> I have seen no aliens, and as far as Bill Clinton, I thought this
forum was for BSE. As far as real evidence of BSE in the USA, there is no real
evidence of anything with TSE's, other than you die, but there are a few items
to suggest this. Why are you so sure, there is not a BSE type disease in US
cattle? Also what if CWD or TME were to have entered the food chain somehow,
sometime back?
(1986-1988) Marsh and Harsough report that they suspect a scrapie-like
disease of cattle in the USA.
Could it be something different than the U.K. strain?
I agree.
I also agree.
> I disagree, partly for the above reasons in the URL's, and also for
the fact, the US has only checked, as of Aug. 1999, 8,400 cattle brains for BSE
in the U.S., from 1,250,880,700 raised in the U.S. since 1990. 100,000 Downers
annually. With the feeding practices and the rendering practices before the Aug.
4, 1997 partial ban of by-products in the U.S. mirroring that of the U.K.'s, the
950 scrapie infected flocks of sheep, as of Aug. 1999. It would seem to me, that
there is a good chance of some strain of TSE, to be in the U.S. cattle
population. But, gut feeling, I think that a good portion of the deaths from
sporadic CJD in the U.S., has come from Surgery's. At least, that is what I
think killed my Mom hvCJD, and many more. But who know's? I'm still
looking...
Kind Regards, Terry S. Singeltary SR., Bacliff, Texas USA
snip...end...tss
August 21-28, 1988
To be published in the Proceedings of the Fourth International Scientific
Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
R.F. Marsh* and G.R. Hartsough
•Department of Veterinary Science, University of Wisconsin-Madison,
Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville,
Wisconsin 53092
ABSTRACT
Epidemiologic investigation of a new incidence of transmissible mink
encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may
have resulted from feeding infected cattle to mink. This observation is
supported by the transmission of a TME-like disease to experimentally inoculated
cattle, and by the recent report of a new bovine spongiform encephalopathy in
England.
snip...
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville,
Wisconsin reported that many of his mink were “acting funny”, and some had died.
At this time, we visited the farm and found that approximately 10% of all adult
mink were showing typical signs of TME: insidious onset characterized by subtle
behavioral changes, loss of normal habits of cleanliness, deposition of
droppings throughout the pen rather than in a single area, hyperexcitability,
difficulty in chewing and swallowing, and tails arched over their _backs like
squirrels. These signs were followed by progressive deterioration of neurologic
function beginning with locomoior incoordination, long periods of somnolence in
which the affected mink would stand motionless with its head in the corner of
the cage, complete debilitation, and death.
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
***Since previous incidences of TME were associated with common or shared
feeding practices, we obtained a careful history of feed ingredients used over
the past 12-18 months.
***The rancher was a “dead stock” feeder using mostly (>95%) downer or
dead dairy cattle and a few horses. Sheep had never been fed.***
snip...end
Subject: Re: BSE in Germany as a topic at a veterinary conference
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Thu, 2 Nov 2000 10:44:15 +0100
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Dear all,
> BSE in Germany will be the topic of a session of the upcoming
> Bavarian Veterinary Congress next May. I certainly don't consider
> myself an expert in the field, and I confess that I simply don't have
> the time to read through all of the postings of this list. Still I'm
> asking for your help.
> > I plan to present a paper titled "Critical questions with regard
to
> BSE in Germany".
> I welcome it that it is possible that "BSE in Germany" will be the
topic of a session of the upcoming Bavarian Veterinary Congress. Furthermore I
wish Prof. Klee all the best for his investigation and his lecture.
But as a seriously thinking scientist considering himself not as an expert
in the field of BSE-risk research he suggested among his professional
colleagues, to invite me as a speaker about this questions which obviously have
been my special interest for many years. For me somewhat surprising they
initially accepted his proposal and so he asked me to speak in Munich.
I have to confess that I felt not very comfortable with this idea, because
I am always arguing against such conferences and because I already published
most of my kowledge about this special topic on my site. In addition I knew that
giving a lecture at a veterinary congress would mean, that I would have been
very alone against perhaps hundreds of vets which do not love me for what I
publish. I was not really enthusiastic expecting extremely critical and even
aggressive questions and comments.
But after an email and a telephon call from Prof. Klee I accepted his kind
invitation. And now, not really surprizing but disappointing me, Prof. Klee had
to tell me that some of his professional colleagues do not want me to speak on
their conference. They even were not too ashamed to ask him to cancel my
invitation.
You can believe me that I am not really unhappy that I will not have to
discuss with such incorrigible down players. But I am extremely frustrated about
what this means for the attitude of mind about BSE among those German vets, who
are expected - or perhaps somewhat more realistic - officially would have to
report German BSE cases. I am afraid now more than ever, that this might not
always happen to say the least.
To this distressing picture fits the fact that the ministry for agriculture
in North Rhine Westfalia started a so called information campaign with the aim
to ensure the public that German and of course especially the meat of North
Rhine Westfalia is still the safest in the world. Sorry, british members, I know
that this must sound almost too familiar to you, but it seems that every
government thinks like this. Interesting with this information campaign is the
fact that it is full of unbelievable factual mistakes which demonstrate that it
was produced by people who are extremely bad informed about the simple facts.
This is somewhat surprizing, because they have a vey well informed expert there
and knew that they always could ask me or Prof. Riesner who sits in Duesseldorf
like they do. But they did not only produce this very poor information (By the
way, it was produced by a journalist). In addition they decided not to put any
link to Internet sites with warnings about BSE risks, although there are a lot
of links on this site. www.pro-nrw.de
Therefore I am bound to say that we obviously have in Germany of the year
2000 still exactly that climate of secrecy which was just criticized by the
inquiry's final report. There are still authorities and vets who are not
prepared to communicate risks to the public. They still do their very "best" to
exclude critical and independent scientists from the discussion. They even do
not want to discuss with the probably only independent German expert for BSE
safety problems within a closed circle of vets. Instead they prefer to have a
Veterinary Congress about BSE safety problems without any expert who could tell
them what they do not want to hear. We can only hope that they will not cancel
the invitation of Prof. Klee as well.
So it may well be that the idea of beeing so allone only with a few
hundreds of professional colleagues against me, the cruel vet eater, created
panic atacks for some of them. But I can't restrain myself to increase their
slight physical discomfort somewhat further. I think that other EU member states
and the EU commission should know what happens in Germany with regard to
BSE-risk-awareness and risk communication and I just informed the leading
BSE/CJD expert in the German parliament. Now I am very excited about what German
journalists think about this scandal.
I hope that you understand that I am not going to investigate the question
of Prof. Klee, which would be really time consuming. Of course I am interested
in this questions too, but I would not really like it to collect the data for a
lecture which I am not allowed to hold.
kind regards
Roland
Subject: Re: Baby food in Germany
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Mon, 6 Nov 2000 22:16:09 +0100
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Dear Kelly,
> I had written a letter to Hipp, a main manufacturer of baby food in
Germany
> a few months ago and have finally received a response from Dr. Holger
> Kukral from Hipp.
> this sounds good, but he did not really answer all of your
questions.
> 4. What type of slaughtering procedures are used on cattle designated
for
> your products? Are the cattle slaughtered with or without bolt pistol
and
> pithing? Or is electrical stunning used?
> Answer: The animals are slaughtered in accordance with the provisions
of
> the Animal Protection Law and the provisions of the EU Order on
Organic
> Farming, separately from animals that do not come from organic farms.
> Therefore I think that the use stunning and pithing as it is normal in
Germany. This is of course no problem when the animals really do not have
BSE.
> 5. What types of beef are used in the baby foods? Is there any use of
> organs or tissues besides pure muscle beef in your products (ie.
Brain,
> spinal cord, spleen etc)? In France for example on 10 April 1996 under
the
> : Decree no. 96-307, baby food.. and the nutritional supplements
destined
> for human nutrition cannot be made, imported or sold...if they contain
> tissue at risk from bovine origin. These tissues considered at risk
are
> those from the central nervous system (brain and spinal cord),
intestines
> etc. Is there a similar policy regarding the ban of certain bovine
> materials for baby food in operation in Germany and/or at Hipp?
> Answer: Only muscle meat is used. Offal is not processed. As in
France, the
> regulations in Germany are that the use of these special tissues is
not
> permitted.
> In Germany the use of these special tissues was permitted until
recently. Only the EC-decision 2000/418 from 29.6.2000 stopped this from
1.10.2000 on. This does of course not mean that baby food producers used these
tissues.
> 6. Finally, besides beef, I am also wondering about the feeding
policies
> and origin of the chickens and turkeys that are used in your products.
> Answer: Our chicken and turkey meat also comes from organically kept
birds.
> This means that the birds must be kept in a way appropriate for their
> species, are allowed space to run around and have the opportunity to
behave
> as appropriate for their species (e.g. sand baths).
> This does not say anything about the feed.
> The letter continues "In addition to our comprehensive tests, we also
use
> the latest technical analytical facilities to make sure that there is
no
> trace of BSE by means of additional monitoring."
> I wonder what this might mean. I have no idea how one could achieve
this.
> So, that was the letter.... I didn't find my answer to question 6) as
to
> what the chicken and turkey receive as feed in Germany/Hipp. Roland,
what
> happened to the 12000 tons of MBM imported from Britain? Was it
fed/being
> fed to non-ruminants? In France as of 1996 some measures were taken
for
> non-ruminant feed. Basically, organs and tissues of ruminants
identified as
> a potential risk are not recycled for non-ruminant feed (pig, chicken,
> fish), but are instead incinerated. And also as of 1996 the
incorporation
> of animal carcasses is forbidden. In addition, a second level of
security
> calls for a thermal treatment of 133 C during 20 min under 3 bars of
> pressure for feed intended for non-ruminants (decision 96/449 frin
July 18 > 1996).
> I am of course no detective and therefore I cannot say what happened
to British MBM in Germany. But from Swiss investigations I know that some of
this MBM was sold to other countries. Some of the British MBM was used for
German feed for pigs, chicken and fish. Because until now all German federal
governments argued that there is no BSE in Germany and that we therefore don't
need any measurements, we did nothave such measurements. What we have are
exactly the mesurements that we were forced to introduce by the EU, mainly
99/534 and 2000/418.
> Does anyone (Roland?) know what the situation is in Germany for non-
> ruminants? Are chickens/turkeys fed MBM? Is it also the case with organic
> birds, and are you aware whether the SRM's are allowed in their feed? I am
> hoping that the same minimal precations are taken as in France. Especially
> in respect to baby food. > We do not have so many turkeys, but chickens
are fed with MBM. Organic birds does not mean anything. There are certain
organizations like Demeter or Bioland with special regulations, which exclude
potentially dangerous feeds. But what exactly is allowed or forbidden, depends
on the organization.
A main problem in Germany is that it is extremely difficult to get
information. Beside my own site there are no Internet sites where you can find
descriptions of what is allowed or not. Our authorities still have to learn very
much from British, French and Swiss authorities.
All the best,
Roland
Subject: Germany rues 'complacency' over BSE testing strategy
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Thu, 30 Nov 2000 11:46:08 -0800
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Greetings List Members,
you see what happens to a country that INSISTS on being BSE Free. The U.S.
should take heed. Even a small country such as Germany over the past 10 years
has checked more cattle for BSE than that of the U.S. in 10 years. and to
magnify this, compare the number of cattle raised in the two countries. Somebody
needs to start using common sense instead of this 'fuzzy math'. you see, the TSE
agent knows no math.
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
NATURE
November 30, 2000
Germany rues 'complacency' over BSE testing strategy
ALISON ABBOTT AND QUIRIN SCHIERMEIER
[MUNICH] The German government has been prompted to order extensive tests
on cows following the identification last week of two cases of BSE (bovine
spongiform encephalopathy) in German-born cattle. Within the next few weeks it
should learn whether these cases represent only the tip of an iceberg.
Many scientists fear that the true extent of the disease may have been
hidden. Germany had declared itself 'BSE-free', largely because its farmers have
not traditionally fed their cattle on the blood and bone-meal that are thought
to have sparked the crisis in Britain.
The precautions taken have therefore not been as rigorous as in other
countries. When Britain banned the use of bone-meal as feed in all farm animals,
for example, Germany banned its use only in cattle, allowing it to continue in
pigs and poultry.
Moreover, Germany has only carried out BSE tests on animals showing
symptoms of central nervous system disturbance — there have been around 15,000
such tests in the past ten years.
The federal government has now called for testing of all cattle at high
risk of developing BSE, including those dying of unknown causes. Such cases
average 66,000 per year. Cattle slaughtered over the age of 30 months might also
be added to the list, because older cattle have a higher risk of accumulating
the infectious prions thought to cause the disease.
In the wake of last week's discovery, some scientists say that German
complacency was misplaced. Hans Kretzschmar, a prion expert at the University of
Munich, and a member of an ad hoc group of experts called on occasionally to
advise the government, regrets that scientific advice on the matter was not
institutionalized in Germany. "There was a feeling that Germany could never be
affected by BSE, so a standing advisory committee would not be necessary," he
says.
"But when an animal born in Germany in 1996 contracts BSE, even though the
use of blood and bone-meal was banned in cattle in 1994, you start to wonder
what can be believed, Kretzschmar says. He warns that variant Creutzfeldt–Jakob
disease, the human form of BSE, may now arrive in Germany.
"We have been too complacent in assuming that Germany was immune," says
Reinhard Kurth, head of the Robert Koch Institute, the government agency that
researches into infectious diseases. Kurth regrets what he sees as the general
lack of a sound scientific basis in dealing with BSE issues.
Subject: BSE GERMANY -- "The killed animals will be destroyed in a
rendering plant." ???
From: "Terry S. Singeltary Sr." flounder@WT.NET
Reply-To: Bovine Spongiform Encephalopathy BSE-L@UNI-KARLSRUHE.DE
Date: Tue, 26 Dec 2000 11:51:49 –0800
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Greetings again list members,
In Germany, if i am understanding this document correctly, (the confirmed
BSE numbers seem to be outdated, to date, in this posting from oie), it seems
they destroy BSE infected cattle in rendering plants.
my thoughts would be, this would be very careless, and could possibly leave
the infectious agent to be left to 'cross-contaminate'.
is this the normal thing to do, in all countries???
> Control measures:
> - The killed animals will be destroyed in a rendering plant.
thank you, Terry S. Singeltary Sr., Bacliff Texas USA
Subject: Re: BSE GERMANY -- "The killed animals will be destroyed in a
rendering plant." ???
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 26 Dec 2000 21:26:39 +0100
Content-Type: text/plain
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Dear Terry,
> In Germany, if i am understanding this document correctly,
> (the confirmed BSE numbers seem to be outdated, to date,
> in this posting from oie), it seems they destroy BSE infected
> cattle in rendering plants.
> Jan Braakmann always has the actual numbers.
> my thoughts would be, this would be very careless, and could
> possibly leave the infectious agent to be left to
> 'cross-contaminate'.
> I always warned German authorities not to destroy German BSE cattle
within rendering plants. But now German meat-bone-meal and animal fat become
neither exported, nor used in any normal farm animal feed. At the moment, just
because we have winter, they also are not used as fertilizers. In addition , the
German MAFF is going to prepare a new law that will ban animal waste from
fertilizers. Therefore they produce meat-bone-meal only in order to get
something that burns well.
kind regards
Roland
Subject: Re: EU Commission Report Criticizes Feed Production in Bavaria
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 26 Dec 2000 21:08:57 +0100
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Dear Terry,
> sometimes things just happen in cyber-space.
> even your messages come out garbled on my end sometime.
> may be it is problem with your email client. If you transfer one of
your garbled emails into an external editor, you might be able to see that there
is a wrong end of line code. I think it is ASCII code 11 instead of ASCII code
13 plus 10. The problem should be solved if you delete each end of line and
reformat the text within the email client.
> Kurth warned against the danger of blood donations helping the
> spread of Creutzfeldt-Jakob disease, the human form of mad cow
> disease.
> Prof Kurth is no prion scientist, but produced intelligent and careful
statements about BSE/CJD-risks during recent years. But other chiefs of
important German governmental research institutes (non-prion-scientists, but
scientific advisers of the government) became aware of important risk factors
only during the last weeks. They obviously did not read the FSA report and of
course not my articles.
> German officials said Sunday they had detected another case of
> suspected mad cow disease, raising the number of suspected or
> confirmed cases to nine.
> You should not only count all suspections, but also see when they are
not confirmed. Until now we have five confirmed cases and one very likely, but
not finally confirmed case in addition to the six imported cases.
kind regards,
Roland
Subject: Re: Fwd: Re: risks of BSE to US, Canada, Germany, ...
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Thu, 28 Dec 2000 03:06:55 +0100
Content-Type: text/plain
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Robert,
my position did not change a millimetre.
>>> "New Scientist 10.6.00 What Mad Cows? The editorial
>>> explaining how the European Commission decided that
>>> some countries are really harbouring some BSE and yet
>>> have not reported any cases. It says just why countries
>>> are determined not to find any.
> >> in BSE-L and on my Internet site I repeatedly explained
>> that we have very poor measurements to prevent the spread
>> of imported TSE-infectivity in Germany. But until now there
>> is no proof for hidden BSE in Germany. Therefore in my
>> opinion no commision can decide that this country is really
>> harbouring some BSE.
> This was absolutely correct at that time, because even the SSC did not
find a single German BSE case until then. It was my position that we were likely
to have BSE, but that it was wrong to say that we had BSE. This was simply the
only scientific founded position and therefore correct.
>>> For instance Germany imported 13000 British cattle at the
>>> height of the British epidemic, plus 1200 tonnes of UK
>>> MBM and the figures for Spain and Italy were similar. Again,
>>> some of the offal from these cattle were fed to local
>>> animals without adequate pressure cooking. Spain, Germany
>>> and Italy have all refused EC requests to remove high
>>> risk tissue from human diets after insisting that they
>>> are BSE free.
> >> Unfortunately this is true and I unsuccessfully tried to
>> explain this to the responcible politicians in Berlin.
>> But 13000 imported British cattle and 1200 tonnes of UK
>> MBM are not simply comparable with the same amounts staying
>> in the UK. As far as I know it German farmers mainly imported
>> cattle races like Galloways, Angus and other extensive races.
>> Although 5 of our 6 reported BSE cases had been Galloways,
>> this race was at a much lower risk in the UK. Therefore it
>> is not correct to extrapolate from the whole UK BSE incidence
>> to the incidence among this 13000 imported cattle.
>> In addition it seems to be an important factor, that we do
>> not use Phosmet in Germany. Nobody can quantify this factor,
>> but I think that this may be a main reason for the irritating
>> fact that we have so few BSE cases in Germany.
>> The imported British MBM had little effect in Germany, because
>> it was simply not feed to German cattle. It was sold to other
>> countries like Switzerland or mixed into food for German pigs,
>> chicken and farm fish. Therefore we "only" had the problem
>> of cross contamination within the feed mills.
> And what is wrong with this position or ddifferent from what I wrote
more recently? I think you simply have to accept that reallity is somewhat more
complicated than you like it. My position was and is that I try to understand as
many factors as possible regardless what that might mean for my or your
hypotheses or intentions and that I hate oversimplifications.
>>> The EC simply says that passive surveillance (i.e. allowing
>>> the farmers to report the cases) would not pick up the cases
>>> adequately. (Ed - a good example is the testing of 40,000
>>> cattle in France, which is going on currently. If they are
>>> only expecting to find a similar number to the 89 cases of
>>> 10 million cattle in the country then that represents around
>>> one animal in 100,000 symptomatic and around one in 30,000
>>> including asymptomatic adults. Therefore they should find
>>> just one cow in their 40,000 if they are lucky.
> >> The Swiss active surveillance has shown that this calculation
>> is not correct. Active surveillance of course identifies more
>> cases than reporting from farmers or vets. But I agree that
>> even 40.000 tests are not very much.
>> What I cannot agree with is the often repeated statement that
>> we have had only passive surveillance in Germany. We should
>> not forget that we performed more than 3000 Prionics tests
>> on symptome-free cattle in Nordrhein-Westfalen and that all
>> German cattle with neurological signs become tested by the
>> Groschup surveillance group in Tuebingen.
> Ok, we had not 3000, but 5029 Prionics tests in North-Rhine-Westfalia.
And they did not really test all cattle with neurological signs in Tuebingen,
but only said so. But they tested about 2000 of such animals in Tuebingen and
many more in different states. Therefore my statement that we had not only a
passive surveillance system in Germany was correct, although I did not get
absolutely correct information. And my prediction that they would find more than
1 BSE case with 40.000 tests in France was very correct. Remember I did not
state that everything was wonderful in Germany. You should perhaps read what I
wrote and not what you felt about what I wrote.
>>> A draft has been put on the Web to collect comments from
>>> researchers and government experts.
> >> This is only a public relations trick. I already wasted my
>> time with comments to a former SSC draft. I never got any
>> answer.
> And why is this statement different from what I write now?
> Your position has changed markedly since this post in June, Roland!
> Not at all. Your examples show no change in my positions.
> Perhaps now it is apparent why government officials have also
> changed their stances over relatively short periods of time.
> In sharp contrast to you I am well informed about the positions of
many German politicians, authorities and scientists and I know where they
changed. Most of them did not change their positions, but only had to follow
political pressure. Only five things really changed and the reasons for that are
simple and clear:
1) The consumption of meet decreased significantly first because of the BSE
crisis in France.
2) In order to reassure the consumers, many German butchers started to test
their cattle with the Prionics Check and increased the presure on other butchers
to do the same. At the end the government had to follow the facts.
3) As a consequence of testing we got our first German BSE cases.
4) It became impossible to argue with the BSE-free-status according to OIE
and therefore authorities had to introduce measurements against BSE-infections.
5) Only this political activities, not interest in public health, made BSE
interesting for the media and their pressure made it possible for unwelcome
critics like Byrne and me to make their positions public.
By the way, it would be very naiv to believe that the MAFF people changed
their main positions. They are still in a battle with the ministry of health and
the end is open.
Roland
Subject: Re: GERMANY--Government May Order BSE Tests for Sheep
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Sun, 31 Dec 2000 10:28:27 +0100
Content-Type: text/plain
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Hello Terry,
> we understand you are under a lot of pressure about
> your Country's stupidity to TSEs. We have same problem.
> are you now speaking for the whole list?
> but you don't have to be disrespectful.
> not only to me, but others.
> You were the one who was disrespectful, when you answered my detailed
description of the new German measurements with a totally unfounded suspicion
about my motives.
> this seems to be a big problem with you.
> i have always respected your science.
> but you are not a very nice person.
> I am a nice person for my friends and even for most people who I do
not know. But I see no reason to keep smiling whereas you are trying to accuse
me of a conspiration with our ministers, instead of arguing against my
arguments. And I repeated my arguments and you are still not prepared to argue.
Therefore you are the impudent person and it is quit normal that this makes my
angry. How would you react when I would claim that you must be paid by your
governmnt for beeing quiet about your mothers dead, just because you did not
post anything about this for 14 days? It is always the same with you. First
everything within the UK was bad, then it was France although they only made
more tests than others, and now Germany is the center of the hell. You always
argue against the countries after they improved BSE-measurements.
> you should try loosing your chip on shoulder.
> Would probably help your science.
> the pressure can be seen.
> you should take a chill pill, the worst is yet to come for you.
> I think you describe your own problem, with the exception of science
of course. You are one of the most unfriendly members of this list, you totally
ignore understandable wishes like those of Oz and you attacked me personally
instead of discussing about my arguments. You are the problem.
> you said "but now we have the best in the world" >
> I was just afraid you had started to sound like the
> French;
> Indeed you are always afraid about sounds instead of rationally
analysing what people actually write. And it is always "the French" or "the
Germans". I have no problem to sound like for example Vincent Dedet or Prof.
Brugere- Picoux or Mark Barbier in this list. French is still not a synonym for
mad.
> no need to continue to debate this with me,
> you make no sense now, loose the chip on
> your shoulder, and we can then debate
> human/animal TSE, and BSE in Germany
> and elsewhere around the globe, even in
> U.S., when they start looking...
> I am not at all interested in further debates with you. I am
interested in facts, arguments and discussion and one needs an open mind for
this.
> The Welt am Sonntag newspaper quoted Byrne as criticizing Funke for
long
> saying Germany had no BSE problem despite that report.
> ``I just cannot explain such a statement,'' Byrne said. ``There are
> presumably many motivations, but I would not like to speculate about >
them.'' > -------------
> sure there are many motivations, i just don't think the Germans are
> that stupid, so what other reason would there have been ??? COVER-UP >
AND LIES for Industry. same as everywhere else.
> > someone needs to 'learn and understand'
> Everybody who is interested to argue honestly, knows that I repeatedly
argued within this list against this "Germany has no BSE problem". For years I
have been one of only very few who said in public that there was no proof for
that. I described on my site in detail why this statement was wrong. Therefore I
am not the one who needs to learn something about this.
> it looks as if Germany did not to date, one can only hope for furture.
> It is absolutely nonsense to claim that Germany did not learn from the
mistakes of the past. One has to be as blind as Terry to think so instead of
beeing happy about what improved this year. Whereas we are working hard in order
to stop all German TSE amplification mechanisms and transmission pathways and
whereas we are reorganizing our political and scientific risk communication
structures, he is only concerned about the sound of my words - possibilities to
misunderstand me. This is sick.
> German Minister Admits Mistakes in Mad Cow Scare
> > BERLIN (Reuters) - German Agriculture Minister Karl-Heinz Funke
> admitted mistakes on Saturday in his country's reaction to mad cow
> disease as a European Union (news - web sites) official criticized him
> for ignoring warnings earlier in the year.
> Ministers do not admit mistakes every day.
> ``Had we known earlier what we now know, my colleagues and I on a
> European level should have pushed ahead with a Europe-wide ban on
> animal feed earlier,'' Funke told German radio.
> Of course he could have known earlier and could now know more, but he
is now in serious problems because of this and only tries to hold his job. This
is quit normal and does make the improvements smaller.
> Yet in an interview released on Saturday, European Union food safety
> commissioner David Byrne said the EU had already distributed a
> scientific study last March warning of the possibility of BSE in
> Germany.
> This is correct and there were such warnings from several German
experts much earlier.
> The Welt am Sonntag newspaper quoted Byrne as criticizing Funke for
long
> saying Germany had no BSE problem despite that report.
> > ``I just cannot explain such a statement,'' Byrne said. ``There
are
> presumably many motivations, but I would not like to speculate about
> them.''
> It was indeed a mistake of Funke and his ministry to react only on
scientifically proven dangers, not already on plausible risks. But this is not
really far away from what Byrnes still does. The reason for this is simple. They
were afraid to run into trouble by causing costs for the industry without
reliable scientific foundation.
> In another interview with the online edition of the weekly news
magazine
> Der Spiegel, Funke said Germany had tested 19,000 cattle brains
between
> 1991 and 1999 without finding a single case of BSE.
> This is not true and will be investigated. But this is a
misinformation which the minister got from his ministry. The German chancellor
already said that such mistakes will have serious consequences next year. He
just introduced something like the British Inquiry and said that there will be
fundamental reorganizations of several ministries.
> ``In early 2000, we did not count on BSE cases in Germany,'' he said,
> adding that experts had been seeking more hard data after the EU
report.
> > Consumer groups and others have stepped up criticism of the
government
> in recent weeks for its handling of the mad cow scare, saying it had
> reacted too late to expert advice to introduce nationwide BSE testing.
> This is correct, but only Switzerland and France did test more and now
there is no country testing as intensive as Germany. Until December the German
government was very ignorant, but then it was forced to react and did this very
fast and efficiently. Many mistakes have been made in the past, but most of them
are already corrected and the rest will be corrected soon. It is therefore
somewhat unlogical to criticize just now the German BSE-safety situation and
governmental actions. But it was exactly the same when the UK and France
improved their measurements. Whereas people like Terry now react hysterical on 7
German BSE cases and the results of our now intensified controls, they do not
see the bigger BSE problems in Poland, Czechia, Slovakia and other European
countries. I argue against such overreactions, because I do not want governments
to be afraid to discuss problems openly. It is no good situation when the
reactions on test results become a more serious problem than the disease
itself.
> Funke said this week he wanted to widen testing to include sheep and
> called for a European Union plan to examine the possibility that sheep
> could be linked to mad cow disease.
> We should not use too much time and money for a BSE in sheep
investigation. We should just test for scrapie and eradicate all variants of the
disease.
regards,
Roland
Subject: Re: SV: GERMANY--Government May Order BSE Tests for Sheep
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Sun, 31 Dec 2000 12:10:53 +0100
Content-Type: text/plain
Parts/Attachments: Parts/Attachments text/plain (97 lines) Reply Reply
######### Bovine Spongiform Encephalopathy
#########
Dear Karin,
> "For _practical reasons_ and taking into account the present technical
> limits of detection as well as a risk analyses based on present
knowledge,
> the SSC considers that levels of cross-contamination of ruminant feeds
with
> mammalian meat-and-bone meal - derived from raw materials sourced and
> processed according to the conditions laid down in the SSC's opinion
on the
> safety of MBM - which exceeds 0.50% MBM (or 0.15% animal bone
fragments or
> 0.25% proteins, whichever is the lowest) should be condemned."
> > This has been interpreted by several countries as "it is OK" as
long as
> cross contaminations do not exceed 0,5%. There have been cross
> contaminations probably in all European countries and, according to
the SSC:
> "most European feed production systems are of a mixed type, meaning
that in
> 90% of cases the same facilities and the same conveying systems are
used for
> the production of feed for both ruminants and monogastrics".
> it is indeed one of our major problems now, that not all German
countries had a zero tolerance policy against cross contamination. Now this is
no longer a problem, because no German feed mill uses MBM, blood products or
animal fat.
> In my opinion, avoiding cross-contaminations by so-called "appropriate
> measures" will not work in such conditions, only complete separation
of
> manufacturing and transport for monogastric feeds and ruminant feeds
will
> avoid cross-contaminations. This is what they do in Ireland, where
they have
> 122 feed manufacturers of which only 2 are allowed to make feeds
containing
> MBM for pigs and poultry (they exported most of their MBM, they will
have to
> burn it now).
> I think that even separation on the production and transport level is
not enough, because cross contamination is also possible within the farms.
> Also remember that gelatin and blood meal was still allowed in many
> countries (even countries where pithing was allowed).
> Animal fat is also still allowed in most countries so that we now have
the problem that imported feedstuff can include risk material that has been
banned in Germany.
> All European countries have had a ban against mammalian MBM for
> ruminants, but this may have been only slightly better than no ban
> at all: if normal inclusion of MBM in ruminant feeds before the ban
> was 3-5% and they have considered as "OK" to have a cross
contamination
> of 0,3 to 0,5%, the difference is only a factor 10 in
cross-contaminated
> batches. And this cross-contamination has been going on for many
years,
> even before the formal bans in 1990-1994 in countries such as Austria,
> Germany or Norway, where MBM was "never voluntarily" included in
> ruminant feeds.
> I am not so sure that MBM has never been voluntarily included in
German ruminant feeds. But the ban against mammalian MBM for ruminants was not
only slightly better than no ban at all in the UK. It was not complete and
should have been better, but it had a dramatic effect on the British BSE
numbers.
> The situation would be even worse in non European countries such as
the USA,
> where SRM are not removed, heat treatments are lower than 133
degrees/3 bar. > BSE or any other TSE would easily be recycled if present,
and the very
> delayed US ban (1997) concerns only ruminant MBM, not mammalian MBM.
> It would be interesting to know more about the situation of the
eastern European countries, which imported most of the German meat-and-bone-meal
and perhaps large amounts of British MBM.
> When will the USA start removing SRM ? Will they ever start a serious
active
> surveillance ? The USA will have an increasing problem of credibility,
as
> importing countries maybe start to read the SSC risk assessment for
the USA.
> The problem is that the US beef industry has no problem with BSE at
the moment. Only when the government introduces risk measurements this will
produce costs. When they perform a BSE screening with one of the evaluated
tests, they will probably find cases and the US beef industry will run into a
serious crisis. They have to decide between waiting and hoping or finishing
completely the recycling of animal wastes despite massive protests from the
industry in order to reduce the risk of extermination of the whole beef
industry. If a government becomes active, it will have serious problems. If it
waits, the first BSE case may hurt the next president.
> First of all they have to start looking for scrapie, and I
> really hope they will develop/use methods for detection in blood or
> intestines or other tissues in early incubation. What is happening
with the
> Schmerr test ? Does any of you know if Prionics or CEA or any other
> BSE-rapid test method has been really validated for active
surveillance in
> sheep populations ? There was also a tonsil test and an eyelid-test,
what
> happened to those, are they used, and if so where ?
> I think that the German authorities will simply use the Prionics test
for a scrapie surveillance early in next year. Probably the Lelystad tonsil test
would be better, but it seems to be not available commercially.
Best regards, Roland
Subject: Re: SV: GERMANY--Government May Order BSE Tests for Sheep
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Mon, 1 Jan 2001 11:57:18 +0100
Content-Type: text/plain
Parts/Attachments: Parts/Attachments text/plain (63 lines) Reply Reply
######### Bovine Spongiform Encephalopathy
#########
Dear Tom,
>>> government testing of
>>> lyodura is needed to determine the species of origin in
material used for
>>> human implantation.
> >> I think the Japanese should do that But this
>> is a compensation problem between Braun Melsungen and the victims.
> > Yes but it is important for global policy on scrapie to know that
it
> transmits to humans. Countries like the UK, Canada, and US are awash
> in scrapie and there is no real effort to keep it out of the human
> food supply
> I agree that this would be interesting, but do you think that there
are still samples of the duras that caused diseases?
>>> if the iatrogenic dura mater CJD is associated with German
sheep
>>> brain then the incidence of subclinical scrapie has to be much
>>> higher than they are letting on.
> >> Why do you think that all or many of the Lyodura cases are
caused
>> by sheep brains and not by human dura mater?
> > There could be both. After all, we have no real idea of the
normal
> incidence of preclinical CJD infectivity. But the species origin of
> dura mater is easily and rapidly settled by routine experiment.
> I agree, but I doubt that Braun Melsungen or the Japanese hospitals
still have material of the infective duras.
> However, how does the German government account for all the "isolated"
> scrapie outbreaks below?
Yes, one was sheep imported from France. Note
> also that only 2 states have a record of reporting scrapie at all.
> Bavaria, the center of BSE, is reporting nothing. I find it most
> implausible that Germany is seeing spontaneous de novo independent
origins
> of scrapie. In my opinion, scrapie is widespread in Germany but rarely
> reported. And what did the lambs eat during the time the calves ate
BSE
> meal?
> Reporting of scrapie cases is obligatory for all German countries. Of
course this does not mean for me that all cases become reported, but I think it
is unlikely the we actually have as many scrapy cases as the UK has. It is not
necessary to asume spontaneous de novo independent origins of scrapie in
Germany. John Hazelwood in this list told me that we had many scrapie cases in
Germany 80 years ago and Dr. Wiemer in the German MAFF confirmed that this is
correct.
> Gutersloh -- what is going on there -- just one totally infested farm
or a
> whole district?
> I do not have details about this although Dr. Wiemer promissed to give
me details repeatedly during the last half year. But thee cases seem to be from
different herds within this district.
kind regards
Roland
Subject: Re: USDA/APHIS response to ROLAND AND GERMANY Statement of
Commissioner Byrne on new BSE-cases in Germany
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Thu, 11 Jan 2001 09:02:09 -0800
Content-Type: text/plain
Parts/Attachments: Parts/Attachments text/plain (179 lines) Reply Reply
######### Bovine Spongiform Encephalopathy
#########
Dear Roland,
> you should try to become somewhat > more up to date in order not to
> write such complete nonsense.
i am tired of your insults and lies. it is you and your country that have
been saying for the past few years, that Germany is BSE Free. NO PROBLEM. wake
up and smell the roses Roland. You are now just doing your Governments PR
work.
it is not difficult for me to understand that if Germany would have
listened years ago, they would not be in the mess they are in now, same with
other countries, including the U.S.
> but then you should not write > about things you don't
understand.
i understand full well what i speak of.
> In Germany we now have ...
yea, you now have, correct, after the fact, after your country stumbled
across a case by accident, and the 'cow was out of the barn' so to speak. now
your country all of a sudden gets religious about BSE. what took so long?
this is the problem with all countries, once they wait til they come across
a BSE case from 'passive' surveillance, then its too late. Passive surveillance
does not work, and we all knew it would not work. all the religion in the world
will not fix it. man did it, only man can fix.
> not only because I am familiar with her sister.
great, i am glad you are not only rubbing elbows with the gods now, but are
are now friends with the Government. but you are starting to now sound as they
do.
> There are of course still some problems, > but it is really stupid
and ignorant to > describe the actual German BSE handling as > "acting as
stupid as Germany".
Roland, before you went religious on us, or before you were not in the
'click', you just about called everybody stupid. now all of a sudden, everything
in Germany is o.k. and BSE is under control. you have nothing under control
yet.
i stand by what i said, Germany was stupid in its past handling of BSE, as
with other countries including the U.S. until this stupidity stops, and there is
GLOBAL regulations that are regulated very strictly, only then will the world
get a handle on human/animal TSEs.
regards, Terry S. Singeltary Sr., Bacliff, Texas USA
Brussels, 18 December 2000
Statement of Commissioner Byrne on new BSE-cases in Germany
It gives me no pleasure to say that I am not surprised by the discovery of
BSE in Bavaria. Public authorities must take all the measures necessary to
protect public health and to inform their citizens. Even if Germany has only
recently realized the risk that BSE has posed they must ensure that all EU
legislation is fully implemented. If this is done then the consumer can have
confidence in the beef they eat. There must be no half measures in regards to
public health and safety. I call upon them to take any necessary step to protect
consumers. Denmark for example has after the discovery of its first BSE-case
withdrawn from the market all products which were still produced with materials
like cattle brain and spinal cord. These "risk materials" are the ones which
carry most of the infectivity.
I also want to ensure that consumers are properly informed. Meat- and bone
meal has been identified as the clear source of the BSE-infection. A ban of
feeding to ruminants has been EU-wide in place since 1994. But we have serious
doubts it was respected. That is why we have now a temporary total ban on
meat-and bone meal in place from 1 January 2001 onwards. There is also the
possibility that compound feed might have been contaminated with traces of
meat-and bone meal in plants where there were no dedicated manufacturing lines.
It is of no help for consumers to speculate now about other possible ways of
transmission which are all not scientifically backed up. It is much more
important to tell people the truth and to force industry and farmers to respect
laws.
Released on 10/01/2001
Roland Heynkes wrote:
> > ######### Bovine Spongiform Encephalopathy
#########
> > Dear Terry,
> > > BUT, they should be reported, some are infected with TSE.
> > The U.S. is just acting as stupid as Germany and other
> > Countries that insist they are free of BSE.
> > > you should try to become somewhat more up to date in order
not to
> write such complete nonsense.
> > German governments not only do not state to be BSE-free, they
also
> do not act stupid against BSE-risks. It might be difficult for you
> to see the fundamental changes in Germany, but then you should not
> write about things you don't understand.
> > In Germany we now have a very complete ban of mammalian slaughter
> waste products in farm animals feed and an extension of this ban to
> fertilizers is coming. Nearly every fallen or sick slaughtered cattle
> is being tested with the Prionics-Check. All over 30 months old, all
> cattle slaughtered in Nordrhein-Westfalen and many additional younger
> animals in other German countries are tested with the Prionics or
BioRad
> tests. We already had about 70000 BSE tests during the last weeks.
> > The ignorant ministers for health and agriculture resigned and
the
> ministries became reorganized. Instead of a ministry for agriculture
we
> now have a ministry for consumer safety, food and agriculture and the
> new minister is from the green party and does not come from a farm.
> This dramatically reduces the lobbying power of the farmers and this
> will totally change the German agriculture policy within the EU.
> > Our new minister for health (Ulla Schmitt from Aachen) is much
more
> communicative and perceptive. I now see a very good chance to make her
> aware of still existing risks of human-to-human transmission of CJD
> (not only nvCJD), not only because I am familiar with her sister.
> > We now have a German Inquiry for structural reasons for the
mismanagement
> of the BSE problem and this will result in further organizational
> improvements. In addition we now have a massive push of prion science
> and governmental research institutes now publicly discuss BSE-risks
and
> ask for improvements in many industrial and research processes. More
and
> more German scientists become prepared to use modern communication
methods
> and to discuss even with independent scientists. And German ministries
> are going to organize much more open mechanisms of scientific
advisory.
> > In addition we now have very tight controls of animal feed,
production
> processes and meat products. And the results of this inspections
become
> published immediately.
> > This and many other changes came and come extremely fast and are
really
> fundamental. There are of course still some problems, but it is really
> stupid and ignorant to describe the actual German BSE handling as
> "acting as stupid as Germany". It is absolutely OK and necessary to
> criticize existing safety problems, but it is not constructive to
> ignore improvements. The latter is exactly what the former German
> ministers did when they constantly ignored the huge improvements in
the
> UK, Switzerland and France.
> > regards
> > Roland
Subject: no chance to conseal BSE cases in Germany
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
Date: Fri, 26 Jan 2001 15:20:15 +0100
Content-Type: text/plain
Parts/Attachments: Parts/Attachments text/plain (37 lines) Reply Reply
######### Bovine Spongiform Encephalopathy
#########
Dear all,
in Germany we now have 19 cases of BSE-positive tested German cows, which
had shown BSE-symptomes in only two cases.
And the new minister for consumer safety and agriculture Renate Kuenast of
the Green Party decided officially today, that all at least 2 years old
slaughtered cattle have to become tested for BSE with the Prionics Western Blot
or with the Bio-Rad ELISA.
In addition all cows (regardless how old) and all male cattle over 30
months that are found dead (downer cattle) and all for exceptional reasons (sick
or injured) slaughtered cattle over 24 months are BSE-tested in accordance the
EU regulation a somewhat more stringent German regulation.
In Nordrhein-Westfalen all healthy, sick, injured and fallen cattle over 24
months become tested for BSE.
In addition many butchers decide to test even younger cattle, because
otherwise their customers would not buy the meat.
This does not mean that we will be able to identify all BSE- infected
cattle now, but at least it means that there is now nearly no chance even for
criminal farmers to conceal BSE cases.
kind regards
Roland
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
BSE INQUIRY DFAs
Sunday, May 18, 2008
BSE Inquiry DRAFT FACTUAL ACCOUNT DFA
BSE Inquiry DRAFT FACTUAL ACCOUNTS DFA's
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
Sunday, May 18, 2008
MAD COW DISEASE BSE CJD CHILDREN VACCINES
Creutzfeldt Jakob Disease Germany 1993 - 2014
suspected CJD cases ≤50 years
Year suspected cases≤50 definite & probable cases ≤50
1993 0 0
1994 20 3
1995 14 3
1996 32 5
1997 13 6
1998 20 7
1999 12 7
2000 9 4
2001 15 5
2002 15 4
2003 19 9
2004 10 4
2005 18 8
2006 26 5
2007 28 7
2008 40 4
2009 27 4
2010 20 7
2011 14 4
2012 8 4
2013 8 3
2014 1 1
Gesamt 369 104
Friday, November 06, 2009
CJD GERMANY UDPATE 2009
----- Original Message -----
From: Terry S. Singeltary Sr.
To: TERRY SINGELTARY
Sent: Tuesday, October 27, 2009 12:36 PM
Subject: CJD GERMANY
CJK in Deutschland
Stand 06.10.2009
Jahr sicher wahrscheinlich möglich GSS FFI genetische
CJD
Iatrogen vCJK Inzidenz
1993 24 8 4 1 0 0 0 - 0,7
1994 45 27 26 0 2 4 1 - 0,9
1995 64 23 15 1 2 2 0 - 1,1
1996 55 34 22 1 5 5 1 - 1,1
1997 73 34 31 1 1 6 1 - 1,3
1998 63 54 11 1 3 7 0 - 1,4
1999 68 35 5 0 1 9 1 - 1,3
2000 53 55 4 2 1 7 1 - 1,3
2001 69 55 11 0 3 8 0 - 1,5
2002 52 46 6 0 2 7 0 - 1,2
2003 52 63 8 1 1 3 3 - 1,4
2004 80 60 5 1 4 4 0 - 1,7
2005 62 82 9 0 5 9 2 - 1,8
2006 61 80 8 0 4 5 1 - 1,7
2007 48 83 14 0 3 1 0 - 1,6
2008 57 78 9 0 3 0 0 - 1,6
2009 16 70 8 1 4 1 0 - 1,4*
see chart...tss
suspected CJD cases <50 div="" years="">
vCJD cases worldwide
see links ;
----- Original Message -----
From: Terry S. Singeltary Sr.
To: TERRY SINGELTARY
Sent: Tuesday, October 27, 2009 12:36 PM
Subject: CJD GERMANY
Journal of Neurology September 2014, Volume 261, Issue 9, pp 1811-1817
Date: 15 Jul 2014
First symptom and initial diagnosis in sporadic CJD patients in Germany
Anna Krasnianski, Judith Kaune, Klaus Jung, Hans A. Kretzschmar, Inga Zerr
…
Abstract
To describe the first symptom/sign and first diagnosis in patients with
sporadic Creutzfeldt-Jakob disease (sCJD) in Germany with respect to M129V
polymorphism of the prion protein gene and prion protein type. Data on the first
symptom/sign and first diagnosis were studied in 492 sCJD patients with probable
and definite sCJD and known M129V polymorphism. Unspecific prodromal symptoms
such as headache, fatigue, sleep disturbances, “peculiar feeling in the head”,
photophobia or weight loss were found in about 10 % of the patients. No
prodromal symptoms were found in MV2 and VV1 patients. Dementia was the most
common first symptom (37 %) followed by cerebellar (34 %), visual (15 %), and
psychiatric disturbances (14 %). The CJD diagnosis was the first diagnosis in
only 35 % of the patients (in 42 % of MM, 28 % of MV, and 24.5 % of VV
patients). We provide a detailed analysis on clinical presentation and first
diagnosis in a large group of patients with sCJD with respect to M129V genotype
and prion protein type. These data emphasize the importance of knowledge about
CJD and especially rare CJD types among physicians of different specializations.
Our findings may improve early recognition of atypical CJD forms.
Date: 26 Feb 2014
Diagnostic profiles of patients with late-onset Creutzfeldt–Jakob disease
differ from those of younger Creutzfeldt–Jakob patients: a historical cohort
study using data from the German National Reference Center
André Karch, Lena Maria Raddatz, Claudia Ponto, Peter Hermann, David
Summers, Inga Zerr …
Abstract
In contrast to other neurodegenerative diseases, sporadic Creutzfeldt–Jakob
disease (sCJD) is rarely diagnosed in patients older than 75 years. Data
describing the characteristics of sCJD in the very old are rare and
inconclusive. Therefore, a historical cohort study was designed to evaluate
clinical, cerebrospinal fluid (CSF), electroencephalography (EEG), and magnetic
resonance imaging (MRI) features of this group. Patients older than 75 years
identified via the German surveillance program from 2001 to 2012 (n = 73) were
compared to a random subsample of sCJD patients younger than 75 (n = 73) from
the same time period using an historical cohort design. Older patients showed a
faster disease progression represented by an earlier point of diagnosis and a
shorter survival time (p < 0.001). In the early stages of disease, older
patients presented slightly more often with dementia (p = 0.127) or dysarthria
(p = 0.238), whereas disorders of the extrapyramidal (p = 0.056) and visual
system (p = 0.015) were more common in the younger group. Atypical MRI profiles
such as MRI lesions restricted to one hemisphere (p < 0.001) or cortical
lesions only (p = 0.258) were found more frequently in patients older than 75
years, whereas typical cortical and basal ganglia hyperintensities were more
common in the younger group (p = 0.001). We demonstrated for the first time that
patients with late-onset sCJD differ from younger sCJD patients with respect to
MRI profiles and initial clinical presentation, but not among CSF markers.
Misclassification of Creutzfeldt–Jakob disease cases in patients older than 75
years seems likely due to atypical clinical and radiological presentation. This
might contribute to lower sCJD incidence rates in this age group.
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
5.195 Among occupational groups exposed to BSE, farmers remain unusual in
having such an excess over the incidence of CJD for the population as a whole.
No cases of CJD have been reported amount veterinarians exposed to BSE. Four
people in the meat industry (butchers, abattoirs, rendering plants, etc) have
been reported to have vCJD.386 The present evidence has been accepted by some as
reassuring in that such occupations may not pose as serious a risk as might have
been expected.
This was not simply another farmer but the third farmer......
suspect case of CJD in a farmer who has had a case of BSE in his beef
suckler herd.
cover-up of 4th farm worker ???
CONFIRMATION OF CJD IN FOURTH FARMER
now story changes from;
SEAC concluded that, if the fourth case were confirmed, it would be
worrying, especially as all four farmers with CJD would have had BSE cases on
their farms.
to;
This is not unexpected...
was another farmer expected?
4th farmer, and 1st teenager
2. snip...
Over a 5 year period, which is the time period on which the advice from
Professor Smith and Dr. Gore was based, and assuming a population of 120,000
dairy farm workers, and an annual incidence of 1 per million cases of CJD in the
general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an
individual in the general population to develop CJD. Using the actual current
annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5
TIMES.
3. You will recall that the advice provided by Professor Smith in 1993 and
by Dr. Gore this month used the sub-population of dairy farm workers who had had
a case of BSE on their farms - 63,000, which is approximately half the number of
dairy farm workers - as a denominator. If the above sums are repeated using this
denominator population, taking an annual incidence in the general population of
1 per million the observed rate in this sub-population is 10 TIMES, and taking
an annual incidence of 0.7 per million, IT IS 15 TIMES (THE ''WORST CASE''
SCENARIO) than that in the general population...
CJD FARMERS WIFE 1989
20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19
year old died from sCJD in France in 1985. There is no evidence of an iatrogenic
cause for those cases....
THE COVER UP OF MAD COW DISEASE IN FARMERS, FARMERS WIVES, AND VICKY
RIMMER, THE DAY MAD COW SCIENCE CHANGED $$$
Monday, May 19, 2008
*** SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND
ABATTOIRS ***
DOES ANYONE BESIDES ME SEE A PATTERN YET ???
Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of sporadic
CJD, whatever the hell that is. and there have been 16 year old die from
sporadic CJD in the USA as well.
SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. the elderly
are expendable, pets and kids are not.
Science was dictated by 'big buisness' after the Vickey Rimmer case with
the ukbsenvcjd only myth.
and there have been 16 year old die from sporadic CJD in the USA as
well.
snip...
I have interviewed Mrs Rimmer at my constituency surgery
IF there is nothing to hide, why is there so much SECRECY? WHY is the
Government and other Bodies trying to stop any CHANCE OF PEOPLE CONNECTING THE
TWO DISEASES. The B.S.E. problem is obvious, but if the correct measures are
taken, surely the problem could be contained, however, as it stands the lack of
investigation and interest of the possibility of B.S.E. and C.J.D. being linked
is open for speculation and surely someone has to account for peoples lives! WHY
is so much trouble being taken to convice people that B.S.E. and C.J.D. are not
linked? Guilty Conscience perhaps ? - or cover up?
HOUSE OF COMMONS
FROM BARRY JONES, M.P.
22 FEBRUARY 1994
Alleged Case of Creutzfeld Jakob Disease: Victoria Rimmer.
(now story changes that biopsy shows she does not have CJD...tss)
now story changes to ;
Advice
7. The Parliamentary Secretary is invited to note the recent statements
made on __________ and the present position which remains that CJD cannot be
confirmed, in this case at this stage.
3. The Medical Director at ___________________ Hospital advised the
Department on 6 June that the results of ___________________ brain biopsy had
been received and that it showed NO EVIDENCE OF CJD. ______________ Hospital
subsequently issued a statement to the press to this effect and this was
publicised widely in the press (doc 1). News coverage which followed suggested
that the statement made by ________________ Hospital had been misleading (doc
2). Enquires have been made of the Medical Director at _______________ Hospital
who has CONFIRMED THAT THE STATEMENT ISSUED BY THE HOSPITAL WAS ISSUED IN ERROR.
The facts are that two pathology reports on the same piece of brain tissue were
recieved. The first report indicated that CJD was unlikely, The second report
indicated that CJD was possible, PERHAPS EVEN LIKELY, but that no definitive
diagnosis could be made before a post mortem was undertaken.
MAD COW MEAL DESTROYED MY DAUGHTERS LIFE
A TEENAGE GIRL may have caught the human form of MAD COW DISEASE by eating
a contaminated burger it was claimed last night.
VICKY RIMMER, 16, has the killer Creutzfeldt-Jakob disease (CJD).
GIVE ME BACK MY LIFE
THEY BEGGED ME TO HUSH IT UP – GRAN’S AGONY
HUSH UP! GOVERNMENT TOLD GRAN: ''YOU MUST THINK OF THE ECONOMY''
WHY IS MY GIRL DYING ? '' IT WAS LIKE SOMEBODY OLD INSIDE A YOUNG PERSON'S
BODY
ONLY PROBLEM IS, VICKY RIMMER, 16, DID NOT DIE FROM nvCJD, SHE DIED FROM
SPORADIC CJD, supposedly. ...
Tuesday, November 04, 2014
*** The pathological and molecular but not clinical phenotypes are
maintained after second passage of experimental atypical bovine spongiform
encephalopathy in cattle
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Thursday, October 02, 2014
[Docket No. APHIS-2013-0064] Concurrence With OIE Risk Designations for
Bovine Spongiform Encephalopathy
Saturday, August 14, 2010
*** BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama)
and VPSPr PRIONPATHY
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
full text ;
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been
discovered in a wide verity of species across North America. typical C-BSE,
atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine,
typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98
Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD
in cervid is slowly spreading without any stopping it in Canada and the USA and
now has mutated into many different strains. Transmissible Mink Encephalopathy
TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease
have been silently mutating and spreading in different species in North America
for decades.
The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion
Firewall, of which we now know without a doubt, that it was nothing but ink on
paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of
banned mad cow feed has been put out into commerce, never to return, as late as
December of 2013, serious, serious breaches in the FDA mad cow feed ban have
been documented. The 2004 enhanced BSE surveillance program was so flawed, that
one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown,
who is preparing a scientific paper based on the latest two mad cow cases to
estimate the maximum number of infected cows that occurred in the United States,
said he has "absolutely no confidence in USDA tests before one year ago" because
of the agency's reluctance to retest the Texas cow that initially tested
positive.
The BSE surveillance and testing have also been proven to be flawed, and
the GAO and OIG have both raised serious question as to just how flawed it has
been (see GAO and OIG reports). North America has more documented TSE prion
disease, in different documented species (excluding the Zoo BSE animals in the
EU), then any other place on the Globe. This does not include the very
likelihood that TSE prion disease in the domestic feline and canine have been
exposed to high doses of the TSE prion disease vid pet food. To date, it’s still
legal to include deer from cwd zone into pet food or deer food. Specified Risk
Material i.e. SRM bans still being breach, as recently as just last month. nvCJD
or what they now call vCJD, another case documented in Texas last month, with
very little information being released to the public on about this case? with
still the same line of thought from federal officials, ‘it can’t happen here’,
so another vCJD blamed on travel of a foreign animal disease from another
country, while ignoring all the BSE TSE Prion risk factors we have here in the
USA and Canada, and the time that this victim and others, do spend in the USA,
and exposed to these risk factors, apparently do not count in any way with
regard to risk factor. a flawed process of risk assessment.
sporadic CJD, along with new TSE prion disease in humans, of which the
young are dying, of which long duration of illness from onset of symptoms to
death have been documented, only to have a new name added to the pot of prion
disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a
familial type disease could be sporadic with no genetic link to any family
member? when the USA is the only documented Country in the world to have
documented two different cases of atypical H-type BSE, with one case being
called atypical H-G BSE with the G meaning Genetic, with new science now showing
that indeed atypical H-type BSE is very possible transmitted to cattle via oral
transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada,
USA, and the UK, with the same old excuse, better surveillance. You can only use
that excuse for so many years, for so many decades, until one must conclude that
CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a
blip or a reason of better surveillance, it is a mathematical rise in numbers.
More and more we are seeing more humans exposed in various circumstance in the
Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same
time in North America, more and more humans are becoming exposed to the TSE
prion disease via consumption of the TSE prion via deer and elk, cattle, sheep
and goats, and for those that are exposed via or consumption, go on to further
expose many others via the iatrogenic modes of transmission of the TSE prion
disease i.e. friendly fire. I pondered this mode of transmission via the victims
of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone
sub-clinical with sFFI or sGSS ? what if?
Two decades have passed since Dr. Ironside first confirmed his first ten
nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first
ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is
transmissible. yet all these TSE prion disease and victims in the USA and Canada
are being pawned off as a spontaneous event, yet science has shown, the
spontaneous theory has never been proven in any natural case of TSE prion
disease, and scientist have warned, that they have now linked some sporadic CJD
cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about
this in the public domain. We must make all human and animal TSE prion disease
reportable in every age group, in ever state and internationally, we must have a
serious re-evaluation and testing of the USA cattle herds, and we must ban
interstate movement of all cervids. Any voluntary effort to do any of this will
fail. Folks, we have let the industry run science far too long with regards to
the TSE prion disease. While the industry and their lobbyist continues to funnel
junk science to our decision policy makers, Rome burns. ...end
REFERENCES Sunday, June 29, 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
TSS
Friday, November 28, 2014
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE AKA MAD COW DISEASE PORTUGAL
CONFIRMED
Thursday, February 14, 2013
Unique Properties of the Classical Bovine Spongiform Encephalopathy Strain
and Its Emergence From H-Type Bovine Spongiform Encephalopathy Substantiated by
VM Transmission Studies
Saturday, December 15, 2012
*** Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Saturday, August 14, 2010
***BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama)
and VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
However, a BSE expert said that consumption of infected material is the
only known way that cattle get the disease under natural conditons.
***“In view of what we know about BSE after almost 20 years experience,
contaminated feed has been the source of the epidemic,” said Paul Brown, a
scientist retired from the National Institute of Neurological Diseases and
Stroke.
BSE is not caused by a microbe. It is caused by the misfolding of the
so-called “prion protein” that is a normal constituent of brain and other
tissues. If a diseased version of the protein enters the brain somehow, it can
slowly cause all the normal versions to become misfolded. It is possible the
disease could arise spontaneously, though such an event has never been recorded,
Brown said.
*** What irks many scientists is the USDA’s April 25 statement that the
rare disease is “not generally associated with an animal consuming infected
feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown,
one of the world’s experts on this type of disease who retired recently from the
National Institutes of Health. "(The agency) has no foundation on which to base
that statement.”
Wednesday, February 12, 2014
*** USDA/APHIS NOTICE: Final Rule Regarding Imports and BSE Effective March
4, 2014
Thursday, February 20, 2014
Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr.
Linda Detwiler 2014
I ask Professor Kong ; Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform
Encephalopathies (BSE): Public Health Risk Assessment ''IS the h-BSE more
virulent than typical BSE as well, or the same as cBSE, or less virulent than
cBSE? just curious.....'' Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or
another, but we have found that H-BSE can infect humans. I hope we could publish
these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong, PhD Associate Professor Department of
Pathology Case Western Reserve University Cleveland, OH 44106 USA END...TSS
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
BSE-H is also transmissible in our humanized Tg mice. The possibility of
more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
please see below from PRION2013 ;
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
AD.56: The emergence of novel BSE prions by serial passages of H-type BSE
in bovinized mice
Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki
Okada, Shirou Mohri and Takashi Yokoyama National Institute of Animal Health;
Tsukuba, Japan
H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE,
and has been detected in several European countries, and North America.
Transmission studies of H-type BSE led to the emergence of the classical BSE
(C-BSE) phenotypes during passages in inbred wild type and bovinized
PrP-overexpressing transgenic mice. In this study, we conducted serial passages
of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice
(TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods
of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage
were constant (~= 220 d), no clear differences were observed in their biological
and biochemical properties. However, at the forth passage, 2 different BSE
phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the
other is longer survival times. TgBoPrP mice with longer incubation period
showed the H-type phenotype of PrPsc profile and pathology. However, those of
shorter incubation period were different phenotypes from previously existed BSE
prions (C-BSE, L-type BSE, and H-type BSE).
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
www.landesbioscience.com
please see ;
Thursday, August 15, 2013
The emergence of novel BSE prions by serial passages of H-type BSE in
bovinized mice
Sunday, September 1, 2013
*** Evaluation of the Zoonotic Potential of Transmissible Mink
Encephalopathy
We previously described the biochemical similarities between PrPres derived
from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations
suggest a link between these two uncommon prion phenotypes in a primate model
(it is to note that such a link has not been observed in other models less
relevant from the human situation as hamsters or transgenic mice overexpressing
ovine PrP [28]). We speculate that a group of related animal prion strains
(L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion
diseases in humans with a type 2 PrPres molecular signature (and more
specifically type 2B for vCJD)
snip...
Together with previous experiments performed in ovinized and bovinized
transgenic mice and hamsters [8,9] indicating similarities between TME and
L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME
outbreaks in North America and Europe during the mid-1900s.
Sunday, December 15, 2013
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE ***
Saturday, August 4, 2012
*** Final Feed Investigation Summary – California L-type BASE BSE Case -
July 2012
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical BSE
in these countries.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
The present study demonstrated successful intraspecies transmission of
H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc
in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be
minimally defined by oral transmission of different TSE agents (C-type, L-type,
and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected
cattle have been initiated and are underway to provide information regarding the
extent of similarity in the immunohistochemical and molecular features before
and after transmission.
In addition, the present data will support risk assessments in some
peripheral tissues derived from cattle affected with H-type BSE.
in the url that follows, I have posted
SRM breaches first, as late as 2011.
then
MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until
2007, when they ceased posting them.
then,
MAD COW SURVEILLANCE BREACHES.
Friday, May 18, 2012
Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy
(BSE) in the United States Friday May 18, 2012
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
Wednesday, May 30, 2012
PO-028: Oral transmission of L-type bovine spongiform encephalopathy
(L-BSE) in primate model Microcebus murinus
Monday, June 18, 2012
R-CALF Submits Incomplete Comments Under Protest in Bizarre Rulemaking
“Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products”
Tuesday, July 17, 2012
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th
General Session, 20 - 25 May 2012
Saturday, December 21, 2013
**** Complementary studies detecting classical bovine spongiform
encephalopathy infectivity in jejunum, ileum and ileocaecal junction in
incubating cattle ****
Wednesday, December 4, 2013
*** Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine
Products; Final Rule Federal Register / Vol. 78 , No. 233 /
Wednesday, December 4, 2013
Saturday, November 2, 2013
*** APHIS Finalizes Bovine Import Regulations in Line with International
Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type
disease around the Globe
UPDATE NORTH AMERICA MAD COW DISEASE
Monday, March 19, 2012
Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform
Encephalopathy
PLoS One. 2012; 7(2): e31449.
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...
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 ;
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...
Sunday, November 23, 2014
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in
June 2014 confirmed as USA case NOT European
The completed investigation did not support the patient's having had
extended travel to European countries, including the United Kingdom, or travel
to Saudi Arabia. The specific overseas country where this patient’s infection
occurred is less clear largely because the investigation did not definitely link
him to a country where other known vCJD cases likely had been infected.
Monday, November 3, 2014
USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014
National Prion Disease Pathology Surveillance Center Cases Examined1
(October 7, 2014)
***6 Includes 11 cases in which the diagnosis is pending, and 19
inconclusive cases;
***7 Includes 12 (11 from 2014) cases with type determination pending in
which the diagnosis of vCJD has been excluded.
***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob
disease (sCJD),
***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)
***and 21 cases of sporadic Fatal Insomnia (sFI).
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis *video*
Jeff Schwan, sporadic cjd, clustering, and BSE aka mad cow type disease, is
there a link ? *video*
1997-11-10: Panorama - The british disease *video*
Sunday, September 6, 2009
MAD COW USA 1997 *video*
Singeltary submission to PLOS ;
RE: re-Human Prion Diseases in the United States part 2 flounder replied to
flounder on 02 Jan 2010 at 21:26 GMT
No competing interests declared.
see full text ;
FACT is, BSE cases in Europe of the past years have dropped dramatically
due to feed ban that was enforced, and extensive BSE testing, in large numbers.
just the opposite has happened in the USA. it’s all been documented. there is
ample evidence that there is as much of a chance (if not more), that this victim
contracted human mad cow disease from sources right here in the USA. this PR
push to alienate a USA source factor for human BSE in the USA is a PR stunt by
the USDA inc., and not justified now, in my opinion. compare BSE testing figures
in the EU compared to the USA, compare mad cow feed ban breaches, and you will
see. hell, the 2004 enhanced BSE surveillance program was flawed so bad, the top
Prion God at the NIH TSE prion expert Paul Brown, says he does not trust
anything from the USDA since Texas covered up a mad cow for 7 months, on a 48
hour confirmation turn around. it’s all documented below in link. USDA inc shut
down the mad cow testing after so many atypical BSE cases started showing up.
...
***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.
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent.
*** Lending support to this hypothesis, pathological and biochemical
similarities have been observed between L-BSE and an sCJD subtype (MV genotype
at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and
another sCJD subtype (MM genotype) [15].
snip...
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion
strains in transgenic mice expressing human prion protein
*** Surprisingly, however, BSE transmission to these transgenic mice, in
addition to producing a vCJD-like phenotype, can also result in a distinct
molecular phenotype that is indistinguishable from that of sporadic CJD with
PrPSc type 2.
These data suggest that more than one BSEderived prion strain might infect
humans;
***it is therefore possible that some patients with a phenotype consistent
with sporadic CJD may have a disease arising from BSE exposure.
snip...
These studies further strengthen the evidence that vCJD is caused by a
BSE-like prion strain.
Also, remarkably, the key neuropathological hallmark of vCJD, the presence
of abundant florid PrP plaques, can be recapitulated on BSE or vCJD transmission
to these mice.
***However, the most surprising aspect of the studies was the finding that
an alternate pattern of disease can be induced in 129MM Tg35 mice from primary
transmission of BSE, with a molecular phenotype indistinguishable from that of a
subtype of sporadic CJD. This finding has important potential implications as it
raises the possibility that some humans infected with BSE prions may develop a
clinical disease indistinguishable from classical CJD associated with type 2
PrPSc. This is, in our experience, the commonest molecular sub-type of sporadic
CJD. In this regard, it is of interest that the reported incidence of sporadic
CJD has risen in the UK since the 1970s (Cousens et al., 1997)...
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.
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a
Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have
attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you
will find in the paper, we have managed to associate the alternate phenotype to
type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim
any further sub-classification in respect of Heidenhain variant CJD or Vicky
Rimmer's version. It will take further studies, which are on-going, to establish
if there are sub-types to our initial finding which we are now reporting. The
main point of the paper is that, as well as leading to the expected new variant
CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an
alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can
be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial
College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44
(0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until
9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
____________________________________ END
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis *video*
Jeff Schwan, sporadic cjd, clustering, and BSE aka mad cow type disease, is
there a link ? *video*
1997-11-10: Panorama - The british disease *video*
Sunday, September 6, 2009
MAD COW USA 1997 *video*
Wednesday, October 09, 2013
*** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY,
£41,078,281 in compensation ***
Monday, November 3, 2014
USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014
National Prion Disease Pathology Surveillance Center Cases Examined1
(October 7, 2014)
***6 Includes 11 cases in which the diagnosis is pending, and 19
inconclusive cases;
***7 Includes 12 (11 from 2014) cases with type determination pending in
which the diagnosis of vCJD has been excluded.
***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob
disease (sCJD),
***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)
***and 21 cases of sporadic Fatal Insomnia (sFI).
Monday, November 3, 2014
The prion protein protease sensitivity, stability and seeding activity in
variably protease sensitive prionopathy brain tissue suggests molecular overlaps
with sporadic Creutzfeldt-Jakob disease
Sunday, November 23, 2014
Transmission Characteristics of Variably Protease-Sensitive Prionopathy
* We concluded that VPSPr is transmissible; thus, it is an authentic prion
disease.
Thursday, August 12, 2010
Seven main threats for the future linked to prions
***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...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
*** 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...
Singeltary submission to PLOS ;
RE: re-Human Prion Diseases in the United States part 2 flounder replied to
flounder on 02 Jan 2010 at 21:26 GMT
No competing interests declared.
No competing interests declared.
see full text ;
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL
TEXT
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember,
the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been
documented in North America, along with the typical scrapie's, and atypical
Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these
TSE in different species have been rendered and fed to food producing animals
for humans and animals in North America (TSE in cats and dogs ?), and that the
trading of these TSEs via animals and products via the USA and Canada has been
immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances
and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD
only theory in 2009. With all the science to date refuting it, to continue to
validate this old myth, will only spread this TSE agent through a multitude of
potential routes and sources i.e. consumption, medical i.e., surgical, blood,
dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and
the urgent need to make all human TSE in the USA a reportable disease, in every
state, of every age group, and to make this mandatory immediately without
further delay. The ramifications of not doing so will only allow this agent to
spread further in the medical, dental, surgical arena's. Restricting the
reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO
age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al
and many more, that the world of TSE Transmissible Spongiform Encephalopathy is
far from an exact science, but there is enough proven science to date that this
myth should be put to rest once and for all, and that we move forward with a new
classification for human and animal TSE that would properly identify the
infected species, the source species, and then the route.
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
Singeltary comment ;
TSS
