in support of a transmissible nature of Aβ aggregates, a clear, molecular-level understanding of this intriguing mechanism is lacking. Recently, we reported the characterization of unique replicating oligomers of Aβ42 (12–24 mers) in vitro called Large Fatty Acid-derived Oligomers (LFAOs) (Kumar et al., 2012, J. Biol. Chem). In the current report, we establish that LFAOs possess physiological activity by activating NF-κB in human neuroblastoma cells, and determine the experimental parameters that control the efficiency of LFAO replication by self-propagation. These findings constitute the first detailed report on monomer – oligomer lateral propagation reactions that may constitute potential mechanism governing transmissibility among Aβ oligomers. These data support the previous reports on transmissible mechanisms observed in transgenic animal models.

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0111492

O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?

re-Self-Propagative Replication of Aβ Oligomers Suggests Potential Transmissibility in Alzheimer Disease

Alzheimer's disease

let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...

Singeltary Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic,  what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Background

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

Methods

Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

Results

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

Conclusions

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

end...tss

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT


Ann N Y Acad Sci. 1982;396:131-43.

Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).

Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.

Abstract

Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.


CJD1/9 0185 Ref: 1M51A

IN STRICT CONFIDENCE

Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:

i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;

ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and

iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1


BSE101/1 0136

IN CONFIDENCE

5 NOV 1992 CMO From: Dr J S Metters 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 recognized 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 emphasizes 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.

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.

JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2


CJD1/9 0185

Ref: 1M51A

IN STRICT CONFIDENCE

From: Dr. A Wight Date: 5 January 1993

Copies:

Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES


''on the possible transmissibility of Alzheimer's''

9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly

(1) concerning a farmer with CJD who had BSE animals,

(2) on the possible transmissibility of Alzheimer's and

(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic,  what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT




Singeltary 2001

Subject: CJD or Alzheimer's or the same ???

Date: Sun, 29 Apr 2001 12:45:28 -0700

From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

Bovine Spongiform Encephalopathy

Greetings List,

thought some might be interested in this. I have always wondered if CJD and or all TSEs and Alzheimer's could be linked. i have been of the opinion that Alzheimer's is a TSE for a long time, just at the low end of the titre of infectivity scale. i also believe in the accumulation theory. by dose, you could be killed by one sitting, or one injection, or one whatever, depending on the titre of infectivity of that whatever. on the other hand, if the dose is not a lethal dose, over a period of time, the accumulation will become lethal (if consumption continued), and i believe the route/source/titre of infectivity, will be a key roll to the incubation period, and symptoms.

just my opinion...snip…end

Singeltary 2001, CJD or Alzheimer's or the same ???

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic,  what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT

https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Conclusions

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread.

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT

https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d

https://creutzfeldt-jakob-disease.blogspot.com/2023/09/professor-john-collinge-on-tackling.html

Singeltary Nature commentary;

Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)

snip...see full Singeltary Nature comment here;

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)

http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html

I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.

First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.

Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.

where have we all heard this before? its been well documented via the BSE Inquiry. have they not learned a lesson from the last time?

we have seen this time and time again in England (and other Countrys) with the BSE mad cow TSE Prion debacle.

That ‘anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.

The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients ? who got pooled extracts injected from thousands of cadavers ? were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.

That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find ‘alarming’ is pathetic.

Sounds like the journalists had it right in the first place: ‘Alzheimers may be a transmissible infection’ in The Independent to ‘You can catch Alzheimers’ in The Daily Mirror or ‘Alzheimers bombshell’ in The Daily Express

if not for the journalist, the layperson would not know about these important findings.

where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?

when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.

to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimers, the price of poker goes up drastically.

so, who makes that final decision, and how many more decades do we have to wait?

the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?

Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.

FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.

in my opinion, it’s one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.

greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it’s bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.

my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimers of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.

I kindly wish to remind the public of the past, and a possible future we all hopes never happens again…

[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer?s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media attention.]





please see more of this history and references there from (these blogs are for educational use, I do not advertise or make money from this. just made a promise to mom dod 12/14/97 hvCJD, never forget, and never let them forget.)

re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

Singeltary Submission to Nature;



Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'

Your preliminary abstract number: 670

Dear Mr. Singeltary,

On behalf of the Scientific Committee, I am pleased to inform you that your abstract

'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'

WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.

Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.

Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Author: T. Singeltary; Bacliff, TX/US

Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange

This abstract has been ACCEPTED.

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Authors: T. Singeltary; Bacliff, TX/US

Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Body: Background

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods

12 years independent research of available data

Results

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.

I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion

page 114 ;

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf


http://www.isid.org/14th_icid/

http://www.isid.org/publications/ICID_Archive.shtml

http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf

Singeltary iatrogenic what if

“I say again, what if, iatrogenic, what if, with all these neurological disorders, with a common denominator that is increasingly showing up in the picture, called the prion.”

“I urge all scientist to come together here, with this as the utmost of importance about all these neurological disease that are increasingly showing up as a prion mechanism, to put on the front burners, the IATROGENIC aspect and the potential of transmission there from, with diseases/disease??? in question.”

“by definition, could they be a Transmissible Spongiform Encephalopathy TSE prion type disease, and if so, what are the iatrogenic chances of transmission?”

“this is very important, and should be at the forefront of research, and if proven, could be a monumental breakthrough in science and battle against the spreading of these disease/diseases.”

FRIDAY, JANUARY 10, 2014

vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???

Greetings Friends, Neighbors, and Colleagues,

vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???

Confucius is confused again.

I was just sitting and thinking about why there is no genetic link to some of these TSE prion sGSS, sFFi, and it’s really been working on my brain, and then it hit me today.

what if, vpspr, sgss, sffi, TSE prion disease, was a by-product from iatrogenic gss, ffi, familial type prion disease ???

it could explain the cases of no genetic link to the gss, ffi, familial type prion disease, to the family.

sporadic and familial is a red herring, in my opinion, and underestimation is spot on, due to the crude prehistoric diagnostic procedures and criteria and definition of a prion disease.

I say again, what if, iatrogenic, what if, with all these neurological disorders, with a common denominator that is increasingly showing up in the picture, called the prion.

I urge all scientist to come together here, with this as the utmost of importance about all these neurological disease that are increasingly showing up as a prion mechanism, to put on the front burners, the IATROGENIC aspect and the potential of transmission there from, with diseases/disease??? in question.

by definition, could they be a Transmissible Spongiform Encephalopathy TSE prion type disease, and if so, what are the iatrogenic chances of transmission?

this is very important, and should be at the forefront of research, and if proven, could be a monumental breakthrough in science and battle against the spreading of these disease/diseases.


So, this is what we leave our children and grandchildren?

2001 Singeltary on CJD, Journal of American Medical Association

February 14, 2001

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Terry S. Singeltary, Sr

Author Affiliations

JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214

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.

February 14, 2001

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Terry S. Singeltary, Sr

Author Affiliations

JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214


RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 Singeltary Journal of Neurology

26 MARCH 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States

Terry S. Singeltary, retired (medically)

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?


2023


***> With the recent findings of wild pigs carrying the CWD TSE PrP from Texas and Arkansas, the fact CWD will transmit to pigs by blood, and CWD transmission by oral routes to pigs, sheep, cattle, and primates, might be interesting to review blood products risk factors again from the BSE Inquiry, let’s look and see shall we…terry

***> TSE PrP and blood, blood products, what if?

Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.


CONFIDENTIAL

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...


we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.


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.....


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


IN CONFIENCE

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. ...


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.....


BSE TO PIGS NEWS RELEASE


CONFIDENTIAL

BSE: PRESS PRESENTATION






INDUSTRY RESPONSE TYPICAL


DEFENSIVE BRIEFING


CONFIDENTIAL

pigs & pharmaceuticals





COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP

There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............


snip...

7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;

1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,

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 1-2weeks 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]


“While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle.”

Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak Assessment DEFRA 26 January 2026 Department for Environment, Food and Rural Affairs

Preliminary Outbreak Assessment

Chronic wasting disease prions in cervids and wild pigs in North America

26 January 2026

Disease report

“They analysed over 300 brain and lymph node samples from 178 wild pigs living across Arkansas and Texas, USA…the researchers identified CWD prions in up to 37% of the lymph node samples and 15% of brain samples. The lowest detection rates were in the Texas samples (below 16%), matching the lower CWD prevalence in the state’s cervid population.”


Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United State Volume 31, Number 1—January 2025


WEDNESDAY, JANUARY 28, 2026

Chronic wasting disease prions in cervids and wild pigs in North America Preliminary Outbreak





Prion Conference 2023

Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure

Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA

Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.

Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).

Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.

“Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.”

Strain characterization of chronic wasting disease in bovine-PrP transgenic mice

Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.

Prion 2023 Congress Organizing Committee and the NeuroPrion Association, we invite you to join us for the International Conference Prion2023 from 16-20 October 2023 in Faro, Portugal.

https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf



cwd to sheep

Chronic Wasting Disease CWD vs Scrapie TSE Prion


Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.





Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies

Location: Virus and Prion Research

Title: Differentiation of scrapie from chronic wasting disease in white-tailed deer

Accomplishments

1. 01 Determined that white-tailed deer (WTD) infected with scrapie from sheep can transmit the disease to other deer under conditions mimicking natural exposure. It has long been suggested that prion disease in deer (chronic wasting disease (CWD)) was caused by the prion agent from sheep. The prion disease that affects sheep, scrapie, has been recognized for hundreds of years. However, chronic wasting disease, a similar disease found in WTD, has only been recognized since the 1960s. ARS researchers in Ames, Iowa, showed that white-tailed deer sick with scrapie from sheep can infect other deer under conditions mimicking natural exposure. Furthermore, this work shows that CWD is difficult to differentiate from WTD infected with scrapie. WTD scrapie prions accumulate in the lymphoreticular system in a manner similar to CWD, meaning that environmental contamination may occur through feces, saliva, and other body fluids of scrapie affected WTD as has been shown for CWD. The presence of WTD infected with scrapie could confound mitigation efforts for chronic wasting disease. This information informs regulatory officials, the farmed cervid industry, and officials tasked with protecting animal health such as state Departments of Agriculture, Natural Resources, or Parks and Wildlife with regard to a disease similar to CWD but arising from sheep scrapie that could be present in WTD that have contact with scrapie affected sheep and/or goats.


Chronic Wasting Disease CWD TSE Prion, Economical, Environmental, Zoonotic, Risk Factors 2026


***> USA Report, Scrapie, CWD, BSE, TSE, Cattle, Sheep, Pigs, Cervid, Humans, Zoonotic, 2026

April 2026



TUESDAY, AUGUST 1, 2017

BSE INQUIRY DFA 17 Medicines and medical devices

DFA 17


TWA LITTLE minute

2. We have identified one problem over where we are unable to act and this is the use of gonadotrophins in embryo transfer work. Some veterinary surgeons are quite legally using this exemption from the Medicines Act contained in Section 9(2) to prepare gonadotrophins from pituitary glands from various species, including cattle. These hormones are used to stimulate superovulation in donor cows.


NEW LINK URL 2022



NEW LINK URL 2022



NEW LINK URL 2022


COMMERCIAL IN CONFIDENCE

3.2 Minute 5.3 - 5.4 Bovine Spongiform Encephalopathy

It was reported that some replies had been received from Companies using pituitary glands in their products. Copies of the BSE document had also been sent to DHSS and NIBSC.

and then another 3 + pages of blank space. ...TSS


NEW URL LINK 2022


COMMERCIAL IN CONFIDENCE

BSE - CURRENT POSITION WITH VETERINARY LICENCED PRODUCTS (MA.1968)

There are three areas of particular concern, vaccines (including emergency vaccines), pharmaceuticals which are covered by MA licences and unlicenses hormonal products produced under exemptions claimed under (Section 9(2) Medicines Act).

1) Vaccines

http://collections.europarchive.org/tna/20080103033809/http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf

NEW URL LINK 2022


NOT FOR PUBLICATION

another 6 pages of blank space. ...TSS

http://collections.europarchive.org/tna/20080103032658/http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf

NEW URL LINK 2022


http://collections.europarchive.org/tna/20080103032631/http://www.bseinquiry.gov.uk/files/yb/1988/11/04003001.pdf

NEW URL LINK 2022


http://collections.europarchive.org/tna/20080103033926/http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf

NEW LINK URL 2022


COMMERCIAL IN CONFIDENCE

http://collections.europarchive.org/tna/20080103034137/http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf

NEW URL LINK 2022


COMMERCIAL IN CONFIDENCE

Medicines Act - Veterinary Products Committee

http://collections.europarchive.org/tna/20080103034140/http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf

NEW URL LINK 2022


COMMERCIAL IN CONFIDENCE

http://collections.europarchive.org/tna/20080102164744/http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf

NEW URL LINK 2022


MANAGEMENT IN CONFIDENCE

CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS

http://collections.europarchive.org/tna/20080102184729/http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf

NEW URL LINK 2022


COMMERCIAL IN CONFIDENCE

NOT FOR PUBLICATION

http://collections.europarchive.org/tna/20080102185137/http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf

NEW URL LINK 2022



NEW LINK URL 2022


COMMERCIAL IN CONFIDENCE

NOT FOR PUBLICATION


NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE

snip...

I was quite prepared to believe in unofficial pituitary hormones, also in the 1970's, whether as described by Dr. Little, or in other circumstances, for animal use.

snip...

The fact that there were jars of pituitaries (or extract) around on shelves is attested by the still potent 1943 pituitaries, described in Stockell Hartree et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the trouble to collect them, they were not lightly thrown out...

http://collections.europarchive.org/tna/20090114045856/http://www.bseinquiry.gov.uk/files/ws/s467bx.pdf

NEW URL LINK 2022


more on the 1968 medicine act, they forgot to follow i.e. no Scrapie-like disease. ...TSS

http://web.archive.org/web/20030526124448/http://www.bseinquiry.gov.uk/files/yb/1989/01/30008001.pdf

NEW URL LINK 2022


Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)

CONCERN ABOUT BSE IN HUMAN MEDICINE

Although these materials relate to materials of bovine origin, they should also be considered as applicable to material from SHEEP, GOATS, DEER, AND SOME OTHER ANIMALS SUSCEPTIBLE TO SCRAPIE LIKE AGENTS.

http://collections.europarchive.org/tna/20080103002832/http://www.bseinquiry.gov.uk/files/yb/1989/02/22008001.pdf

NEW URL LINK 2022



(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.)

http://collections.europarchive.org/tna/20080102164725/http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf

NEW URL LINK 2022


http://collections.europarchive.org/tna/20090505223756/http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf

NEW URL LINK 2022


COMMERCIAL IN CONFIDENCE

http://collections.europarchive.org/tna/20080102164736/http://www.bseinquiry.gov.uk/files/yb/1988/06/07010001.pdf

NEW URL LINK 2022


TWA LITTLE STATEMENT 331

http://collections.europarchive.org/tna/20080102163939/http://www.bseinquiry.gov.uk/files/ws/s331.pdf

NEW URL LINK 2022


snip...

Singeltary concerns submitted to FDA;

PDF]Freas, William TSS SUBMISSION

File Format: PDF/Adobe Acrobat -

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...


2003

http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm

NEW URL LINK 2022


http://collections.europarchive.org/tna/20080103032631/http://www.bseinquiry.gov.uk/files/yb/1988/11/04003001.pdf

NEW URL LINK 2022


8. The Secretary of State has a number of licences. We understand that the inactivated polio vaccine is no longer being used. There is a stock of smallpox vaccine. We have not been able to determine the source material. (Made in sheep very unlikely to contain bovine ingredients).

CONFIDENTIAL

http://collections.europarchive.org/tna/20080102164642/http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf

NEW URL LINK 2022


From: TSS 

Subject: How many NHS patients as having received blood from a donor who later developed vCJD were people with haemophilia 

Date: December 21, 2006 at 9:13 am PST

Health: vCJD Lord Morris of Manchester asked Her Majesty's Government:

How many NHS patients identified by the National Blood Service as having received blood from a donor who later developed vCJD were people with haemophilia. [HL750]

19 Dec 2006 : Column WA291

The Minister of State, Department of Health (Lord Warner): No patient with haemophilia or other bleeding disorders have been identified as having received blood from a blood donor who subsequently developed vCJD, nor have there been any reported cases of vCJD associated with receipt of plasma products.

However, all haemophilia patients who received plasma products between 1980 and 2001 sourced from UK donor plasma have been designated as "at risk of vCJD for public purposes". All plasma products are now sourced from non-UK plasma. The United Kingdom Haemophilia Centre Doctors' Organisation is collecting data that will provide an estimate of the number of haemophilia patients who have been exposed to plasma products which may be implicated with vCJD.

Lord Morris of Manchester asked Her Majesty's Government:

What is their response to the findings of Professor John Collinge in the December 2006 edition of the Lancet on the transmission by infected blood of variant CJD; and what action they are planning to take. [HL751]

Lord Warner: The Lancet article refers to the third known case of vCJD transmission via blood transfusion from a vCJD-infected donor. This case was originally notified to the department in January 2006 and announced by the Health Protection Agency in a press release on 9 February 2006, a copy of which has been placed in the Library.

There are 24 living patients in a group of people who had received blood components from donors subsequently known to have developed vCJD. They were all notified in 2005 or earlier, through their GPs, of their risk status and have been provided with information and support. The Health Protection Agency contacted the GPs earlier in the year to notify them of this third case and the agency has ensured that the GPs are fully informed and briefed about the subsequent Lancet publication.

The department has implemented a series of measures to reduce the risk of vCJD being transmitted through the blood supply. Shortly after vCJD was first identified in 1996, the possibility of human-to-human transmission through blood was considered, and the department implemented precautionary measures to reduce what was, at that time, a theoretical risk. These measures have been strengthened since evidence of transmission via blood began to emerge from animal studies, and following the first case of transfusion-associated transmission in humans, reported in December 2003. An important additional step, introduced in March 2004, was to exclude from blood donation those people who had themselves received a blood transfusion since January 1980. Other precautionary measures include:

from December 1997, blood components, plasma products or tissues obtained from any individual who later develops vCJD, were withdrawn/recalled;

19 Dec 2006 : Column WA292

in July 1998, it was announced that plasma for the manufacture of blood products, such as clotting factors, would be obtained from non-UK sources;from November 1999, white blood cells, which may carry a significant risk of transmitting vCJD, were removed from all blood used for transfusion;in August 2002, it was announced that fresh frozen plasma for treating babies and young children born on or after 1 January 1996 would be obtained from the USA; in July 2004, the exclusion criteria for blood donation were extended to include previously transfused platelet donors, and donors who were unsure if they had previously had a blood transfusion;in September 2004, the department announced further precautionary measures for patients who had received certain batches of plasma products;in July 2005, the use of USA-sourced fresh frozen plasma was extended to all children up to the age of 16;in July 2005, the department announced further precautionary measures for those patients who donated blood to three people who later developed vCJD. The department continues to keep all the evidence in relation to transmission of vCJD by blood under close review.



Subject: Re: VACCINES/CHILDREN/TSE'S -- 'CONFIDENTIAL' 

Date: Wed, 6 Sep 2000 18:20:09 -0800 

From: tom 

Reply-To: Bovine Spongiform Encephalopathy 

To: BSE-L@uni-karlsruhe.de References: 1

######### 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/

(please note, toms old mad-cow links don’t work anymore, but some can still be found using wayback machine…terry)

Thus for louping ill (unnecessary cites suppressed):


Paragraph 94 of Dr Maddocks supplementary statement (WS 467A)

(a)A sheep is another sheep’s worst enemy. I agree.

(b)Louping ill vaccine in sheep is associated with scrapie and growth hormone in humans. Someone at CVL would be very qualified to answer questions on the trial of louping ill vaccine which were carried out many years ago. Sheep tissue was used in the preparation. Unfortunately scrapie type symptoms and lesions appeared in the recipients of this vaccine. I am sure our medical colleagues could give more details of the human derived growth hormone, which was reported to have caused CJD symptoms in recipients of treatment with that product.

Vaccines and hormones are species specific prepared. This was not the case in this country. No cow pituitaries were used in the preparation of FSH products compared with the case of louping ill vaccine for scrapie.

http://www.bse.org.uk/witness/htm/stat537.htm

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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.

http://www.mad-cow.org/~tom/fda_late.html#ill

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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

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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 OWhat 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;

Subject: 2 known incidents of iatrogenic scrapie Date: Thu, 7 Sep 2000 09:51:14 -0800 From: tom Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de References: 1

######### Bovine Spongiform Encephalopathy #########

One really has to wonder what went on in veterinary products produced during the peak BSE years. At this point, there are only 2 known incidents, both involving sheep brain vaccines.

I found a better source for needed references for iatrogenic scrapie in a nice review by Ray Bradley at http://www.iica.org.ar/Bse/6-%20Bradley.html. Disclosure has been meagre on the 1998 vaccine incident in Italy. Note 3 of the 5 references are totally off Medline and the other 2 fail to have abstracts or links, due to journal ineptness, burial in conference proceedings, and age of article.

If anyone has the first 3, I would appreciate a fax 542-484-0669 US.

tom

GORDON , W.S., 1959. Scrapie panel. In: Proceedings of 63rd Annual Meeting of the US Livestock Sanitary Association, 63, 286-294. [no medline record]

GORDON, W.S., 1946. Advances in Veterinary Research: Louping ill, tick-borne fever and scrapie. Veterinary Record, 58, 516-525. [no medline record]

GORDON , W.S., BROWNLEE, A.& WILSON, D.R., 1939. Studies in louping-ill, tick-borne fever and scrapie. 3rd International Congress for microbiology, 362-363. [no medline record]

-=-=--=

CAPUCCHIO, M.T., GUARDA,F., ISAIA,M.C., CARACAPPÀ, S. & DiMARCO,V., 1998. Natural occurrence of scrapie in goats in Italy. Veterinary Record, 143, 452-453. [title only]

AGRIMI, U., GLUSOPPE, R.U., CARDONE, F., POCCHIARI, M. & CARAMELLI, M., 1999. Epidemic transmissible spongiform encephalopathy in sheep and goats in Italy. Lancet, 353, 560-561. [title only]

IATROGENIC DISEASE IN ANIMALS

http://www.iica.org.ar/Bse/6-%20Bradley.html

Ray Bradley Private BSE Consultant Veterinary Laboratories Agency, United Kingdom

There have been two reported incidents of iatrogenic disease in animals, both involving scrapie. One was in Great Britain (Gordon, Brownlee and Wilson, 1939, Gordon 1946, 1959) the other in Italy (Capucchio et al, 1998, Agrimi et al, 1999). Both resulted from infection being introduced into vaccines, louping ill vaccine in Great Britain, Mycoplasma agalactiae vaccine in Italy. Each of these vaccines was prepared from tissues that included sheep brain. In both episodes it seems most likely that natural scrapie infection was present unknowingly in some brains used for the purpose. Once prepared and having passed all the conventional vaccine tests large numbers of sheep in Great Britain, and goats and some sheep in Italy were inoculated. After the necessary incubation period large numbers (> 1,000 in each case) of inoculated animals came down with scrapie. In the meantime some inoculated clinically healthy goats and sheep may have entered food and feed chains or have been used for other purposes. In the British outbreak there appears to have been no consequence for humans who may have consumed infected sheep. It is too early to say what may be the consequences in Italy but measures have been taken to reduce any risk there may have been. .........end

Louping-ill vaccine documents from November 23rd, 1946 FULL TEXT

THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946

NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND

ANNUAL CONGRESS, 1946

The annual Congress, 1946, was held at the Royal Veterinary College, Royal College Street, London, N.W.I. from September 22nd to September 27th.

Opening Meeting

[skip to scrapie vaccine issue...tss]

Papers Presented to Congress

SNIP...FULL TEXT ;


although 176 products do _not_ conform to the CSM/VPC guidelines.

COMMERCIAL IN CONFIDENCE

NOT FOR PUBLICATION


8. The Secretary of State has a number of licences. We understand that the inactivated polio vaccine is no longer being used. There is a stock of smallpox vaccine. We have not been able to determine the source material. (Made in sheep very unlikely to contain bovine ingredients).

CONFIDENTIAL

http://collections.europarchive.org/tna/20080102164642/http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf

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CONFIDENTIAL

http://collections.europarchive.org/tna/20080103002544/http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf

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more on the 1968 medicine act, they forgot to follow

http://web.archive.org/web/20030526124448/http://www.bseinquiry.gov.uk/files/yb/1989/01/30008001.pdf

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Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)

http://collections.europarchive.org/tna/20080103002832/http://www.bseinquiry.gov.uk/files/yb/1989/02/22008001.pdf

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http://collections.europarchive.org/tna/20080102155758/http://www.bseinquiry.gov.uk/files/yb/1989/02/22011001.pdf

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2.3.Iatrogenic exposure

Iatrogenic exposure of scrapie has probably occurred twice. The first report determined that the vehicle was a louping ill vaccine prepared from sheep tissues and this infected a large number of sheep sheep (Gordon, 1946, Greig, 1950). The second was more recent and in this case a vaccine against Mycoplasma agalactiae prepared from sheep tissues was incriminated (Agrimi et al 1999, Capucchio, 1998) but not all outbreaks could be linked to the use of the vaccine. In this episode goats were predominantly affected10.

http://ec.europa.eu/food/fs/sc/ssc/out170_en.pdf


http://ec.europa.eu/food/fs/sc/ssc/out247_en.pdf


5.3.3 The greatest risk, in theory, would be from parenteral injection of material derived from bovine brain or lymphoid tissue. Medicinal products for injection or surgical implantation which are prepared from bovine tissues, or which utilise bovine serum albumin or similar agents in their manufacture, might also be capable of transmitting infectious agents. All medicinal products are licensed under the Medicines Act by the Licensing Authority following guidance, for example from the Committee on Safety of Medicines (CSM), the Committee on Dental and Surgical Materials (CDSM) and their subcommittees. The Licensing Authority have been alerted to potential concern about BSE in medicinal products and will ensure that scrutiny of source materials and manufacturing processes now takes account of BSE agent.

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BEFORE the BSE Inquiry went online, i was requesting the daily hearings and submissions, and they were sending them to me via air mail. then, when the BSE Inquiry finally went online, i was then able to go back and match up some of what i had with the YB numbers (above), with the official documents. ...TSS

BSE offals used in cosmetics, toiletry and perfume industry Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas Miss Marion Kelly Cosmetic, Toiletry and Perfumery Association 35 Dover Street London W1X3RA

Department of Trade and Industry 10-18 Victoria Street London SW1H ONN Enquiries 01-215 5000Telex 8811074 DTHQ G 01 215 3324 1February 1990

http://www.mad-cow.org/00/sep00_news.html#bbb


40,000 human heart valves a year from BSE herds Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas

Opinion (webmaster): Below are some shocking documents. Here is a British company preparing 40,000 heart valves a year from bovine pericardium, primarily for export, and they are not required to source this material from BSE-free herds even in peak epidemic years. It is amazing to watch health "authorities" grovelling on their bellies to wring petty concessions from middle management at obscure little companies. The main worry is not the practise of using 800 potentially infected cows a week for human heart transplant material but that the press or recipients will get wind of it, hurting business.

BSE wasn't the problem, it was awkward queries from importing countries like the US. The cows are stunned using brain penetration -- can't do anything about the chunks of bovine brain blasted into the circulatory system, it's the norm. Can't use younger lower-risk animals either, patch would not be big enough. It is fascinating to see the British government worrying about, but doing nothing, with pigs with BSE 10 years ago.

While scrapie was long used as an excuse for continuing with human use of BSE-tainted material, little sheep material was used medically. Bovine transplants, vaccines, insulin doeses, etc. are far more dangerous than dietary material as injections, and are done on a very wide scale. So scrapie was never a valid analogy to BSE, as MAFF knew full well.

The British government deferred to the manufacturer's rep for an opinion on how contaminated pericardium might be, just as this appeared showing that this tissue is extremely dangerous:

http://www.mad-cow.org/00/sep00_news.html#hhh


England worried briefly about infecting other countries 27 Aug 00 confidential correspondence obtained by Terry S. Singeltary Sr.

BSE11/2 020;

SC1337p

DEPARTMENT OF HEALTH AND SOCIAL SECURITY Richmond House, 79 Whitehall, London SWIA 2NS Telephone 01-210 3000 From the Chief Medical Officer Sir Donald Achson KBE DM DSc FRCP FFCM FFOM

Mr K C Meldrum Chief Veterinary Officer Ministry of Agriculture, Fisheries and Food Government Buildings Hook Rise South Tolworth Surbiton Surrey KT6 7NG 3 January 1990

Dear Mr Meldrum

BOVINE SPONGIFORM ENCEPHALOPATHY

You will recall that we have previously discussed the potential risks of BSE occurring in other countries as a result of the continuing export from the UK of meat and bone that may be contaminated by scrapie or possibly BSE.

I remain concerned that we are not being consistent in our attempts to contain the risks of BSE. Having banned the feeding of meat and bone meal to ruminamts in 1988, we should take steps to prevent these UK products being fed to ruminants in other countries. This could be achieved either through a ban on the export of meat and bone meal, or at least by the proper labelling of these products to make it absolutely clear they should not be fed to ruminants [or zoo animals, including rare and endangered primates -- webmaster]. Unless some such action is taken the difficult problems we have faced with BSE may well occur in other countries who import UK meat and bone meal. Surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries.

http://www.mad-cow.org/00/aug00_last_news.html#fff


The documents below were provided by Terry S. Singeltary Sr on 8 May 2000. They are optically character read (scanned into computer) and so may contain typos and unreadable parts.

TIP740203/l 0424 CONFIDENTIAL

Mr Cunningham CMP3 From: D O Hagger MBI Dr Salisbury MED/IMCD3 Mr Burton PD/STB/PG1B B/17/2 Date: 15.02.1989 Mr Dudley PD/AD4

BOVINE SPONGIFORM ENCEPHALOPATHY

http://www.mad-cow.org/00/may00_news.html#aaa


Other US BSE risks: the imported products picture 24 Jul 00 Trade Statistics: UK to US Compiled by Terry S. Singeltary Sr of Bacliff, Texas

[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these?

Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.

Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]

10 January 1990 COMMERCIAL IN CONFIDENCE

NOT FOR PUBLICATION

COMMITTEE ON SAFETY OF MEDICINES WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY

SURGICAL CATGUT SUTURES 2.1 At the first meeting of the Working Party on Bovine Spongiform Encephalopathy on 6 September 1989, detailed consideration was given to XXXXX Surgical Catgut. This arose from the Company's response to the Letter to Licence Holders, indicating that the bovine small intestine source material was derived from UK cattle, unlike 8 other licenced catgut sutures. In contrast XXXXX Surgical Catgut was stated to hold over 90% share of the market for catgut sutures, and to constitute approximately 83% of all sutures used in U.K. IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY;

http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh


The documents below were provided by Terry S. Singeltary Sr on 8 May 2000. They are optically character read (scanned into computer) and so may contain typos and unreadable parts.

TIP740203/l 0424 CONFIDENTIAL

Mr Cunningham CMP3 From: D O Hagger MBI Dr Salisbury MED/IMCD3 Mr Burton PD/STB/PG1B B/17/2 Date: 15.02.1989 Mr Dudley PD/AD4

BOVINE SPONGIFORM ENCEPHALOPATHY

1. The purpose of this minute is to alert you to recent developments on BSE as they affect medicines and to invite representatives to a meeting in Market Towers on 22 February 1989.

2. The report of the Working Party on Bovine Spongiform Encephalopathy (BSE) was submitted by the CMO to the Secretary of State for Health and Minister for Agriculturer on 9 February.

3. The summary at the end of the report records, inter alia: 'we have drawn the attention of the Licensing Authority to the potential of transfer of BSE agent in human and veterinary medicinal products. In paragraph 7 of his submission (Annex A), the CMO notes:

"I am also putting work urgently in hand to satisfy myself that everything possible has been done to ensure .... that transfer of the BBE agent in human and veterinary medicinal products does not occur."

4. The Veterinary products Committee meets on 16 February and The committee on Safety of Medicines on 23 February when each will be considering a draft of some joint guidelines for manufacturers of medicinal products which use bovine material as an ingredient or an intermediate in the manufacturing process (Annex B).....

6. Although a wide range of medicines may be implicated - and the present proposal is to write to companies for more information - an "instant" telephone survey of manufacturer of vaccines used for children has already been undertaken in response to a request from Dr Harris. The results are in Dr Adams' minute of 14 February (Annex C) - the proviso in his second paragraph, last sentence should be noted. 89/02.15/11.1

89/02.15/11.2 MF580439/1 0584 SOUTHWOOD REPORT: BSE AND MEDICINAL PRODUCTS

1. I attach a list of questions on BSE and medicines compiled with the aim of providing question and answer briefing to DH and MAFF Ministers upon publication of the Southwood Report. I have suggested names of those who may be able to provide answers. All recipients are invited to consider which if any important areas have been missed. Also attached is copy QA briefing being proposed by MAFF. I understand MAFF have produced General QA briefing on the reports as a whole. ..

MF580439/1 0585 Question

1. Which medicines are affected? (person to provide reply) Dr. Jefferys

2. Are the risks greater with some medicines than others? Dr. Jefferys

3. Why are medicines affected? Dr. Jefferys

4. Are some affected products available over the counter from pharmacies or shops? Dr. Purves

5. Are only UK products at risk? Dr. Jefferys

6. Are existing stocks safe? Dr. Jefferys

7. Are pre 1980 stocks available? Mr. Burton

8. Are these alternatives to the use of bovine material? Dr. Purves

9. Why can't we throw away suspect stock and import or manufacture safe medicines? Dr. Jefferys

10. Which patients are at risk? Dr. Jefferys

11. Are some patients particularly vulnerable? Dr Jefferys

12. What risks exist to those who have already used these medicines? Dr. Jefferys

13. HOW might patients be affected? Dr. Jefferys

14. Can BSE be transmitted to patients by medicines? Dr. Jefferys

15. How long will it be before risks are quantified? Dr. Jefferys

100 89/02.17/10.2 MF580439/1 0586

16. What research is going on to find out if medicines can transmit this disease and if any patients have been affected? Dr Jefferys

17. Could recent cases of Creuuzfeld Jacob Disease have been caused by transmission of BSE through medicines? Dr. Jefferys

18. What action is the Licensing Authority taking to ensure proper scrutinising of source materials and manufacturing processes? Dr. Jefferys/Dr. Purves

19. Are the guidelines practical? Dr. Jefferys/Dr. Purves

20. Will the guidelines remove the risk? Dr. Jefferys

21. How will the guidelines be enforced? Dr. Jefferys/Dr. Purves

22. How soon will they come into force? Dr. Jefferys

23. Will the guidelines be published? Mr. Hagger

24. What is being done to reassure patients, parents etc? Mr. Hagger/Dr. Salisbury

25. What advice is being given to doctors, pharmacists etc? Mr. Hagger

26. What advice is the Government giving about its vaccination programme? Dr. Salisbury

27. Is the vaccination programme put at risk because of BSE? Dr. Salisbury

89/02.17/10.3

Q. Will government act on this?

A. Yes - thymus is not used in preparation of baby foods but it is contacting all manufacturers to seek their urgent views on use of kidneys and liver from ruminants. Will consider any necessary measures in the light of their response.

VETERINARY MEDICINES

Q. Can medicines spread BSE to other cattle/animals?

A. The report describes any risks as remote.

Q. How can risks be avoided?

A. In liaison with the DOH the Veterinary Products Committee is examining guidelines for the veterinary pharmaceutical industry which will be issued shortly.

Q. What will Guidelines say?

A. In essence they call for non-bovine sources to be used if possible, including synthetic material of biotechnological origin. Where this is not possible the industry should look for sources which are free of BSE and which are collected in a manner which avoids risk of contamination by the BSE agent.

89/02.17/10.4 MF580439/1 0588

A. Bovine source material is used in [garbled, cannot read...TSS] and some other medicines.

Q. How many medicines are involved?

A. Computer records show that about 300 of the 3,050 veterinary medicines licensed in the U.K. are manufactured directly from bovine source material. However, other medicines may be produced from bovine sources and a letter is going to all license holders so that a comprehensive list can be drawn up.

89/06.19/8.1 BSE3/1 0191 Hr J Maslin (MAFF) Ref: Maslin3g

From: Dr H Pickles Med SEB/B Date: 3 July 1989

CATTLE BY-PRODUCTS AND BSE

I was interested to see the list of by-products sent to the HSE. Those of particular concern included:

* small intestines: sutures (I thought the source was ovine but you are checking this)

* spinal cord: pharmaceuticals

* thymus: pharmaceuticals

Are you able to give me more information on which UK manufacturers use these materials? Our proposed ban on bovine offal for human consumption would not affect these uses, I assume.

Id No. 1934/RD/1 89/08.10/6.1 117A

BOVINE SPONGIFORM ENCEPHALAPATHY MEETING HELD ON 21 AUGUST 1989 AT 2;15 IN ROOM 720 Miss M Duncan (Chairman) Mr W Burton Dr E Hoxey Mrs J Dhell Ms K Turner Dr S Whittle Mr N Weatherhead ... 5. The MCA had sent 2700 questionnaires out, 1,124 had made valid returns; of these 122 use animal material of some kind and there are 582 products involved. ... 6. The MCA/BSE working group will meet on 6th September. Their aim is to review responses from professional officers in MCA who have suggested seven categories of importance (with 1 being the most important} for medical products:

ID 2267/NRE/1 89/08.21/10.1

1. Products with Bovine brain/lymph tissue administered by injection.

2. Products with bovine tissue other than brain/lymph administered by inection.

3. Tissue implants/open wound dressing/surgical materials/dental and ophthlamic products with bovine ingredients.

4. Products with bovine ingredients administered topically.

5. Products with bovine ingredients administered orally.

6. Products with other animal/fish/insect/bird ingredients administered by injection/topically/oral routes.

7. Products with ingredients derived from animal material by chemical processing (eg stearic acid, gelatine, lanolin ext.

The BSE working group will decide which of these are important, and should be examined more closely, and which categories can be eliminated.

The responses by the companies were presented by Ms Turner and were categorised by MCA standards, the products that were discussed were all low volume usage products eg sutures, heart valves.

8. As the responses included some materials of human origin it was decided that more information should be sought about CJD. There had been 2 recent deaths reported associated with human growth hormone. These were being investigated.

9. Re-editing of the Paper on "Incubation of Scrapie-like Agents"

It was suggested that the document could be sent out to companies with the non-standard sterilization Document. The document could have severe implications on the companies whose products have a high risk factor as decided by the MCA working group....

11. The Need for a list of High Priority Implantables The commitee decided that no list is necessary as all implantables, including ones from a human source are of high priority. Concern was shown over Killingbeck who use human material but had not yet responded. The company will be chased for a response. Concern was shown over the fact that there may be other scrapie-like organisms in other animals and further enquiries should be made.

2334q/RD/4 89/08.21/10.7

BOVINE MATERIAL USED IN THE MANUFACTURE OF SURGICAL IMPLANTS AND BLOOD CONTACT MEDICAL DEVICES

Glutaraldehyde, formaldehyde, and ethylene oxide are used in the sterilization of these devices.

However, glutaraldehyde 4,10,12,19 formaldehyde 5,10,11,13,19 and ethylene oxide 19,23 are all reported to be ineffective methods for sterilization of material infected with the agents of CJD or scrapie.

Previous advice and research using the agents of CJD and scrapie, has concentrated on the decontamination of equipment; protection of health care workers from contaminated human material; human growth hormone; and dura mater. The methods developed may not be directly applicable or transferable to material of bovine origin for use in human implantation.

2334q/RD/7 89/08.21/10.10 BSE11/2 020 SC1337

DEPARTMENT OF HEALTH AND SOCIAL SECURITY Richmood House 79 Whitehall, London SW1A 2NS Telephone 01-210-3000 From the Chief Medical Officer Sir Donald Acheson KBE DM DSc FRCP FFCM FFOM

Mr K C Meldrum Chief Veterinary Officer Ministry of Agriculture, Fisheries and Food Government Buildings Hook Rise South Tolworth Surbiton Surrey KT6 7NG

3 January 1990

Dear Mr. Meldrum,

BOVINE SPONGIFORM ENCEPHALOPATHY

You will recall that we have previously discussed the potential risks of BSE occurring in other Countries as a result of the continuing export from the UK of meat and bone that may be contaminated by scrapie or possibly BSE.

I remain concerned that we are not being consistent in our attempts to contain the risks of BSE. Having banned the feeding of meat and bone meal to ruminants in 1988, we should take steps to prevent these UK products being fed to ruminants in other countries. This could be achieved either through a ban on the export of meat and bone meal, or at least by the proper labelling of these products to make it absolutely clear they should not be fed to ruminants. Unless some such action is taken the difficult problems we have faced with BSE may well occur in other countries who import UK meat and bone meal. Surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries.

I would be very interested to hear how you feel this gap in the present prcautionary measures to eliminate BSE should be closed. We should be aiming at the global elimination of this new bovine disease. The export of our meat and bone meal is a continuing risk to other countries.

Signed Sincerely Donald Acheson

Did the US import fetal calf serum and vaccines from BSE-affected countries? 3002.10.0040: FETAL BOVINE SERUM (FBS) U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 ---> <--- 1998 YTD ---> Country Quantity Value Quantity Value

================================================================= WORLD TOTAL . . . . . . . 2,727 233 131,486 8,502 Australia . . . . . . . . --- --- 19,637 2,623 Austria . . . . . . . . . --- --- 2,400 191 Belgium . . . . . . . . . --- --- 17 32 Canada . . . . . . . . . 900 110 30,983 3,220 Costa Rica . . . . . . . 500 20 4,677 169 Federal Rep. of Germany --- --- 105 21 Finland . . . . . . . . . 1 8 9 83 France . . . . . . . . . --- --- 73 7 Guatemala . . . . . . . . --- --- 719 42 Honduras . . . . . . . . --- --- 1,108 88 Israel . . . . . . . . . --- --- 24 165 Netherlands . . . . . . . --- --- 1 5 New Zealand . . . . . . . 26 5 65,953 913 Panama . . . . . . . . . --- --- 1,195 64 Switzerland . . . . . . . 971 8 1,078 23 United Kingdom . . . . . 329 82 743 756 Uruguay . . . . . . . . . --- --- 2,764 98 ------------------------------------------------------------------ 3002.20.0000: VACCINES FOR HUMAN MEDICINE U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 ---> <--- 1998 YTD ---> Country Quantity Value Quantity Value ================================================================= WORLD TOTAL . . . . . . . 25,702 26,150 550,258 378,735 Austria . . . . . . . . . --- --- 45 225 Belgium . . . . . . . . . 14,311 12,029 248,041 199,036 Canada . . . . . . . . . 1,109 1,527 15,798 16,305 Denmark . . . . . . . . . 80 234 246 682 Federal Rep. of Germany 1,064 4,073 12,001 6,329 France . . . . . . . . . 3,902 4,859 87,879 92,845 Ireland . . . . . . . . . --- --- 120 478 Italy . . . . . . . . . . --- --- 2,359 81 Japan . . . . . . . . . . 445 1,903 11,350 11,298 Netherlands . . . . . . . --- --- 94 6 Republic Of South Africa --- --- 2 1 Spain . . . . . . . . . . --- --- 60 30 Switzerland . . . . . . . 716 353 9,303 4,271 United Kingdom . . . . . 4,075 1,172 162,960 47,148 ------------------------------------------------------------------ 3002.30.0000: VACCINES FOR VETRINARY MEDICINE U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 ---> <--- 1998 YTD ---> Country Quantity Value Quantity Value ================================================================= WORLD TOTAL . . . . . . . 6,528 237 87,149 2,715 Canada . . . . . . . . . --- --- 2,637 305 Federal Rep. of Germany --- --- 104 5 Netherlands . . . . . . . 138 64 472 192 New Zealand . . . . . . . 6,390 173 83,882 1,895 United Kingdom . . . . . --- --- 54 318

http://www.mad-cow.org/00/may00_news.html


Procedures Manual

Bovine Spongiform Encephalopathy (BSE)

Ongoing Surveillance Plan

Ongoing Surveillance Plan Implementation July 20, 2006

snip...

Personal Safety

If BSE is transmissible to humans in the occupational setting, the most likely routes would be through contact with infective tissues through wounds or open lesions on the skin, contact with mucous membranes (eyes and mouth), or exceptionally, by swallowing. .....snip...end

http://www.aphis.usda.gov/vs/nvsl/PDFs/BSE%20Ongoing%20Surveillance%20SOP%207-20-06.doc



SO, looks like to me the most likely route of transmission of BSE to humans would be through inoculation i.e.

the most likely routes would be through contact with infective tissues through wounds or open lesions on the skin,

IF you look at all the successful transmission studies in the lab with TSE, inoculations was the most successful route.

BSE-L@LISTS.AEGEE.ORG

Bovine Spongiform Encephalopathy

BSE-L is a discussion forum for scientists who are interested in Bovine Spongiform Encephalopathy (BSE). BSE-L has been created on 20th July, 1994 by Siegfried Schmitt. Impressum: http://www.kaliv.de/impressum.html

LISTS.AEGEE.ORG ( BSE-L: 484 matches (only the first 50 will be shown).. )

From: TSS (216-119-138-163.ipset18.wt.net) Subject: Louping-ill vaccine documents from November 23rd, 1946 Date: September 10, 2000 at 8:57 am PST

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

The annual Congress, 1946, was held at the Royal Veterinary College, Royal College Street, London, N.W.I. from September 22nd to September 27th.

Opening Meeting

[skip to scrapie vaccine issue...tss]

Papers Presented to Congress

The papers presented to this year's Congress had as their general theme the progressive work of the profession during the war years. Their appeal was clearly demonstrated by the large and remarkably uniform attendance in the Grand Hall of the Royal Veterinary College throughout the series; between 200 and 250 members were present and they showed a keen interest in every paper, which was reflected in the expression of some disappointment that the time available for discussion did not permit of the participation of more than a small proportion of would-be contributors.

In this issue we publish (below) the first to be read and discussed, that by Dr. W. S. Gordon, M.R.C.V.S., F.R.S.E., "Advances in Veterinary Research." Next week's issue will contain the paper on "Some Recent Advances in Veterinary Medicine and Surgery in Large-Animal Practice" by Mr. T. Norman Gold, M.R.C.V.S. In succeeding numbers of the Record will be reproduced, also with reports of discussions, that by Mr. W. L. Weipers, M.R.C.V.S., D.V.S.M., on the same subject as relating to small-animal practice, and the papers by Mr. J. N. Ritchie, B.SC., M.R.C.V.S., D.V.S.M., and Mr. H.W. Steele-Bodger, M.R.C.V.S., on "War-time Achievements of the British Home Veterinary Services."

The first scientific paper of Congress was read by Dr. W. S. Gordon, M.R.C.V.S., F.R.S.E. on Monday, September 23rd, 1946, when Professor J. Basil Buxton, M.A., F.R.C.V.S, D.V.H., Prinicipal of the Royal Veterinary College, presided.

Advances in Veterinary Research

by

W.S. GORDON, PH.D., M.R.C.V.S., F.R.S.E.

Agriculteral Research Council, Field Station, Compton, Berks.

Louping-ill, Tick-borne Fever and Scrapie

In 1930 Pool, Browniee & Wilson recorded that louping-ill was a transmissible disease. Greig et al, (1931) showed that the infective agent was a filter-passing virus with neurotropic characters and Browniee & Wilson (1932) that the essential pathology was that of an encephalomyelitis. Gordon, Browniee, Wilson & MacLeod (1932) and MacLeod & Gordon (1932) confirmed and extended this work. It was shown that on louping-ill farms the virus was present in the blood of many sheep which did not show clinical symptoms indicating involvement of the central nervous system and that for the perpetuation and spread of the disease these subclinical cases were probably of greater importance that the frank clinical cases because, in Nature, the disease was spread by the tick, lxodes ricinus L. More recently Wilson (1945, 1946) has described the cultivation of the virus in a chick embryo medium, the pathogenic properties of this culture virus and the preparation of louping-ill antiserum.

Between 1931 and 1934 I carried out experiments which resulted in the development of an effective vaccine for the prevention of louping-ill.* This vaccine has been in general use since 1935 and in his annual report to the Animal Diseases Research Association this year, Dr. Greig stated that about 227,000 doses of vaccine had been issued from Moredun alone.

Dr. Gordon illustrated this portion of his paper by means of graphs and diagrams projected by the epidiascope.

This investigation, however, did not begin and end with the study of louping-ill; it had, by good fortune, a more romantic turn and less fortunately a final dramatic twist which led almost to catastrophe. After it had been established that a solid immunity to louping-ill could be induced in sheep, a group of immunized and a group of susceptible animals were placed together on the tick-infected pasture of a louping-ill farm. Each day all the animals were gathered and their temperatures were recorded. It was anticipated that febrile reactions with some fatalities would develop in the controls while the louping-ill immunes would remain normal. Contrary to expectation, however, every sheep, both immune and control, developed a febrile reaction. This unexpected result made necessary further investigation which showed that the febrile reaction in the louping-ill immunes was due to a hitherto undescribed infective agent, a Rickettsia-like organism which could be observed in the cytoplasm of the granular leucocytes, especially the neutrophil polymorphs (MacLeod (1932), Gordon, Browniee, Wilson & MacLeod. MacLeod & Gordon (1933). MacLeod (1936). MacLeod collected ticks over many widely separated parts of Scotland and all were found to harbour the infective agent of tick-borne fever, and it is probable that all sheep on tick-infested farms develop this disease, at least on the first occasion that they become infested with ticks. When the infection is passed in series through susceptible adult sheep it causes a sever, febrile reaction, dullness and loss of bodily condition but it rarely, if ever, proves fatal. It is clear, however, that it aggravates the harmful effects of a louping-ill infection and it is a serious additional complication to such infections as pyaemia and the anacrobic infections which beset lambs on the hill farms of Northern Britain.

Studying the epidemiology of louping-ill on hill farms it became obvious that the pyaemic condition of lambs described by M'Fadyean (1894) was very prevalent on tick infested farms Pyaemia is a crippling condition of lambs associated with tick-bite and is often confused with louping-ill. It is caused by infection with Staphylococcus aureus and affected animals may show abscess formation on the skin, in the joints, viscera, meninges and elsewhere in the body. It was thought that tick-borne fever might have been a predisposing factor in this disease and unsuccessful attempts were made by Taylor, Holman & Gordon (1941) to reproduce the condition by infecting lambs subcutaneously with the staphylococcus and concurrently producing infections with tickborne fever and louping-ill in the same lambs. Work on pyaemia was then continued by McDiarmid (1946a, 1946b, 1946c), who succeeded in reproducing a pyaemic disease in mice, guinea-pigs and lambs similar to the naturally occurring condition by intravenous inoculation of Staphylococcus aureus. He also found a bacteraemic form of the disease in which no gross pyaemic lesions were observed. The prevention or treatment of this condition presents a formidable problem. It is unlikely that staphylococcal ???oid will provide an effective immunity and even if penicillin proved to be a successful treatment, the difficulty of applying it in adequate and sustained dosage to young lambs on hill farms would be almost insurmountable.

From 1931 to 1934 field trials to test the immunizing value and harmlessness of the loup-ill vaccine were carried out on a gradually increasing scale. Many thousands of sheep were vaccinated and similar numbers, living under identical conditions were left as controls. The end result showed that an average mortability of about 9 percent in the controls was reduced to less than 1 percent in the vaccinated animals. While the efficiency of the vaccine was obvious after the second year of work, previous bitter experience had shown the wisdom of withholding a biological product from widespread use until it had been successfully produced in bulk, as opposed to small-scale experimental production and until it had been thoroughly tested for immunizing efficiency and freedom from harmful effects. It was thought that after four years testing this stage had been reached in 1935, and in the spring of that year the vaccine was issued for general use. It comprised a 10 percent saline suspension of brain, spinal cord and spleen tissues taken from sheep five days after infection with louping-ill virus by intracerebral inoculation. To this suspension 0-35 percent of formalin was added to inactivate the virus and its safety for use as a vaccine was checked by intracerbral inoculation of mice and sheep and by the inoculation of culture medium. Its protective power was proved by vaccination sheep and later subjecting them, along with controls, to a test dose of living virus.

Vaccine for issue had to be free from detectable, living virus and capable of protecting sheep against a test dose of virus applied subcutaneously. The 1935 vaccine conformed to these standards and was issued for inoculation in March as three separate batches labelled 1, 2, and 3. The tissues of 140 sheep were employed to make batch 1 of which 22,270 doses were used; 114 to make batch 2 of which 18,000 doses were used and 44 to make batch 3 of which 4,360 doses were used. All the sheep tissues incorporated in the vaccine were obtained from yearling sheep. During 1935 and 1936 the vaccine proved highly efficient in the prevention of loup-ill and no user observed an ill-effect in the inoculated animals. In September, 1937, two and a half years after vaccinating the sheep, two owners complained that scrapie, a disease which had not before been observed in the Blackface breed, was appearing in their stock of Blackface sheep and further that it was confined to animals vaccinated with louping-ill vaccine in 1935. At that stage it was difficult to conceive that the occurrence could be associated with the injection of the vaccine but in view of the implications, I visited most of the farms on which sheep had been vaccinated in 1935. It was at this point that the investigation reached its dramatic phase; I shall not forget the profound effect on my emotions when I visited these farms and was warmly welcomed because of the great benefits resulting from the application of louping-ill vaccine, wheras the chief purpose of my visit was to determine if scrapie was appearing in the inoculated sheep. The enquiry made the position clear. Scrapie was developing in the sheep vaccinated in 1935 and it was only in a few instances that the owner was associating the occurrence with louping-ill vaccination. The disease was affecting all breeds and it was confined to the animals vaccinated with batch 2. This was clearly demonstrated on a number of farms on which batch 1 had been used to inoculate the hoggs in 1935 and batch 2 to inoculate the ewes. None of the hoggs, which at this time were three- year-old ewes. At this time it was difficult to forecast whether all of the 18,000 sheep which had received batch 2 vaccine would develop scrapie. It was fortunate, however, that the majority of the sheep vaccinated with batch 2 were ewes and therfore all that were four years old and upwards at the time of vaccination had already been disposed of and there only remained the ewes which had been two to three years old at the time of vaccination, consequently no accurate assessment of the incidence of scrapie could be made. On a few farms, however, where vaccination was confined to hoggs, the incidence ranged from 1 percent, to 35 percent, with an average of about 5 percent. Since batch 2 vaccine had been incriminated as a probable source of scrapie infection, an attempt was made to trace the origin of the 112 sheep whose tissues had been included in the vaccine. It was found that they had been supplied by three owners and that all were of the Blackface or Greyface breed with the exception of eight which were Cheviot lambs born in 1935 from ewes which had been in contact with scrapie infection. Some of these contact ewes developed scrapie in 1936-37 and three surviving fellow lambs to the eight included in the batch 2 vaccine of 1935 developed scrapie, one in September, 1936, one in February, 1937, and one in November, 1937. There was, therefore, strong presumptive evidence that the eight Cheviot lambs included in the vaccine although apparently healthy were, in fact, in the incubative stage of a scrapie infection and that in their tissues there was an infective agent which had contaminated the batch 2 vaccine, rendering it liable to set up scrapie. If that assumption was correct then the evidence indicated that:-

(1) the infective agent of scrapie was present in the brain, spinal cord and or spleen of infected sheep: (2) it could withstand a concentration of formalin of 0-35 percent, which inactivated the virus of louping-ill: (3) it could be transmitted by subcutaneous inoculation; (4) it had an incubative period of two years and longer.

Two Frenchmen, Cuille & Chelle (1939) as the result of experiments commenced in 1932, reported the successful infection of sheep by inoculation of emulsions of spinal cord or brain material by the intracerebral, epidural, intraocular and subcutaneous routes The incubation period varied according to the route employed, being one year intracerebrally, 15 months intraocularly and 20 months subcutaneously. They failed to infect rabbits but succeeded in infecting goats. Another important part of their work showed that the infective agent could pass through a chamberland 1.3 filter, thus demonstrating that the infective agent was a filtrable virus. It was a curious coincidence that while they were doing their transmission experiments their work was being confirmed by the unforeseeable infectivity of a formalinized tissue vaccine.

As a result of this experience a large-scale transmission 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 inoculated 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 77518


iatrogenic TSE






***> Prion protein (PrP) profiles in blood and CSF: insights into pre-symptomatic and symptomatic prion disease

Tuesday, June 9, 2026

Hazard identification for the risks to terrestrial animal health from the import of hay and straw, BSE, CWD, Scrapie, TSE, Prion



Cervid CWD TSE PrP Transmission to Humans, has it already happened and being masked as sporadic CJD, What if? July 2026 Review



HUMAN TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: A CRITICAL SCIENTIFIC INVESTMENT

Final Report of the National Prion Research Program

US Army Medical Research and Materiel Command Congressionally Directed Medical Research Programs

Fort Detrick, Maryland

2007

Snip…

*** 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.

Snip…


one of the old studies that has always stuck out in my mind, one that the late great Dr. Gibbs, Gajdusek, et al did way back, and to this day is still amazes me...terry

*** 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.


France issues moratorium on prion research after fatal brain disease strikes two lab workers

By Barbara CasassusJul. 28, 2021 , 4:35 AM

PARIS—Five public research institutions in France have imposed a 3-month moratorium on the study of prions—a class of misfolding, infectious proteins that cause fatal brain diseases—after a retired lab worker who handled prions in the past was diagnosed with Creutzfeldt-Jakob disease (CJD), the most common prion disease in humans. An investigation is underway to find out whether the patient, who worked at a lab run by the National Research Institute for Agriculture, Food and Environment (INRAE), contracted the disease on the job.

If so, it would be the second such case in France in the past few years. In June 2019, an INRAE lab worker named Émilie Jaumain died at age 33, 10 years after pricking her thumb during an experiment with prion-infected mice. Her family is now suing INRAE for manslaughter and endangering life; her illness had already led to tightened safety measures at French prion labs.

Posted in: EuropeHealthScientific Community

doi:10.1126/science.abl6587


Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure

Variant Creutzfeldt–Jakob disease was identified in a technician who had cut her thumb while handling brain sections of mice infected with adapted BSE 7.5 years earlier. The long incubation period was similar to that of the transfusion-transmitted form of the disease.

Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure

TO THE EDITOR:

We report a case of variant Creutzfeldt–Jakob disease (CJD) that was plausibly related to accidental occupational exposure in a technician who had handled murine samples contaminated with the agent that causes bovine spongiform encephalopathy (BSE) 7.5 years earlier.

In May 2010, when the patient was 24 years of age, she worked in a prion research laboratory, where she handled frozen sections of brain of transgenic mice that overexpressed the human prion protein with methionine at codon 129. The mice had been infected with a sheep-adapted form of BSE. During this process, she stabbed her thumb through a double pair of latex gloves with the sharp ends of a curved forceps used to handle the samples. Bleeding was noted at the puncture site.

In November 2017, she began having burning pain in the right shoulder and neck. The pain worsened and spread to the right half of her body during the following 6 months. In November 2018, an examination of a sample of cerebrospinal fluid (CSF) obtained from the patient was normal. Magnetic resonance imaging (MRI) of the brain showed a slight increase in the fluid-attenuated inversion recovery (FLAIR) signal in the caudates and thalami (Fig. S1A and S1B in the Supplementary Appendix, available with the full text of this letter at NEJM.org). In January 2019, she became depressed and anxious and had memory impairment and visual hallucinations. There was hypertonia on the right side of her body. At that time, an analysis of CSF for 14-3-3 protein was negative. In March 2019, MRI showed an increased FLAIR signal in pulvinar and dorsomedial nuclei of thalami (Fig. S1C through S1E).

Figure 1.

Detection of Abnormal Prion Protein in Biologic Fluid Samples and Postmortem Findings.

The patient was found to be homozygous for methionine at codon 129 of the prion protein gene without mutation. An analysis of a sample of CSF on real-time quaking-induced conversion analysis was negative for a diagnosis of sporadic CJD. However, an analysis of plasma and CSF by means of protein misfolding cyclic amplification was positive for the diagnosis of variant CJD (Figure 1A and 1B). The patient died 19 months after the onset of symptoms. Neuropathological examination confirmed the diagnosis of variant CJD (Figure 1C and 1D). Western blot analysis showed the presence of type 2B protease-resistant prion protein in all sampled brain areas. The clinical characteristics of the patient and the postmortem neuropathological features were similar to those observed in 27 patients with variant CJD who had previously been reported in France.1 (Additional details are provided in the Supplementary Appendix.)

There are two potential explanations for this patient’s condition. Oral transmission from contaminated cattle products cannot be ruled out because the patient was born at the beginning of the French BSE outbreak in cattle. However, the last two patients who had confirmed variant CJD with methionine homozygosity at codon 129 in France and the United Kingdom died in 2014 and 2013, respectively, which makes oral transmission unlikely. In France, the risk of variant CJD in 2019 was negligible or nonexistent in the post-1969 birth cohort.2

Percutaneous exposure to prion-contaminated material is plausible in this patient, since the prion strain that she had handled was consistent with the development of variant CJD.3 The 7.5-year delay between the laboratory accident and her clinical symptoms is congruent with the incubation period in the transfusion-transmitted form of the disease. The ability of this strain to propagate through the peripheral route has been documented, and experimental studies with scrapie strains have shown that scarification and subcutaneous inoculation are effective routes.4,5 The last known Italian patient with variant CJD, who died in 2016, had had occupational contact with BSE-infected brain tissues, although subsequent investigation did not disclose a laboratory accident (Pocchiari M, Italian Registry of CJD: personal communication). Thus, the last two cases of variant CJD outside the United Kingdom have been associated with potential occupational exposure. Such cases highlight the need for improvements in the prevention of transmission of variant CJD and other prions that can affect humans in the laboratory and neurosurgery settings, as outlined in the Supplementary Appendix.

Jean-Philippe Brandel, M.D. Assistance Publique–Hôpitaux de Paris, Paris, France

M. Bustuchina Vlaicu, M.D. Groupe Hospitalier Nord-Essonne, Orsay, France

Audrey Culeux, B.Sc. INSERM Unité 1127, Paris, France

Maxime Belondrade, M.Sc. Daisy Bougard, Ph.D. Etablissement Français du Sang, Montpellier, France

Katarina Grznarova, Ph.D. Angeline Denouel, M.Sc. INSERM Unité 1127, Paris, France

Isabelle Plu, M.D. Elodie Bouaziz-Amar, Pharm.D., Ph.D. Danielle Seilhean, M.D., Ph.D. Assistance Publique–Hôpitaux de Paris, Paris, France

Michèle Levasseur, M.D. Groupe Hospitalier Nord-Essonne, Orsay, France

Stéphane Haïk, M.D., Ph.D. INSERM Unité 1127, Paris, France stephane.haik@upmc.fr

Supported by a grant (ANR-10-IAIHU-06) from Programme d’Investissements d’Avenir and Santé Publique France.

Disclosure forms provided by the authors are available with the full text of this letter at NEJM.org.

5 References

July 2, 2020

N Engl J Med 2020; 383:83-85

DOI: 10.1056/NEJMc2000687

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Terry S. Singeltary Sr.

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