Review of the Human Pituitary Trust Account and CJD

Issue 20
January
2010


News from the Department of Health and Ageing

Review of the Human Pituitary Trust Account

Since the Human Pituitary Hormone Program ceased in 1985, the Commonwealth has provided funds for counselling for recipients and their families, a support group network for recipients, and a number of medical research projects from the Pituitary Hormone Trust Account (PHTA). The Department also provides funding to support the Australian National CJD Registry (ANCJDR).

In 1994, Professor Margaret Allars conducted the Report of the Inquiry into the use of Pituitary Derived Hormones in Australia and Creutzfeldt-Jakob (CJD) disease known as the Allars Report. The Allars Report recommended that the PHTA and the Creutzfeldt-Jakob Disease Support Group Network (CJDSGN) be reviewed by 2010. A review is currently underway and the reviewer has been in contact with both the ANCJDR and the CJDSGN. The review will assess the appropriateness, effectiveness and efficiency of support to the CJDSGN and Registry and make recommendations regarding future funding.

CJD Nationally Notifiable

In September 2003, the Communicable Disease Network Australia endorsed the latest version of the list of communicable diseases to be notified nationally which included Creutzfeldt-Jakob Disease (CJD). Tasmania, Victoria, Western Australia, South Australia and New South Wales have included CJD in their State notifiable diseases list, the remaining States and Territories are expected to follow. In some jurisdictions this has meant a lengthy process associated with amendment to existing legislation.
The reporting of diseases such as CJD enables monitoring and investigation of these diseases in the community in order to prevent the spread of these diseases and reduce their impact on others.

Medical in confidence letter

The ‘Medical-In-Confidence - To Whom It May Concern Letter’ letter was developed to assist recipients in accessing medical care, this letter was revised in 2008 to reflect the changes to current infection control standards and best practice. Just as a reminder if you would like to receive the updated ‘Medical-In-Confidence - To Whom It May Concern Letter’ please contact the free call line 1800 802 306 and a copy will be sent to you.

When this letter is updated in future to reflect infection control standards, the Department will automatically send the latest version to recipients who have previously requested a copy.
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Infection Control Guidelines (ICGs)

The ICGs are available to the public and provide guidance on infection control strategies, environmental cleaning and protection of health care workers in health care facilities. The ICGs cover all kinds of transmissible diseases including viruses (eg. hepatitis C, rotavirus), bacteria (eg. staphylococcus, tuberculosis) and other diseases like classical CJD (cCJD).The ICGs are designed to be used by all health care workers, such as hospital and clinic infection control staff, nurses, clinicians and dentists.
Chapter 31 of the ICGs relates to cCJD, including sporadic CJD, inherited CJD and iatrogenic CJD, but excluding variant CJD (vCJD).

During 2007, the cCJD Chapter of the ICGs was reviewed by an expert panel and revised to ensure a more concise format. The procedures and processes which infection control staff use to evaluate a patient and determine the best way to protect them and subsequent patients has been simplified into a dichotomy for classification of transmission risk based on the tissues exposed during a procedure and the risk status of the patient. The precautions which need to be taken when a patient at risk of cCJD is identified have also been simplified to minimise the risk of transmission of cCJD and minimise occupational hazards for health care workers. The result is more user-friendly ICGs.
The entire ICGs are currently undergoing further review by the National Health and Medical Research Council on behalf of the Australian Commission for Quality and Safety in Healthcare and expect to be finalised this year.

If you are undergoing a procedure, your healthcare provider can download a copy of the cCJD Chapter of the ICG free of charge from the Department of Health and Ageing website (www.health.gov.au). The CJDSGN or the State or Territory Health Department can also provide further advice on infection control in your situation.

CJD Support Group News

2010 ‘Understanding CJD’ Conference

The CJD Support Group Network (CJDSGN) is currently organising the third annual conference to be held in Melbourne in May 2010.

The first conference was held in Melbourne in 2008 followed by the conference this year in Sydney. Attendance at the annual conference is free for all members of the CJDSGN, their families and friends. All recipients of human pituitary hormones and their families, who are not currently members of the CJDSGN, are also welcome to attend the conference free of charge.

Since the restructure of the CJDSGN in 2004 the focus and work of the network has grown. The funding agreement with the Department of Health and Ageing has been expanded to support all Australians affected by CJD or other prion diseases. This includes other ‘at risk of CJD’ groups and families who are dealing with or have lost a loved one to CJD.

It has been encouraging at meetings to see how supportive recipients have been of families affected by sporadic or genetic forms of CJD. As CJD occurs at random in about one person per million of the population each year there are about 25 – 30 families each year who lose a family member to this devastating disease.

The support and resources available for families has been crucial and the expansion has meant that the CJDSGN continues to provide for recipients needing advice and assistance, an active and well connected network. The CJDSGN provides an informative website, resource material and an education/awareness program for health care professionals aimed at reducing the infection control problems that we often face when accessing health care.

At the 2008 and 2009 conferences we were fortunate to have Australia’s leading researchers and experts attending as speakers giving our audience the opportunity to learn

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more about research on prion disease being conducted in Australia and overseas as well as information on many topics of interest including infection control, experimental treatments for CJD patients and the management of CJD.

Professor Colin Masters, Associate Professor Steven Collins, Professor Andrew Hill and Dr Victoria Lawson from the University of Melbourne, Professor Simon Hawke from the University of Sydney and Ms Alison Boyd from the Australian National CJD Registry gave freely of their time to present current information for our members.

This year we were also honoured to welcome Professor Richard Knight from the National CJD Surveillance Unit, Edinburgh UK, and for the second year Ms Margaret Leitch, who is the national coordinator for CJD patients in the UK. Both Professor Knight and Ms Leitch funded their travel to Australia to share information on surveillance, research and the situation in the UK.

For the 2010 conference we are delighted to have the interest of a number of overseas experts keen to attend and to provide a variety of information for you all. We are hopeful of welcoming representatives of the member organisations of the CJD International Support Alliance (CJDISA). The CJDSGN was a founding member of the CJDISA in 2006 and working with, and sharing resources, with like organisations around the world has greatly enhanced the services that we are now able to provide as well as encouraging and giving us the confidence to hold an annual conference.

For the past two years attendees at the conferences have included people from every state and territory in Australia as well as from New Zealand. Although the conference is designed to supply information for members we do encourage any interested health care professionals to attend providing they cover the cost of their attendance.

In order to provide availability for as many people as possible we are planning in 2010 to hold a full day meeting in Perth prior to the Melbourne conference and we are hopeful that we can encourage several of the speakers to join us for this meeting. Following the Melbourne conference there will also be an information afternoon held in Sydney. If we are able to continue to provide an annual conference in the future we will be mindful of providing access for members in other areas of Australia.

If you are not already a member but would like to receive an invitation to the conference please email contactus@cjdsupport.org.au or ring our toll free number 1800 052466.

Copies of our DVD ‘Understanding CJD’ are available free of charge for members. The DVD provides an excellent resource tool for your GP or any other health care professional and covers the current infection control guidelines.

We have an extensive electronic ‘Interested Party’ list of health care professionals interested in receiving up to date information or resources to which you are welcome to add your doctor or dentist.

Suzanne Solvyns
Director

The CJD Support Group Network

Incident Panel Report for 2009 activities

Over 2009, the National CJD Incident Panel (CJDIP) was convened to assess and advise on a number of issues. The first was in relation to surgery after a suspect CJD diagnosis had been made. The remaining six requests were made for advice before surgery, when medical staff were planning to undertake procedures and were seeking clarification of patient’s CJD risk status and the appropriate infection control measures needed. The following summarise the Incident Panel’s requests and the advice provided.
1. A patient with recurrent eye infections underwent draining of intra-ocular fluid on two occasions for diagnosis and treatment. Several weeks after the eye procedures, an acute illness which involved cognitive impairment emerged, which led to the clinical suspicion of CJD shortly before death. There

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was no referral for autopsy. A routine medical risk assessment identified the ocular procedures during the patient’s possible CJD illness. The procedure was reviewed and the instruments involved identified as a part of the risk assessment, and promptly placed in quarantine by the hospital. The local health authority concerned sought the CJD Incident Panel’s advice on the assessment of the CJD risk for these instruments. The assessment revealed the procedure only involved the anterior chamber of the eye, and as a consequence no additional infection control measures were necessary. The quarantined instruments were safely returned to general use.

2. Four patients presented separately over 2009 for either spinal or cranial surgery after previously being notified by a local health department about a possible CJD exposure from previous surgery they have undergone. The initial CJD risk notification by the hospital and local health authority had alerted several hundred patients treated by the health service of their “low risk” CJD status when the potential for a surgical exposure to CJD had been identified, several years earlier. The risk status advice was based on the Australian infection control guidelines and current scientific knowledge about CJD. The local health authorities and /or treating medical staff requested the Incident Panel advise on these four patients’ current risk status for CJD, and also for sterilisation advice for the management of any neuro-surgical equipment used in their future surgical procedures. The Incident Panel reported that the risk assessment to these four patients’ could be downgraded from a “low risk” status, to a background population risk level. Consequently, after careful review of the initial CJD patient surgery event, the dates involved for all these patient’s surgeries, and the sterilisation of the surgical equipment, these four patients were considered to require only routine sterilisation measures for all their future surgery.

3. Hospital medical staff requested advice from the Incident Panel in relation to clarifying the risk group classification for a further two patients requiring surgery involving the central nervous system. One patient had reported a suspicion of a family history of CJD and a second raised the possibility of a growth hormone treatment when younger. The Incident Panel was able to clarify the CJD risk levels and advised on appropriate infection control measures.

Infection control developments for surgery

Pre-surgical assessment of patients according to either a high, low or background population risk for CJD has been relied on around the world, to assist hospitals and health care services manage CJD transmission risks, particularly for patient’s undergoing neuro-surgical procedures. Because the disease associated transmissible agent causing CJD is difficult to destroy by routine hospital sterilisation methods, additional management methods of patients with a higher or lower risk for CJD will need to continue. Consequently, the pre-surgical risk assessment will continue as an important basis for minimising the surgical transmission of CJD in hospitals.

During 2009, the Australian bio-pharmaceutical group Novapharm Research P/L released two new products that they claim are prionicidal agents. These new enzymatic cleaning products are released under the trade-names Asepti RAPIDZYME Pr and Asepti AUTOZYME Pr. They are designed to augment routine cleaning and sterilisation methods already used on surgical and endoscopic equipment in the health care setting. The Novapharm Research P/L Asepti solutions are claimed to be the first prionicidal cleaning products that can be easily incorporated into hospitals routine sterilisation procedures on surgical and endoscopic equipment. These products are intended to provide a greater level of reassurance for the management of routine sterilisation methods and for inadvertent surgical transmission events, when higher level infection control sterilisation methods are needed.

Authors:
ANCJDR/CJDIP


http://www.health.gov.au/internet/main/publishing.nsf/Content/ohp-phi-newsletter-20/$File/hph-20.pdf



Opinion

Bioethics Research Notes 9(2): June 1997

AUSTRALIAN SENATE INQUIRY INTO TREATMENT OF HORMONE RECIPIENTS HEARS NEGLIGENCE ALLEGATIONS

By Melinda Tankard Reist

"It was a shocking product, I can't believe this had ever been marketed" - Dr Wes Whitten, reproductive physiologist, former assistant director, National Biological Standards Laboratory (now known as the Therapeutic Goods Administration Authority).

"..it is my opinion that not one batch of fertility hormone met all the regulatory standards and many did not even meet CSL's own rudimentary standards." - Dr Frank Peters -former assistant and acting director, NBSL.

"It is the consumers who will pay the heaviest price...when the duty of care plays second fiddle to other imperatives...- Dr David Howes, former chief virologist and head of biologicals branch, NBSL
An Australian Senate Committee has heard evidence of breaches of proper procedure in the processing of pituitary hormones used in infertility and growth treatments and linked with the rare fatal brain disorder Creutzfeldt-Jacob Disease (CJD). It is alleged Australian Government bodies failed in their responsibility to ensure the highest standards in the regulation and manufacture of biological products.

The Senate Community Affairs References Committee was appointed to examine the Australian Federal Government's treatment of recipients of human pituitary hormones, whether the Government's response to the 1994 Allars inquiry into the pituitary hormone program was fair and adequate, whether documents related to the inquiry were withheld and why legal aid was denied to "APQ", a claimant in a land-mark test case for compensation.

The inquiry is also examining whether the Commonwealth Serum Laboratory (CSL) or CSL Ltd, the National Health and Medical Research Council, the Department of Health and Family Services or any other Commonwealth department, agency or employee failed to adequately protect public safety in relation to the Human Pituitary Hormone Program.

A Commonwealth Ombudsman investigation is also underway into the handling of the CJD matter by the Department of Health and the Australian Government Solicitor.

The test case seeking compensation for nervous shock involving 132 recipients of hormones manufactured by CSL, and distributed at the direction of the Department of Health from1967-1985, was settled in April on the eve of what was to be a 15-week jury trial. The case was hampered by denial of legal aid by the Commonwealth and
problems securing necessary documents. An out-of -court settlement involved no immediate money and no admission of liability on the part of the Commonwealth.

Australia was the only country providing a government sponsored program using human pituitary hormone (hPG). It was banned in the US. CSL collected, manufactured, and distributed the glands which were derived from dead bodies. A total of 171,091 pituitary glands were collected with removal carried out mainly by mortuary staff who were paid fifty cents for each gland collected. Relatives had not given their consent. Dr P Schiff of CSL's representative on the Human Pituitary Hormone Advisory Committee (HPAC), and responsible to the Minister for Health in overseeing the program, advised gland collectors that "unless the body is badly decomposed it is never too late to take the gland." In other words, decomposing body parts could be removed and processed for use in living humans.

There was enough information in 1966 to indicate that the program should not have been allowed to proceed. However it continued until May 1985 when two US recipients died of CJD, a form of bovine spongiform encephalopathy (BSE) or mad cow disease which causes spongy formations in the brain. It has so far killed four Australian women and one man - another woman is being assessed for CJD and believed to be dying.

The Senate Committee heard damning evidence against CSL.

CSL did not follow world's best practice in the pooling and homogenising of glands, had failed to comply with the Code of Good Manufacturing Practice and told pathologists to ignore the exclusion criteria about possible Hepatitis infected glands. CSL had also failed to utilise a simple technique to destroy the infectivity of enveloped viruses such as Hepatitis B in pituitary hormones. The Department had not taken steps to monitor the health of recipients during and after treatment to determine whether the virus had been transmitted, nor sought to find out if recipients suffered hepatitis or liver problems.

Less harmful techniques for ovarian stimulation such as the use of gonadotrophin from menopausal urine, a standardised product with lesser side effects including fewer multiple births and the preferred treatment in almost all other countries, were not used (even though CSL described hPG as a treatment of "last resort").

The Committee also heard that in addition to the 2000 hormone recipients on the official program, possibly another 500-600 unofficial recipients were treated with "leftover" product and in other experimental programs.

Disturbing evidence was given by reproductive physiologist, Dr Wes Whitten, that batches of pituitary hormones were 99.9 percent impure, i.e only one tenth of one percent pure.

The lack of informed consent is a constant issue in the thousands of pages of submissions and transcripts.

Hormone recipients believed the hormones were safe and "natural". They did not know they were guinea pigs in an unlawful, experimental program using hormones processed from the glands of cadavers. They did not know that hPG had not been evaluated for clinical use before the program started. They were not informed of a risk per treatment cycle of ovarian hyperstimulation of 30 percent. The first guidelines for selecting women for the program was that they should not be ovulating. However ovulating women were given hPG.

It has only come to light recently that some hormone batches were contaminated with Hepatitis B, others were unsterile, and there is the possibility of mother to child transmission of CJD.
Conflicts of interest were also alleged. Convenor of the CJD support group and a recipient, Sue Byrne told the hearing: "Four people who were intimately involved with the program are actually controlling the program. The regulation of product is being conducted by somebody who works for the organisation who is controlling the products and who invented the process. There were no checks and balances. There was no independent review. There was no scope of expertise. It was a very narrow, a very self-interested group, who were running the ... Program"

All overseas cases involving hormone recipients have settled in favour of the recipients. France has gaoled two doctors for manslaughter and a pathologist in charge of the program for poisoning. But in Australia, no-one has been prosecuted and no one has admitted fault. Ted Allender whose former wife Jane and mother of his two children died of CJD has written to prosecutors asking them to consider laying criminal charges against HPAC members. Hormone recipient Samantha Ogilvie told the committee: "It is not the money that matters. It is the fact that people should be accountable for what they did to us."

Geraldine Brodrick gave birth to nontuplets in 1971. The six babies born alive died within two days. She told the committee "All who conspired to force this terrible legacy on hPG and hGH [human growth hormone] recipients are now being protected by a government and its officers who would rather see innocent recipients denied justice than admit to the ineptitude and negligence of those involved in producing these treatments and administering this program."

Public confidence in experimental programs is at an all time low in the wake of recent revelations about questionable experiments on orphanage babies, the elderly, "tall girls" and other vulnerable groups. It is hoped the CJD inquiry will lead to a serious tightening of the rules governing human experimentation in Australia.

The Committee's report will be released in October.

© 1997 Southern Cross Bioethics Institute
Adelaide, South Australia



http://www.bioethics.org.au/Resources/Online%20Articles/Opinion%20Pieces/0902%20Australian%20Senate%20inquiry%20into%20treatment%20of%20hormone%20recipients%20hears%20negligence%20allegations.pdf




Creutzfeldt-Jakob Disease, CJD Support Group for short statured children of the 1970's and 1980's. Recommendations for Unapproved/Unregistered recipiants


http://mc2.vicnet.net.au/home/shortboys/web/cjdaustralia.html



http://mc2.vicnet.net.au/home/shortboys/web/index.html



http://creutzfeldt-jakob-disease.blogspot.com/2008/01/cjd-hgh-body-snatchers.html




Report of a WHO Consultation on Medicinal and other
Products in Relation to Human and Animal Transmissible
Spongiform Encephalopathies

With the participation of the Office International des Epizooties
(OIE)

Geneva, Switzerland
24-26 March 1997


http://www.who.int/biologicals/publications/en/BTSE97mar24.pdf




Early cognitive decline in Creutzfeldt-Jakob disease associated with human growth hormone treatment

R J Cordery, M Hall, L Cipolotti, S Al-Sarraj, D G O’Donovan, L Davidson, P Adlard, M N Rossor


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1757404/pdf/v074p01412.pdf




SHORT REPORT

Creutzfeldt-Jakob disease 38 years after diagnostic use of human growth hormone

E A Croes, G Roks, G H Jansen, P C G Nijssen, C M van Duijn ...............................................................

J Neurol Neurosurg Psychiatry 2002;72:792-793

A 47 year old man is described who developed pathology proven Creutzfeldt-Jakob disease (CJD) 38 years after receiving a low dose of human derived growth hormone (hGH) as part of a diagnostic procedure. The patient presented with a cerebellar syndrome, which is compatible with iatrogenic CJD. This is the longest incubation period described so far for iatrogenic CJD. Furthermore, this is the first report of CJD after diagnostic use of hGH. Since the patient was one of the first in the world to receive hGH, other cases of iatrogenic CJD can be expected in the coming years.

Prion diseases are potentially transmissible. Human to human transmission was first reported in 1974, when a 55 year old woman was described who developed symptoms of Creutzfeldt-Jakob disease (CJD) 18 months after a corneal transplant.1 Since then, transmission has been reported after stereotactic electroencephalographic (EEG) depth recording, human growth hormone (hGH) and gonadotrophin treatment, and dura mater transplantation.2-5 More than 267 patients with iatrogenic CJD are known today and their number is growing.6 The most important iatrogenic cause of CJD is still contaminated cadaveric hGH. Exposure to contaminated hGH occurred before 1985, when recombinant growth hormone became available. In a recent study, incubation periods in 139 patients with hGH associated CJD were found to range from 5-30 years, with a median of 12 years.6 One of the factors influencing incubation time is genotype on polymorphic codon 129 of the prion protein gene.7 The incubation time is significantly shorter in people who are homozygous for either methionine or valine on this polymorphism.7

We describe the second patient with hGH related CJD in the Netherlands. The patient developed the disease 38 years after hGH injections. To our knowledge, this is the longest incubation period described for any form of iatrogenic CJD. Further-more, our patient was not treated with hGH but only received a low dose as part of a diagnostic procedure.

CASE REPORT

This patient presented at the age of 47 years with paraesthesia in both arms for six months, difficulty with walking for four weeks, and involuntary movements of mainly the upper extremities of two weeks' duration. He did not notice any change in cognitive function, although his twin sister had noticed minor memory disturbances. There was no family history of neurological disease. During childhood the patient had experienced a growth delay compared with his twin sister and with the average in the Netherlands. When he was 9 years old, a nitrogen retention test with 6 IU hGH over five days was performed to exclude growth hormone deficiency. Since the result was not decisive, a quantitative amino acid test was performed, which measures 30 amino acids during fasting and one, two, and three hours after growth hormone injection. No abnormal amino acid concentrations were found making the diagnosis of primordial dwarfism most likely. Therefore, no treatment with hGH was given.

On neurological examination we found a slight dysarthria without aphasia. Cranial nerve function was normal. Walking was unstable and wide based. During movements of the upper extremities myoclonic jerks were present. Sensation, muscle tone, and strength were normal. Co-ordination was impaired in all four limbs with a disturbed balance. Tendon reflexes were brisk at the arms and increased at the legs with a clonus in the ankle reflex. Plantar responses were both normal. On the mini mental state examination, the patient scored 30/30. Routine laboratory investigation, thyroid function, vitamin concentrations (B-1, B-6, B-12, and E), and copper metabolism were normal. Admission EEG examination showed generalised arrhythmic slow activity with diffuse spikes and spike waves. EEG examination two months later showed a further slowing of the rhythm with bilateral diphasic sharp waves but was not typical for CJD. Cerebral magnetic resonance imaging was normal. Cerebrospinal fluid examination showed 1 cell/3 µl, normal glucose and protein concentrations, and a strongly positive 14-3-3 protein test. The patient was homozygous for methionine on the PRNP codon 129 polymorphism. On clinical grounds, CJD was diagnosed. Within one month the patient's condition deteriorated rapidly and because of severe disturbances in coordination and progressive myoclonus he became bedridden. An eye movement disorder developed with slow saccadic and dysmetric eye movements. Temperature became unstable with peaks of 39°C without an infectious focus, for which a disorder of autoregulation was presumed. Until a very advanced stage, cognitive function was intact. The patient died five months after admission. The diagnosis of CJD was confirmed at necropsy. The brain weighed 990 g and showed clear cortical and cerebellar atrophy. Spongiosis, neuronal loss, and gliosis were found predominantly in the putamen, caudate nucleus, and basotemporal and cerebellar cortex; the cerebellum was the most severely affected of these. Vacuoles ranged from 2-12 µm. No amyloid or Kuru plaques were found. Immunohistochemical staining (3F4 antibody 1:1000, Senetek, USA) was clearly positive for prion protein accumulation in a "synaptic" distribution. Most deposition was found in the stratum moleculare of the cerebellum.

DISCUSSION

We describe a 47 year old patient who developed pathology proven CJD 38 years after hGH injections. The patient was never treated with hGH but received a small dose as part of a diagnostic procedure. The onset of CJD was signalled by prodromal symptoms of paraesthesia followed by a rapidly progressive ataxia. The disease presentation and course with predominantly cerebellar and eye movement disorders are compatible with iatrogenic CJD caused by hGH treatment.6 8

Growth hormone treatment was first described in 1958 but hGH was not produced on a larger scale from human pituitary glands until the beginning of the 1960s. In the Netherlands growth hormone extraction started in 1963 and was soon centrally coordinated. Until 1979 growth hormone was extracted non-commercially from pituitaries by a pharmaceutical company. In 1971 commercial products also became available. Our patient was one of the first to receive hGH in the Netherlands but the origin of this product was not recorded. A causal relation can therefore not be established with full certainty, but coincidentally receiving growth hormone and developing this very rare disease is unlikely. Since the clinical course in this relatively young patient is in accordance with an iatrogenic cause, we think the probability is high that the hGH injections explain the development of CJD in this patient.

The first Dutch patient with hGH related CJD died in 1990. 9 During several periods from 1963 to 1969 she received intramuscular injections of hGH. During an unknown period the hGH was derived from South America. At age 39, 27 years after starting the treatment, she developed an ataxic gait, slurred speech, sensory disorders, and myoclonus, but her cognitive function remained normal. Postmortem examination of the brain confirmed the diagnosis of CJD.9 Following the identification of this patient, a retrospective study was started to trace all 564 registered hGH recipients who were treated before May 1985. Until January 1995, none of these was suspected of having CJD.10 Since 1993 prospective surveillance for all forms of human prion disease has been carried out in the Netherlands and, apart from the patient described above, a further two patients with iatrogenic CJD have been identified, who developed the disease after dura mater transplantation.11

An incubation period as long as 38 years had never been reported for iatrogenic CJD. Huillard d'Aignaux et al7 studied the incubation period in 55 patients with hGH related CJD in a cohort of 1361 French hGH recipients. The median incubation period was between 9 and 10 years. Under the most pessimistic model, the upper limit of the 95% confidence interval varied between 17 and 20 years. Although the infecting dose cannot be quantified, it can be speculated that the long incubation period in our patient is partly explained by the administration of a limited amount of hGH. This hypothesis is supported by experimental models, in which higher infecting doses usually produce shorter incubation periods.6 Since our patient was one of the first in the world to receive hGH, this case indicates that still more patients with iatrogenic CJD can be expected in the coming years. Another implication of our study is that CJD can develop even after a low dose of hGH. This case once more testifies that worldwide close monitoring of any form of iatrogenic CJD is mandatory.

ACKNOWLEDGEMENTS

We are grateful to M Jansen PhD MD for his search for the origin of the growth hormone and P P Taminiau MD. CJD surveillance in the Netherlands is carried out as part of the EU Concerted Action on the Epidemiology of CJD and the the EU Concerted Action on Neuropathology of CJD, both funded through the BIOMED II programme, and is supported by the Dutch Ministry of Health. This surveillance would not have been possible without the cooperation of all Dutch neurologists and geriatricians. ........................................

Authors' affiliations

E A Croes, G Roks*, C M van Duijn, Genetic Epidemiology Unit, Department of Epidemiology and Biostatistics, Erasmus University Medical Centre Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands

P C G Nijssen, Department of Neurology, St Elisabeth Hospital, PO Box 90151, 5000 LC Tilburg, Netherlands

G H Jansen, Department of Pathology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands

*Also the Department of Neurology, St Elisabeth Hospital

Correspondence to: Professor C M van Duijn, Genetic Epidemiology Unit, Department of Epidemiology and Biostatistics, Erasmus University Medical Centre Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands; vanduijn@epib.fgg.eur.nl

Received 27 December 2001 In revised form 1 March 2002 Accepted 12 March 2002

Competing interests: none declared

REFERENCES

1 Duffy P, Wolf J, Collins G, et al. Possible person-to-person transmission of Creutzfeldt-Jakob disease. N Engl J Med 1974;290:692-3.

2 Bernoulli C, Siegfried J, Baumgartner G, et al. Danger of accidental person-to-person transmission of Creutzfeldt-Jakob disease by surgery. Lancet 1977;i:478-9.

3 Koch TK, Berg BO, De Armond SJ, et al. Creutzfeldt-Jakob disease in a young adult with idiopathic hypopituitarism: possible relation to the administration of cadaveric human growth hormone. N Engl J Med 1985;313:731-3.

4 Cochius JI, Burns RJ, Blumbergs PC, et al. Creutzfeldt-Jakob disease in a recipient of human pituitary-derived gonadotrophin. Aust NZ J Med 1990;20:592-3.

5 Thadani V, Penar PL, Partington J, et al. Creutzfeldt-Jakob disease probably acquired from a cadaveric dura mater graft: case report. J Neurosurg 1988;69:766-9.

6 Brown P, Preece M, Brandel JP, et al. Iatrogenic Creutzfeldt-Jakob disease at the millennium. Neurology 2000;55:1075-81.

7 Huillard d'Aignaux J, Costagliola D, Maccario J, et al. Incubation period of Creutzfeldt-Jakob disease in human growth hormone recipients in France. Neurology 1999;53:1197-201.

8 Billette de Villemeur T, Deslys JP, Pradel A, et al. Creutzfeldt-Jakob disease from contaminated growth hormone extracts in France. Neurology 1996;47:690-5.

9 Roos RA, Wintzen AR, Will RG, et al. Een patiënt met de ziekte van Creutzfeldt-Jakob na behandeling met humaan groeihormoon. Ned Tijdschr Geneeskd 1996;140:1190-3.

10 Wientjens DP, Rikken B, Wit JM, et al. A nationwide cohort study on Creutzfeldt-Jakob disease among human growth hormone recipients. Neuroepidemiology 2000;19:201-5.

11 Croes EA, Jansen GH, Lemstra AF, et al. The first two patients with dura mater associated Creutzfeldt-Jakob disease in the Netherlands. J Neurol 2001;248:877-81.



http://jnnp.bmj.com/content/72/6/792.abstract




Acquittals in CJD Trial Divide French Scientists


by Barbara Casassus on January 14, 2009 4:10 PM


PARIS--Few criminal investigations go on so long that one of the accused dies of old age, and fewer draw upon the opinions of someone soon to win a Nobel Prize, but a court case in which both happened ended here today. Three French judges rejected charges of involuntary homicide and aggravated fraud against six doctors and pharmacists, which may end a stunningly prolonged investigation centering on the distribution of human growth hormone apparently contaminated with deadly prions.

The hormone had been isolated from cadavers, and much of the trial centered on whether appropriate purification standards were used, an issue that resulted in several prominent scientists being called to the witness stand. The Pasteur Institute, located here, which was involved in purifying the hormone, had already been fined by a civil court that held it responsible for the contamination, but whether someone had done anything criminal remained an open matter.

The defendants' acquittals today come more than 25 years after high-risk batches of the hormone were administered to 968 children in France and 18 years after the criminal investigation began. (Science's original stories from the early 1990s are available here and here.) So far, 117 of the youngsters have died from Creutzfeldt-Jakob disease (CJD), the human form of mad cow disease, and three more have recently shown symptoms.

For virologist Luc Montagnier, a witness in the trial and a winner of this year's Nobel Prize in physiology or medicine, the ruling arouses concern. "I fear we may have not learned any lessons from this case and will face other and bigger public health scandals in the absence of adequate scientific and medical caution over the effects of new treatments on young people and future generations," he says.

In 1980, Montagnier recommended a series of precautions to be taken in the gathering and processing of the pituitary gland but was ignored. He says that the authorities should have halted the use of cadaver-derived human growth hormone when the first case of CJD was linked to the substance and detected in the United States.

"This disaster could have been partly avoided," Montagnier told Science.

Montagnier said he was "surprised and saddened" by the court's failure to attribute responsibility, and is also critical of the fact that since the scandal, there has been little research into technology that could detect early signs of CJD.

But the French scientific community is split on whether today's ruling was just. "No one committed a real fault or negligence," says another witness, neurologist Yves Agid, who was formerly in charge of monitoring CJD cases in France and is scientific director at the Institute of Brain and Spinal Cord Disorders here. "At the time, no one could imagine that patients would contract CJD from human growth hormone."

The public prosecutor had demanded 4-year suspended sentences for the two main protagonists, pediatrician-endocrinologist Jean-Claude Job, who headed the defunct association in charge of collecting the hormone-containing pituitary glands from cadavers and who died after the trial ended, and Fernand Dray, who was in charge of purifying the material at the Pasteur Institute. Dray was also accused of corruption over purchases of human growth hormone from abroad, but the charges were dropped under the statute of limitations.

The criminal court case had proceeded despite a dismissive 2005 report from the French National Institute for Health and Medical Research (INSERM) that had concluded: "It is not reasonable to expect the players involved in the production of growth hormone to have guessed there was a possible risk of CJD from a treatment used since the 1960s" without a single incidence of disease. That report was prepared by an international group of experts including Stanley Prusiner, who won the Nobel Prize for his discovery of prions, and another prion expert, Paul Brown, formerly of the U.S. National Institutes of Health in Bethesda, Maryland.

In contrast to the INSERM report, in 2003 a French civil appeal court upheld an earlier court ruling that the Pasteur Institute was responsible for the 2001 death of 30-year-old Pascale Fachin from CJD contracted from contaminated human growth hormone administered in 1985 and imposed a fine of €322,000.

The prosecutor of the criminal case that just ended has 10 days to appeal the ruling. The families of victims have no right of appeal, but they hope to meet Justice Minister Rachida Dati to elicit her support, according to Bernard Fau, a victims' lawyer. The court did award civil damages to the families who hadn't already accepted an indemnity from the state.


http://news.sciencemag.org/scienceinsider/2009/01/acquittals-in-c.html



Friday, November 06, 2009

Surveillance of Creutzfeldt-Jakob disease in Australia: 2009 update

http://creutzfeldt-jakob-disease.blogspot.com/2009/11/surveillance-of-creutzfeldt-jakob.html




National Hormone and Pituitary Program: Information for People Treated with Pituitary Human Growth Hormone (Comprehensive Report)

http://endocrine.niddk.nih.gov/pubs/creutz/updatecomp.htm




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://www.bseinquiry.gov.uk/files/ws/s467bx.pdf



http://collections.europarchive.org/tna/20080102174454/http://www.bseinquiry.gov.uk/files/ws/s467bx.pdf




(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://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf


http://collections.europarchive.org/tna/20081105233552/http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf




PITUITARY EXTRACT

This was used to help cows super ovulate. This tissue was considered to be of GREATEST RISK OF CONTAINING BSE AND CONSEQUENTLY TRANSMITTING THE DISEASE.


http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf



3. The extraction is from a pool of pituitary glands collected from abbatoirs and the process used is unlikely to have any effect on the BSE agent. Hormones extracted from human pituitary glands have been responsible for a small number of Creutzfeldt Jacob disease in man.


http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf




SEE LOOPHOLE ;


http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/13008001.pdf




SEE LOOPHOLE SHOULD BE CLOSED ;


http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf



http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf




STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH OR DEVELOPMENT

[0002]Not Applicable

BACKGROUND OF THE INVENTION

[0003]The field of embryo transfer is growing in each animal sector in which multiple offspring are desirable. There were over 130,000 donor cattle superovulated worldwide in 2006 and the number of transferred embryos increased by 10% to over 670,000 (IETS Newsletter December 2007). In the United States, there were an estimated 52,000 donors superovulated in 2006 (AETA Annual Report 2006). The current superovulation protocols all require multiple injections of Follicle Stimulating Hormone (FSH) twice daily over the course of at least 4 days. The FSH currently used is animal derived, impure and has the propensity to be infectious. The invention described herein is a long-acting FSH analog that is effective in causing superovulation with a single injection. Furthermore, this FSH analog is highly purified and free of infectious vectors and other contaminants.

[0004]There are over nine million dairy cows in the United States, over one million in Canada and over fifty million worldwide. The dairy industry is extremely competitive and the ability of a dairy to increase the efficiency of breeding and to maintain pregnancies post insemination is critical to the profitability of the producer. It is estimated that the cost of a non-pregnant cow is about five dollars per day. It is further estimated that current inseminations result in approximately twenty to thirty-five percent pregnant cows at day 45 and of those cows ninety to ninety-five percent deliver calves at the end of the 283-day gestation period. However, reproductive efficiency in dairy cattle has been declining steadily over a prolonged period of time. The magnitude and the consistency of this trend are of great importance to the dairy industry and amount to a steady decline of approximately one percent in first service conception rates per year for the last ten years. The impact of this change in productivity has not been readily apparent, because individual cow milk production has increased by twenty percent over the same period. In the long run, the dairy industry cannot afford to continue the current rate of declining reproductive performance.

[0005]Declining reproductive efficiency of dairy cattle has been observed throughout the United States, and other parts of the world where milk production has been increasing (Lucy, M. C. (2001) "Reproductive loss in high-producing dairy cattle: Where will it end?," J. Dairy Sci., 84:1277-1293; Roche et al. (2000) "Reproductive management of postpartum cows," Anim. Reprod. Sci., 60-61:703-712; Royal et al. (2000) "Declining fertility in dairy cattle: changes in traditional and endocrine parameters of fertility," Anim. Sci., 70:487-502; and Macmillan et al. (1996) "The effects of lactation on the fertility of dairy cows" Aust. Vet. J, 73:141-147). Numerous features may negatively influence fertility in dairy cows, including negative energy balance and disease events such as retained placenta, ketosis, cystic ovary, and mastitis (Lucy 2001, supra; and Staples et al. (1990) "Relationship between ovarian activity and energy status during the early postpartum period of high producing dairy cows," J. Dairy Sci., 73:938-947). Furthermore, a prominent trend in the U.S. dairy industry is decreased number of dairy farms, steadily increasing herd size, and movement of dairy production to the western states (USDA National Agricultural Statistics Service, http//www.usda.gov/nass). Larger herd size may contribute to decreased reproductive performance because of the associated changes in the dairy labor force and cow management, resulting in poorly trained or over tasked workers identifying estrus behavior, performing artificial insemination, conducting estrus synchronization programs, and identifying and treating sick cows (Lucy 2001, supra). Heat stress, which occurs throughout much of the year in western and southwestern US dairy herds, has significant negative impact on cattle fertility (Wolfenson et al. (2000) "Impaired reproduction in heat-stressed cattle: basic and applied aspects," Anim. Reprod. Sci., 60-61:535-547).

[0006]The primary revenue source in the dairy industry is milk production. Progress in genetics and management of dairy cows has led to remarkable increases in milk production throughout the last several decades, with a twenty percent increase in per-cow production in the last ten years alone (USDA National Agricultural Statistics Service, http//www.usda.gov/nass). In order to maintain high herd productivity, however, cows must become pregnant and deliver a calf so that the lactation cycle is renewed. Additionally, sufficient numbers of heifers must be produced to replace older cows. Therefore, the future productivity of the dairy industry is very dependent on the maintenance of fertility and reproduction.

[0007]The ability to increase reproductive performance in horses, cattle or other ungulates would have a significant economic benefit to owners. This can be achieved through increasing fertility as well as improving pregnancy maintenance throughout the gestation period to prevent pregnancy losses. Recent studies with ultrasonic pregnancy detection demonstrate embryonic losses in cattle of at least 20% between 28 and 60 days of pregnancy (Pursley et al. (1998) "Effect of time of artificial insemination on pregnancy rates, calving rates, pregnancy loss, and gender ratio after synchronization of ovulation in lactating dairy cows," J. Dairy Sci., 81:2139-2144; and Vasconcelos et al. (1997) "Pregnancy rate, pregnancy loss, and response to heat stress after AI at 2 different times from ovulation in dairy cows" Biol. Reprod., 56 (Supp. 1):140). There are likely even higher losses prior to 28 days that are undetected by ultrasound examination (Lucy 2001, supra). Data suggest that modern dairy cows fail to establish pregnancy because of suboptimal uterine environment (Gustafsson, H. and K. Larsson (1985) "Embryonic mortality in heifers after artificial insemination and embryo transfer: differences between virgin and repeat breeder heifers," Res. Vet. Sci., 39:271-274). Although there are numerous possible factors that could be responsible for embryonic losses, one potential cause is low blood progesterone concentration.

[0008]Currently, several hormone therapies are used to increase fertility or to maintain pregnancy. Thatcher et al. (2001 Theriogenology 55:75-89) describes the effects of hormonal treatments on the reproductive performance of cattle. Hormonal treatments include administration of bovine somatotrophin (bST) and human chorionic gonadotropin (hCG). D'Occhio et al. (2000 Anim. Reprod. Sci. 60-61:433-442) describes various strategies for beef cattle management using gonadotropin releasing hormone (GnRH) agonist implants. De Rensis et al. (2002 Theriogenology 58(9):1675-1687) describes the effect on dairy cows of administering GnRH or hCG before artificial insemination. Martinez et al. (1999 Anim. Reprod. Sci. 57:23-33) describes the ability of porcine luteinizing hormone (LH) and GnRH to induce follicular wave emergence in beef heifers on Days 3, 6, and 9 of the estrus cycle, after ovulation (Day 0), without insemination. Santos et al. (2001 J. Animal Science 79:2881-2894) describes the effect on reproductive performance of intramuscular administration of 3,300 IU of hCG to high-producing dairy cows on Day 5 after artificial insemination. Lee et al. (1983 Am. J. Vet. Res. 44(11):2160-2163) describes the effect on dairy cows of administering GnRH at the time of artificial insemination. U.S. Pat. Nos. 5,792,785 (issued Aug. 11, 1998) and 6,403,631 (issued Jun. 11, 2002) describe methods and compositions for administering melatonin before and after insemination to enhance pregnancy success in an animal. Chagas e Silva et al. (2002 Theriogenology 58(1):51-59) describes plasma progesterone profiles following embryo transfer in dairy cattle. Weems et al. (1998 Prostaglandins and other Lipid Mediators) describes the effects of hormones on the secretion of progesterone by corpora lutea (CL) from non-pregnant and pregnant cows. U.S. Pat. No. 4,780,451 (issued Oct. 25, 1988) describes compositions and methods using LH and follicle stimulating hormone (FSH) to produce superovulation in cattle. Farin et al. (1988 Biol. Reprod. 38:413-421) describes the effect on ovine luteal weight of intravenous administration of 300 IU of hCG on Days 5 and 7.5 of the estrus cycle, without insemination. Hoyer and Niswender (1985 Can. J. Physiol. Pharmacol. 63(3):240-248) describe the regulation of steroidogenesis in ovine luteal cells. Juengel and Niswender (1999 J. Reprod. Fertil. Suppl. 54:193-205) describe the molecular regulation of luteal progesterone in domestic ruminants. U.S. Pat. No. 5,589,457 (issued Dec. 31, 1996) describes methods for synchronizing ovulation in cattle using GnRH, LH, and/or hCG and PGF2a.

[0009]Many of these treatments use hormones or hormone analogs from the glycoprotein hormone family, which consists of the pituitary proteins luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid stimulating hormone (TSH) and chorionic gonadotropin (CG). The gonadotropins, which include CG, FSH and LH, are essential for reproductive function. They are heterodimers composed of two non-covalently associated a and ß subunits. Both subunits are glycosylated, containing asparagine (N)-linked oligosaccharides and, in the case of the CGß subunit, O-linked carbohydrates are also present in a cluster of amino acids at the C-terminus. The individual human ß subunits are encoded by separate genes, and the LHß and CGß proteins are structurally and functionally similar; having more than 80% amino acid identity (Pierce J G, Parsons (1981) "Glycoprotein hormones: structure and function," Biochem. 50:465-495). Within a species, the a subunit amino acid sequence is common to all four hormones (Pierce J G, Parsons (1981) Biochem. 50:465-495).

[0010]In order to use gonadotropins to improve reproduction efficiency in animals, the availability of purified proteins is essential. Currently, the sources for gonadotropins are serum and whole pituitary extracts. To obtain sufficient quantities of these native hormones for such work is expensive and difficult. Pituitary extracts can be effective reproductive therapeutics but contain contaminants and may vary in their amounts of LH and FSH. Preparations of pure pituitary gonadotropins without cross-contamination are not readily available. Given the problem of animal-to-animal variation of native gonadotropins and the charge heterogeneity in the N-linked carbohydrates, the ability to generate the corresponding recombinant proteins will yield gonadotropins of a more homogeneous composition that can be standardized with respect to mass and bioactivity. Such proteins will be critical for calibrating clinical laboratory assays and for breeding management, such as shortening the time to ovulation in transitional and cycling mares for natural breeding and artificial insemination. The use of recombinant forms, as opposed to hormones extracted from serum and pituitary tissue, would avoid the co-contamination of pathogens and agents with a propensity to cause prion related diseases.

Read more: http://www.faqs.org/patents/app/20080312151#ixzz0mybW04wX



http://www.faqs.org/patents/app/20080312151





Review Risks of transmitting ruminant spongiform encephalopathies (prion diseases) by semen and embryo transfer techniques

References and further reading may be available for this article. To view references and further reading you must purchase this article.

A.E. Wrathalla, , , G.R. Holyoakb, I.M. Parsonsonc and H.A. Simmonsa

aAnimal Services Unit, Veterinary Laboratories Agency, Woodham Road, New Haw, Addlestone, Surrey KT15 3NB, United Kingdom

bOklahoma State University, Center for Veterinary Health Sciences, Stillwater, OK 74078, USA

c1 Coape St., Cheltenham, Victoria 3192, Australia

Received 18 March 2008; revised 12 May 2008; accepted 14 May 2008. Available online 30 June 2008.

Abstract Early experiments suggested that scrapie transmission via sheep embryos was a possibility, and gave rise to much controversy. However, when account is taken of the complex genetic effects on ovine susceptibility to scrapie, and of the several different scrapie strains with different clinical and pathological effects, the overall conclusion now is that transmission of classical scrapie by embryo transfer is very unlikely if appropriate precautions are taken. Recent embryo transfer studies have confirmed this. Other studies in sheep have shown that from about the middle of pregnancy the placental trophoblast is liable to scrapie infection in genetically susceptible ewes if the fetus is also susceptible. Since the contrary is also true, use of resistant ewes as embryo recipients could add to the safety of the embryo transfer, at least for classical scrapie. There has been little recent research on scrapie transmission via semen in sheep, and, with hindsight, the early studies, though negative, were inadequate. There is scant information on scrapie transfer via goat semen or embryos, although one study did find that bovine spongiform encephalopathy (BSE) was not transmitted via goat embryos. In cattle it has been shown that, if appropriate precautions are taken, the risks of transmitting BSE via semen and in vivo-derived embryos are negligible, and this conclusion has gained worldwide acceptance. Research on TSE transmission via reproductive technologies in deer has not yet been done, but information on the pathogenesis and epidemiology of chronic wasting disease (CWD) of deer, and on transmission risks in other species, provides optimism that transmission of CWD via semen and embryos of deer is unlikely. The presence of TSE infectivity in blood and various other tissues of infected animals, particularly sheep, gives rise to concerns that certain biological products currently used in reproductive technologies, e.g. pituitary gonadotrophins for superovulation, and certain tissue and blood products used in semen and embryo transfer media, could carry TSE infectivity. Instruments such as laparoscopes used for insemination, and for collection and transfer of embryos, especially in small ruminants, are also a concern because effective decontamination can be very difficult.

Keywords: Semen; Embryos; Placenta; Ruminants; Spongiform encephalopathies; Prion diseases; Import–export



http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCM-4SW858P-1&_user=4973225&_coverDate=09%2F15%2F2008&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=4973225&md5=4dffa4e6fea4d0a4465c84acb2f69772




Wednesday, February 3, 2010

Import Alert 62-07 Sygen Injectable (Bovine-Extracted GMI Monosialoganglioside) manufactured from bovine brain starting material


http://bseusa.blogspot.com/2010/02/import-alert-62-07-sygen-injectable.html






start page 13 of 48 ;



----- Original Message -----

From: Terry S. Singeltary Sr.

To: FREAS@CBER.FDA.GOV

Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov

Sent: Wednesday, November 29, 2006 1:24 PM

Subject: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION]


November 29, 2006

Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,

a kind and warm Holiday Greetings to you all.

i kindly wish to submit the following to the TSE advisory committee for the meeting December 15, 2006, about the assessment for potential exposure to vCJD in human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related communication material ;


http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm



i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;


http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines




however, i seem to disagree. from my primitive ciphering, i see it another way. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million. also, what about the mixed genotypes/mixed susceptibility? what about the silent carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN strain or phenotype? this risk assessment is just more BSe to me. Just another in a long line of industry fed crap. i pray that my assessment is the one that is wrong. but it is THEY who roll the dice with your life. It is THEY who refuse to regulate an industry that has run amok. just from a recall aspect of potentially tainted blood, and these are just recent recalls ;



snip...




MEDICAL IMPLANTS CONTAINING BOVINE MATERIAL SEAC considered the risk to human health from medical implants that include bovine material sourced from the USA. This material was used for a wide range of medical devices, some of which are life saving and for which there are no alternative products. SEAC considered that the source of the animal was crucial to manage the risk. The committee suggested that other precautionary steps be taken where practicable, such as using material from young animals, sourcing material from countries with good surveillance procedures and a low prevalence of disease. ......

snip...


http://www.seac.gov.uk/minutes/final90.pdf




A BIT OF HISTORY ON THIS TOPIC

TWA LITTLE minute


http://www.bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf



COMMERCIAL IN CONFIDENCE


http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf



NOT FOR PUBLICATION


http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf


http://www.bseinquiry.gov.uk/yb/1988/11/04003001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf




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://www.bseinquiry.gov.uk/files/ws/s467bx.pdf



more on the 1968 medicine act, they forgot to follow


http://www.bseinquiry.gov.uk/files/yb/1989/01/30008001.pdf


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).


http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf


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

http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf


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

http://www.bseinquiry.gov.uk/files/yb/1989/02/22008001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/02/22011001.pdf



(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://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/07010001.pdf



TWA LITTLE STATEMENT 331


http://www.bseinquiry.gov.uk/files/ws/s331.pdf



WE know about USA serum and tissue donor herds from the now infamous Jan. 9, 2001 FDA emergency 50 state BSE conference call, that in fact, USA serum and tissue donor herds were eating banned ruminant feed as well ;

Date: Sun, 7 Jan 2001 09:45:19 -0800

Reply-To: Sustainable Agriculture Network Discussion Group

Sender: Sustainable Agriculture Network Discussion Group

From: Beth von Gunten

Subject: [BSE] FDA/IMPORTANT NOTICE: 50 STATE CONFERENCE CALL


IMPORTANT NOTICE: 50 STATE CONFERENCE CALL - BSE

TUESDAY, JANUARY 9, 2001 1:00-2:00 PM EST CALL: 1-888-273-9887

A special "50 STATE CONFERENCE CALL" to discuss BSE (Bovine Spongiform Encephalopathy) issues for Food and Drug Administration (FDA) regulated animal feed products in the United States and imported animal feeds. The conference call will discuss the FDA proposed response to the current BSE issue and the assistance needed from state feed and agriculture programs. THIS ISSUE MAY IMPACT ALL STATES AND ALL ANIMAL FEED AND PRODUCTION INDUSTRIES.

The 50 State call is scheduled for Tuesday, January 9, 2001 from 1:00-2:00 pm EST. Any state agency responsible for animal feed issues wishing to participate should call 1-888-273-9887 and ask to be connected to the "50 State BSE Call". The conference host operator will explain how to participate, including asking questions during the call. If possible, please coordinate within your state to utilize only one phone line per state agency.

We request that you forward this message to your agency management and feed coordinators or other agencies or departments who may be responsible for any animal feed issues related to FDA regulated products.

The agenda will be as follows:

1. Center For Veterinary Medicine (FDA) - Discussion of the problem related to BSE events in Europe and the impact on US feed ingredients for animals and feed operations. Discussion of the proposed actions/inspections/compliance of licensed and unlicensed feed mills, commercial feed manufacturers, animal feed imports, renderer's, protein blenders, on-farm mixers, and ruminant feeders.

2. Office of Regional Operations (FDA) - Discussion of contracting/working with states to inspect the universe of feed mills/industry for "Animal Proteins Prohibited from Use in Animal Feed". Discussion of working with FDA field offices.

3. Questions and answers.

Richard H. Barnes, Director Division of Federal-State Relations (HFC-150) 5600 Fishers Lane Room 1207 Rockville, Md. 20857 ph: (301) 827-6906 FAX: (301) 443-2143


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0101&L=sanet-mg&P=13410





Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001

Date: Tue, 9 Jan 2001 16:49:00 -0800

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de


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


Greetings List Members,


I was lucky enough to sit in on this BSE conference call today and even managed to ask a question. that is when the trouble started. I submitted a version of my notes to Sandra Blakeslee of the New York Times, whom seemed very upset, and rightly so. "They tell me it is a closed meeting and they will release whatever information they deem fit. Rather infuriating."

and i would have been doing just fine, until i asked my question. i was surprised my time to ask a question so quick. (understand, these are taken from my notes for now. the spelling of names and such could be off.) [host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch. [TSS]

yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds? [no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.] [host Richard] could you repeat the question? [TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds? [not sure whom ask this] what group are you with? [TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide. [not sure who is speaking] could you please disconnect Mr. Singeltary [TSS] you are not going to answer my question? [not sure whom speaking] NO from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again; [unknown woman] what group are you with? [TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now? at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference. IF i were another Country, I would take heed to my notes, BUT PLEASE do not depend on them. ask for transcript from; RBARNS@ORA.FDA.GOV 301-827-6906 he would be glad to give you one ;-)

Rockville Maryland, Richard Barns Host


snip...see full text ;




http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8




Friday, April 23, 2010

Upcoming BSE Webinar on Thursday, April 22, 2010 a review


http://bseusa.blogspot.com/2010/04/upcoming-bse-webinar-on-thursday-april.html




Wednesday, April 28, 2010

BSE, Scrapie, CWD, REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 8-12 February 2010

REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL


http://usdameatexport.blogspot.com/2010/04/bse-scrapie-cwd-report-of-meeting-of.html




TSS