Could we face the return of CJD? Experts fear it may lie dormant in thousands
Could we face the return of CJD? Experts fear it may lie dormant in thousands
By Lois Rogers
Last updated at 8:09 AM on 1st November 2011
Holly Mills, aged 15 - three years before she developed the full-blown symptoms of CJD Holly Mills was a lively teenager about to start university. But with her whole life ahead of her, she suddenly found herself in the grip of tragedy.
Within the space of just a few months, the gregarious 18-year-old had become so severely brain damaged that she was unable to move or communicate.
Eight years on, Holly has to be fed through a tube into her stomach and shows no emotion or awareness of her tragic predicament. Her days are spent in heartbreaking, silent immobility.
Holly is one of only three people still alive after developing the full-blown symptoms of Creutzfeldt–Jakob disease (also known as new variant CJD, or vCJD) — the human form of mad cow disease.
Holly’s parents Peter and Linda, both 61, are devoting themselves to their daughter’s full-time care and to a programme of daily mental stimulation, in the belief they are keeping her brain alive until a treatment emerges that will help her.
While they and their three older children live in hope of a cure for Holly, there is growing concern that another CJD outbreak may be imminent.
New evidence collected by the Health Protection Agency (HPA) suggests that one in 4,000 people who were eating meat before 1996 is probably carrying CJD (after that date, cattle infected with mad cow disease were, theoretically, removed from the food chain).
That could mean that as many as 15,000 people nationwide could be affected. While this is in line with a previous survey, the latest findings suggest CJD might be more prevalent in older people.
The findings — which received little publicity when published a few weeks ago — are mid-way results of a programme testing 30,000 samples of tonsil and appendix tissue removed during routine operations across the country.
The aim was to look for evidence of ‘silent’ or symptom-free infection, though scientists admit the method used in the tests cannot identify CJD with total accuracy.
Until recently, a definite diagnosis of the disease in people who have the symptoms could be made only after death, because brain tissue analysis was required.
Holly with her mother Linda, who is devoting herself to her daughter's full-time care and to a programme of daily mental stimulation However, John Collinge, a professor of neurology and a leading expert at the Government’s CJD research unit at University College, London, has developed a blood test which can check if the disease is present by detecting evidence of the so-called prions or infectious proteins known to cause the disease.
He believes the number of people infected could be as high as one in 1,000 and says the CJD situation is ‘very worrying indeed’.
So far, there’s little official interest in investing the several million pounds needed to turn the blood test into the high-speed screening tool needed to bring it into routine use. Critics say this is because the Government fears what it might find.
Mad cow disease, or bovine spongiform encephalopathy (BSE), first emerged in Britain in 1986 as a result of ‘cannibalism’, when beef offal was fed to cattle, which are natural grass-eaters.
The proteins, called prions, that cause BSE were found in large quantities in the brains, spinal cords and spleens of cattle (although they were also subsequently discovered in meat tissue, too). When animal carcasses were ground down to form feed stuff for other cattle, prions were passed on.
They then colonised the brains of the cattle which ate them, and were passed to humans via cheap, mechanically-recovered meat — such as processed sinews and offal that were used at the time in school dinners and baby food.
In humans, the prions triggered the development of a new form of fatal human dementia called new variant CJD, which was first identified in 1996. These prions are entirely new infectious agents, completely different from viruses, bacteria or parasites.
Basically, they are faulty versions of healthy proteins in brain and nervous tissue that then induce their neighbours to become faulty. As a result, the brain cannot function: all signals are disrupted or shut down completely, leading to almost certain death.
Holly was a lively teenager about to start university, but now her days are spent in heartbreaking, silent immobility A ban on using animal remains in livestock feed was imposed in 1989, and 4.4 million cattle were slaughtered to eliminate the disease. At the same time, a ban was imposed on the use of mechanically-recovered meat in products for human consumption.
By the mid-Nineties, when CJD fears were at their height, up to 3.5 million people were believed to possibly be affected. The risk appeared to be greater in younger people, although the reason isn’t clear.
But as new cases failed to materialise (according to official statistics, 168 people have died from CJD in the UK), the view of the Government and medical establishment was that the danger had passed.
However, the new data from the Health Protection Agency suggests the rate of infection is much higher than currently thought.
‘We do not know how many infected people there are or how many of them will develop it,’ Professor Collinge says.
‘The incubation period, where there are no symptoms, can last for decades.’
But it is not only the threat of a widescale re-emergence of the infection that worries experts. There is also the possibility of a new generation being exposed to the disease, as a result of a European Union decision to change the rules on animal feed.
Although CJD emerged from beef, experts say there is evidence of related diseases affecting other meat-producing animals if they are forced into cannibalismContrary to popular belief, BSE has not been wiped out. In fact, 11 cattle were diagnosed with it in Britain last year, although none entered the food chain.
Most young cattle slaughtered for meat are not believed to have developed sufficient infectivity to pose a risk to humans. Any animal more than 30 months old destined for the food chain is checked for BSE after it has been slaughtered.
The new concern is not cattle, however, but pigs and chicken. Earlier this summer, the European Commission announced it was relaxing the ban on using animal remains in livestock feed.
From next year, chicken meat will be used in pig feed and vice versa, to cut costs for farmers who otherwise have to rely on expensive imported soya beans for growth-promoting protein-based animal foods.
Although CJD emerged from beef, experts say there is evidence of related diseases affecting other meat-producing animals if they are forced into cannibalism.
Now a group of CJD-affected families, led by former Labour health secretary Frank Dobson, is to challenge the Government to hasten the development of the new blood test to give people the chance to check if they are infected.
The proposal has been given added urgency by the latest findings about CJD-infected tonsil and appendix tissue, but the Government has been dragging its feet, says Mr Dobson.
‘The projections I was given when I was health secretary in 1998 were that the total number of CJD cases could be anything between a few hundred and 3.5 million people,’ he said.
‘Until now, the only certain way of diagnosing CJD in people who have not yet developed symptoms is to analyse tissue after death.
'Trials show John Collinge’s blood test works, but it needs investment to turn it into a proper screening tool that can quickly deal with a high volume of blood samples.
‘You would have thought the Government would want it to test blood supplies and get an accurate picture of how many people are infected. I can’t understand why they’re not getting on with this.’ Anxiety about CJD transcends party boundaries, with Tory MP Sir Paul Beresford joining Mr Dobson’s cause. The reason Holly and the other two surviving CJD victims are alive is probably because their families fought court battles to be allowed to give them pentosan polysulphate‘We need to find out the extent of the problem and what we need to do about it,’ he said.
‘Otherwise we will potentially see a flood of cases in our grandchildren.’
The parents of Holly, from Thornton Dale in North Yorks, are among those backing the campaign. ‘It’s too big an issue to ignore,’ said Peter Mills. ‘The evidence suggests there will be a second bout of this infection and we need the measures in place to test blood. There is clearly a risk from infected people who have no symptoms. Even if they don’t develop the disease, they can pass it on.’
Normal sterilising techniques do not remove the abnormal proteins which cause CJD from surgical or dental instruments because they survive high temperatures.
There have been at least six transmissions from hospital operations and four cases of CJD infections passed from three different blood donors. All those infected in these ways have died.
In the meantime, Peter and Linda are fully engaged in caring for their sick daughter. When she was diagnosed with the disease aged 18, she was within weeks of leaving home to study midwifery. In fact, her symptoms had been emerging over the previous two years.
At first the family put her fatigue and anxiety down to teenage depression. She had fainting fits two or three times at school when she was 16, but her GP assumed she would grow out of them.
But when Holly began losing weight and having difficulty walking, her parents realised something was wrong.
Her condition quickly worsened, but the CJD diagnosis — based on ruling out everything else — was a dreadful shock.
‘We were devastated,’ says Peter. ‘We think she caught it from the mechanically-recovered meat they used to put in baby food.
'Once Holly became ill, it all happened very fast. Within a few weeks of the diagnosis she couldn’t walk or talk. We treat it like a head injury.
‘We want to stimulate her as much as possible. We talk to her all the time and, although she doesn’t respond, we are convinced she still has some functions.’
Every morning, a system of hoists and pulleys allows Linda to transport Holly from bed to a specially-built bath tub. Once she is washed and dressed, the three embark on an outing into the countryside. Come rain or shine, Holly’s parents guide her wheelchair along the cliff-top paths in the nearby seaside resort of Scarborough, or through the elegant surroundings of one of the local National Trust mansions.
The reason Holly and the other two surviving CJD victims are alive is probably because their families fought court battles to be allowed to give them pentosan polysulphate, an experimental drug currently unlicenced in the UK, injected into the brain which seems to prevent the final stages of the disease.
What lies ahead for Holly and the thousands of other CJD carriers remains to be seen. Campaigning with Frank Dobson, Sir Paul Beresford and the Mills family is Christine Lord, from Southsea, Hampshire, whose son Andy, a radio sports commentator, died aged 24 from CJD three years ago.
Other experts believe up to 60,000 could be affected ‘In one of the last conversations we had, Andy asked me to find out how he got ill and I promised I would,’ says Christine, a BBC journalist who is writing a book about what she believes has been a political cover-up of the extent of the CJD risk. ‘I want to know where this came from. I stopped him eating beef from the age of six because of BSE, but he still got the disease.’
She is organising a protest next month to demand access to the blood test. ‘I think the Government doesn’t want the test out there because of people finding out how prevalent CJD is,’ she says.
A spokesman for the NHS Blood Service said it was in talks with Professor Collinge about using his test to screen the 7,000 blood donations collected daily across the country, but could not say when the work would be done to develop a tool capable of bulk screening.
‘We are spending £40?million a year on a process to remove white blood cells and £200?million a year on synthetic blood-clotting factors to minimise the risk of CJD transmission via blood,’ she told the Mail.
Professor Collinge says blood will certainly already have been donated by infected donors. ‘I think the possibility of a lethal infection in one in 4,000 blood donors is very worrying. People wouldn’t accept that level of risk if it was HIV.’
The Government’s experts have extrapolated the Health Protection Agency’s data and suggested at least 15,000 people are carrying CJD, though they agree the exact figure is unknown and other experts believe up to 60,000 could be affected.
Meanwhile, Azra Ghani, professor of infectious disease epidemiology at London’s Imperial College, says the potential harm from symptom-free CJD carriers is impossible to predict.
‘It’s a waiting game with any new infection. We just don’t know if these people will be infectious or not.’
http://www.dailymail.co.uk/health/article-2055904/Could-face-return-CJD-Experts-fear-lie-dormant-thousands.html
Cow aged over 72 months enters food supply without being tested for BSE Wednesday 26 October 2011
The Agency has been notified that meat has entered the food supply from a cow aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 72 months of age.
It is very unlikely that the cow was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The cow, aged 74 months and 11 days, was slaughtered at Anglo Dutch Meats (Charing) Ltd’s abattoir in Kent, on 11 August 2011. The error was discovered on 6 October in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested cow, plus the one slaughtered before and the two after should not have entered the food supply. However, by the time the failure was discovered, the associated carcases had left the premises.
Subsequent checks indicate that the meat from the carcases was mixed with a large volume of other meat which is no longer in the food supply and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/oct/anglodutch
Cow aged over 48 months enters food supply without being tested for BSE
Tuesday 23 February 2010
The Agency has been notified that meat from a cow aged over 48 months has entered the food supply without being tested for BSE.
It is very unlikely that the cow was infected with BSE and, as specified risk material (SRM) was removed, any risk to human health is extremely low. However, testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.
The cow was slaughtered at Pickstock Ashby Ltd's abattoir in Hartshorne, Derbyshire, on 4 November 2009 aged almost 57 months. The failure was discovered on 28 January during routine cross checks of slaughter and BSE test data. By the time the failure was discovered all of the affected carcasses and offal had left the premises.
The affected carcasses, some edible co-products and offal had been exported. Some meat returned to Britain after processing and some went to other countries. Other edible co-products remained in Britain. Subsequent checks indicate that all of the meat and edible co-product that remained in Britain or that returned to Britain is no longer in the food supply chain. The authorities in the countries that received the exported material have been informed.
Background to BSE testing The BSE testing age was raised to 48 months at the beginning of last year. Cattle aged over 48 months are allowed to enter the food supply provided they have tested negative for BSE. If there is no BSE test, all parts of the carcase must be condemned.
Specified risk material (SRM) is those parts of the animal that contain almost all BSE infectivity, if the animal is infected with BSE.
http://www.food.gov.uk/news/newsarchive/2010/feb/over48monthcow
Cow aged over 48 months enters food supply without being tested for BSE
Tuesday 14 September 2010
The Agency has been notified that meat has entered the food supply from a cow aged over 48 months that had not been tested for BSE.
It is very unlikely that the cow was infected with BSE and, as specified risk material was removed, any risk to human health is extremely low. Nevertheless, a negative BSE test result is mandatory for cattle over 48 months of age slaughtered for human consumption.
The cow was aged one day over 48 months when slaughtered on 9 July at G & GB Hewitt Ltd abattoir in Chester. The error was discovered on 24 August in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested cow, the animal slaughtered before and the two slaughtered after must not enter the food supply. However, by the time the failure was discovered, all of the associated carcasses had left the premises.
Subsequent checks traced one small batch of meat that has since been destroyed and indicate that the rest of the meat from the carcasses is no longer in the food supply chain.
http://www.food.gov.uk/news/newsarchive/2010/sep/otmuntested
Cow aged over 48 months enters food supply without being tested for BSE Monday 2 November 2009
The Agency has been notified that a 58 months old cow has entered the food supply without being tested for BSE. BSE testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.
However, as all the specified risk material (SRM) was removed, and it is unlikely that the cow was infected with BSE, any risk to human health is very low. SRM is those parts of the animal that contain almost all BSE infectivity.
The cow was slaughtered on 28 July 2009 at Dunbia abattoir in Dungannon. The error was discovered by Northern Ireland's Department of Agriculture and Rural Development (DARD) when a routine annual herd TB test revealed that the cow had been misidentified.
DARD has now established the correct identity and age of the cow slaughtered on 28 July. Checks indicate that all the meat and other products from the untested cow are likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2009/nov/over48
Monday, May 12, 2008
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
http://bseinquiry.blogspot.com/2008/05/bse-cjd-and-baby-foods-great-debate.html
NORTH AMERICA USA
PLEASE be aware, for 4 years, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens.
who will watch our children for CJD for the next 5+ decades ???
WAS your child exposed to mad cow disease via the NSLP ???
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
http://downercattle.blogspot.com/2009/05/who-will-watch-children.html
http://downercattle.blogspot.com/
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???
you can check and see here ;
http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
MAD COW DISEASE, TEXAS STYLE
http://www.organicconsumers.org/articles/article_23850.cfm
with an incubation period of up to 50 years or more, we will all just have to wait and see...
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
2006
USA sporadic CJD cases rising ;
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
2008
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
CJD USA RISING, with UNKNOWN PHENOTYPE ;
5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases;
*** 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
Published Date: 2010-04-05 17:00:02
Subject: PRO/AH/EDR> Prion disease update 1010 (04) Archive Number: 20100405.1091
PRION DISEASE UPDATE 2010 (04)
Communicated by: Terry S Singeltary Sr
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed. The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/direct.php?id=20100405.1091
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
(see video here) ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
(see video here)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?
(see video at bottom)
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
Sunday, September 6, 2009
MAD COW USA 1997
(SEE SECRET VIDEO)
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
2010-2011
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Published Date: 2011-06-07 11:47:33
Subject: PRO/AH/EDR> Prion disease update 2011 (06) Archive Number: 20110607.1736
PRION DISEASE UPDATE 2011 (06) ******************************
A ProMED-mail post http://www.promedmail.org
The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
Commentary ---------- Following to a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) and the European Centre for Disease Prevention and Control (ECDC) were asked to deliver a scientific opinion on any possible epidemiological or molecular association between transmissible spongiform encephalopathies (TSEs) in animals and humans. The opinion reviews and discusses the existing scientific evidence that links animal and human TSEs currently known.
The opinion first considers the definition of zoonoses and the principles for the identification of zoonotic diseases, which can be based on evidence gathered from both epidemiological and laboratory studies. The opinion describes the challenges involved in identifying TSEs as zoonoses, due to the specific characteristics of TSE infections/diseases, such as the nature of TSE agents, the occurrence of animal and human TSEs, and the type of monitoring applied, the long incubation period of TSEs etc. The example of the process that led to establishing a link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) is reviewed. The epidemiological and laboratory criteria that can be used to investigate such a link are described in detail, since those criteria might be useful for the identification of links between other animal and human TSEs.
The opinion discusses the strain diversity of the TSE agents described in sheep, goats, cattle, cervids, and humans, based on the current knowledge, which highlights that multiple TSE agents exist in each species. The factors influencing the capacity of TSE agents to cross the species transmission barrier are then considered in detail, including the variability in host and donor PrP gene and protein, the TSE strain type involved and its interaction with the host PrP, and the route of infection.
The opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association between animal and human TSEs. The use of epidemiology is discussed for TSEs in both animals and humans, and the possibility to compare the 2 sources of information is presented as a possible method to study the possible links.
Both in vivo and in vitro laboratory methods are considered and discussed, including neuropathology, transmission experiments involving different animal models (wild type and transgenic mice, primates and other species), biochemical methods, cell-free conversion assays, protein misfolding cyclic amplification (PMCA), and cell culture assays. Characteristics, advantages, and disadvantages of the different methods are reviewed, including the opportunity to collate data from different types of experiments for the study of potential associations between animal and human TSEs.
The opinion then reviews the scientific evidence currently available for the different animal and human TSEs, including classical BSE, atypical BSE (H-type and L-type), classical scrapie, atypical scrapie, chronic wasting disease (CWD), transmissible mink encephalopathy (TME), and human TSEs. In particular, the following aspects are systematically discussed for each TSE agent: epidemiology, pathogenesis, and in vivo and in vitro transmission experiments.
The opinion concludes that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. With regard to human TSEs, detected cases of sporadic CJD are randomly distributed in time and geographical location. These observations have been interpreted as a supportive argument that sporadic CJD is not environmentally acquired. However, the epidemiological evidence in relation to sporadic CJD cannot be regarded as definitive, and the possibility that a small proportion of cases are zoonotic cannot be excluded.
It also concludes that a series of uncertainties in relation to the epidemiological patterns of animal and human TSEs indicate that even a rough comparison of the present epidemiological patterns of human and animal TSEs other than classical BSE is unlikely to be informative. Because of these uncertainties, it is an imperative to continue to carry out systematic surveillance of human TSE diseases, and to continue and improve the surveillance of animal TSE diseases.
The opinion highlights that the active screening has allowed the identification of 3 new forms of animal TSEs (L-type atypical BSE, H-type atypical BSE, and atypical scrapie), but that the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs.
There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential.
Transmission experiments to human PrP transgenic mice suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE and classical BSE in sheep agents) might have zoonotic potential, whereas for other agents there is no evidence provided of a zoonotic potential (H-type atypical BSE and CWD), or no published studies are available (classical and atypical scrapie). In addition, transmission experiments to primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential. In particular, primates are highly permissive to L-type atypical BSE, even by the oral route.
The opinion emphasizes that laboratory transmission experiments indicate that the L-type atypical BSE agent has a significant zoonotic potential, which appears similar or even higher than that of the classical BSE agent. While transmission data for evaluating the zoonotic potential of classical scrapie in primates and human PrP transgenic mice are extremely limited or not yet available, a single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
The opinion concludes that human PrP transgenic mice and primates are currently the most relevant models for investigating the human transmission barrier, but the extent to which such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. It is unpredictable whether a TSE agent will transmit to a new host, and if the transmission principally occurs, what the transmission rate will be.
Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.
-- Communicated by: Terry S Singeltary Sr
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.
It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
******
http://www.promedmail.org/direct.php?id=20110607.1736
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1
http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html
another question, just how long have these atypical BSE TSEs been around in the bovine ???
Subject: atypical BSE reported in 1992 and conviently slaughterd and incinerated and then swept under rug for about 12 years
Date: April 26, 2007 at 1:08 pm PST 1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN THE HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS NOT BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. .......
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf
2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.
3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/29005001.pdf
IN CONFIDENCE
This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/26002001.pdf
COLLINGE THREATENS TO GO TO MEDIA
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS
"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP"
2009 SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
USA MAD COW FEED IN COMMERCE
FDA TRIPLE FIREWALL MAD COW FEED BAN WAS NOTHING MORE THAN INK ON PAPER
10 YEARS (one decade) POST USA FDA MAD COW FEED BAN OF AUGUST 4, 1997, USA STILL FEEDING COWS TO COWS
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR; Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/direct.php?id=20101206.4364
SEE TONNAGE OF MAD COW FEED IN COMMERCE IN 2007 ALONE, A DECADE POST PARTIAL AND VOLUNTARY MAD COW FEED BAN ;
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
Mad Cow Scaremongers
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011
re-2003
"he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease."
http://www.seac.gov.uk/pdf/hol-response091008.pdf
http://bse-atypical.blogspot.com/2009/10/seac-science-and-technology-committees.html
SNIP...SEE FULL TEXT ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html
Tuesday, October 4, 2011
De novo induction of amyloid-ß deposition in vivo
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
http://betaamyloidcjd.blogspot.com/2011/10/de-novo-induction-of-amyloid-deposition.html
layperson
TSS
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
By Lois Rogers
Last updated at 8:09 AM on 1st November 2011
Holly Mills, aged 15 - three years before she developed the full-blown symptoms of CJD Holly Mills was a lively teenager about to start university. But with her whole life ahead of her, she suddenly found herself in the grip of tragedy.
Within the space of just a few months, the gregarious 18-year-old had become so severely brain damaged that she was unable to move or communicate.
Eight years on, Holly has to be fed through a tube into her stomach and shows no emotion or awareness of her tragic predicament. Her days are spent in heartbreaking, silent immobility.
Holly is one of only three people still alive after developing the full-blown symptoms of Creutzfeldt–Jakob disease (also known as new variant CJD, or vCJD) — the human form of mad cow disease.
Holly’s parents Peter and Linda, both 61, are devoting themselves to their daughter’s full-time care and to a programme of daily mental stimulation, in the belief they are keeping her brain alive until a treatment emerges that will help her.
While they and their three older children live in hope of a cure for Holly, there is growing concern that another CJD outbreak may be imminent.
New evidence collected by the Health Protection Agency (HPA) suggests that one in 4,000 people who were eating meat before 1996 is probably carrying CJD (after that date, cattle infected with mad cow disease were, theoretically, removed from the food chain).
That could mean that as many as 15,000 people nationwide could be affected. While this is in line with a previous survey, the latest findings suggest CJD might be more prevalent in older people.
The findings — which received little publicity when published a few weeks ago — are mid-way results of a programme testing 30,000 samples of tonsil and appendix tissue removed during routine operations across the country.
The aim was to look for evidence of ‘silent’ or symptom-free infection, though scientists admit the method used in the tests cannot identify CJD with total accuracy.
Until recently, a definite diagnosis of the disease in people who have the symptoms could be made only after death, because brain tissue analysis was required.
Holly with her mother Linda, who is devoting herself to her daughter's full-time care and to a programme of daily mental stimulation However, John Collinge, a professor of neurology and a leading expert at the Government’s CJD research unit at University College, London, has developed a blood test which can check if the disease is present by detecting evidence of the so-called prions or infectious proteins known to cause the disease.
He believes the number of people infected could be as high as one in 1,000 and says the CJD situation is ‘very worrying indeed’.
So far, there’s little official interest in investing the several million pounds needed to turn the blood test into the high-speed screening tool needed to bring it into routine use. Critics say this is because the Government fears what it might find.
Mad cow disease, or bovine spongiform encephalopathy (BSE), first emerged in Britain in 1986 as a result of ‘cannibalism’, when beef offal was fed to cattle, which are natural grass-eaters.
The proteins, called prions, that cause BSE were found in large quantities in the brains, spinal cords and spleens of cattle (although they were also subsequently discovered in meat tissue, too). When animal carcasses were ground down to form feed stuff for other cattle, prions were passed on.
They then colonised the brains of the cattle which ate them, and were passed to humans via cheap, mechanically-recovered meat — such as processed sinews and offal that were used at the time in school dinners and baby food.
In humans, the prions triggered the development of a new form of fatal human dementia called new variant CJD, which was first identified in 1996. These prions are entirely new infectious agents, completely different from viruses, bacteria or parasites.
Basically, they are faulty versions of healthy proteins in brain and nervous tissue that then induce their neighbours to become faulty. As a result, the brain cannot function: all signals are disrupted or shut down completely, leading to almost certain death.
Holly was a lively teenager about to start university, but now her days are spent in heartbreaking, silent immobility A ban on using animal remains in livestock feed was imposed in 1989, and 4.4 million cattle were slaughtered to eliminate the disease. At the same time, a ban was imposed on the use of mechanically-recovered meat in products for human consumption.
By the mid-Nineties, when CJD fears were at their height, up to 3.5 million people were believed to possibly be affected. The risk appeared to be greater in younger people, although the reason isn’t clear.
But as new cases failed to materialise (according to official statistics, 168 people have died from CJD in the UK), the view of the Government and medical establishment was that the danger had passed.
However, the new data from the Health Protection Agency suggests the rate of infection is much higher than currently thought.
‘We do not know how many infected people there are or how many of them will develop it,’ Professor Collinge says.
‘The incubation period, where there are no symptoms, can last for decades.’
But it is not only the threat of a widescale re-emergence of the infection that worries experts. There is also the possibility of a new generation being exposed to the disease, as a result of a European Union decision to change the rules on animal feed.
Although CJD emerged from beef, experts say there is evidence of related diseases affecting other meat-producing animals if they are forced into cannibalismContrary to popular belief, BSE has not been wiped out. In fact, 11 cattle were diagnosed with it in Britain last year, although none entered the food chain.
Most young cattle slaughtered for meat are not believed to have developed sufficient infectivity to pose a risk to humans. Any animal more than 30 months old destined for the food chain is checked for BSE after it has been slaughtered.
The new concern is not cattle, however, but pigs and chicken. Earlier this summer, the European Commission announced it was relaxing the ban on using animal remains in livestock feed.
From next year, chicken meat will be used in pig feed and vice versa, to cut costs for farmers who otherwise have to rely on expensive imported soya beans for growth-promoting protein-based animal foods.
Although CJD emerged from beef, experts say there is evidence of related diseases affecting other meat-producing animals if they are forced into cannibalism.
Now a group of CJD-affected families, led by former Labour health secretary Frank Dobson, is to challenge the Government to hasten the development of the new blood test to give people the chance to check if they are infected.
The proposal has been given added urgency by the latest findings about CJD-infected tonsil and appendix tissue, but the Government has been dragging its feet, says Mr Dobson.
‘The projections I was given when I was health secretary in 1998 were that the total number of CJD cases could be anything between a few hundred and 3.5 million people,’ he said.
‘Until now, the only certain way of diagnosing CJD in people who have not yet developed symptoms is to analyse tissue after death.
'Trials show John Collinge’s blood test works, but it needs investment to turn it into a proper screening tool that can quickly deal with a high volume of blood samples.
‘You would have thought the Government would want it to test blood supplies and get an accurate picture of how many people are infected. I can’t understand why they’re not getting on with this.’ Anxiety about CJD transcends party boundaries, with Tory MP Sir Paul Beresford joining Mr Dobson’s cause. The reason Holly and the other two surviving CJD victims are alive is probably because their families fought court battles to be allowed to give them pentosan polysulphate‘We need to find out the extent of the problem and what we need to do about it,’ he said.
‘Otherwise we will potentially see a flood of cases in our grandchildren.’
The parents of Holly, from Thornton Dale in North Yorks, are among those backing the campaign. ‘It’s too big an issue to ignore,’ said Peter Mills. ‘The evidence suggests there will be a second bout of this infection and we need the measures in place to test blood. There is clearly a risk from infected people who have no symptoms. Even if they don’t develop the disease, they can pass it on.’
Normal sterilising techniques do not remove the abnormal proteins which cause CJD from surgical or dental instruments because they survive high temperatures.
There have been at least six transmissions from hospital operations and four cases of CJD infections passed from three different blood donors. All those infected in these ways have died.
In the meantime, Peter and Linda are fully engaged in caring for their sick daughter. When she was diagnosed with the disease aged 18, she was within weeks of leaving home to study midwifery. In fact, her symptoms had been emerging over the previous two years.
At first the family put her fatigue and anxiety down to teenage depression. She had fainting fits two or three times at school when she was 16, but her GP assumed she would grow out of them.
But when Holly began losing weight and having difficulty walking, her parents realised something was wrong.
Her condition quickly worsened, but the CJD diagnosis — based on ruling out everything else — was a dreadful shock.
‘We were devastated,’ says Peter. ‘We think she caught it from the mechanically-recovered meat they used to put in baby food.
'Once Holly became ill, it all happened very fast. Within a few weeks of the diagnosis she couldn’t walk or talk. We treat it like a head injury.
‘We want to stimulate her as much as possible. We talk to her all the time and, although she doesn’t respond, we are convinced she still has some functions.’
Every morning, a system of hoists and pulleys allows Linda to transport Holly from bed to a specially-built bath tub. Once she is washed and dressed, the three embark on an outing into the countryside. Come rain or shine, Holly’s parents guide her wheelchair along the cliff-top paths in the nearby seaside resort of Scarborough, or through the elegant surroundings of one of the local National Trust mansions.
The reason Holly and the other two surviving CJD victims are alive is probably because their families fought court battles to be allowed to give them pentosan polysulphate, an experimental drug currently unlicenced in the UK, injected into the brain which seems to prevent the final stages of the disease.
What lies ahead for Holly and the thousands of other CJD carriers remains to be seen. Campaigning with Frank Dobson, Sir Paul Beresford and the Mills family is Christine Lord, from Southsea, Hampshire, whose son Andy, a radio sports commentator, died aged 24 from CJD three years ago.
Other experts believe up to 60,000 could be affected ‘In one of the last conversations we had, Andy asked me to find out how he got ill and I promised I would,’ says Christine, a BBC journalist who is writing a book about what she believes has been a political cover-up of the extent of the CJD risk. ‘I want to know where this came from. I stopped him eating beef from the age of six because of BSE, but he still got the disease.’
She is organising a protest next month to demand access to the blood test. ‘I think the Government doesn’t want the test out there because of people finding out how prevalent CJD is,’ she says.
A spokesman for the NHS Blood Service said it was in talks with Professor Collinge about using his test to screen the 7,000 blood donations collected daily across the country, but could not say when the work would be done to develop a tool capable of bulk screening.
‘We are spending £40?million a year on a process to remove white blood cells and £200?million a year on synthetic blood-clotting factors to minimise the risk of CJD transmission via blood,’ she told the Mail.
Professor Collinge says blood will certainly already have been donated by infected donors. ‘I think the possibility of a lethal infection in one in 4,000 blood donors is very worrying. People wouldn’t accept that level of risk if it was HIV.’
The Government’s experts have extrapolated the Health Protection Agency’s data and suggested at least 15,000 people are carrying CJD, though they agree the exact figure is unknown and other experts believe up to 60,000 could be affected.
Meanwhile, Azra Ghani, professor of infectious disease epidemiology at London’s Imperial College, says the potential harm from symptom-free CJD carriers is impossible to predict.
‘It’s a waiting game with any new infection. We just don’t know if these people will be infectious or not.’
http://www.dailymail.co.uk/health/article-2055904/Could-face-return-CJD-Experts-fear-lie-dormant-thousands.html
Cow aged over 72 months enters food supply without being tested for BSE Wednesday 26 October 2011
The Agency has been notified that meat has entered the food supply from a cow aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 72 months of age.
It is very unlikely that the cow was infected with BSE and as specified risk material (SRM) was removed, any risk to human health is extremely low. SRM is the parts of cattle most likely to carry BSE infectivity.
The cow, aged 74 months and 11 days, was slaughtered at Anglo Dutch Meats (Charing) Ltd’s abattoir in Kent, on 11 August 2011. The error was discovered on 6 October in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested cow, plus the one slaughtered before and the two after should not have entered the food supply. However, by the time the failure was discovered, the associated carcases had left the premises.
Subsequent checks indicate that the meat from the carcases was mixed with a large volume of other meat which is no longer in the food supply and is likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2011/oct/anglodutch
Cow aged over 48 months enters food supply without being tested for BSE
Tuesday 23 February 2010
The Agency has been notified that meat from a cow aged over 48 months has entered the food supply without being tested for BSE.
It is very unlikely that the cow was infected with BSE and, as specified risk material (SRM) was removed, any risk to human health is extremely low. However, testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.
The cow was slaughtered at Pickstock Ashby Ltd's abattoir in Hartshorne, Derbyshire, on 4 November 2009 aged almost 57 months. The failure was discovered on 28 January during routine cross checks of slaughter and BSE test data. By the time the failure was discovered all of the affected carcasses and offal had left the premises.
The affected carcasses, some edible co-products and offal had been exported. Some meat returned to Britain after processing and some went to other countries. Other edible co-products remained in Britain. Subsequent checks indicate that all of the meat and edible co-product that remained in Britain or that returned to Britain is no longer in the food supply chain. The authorities in the countries that received the exported material have been informed.
Background to BSE testing The BSE testing age was raised to 48 months at the beginning of last year. Cattle aged over 48 months are allowed to enter the food supply provided they have tested negative for BSE. If there is no BSE test, all parts of the carcase must be condemned.
Specified risk material (SRM) is those parts of the animal that contain almost all BSE infectivity, if the animal is infected with BSE.
http://www.food.gov.uk/news/newsarchive/2010/feb/over48monthcow
Cow aged over 48 months enters food supply without being tested for BSE
Tuesday 14 September 2010
The Agency has been notified that meat has entered the food supply from a cow aged over 48 months that had not been tested for BSE.
It is very unlikely that the cow was infected with BSE and, as specified risk material was removed, any risk to human health is extremely low. Nevertheless, a negative BSE test result is mandatory for cattle over 48 months of age slaughtered for human consumption.
The cow was aged one day over 48 months when slaughtered on 9 July at G & GB Hewitt Ltd abattoir in Chester. The error was discovered on 24 August in the course of routine cross-checks of slaughter and BSE test data.
According to BSE regulations, the untested cow, the animal slaughtered before and the two slaughtered after must not enter the food supply. However, by the time the failure was discovered, all of the associated carcasses had left the premises.
Subsequent checks traced one small batch of meat that has since been destroyed and indicate that the rest of the meat from the carcasses is no longer in the food supply chain.
http://www.food.gov.uk/news/newsarchive/2010/sep/otmuntested
Cow aged over 48 months enters food supply without being tested for BSE Monday 2 November 2009
The Agency has been notified that a 58 months old cow has entered the food supply without being tested for BSE. BSE testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.
However, as all the specified risk material (SRM) was removed, and it is unlikely that the cow was infected with BSE, any risk to human health is very low. SRM is those parts of the animal that contain almost all BSE infectivity.
The cow was slaughtered on 28 July 2009 at Dunbia abattoir in Dungannon. The error was discovered by Northern Ireland's Department of Agriculture and Rural Development (DARD) when a routine annual herd TB test revealed that the cow had been misidentified.
DARD has now established the correct identity and age of the cow slaughtered on 28 July. Checks indicate that all the meat and other products from the untested cow are likely to have been eaten.
http://www.food.gov.uk/news/newsarchive/2009/nov/over48
Monday, May 12, 2008
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
http://bseinquiry.blogspot.com/2008/05/bse-cjd-and-baby-foods-great-debate.html
NORTH AMERICA USA
PLEASE be aware, for 4 years, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens.
who will watch our children for CJD for the next 5+ decades ???
WAS your child exposed to mad cow disease via the NSLP ???
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
http://downercattle.blogspot.com/2009/05/who-will-watch-children.html
http://downercattle.blogspot.com/
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???
you can check and see here ;
http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
MAD COW DISEASE, TEXAS STYLE
http://www.organicconsumers.org/articles/article_23850.cfm
with an incubation period of up to 50 years or more, we will all just have to wait and see...
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
2006
USA sporadic CJD cases rising ;
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
2008
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
CJD USA RISING, with UNKNOWN PHENOTYPE ;
5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases;
*** 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
Published Date: 2010-04-05 17:00:02
Subject: PRO/AH/EDR> Prion disease update 1010 (04) Archive Number: 20100405.1091
PRION DISEASE UPDATE 2010 (04)
Communicated by: Terry S Singeltary Sr
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed
http://www.promedmail.org/direct.php?id=20100405.1091
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
(see video here) ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
(see video here)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?
(see video at bottom)
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
Sunday, September 6, 2009
MAD COW USA 1997
(SEE SECRET VIDEO)
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
2010-2011
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Published Date: 2011-06-07 11:47:33
Subject: PRO/AH/EDR> Prion disease update 2011 (06) Archive Number: 20110607.1736
PRION DISEASE UPDATE 2011 (06) ******************************
A ProMED-mail post http://www.promedmail.org
The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
Commentary ---------- Following to a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) and the European Centre for Disease Prevention and Control (ECDC) were asked to deliver a scientific opinion on any possible epidemiological or molecular association between transmissible spongiform encephalopathies (TSEs) in animals and humans. The opinion reviews and discusses the existing scientific evidence that links animal and human TSEs currently known.
The opinion first considers the definition of zoonoses and the principles for the identification of zoonotic diseases, which can be based on evidence gathered from both epidemiological and laboratory studies. The opinion describes the challenges involved in identifying TSEs as zoonoses, due to the specific characteristics of TSE infections/diseases, such as the nature of TSE agents, the occurrence of animal and human TSEs, and the type of monitoring applied, the long incubation period of TSEs etc. The example of the process that led to establishing a link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) is reviewed. The epidemiological and laboratory criteria that can be used to investigate such a link are described in detail, since those criteria might be useful for the identification of links between other animal and human TSEs.
The opinion discusses the strain diversity of the TSE agents described in sheep, goats, cattle, cervids, and humans, based on the current knowledge, which highlights that multiple TSE agents exist in each species. The factors influencing the capacity of TSE agents to cross the species transmission barrier are then considered in detail, including the variability in host and donor PrP gene and protein, the TSE strain type involved and its interaction with the host PrP, and the route of infection.
The opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association between animal and human TSEs. The use of epidemiology is discussed for TSEs in both animals and humans, and the possibility to compare the 2 sources of information is presented as a possible method to study the possible links.
Both in vivo and in vitro laboratory methods are considered and discussed, including neuropathology, transmission experiments involving different animal models (wild type and transgenic mice, primates and other species), biochemical methods, cell-free conversion assays, protein misfolding cyclic amplification (PMCA), and cell culture assays. Characteristics, advantages, and disadvantages of the different methods are reviewed, including the opportunity to collate data from different types of experiments for the study of potential associations between animal and human TSEs.
The opinion then reviews the scientific evidence currently available for the different animal and human TSEs, including classical BSE, atypical BSE (H-type and L-type), classical scrapie, atypical scrapie, chronic wasting disease (CWD), transmissible mink encephalopathy (TME), and human TSEs. In particular, the following aspects are systematically discussed for each TSE agent: epidemiology, pathogenesis, and in vivo and in vitro transmission experiments.
The opinion concludes that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. With regard to human TSEs, detected cases of sporadic CJD are randomly distributed in time and geographical location. These observations have been interpreted as a supportive argument that sporadic CJD is not environmentally acquired. However, the epidemiological evidence in relation to sporadic CJD cannot be regarded as definitive, and the possibility that a small proportion of cases are zoonotic cannot be excluded.
It also concludes that a series of uncertainties in relation to the epidemiological patterns of animal and human TSEs indicate that even a rough comparison of the present epidemiological patterns of human and animal TSEs other than classical BSE is unlikely to be informative. Because of these uncertainties, it is an imperative to continue to carry out systematic surveillance of human TSE diseases, and to continue and improve the surveillance of animal TSE diseases.
The opinion highlights that the active screening has allowed the identification of 3 new forms of animal TSEs (L-type atypical BSE, H-type atypical BSE, and atypical scrapie), but that the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs.
There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential.
Transmission experiments to human PrP transgenic mice suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE and classical BSE in sheep agents) might have zoonotic potential, whereas for other agents there is no evidence provided of a zoonotic potential (H-type atypical BSE and CWD), or no published studies are available (classical and atypical scrapie). In addition, transmission experiments to primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential. In particular, primates are highly permissive to L-type atypical BSE, even by the oral route.
The opinion emphasizes that laboratory transmission experiments indicate that the L-type atypical BSE agent has a significant zoonotic potential, which appears similar or even higher than that of the classical BSE agent. While transmission data for evaluating the zoonotic potential of classical scrapie in primates and human PrP transgenic mice are extremely limited or not yet available, a single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
The opinion concludes that human PrP transgenic mice and primates are currently the most relevant models for investigating the human transmission barrier, but the extent to which such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. It is unpredictable whether a TSE agent will transmit to a new host, and if the transmission principally occurs, what the transmission rate will be.
Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.
-- Communicated by: Terry S Singeltary Sr
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.
It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
******
http://www.promedmail.org/direct.php?id=20110607.1736
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1
http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html
another question, just how long have these atypical BSE TSEs been around in the bovine ???
Subject: atypical BSE reported in 1992 and conviently slaughterd and incinerated and then swept under rug for about 12 years
Date: April 26, 2007 at 1:08 pm PST 1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN THE HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS NOT BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. .......
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf
2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.
3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/29005001.pdf
IN CONFIDENCE
This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/26002001.pdf
COLLINGE THREATENS TO GO TO MEDIA
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS
"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP"
2009 SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
USA MAD COW FEED IN COMMERCE
FDA TRIPLE FIREWALL MAD COW FEED BAN WAS NOTHING MORE THAN INK ON PAPER
10 YEARS (one decade) POST USA FDA MAD COW FEED BAN OF AUGUST 4, 1997, USA STILL FEEDING COWS TO COWS
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR; Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/direct.php?id=20101206.4364
SEE TONNAGE OF MAD COW FEED IN COMMERCE IN 2007 ALONE, A DECADE POST PARTIAL AND VOLUNTARY MAD COW FEED BAN ;
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
Mad Cow Scaremongers
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011
re-2003
"he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease."
http://www.seac.gov.uk/pdf/hol-response091008.pdf
http://bse-atypical.blogspot.com/2009/10/seac-science-and-technology-committees.html
SNIP...SEE FULL TEXT ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html
Tuesday, October 4, 2011
De novo induction of amyloid-ß deposition in vivo
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
http://betaamyloidcjd.blogspot.com/2011/10/de-novo-induction-of-amyloid-deposition.html
layperson
TSS
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
3:17 PM
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