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Thread: CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002 Updated 2019

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    Default CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002 Updated 2019

    WEDNESDAY, FEBRUARY 20, 2019

    CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002 Updated 2019

    https://chronic-wasting-disease.blog...ss-serial.html


    terry

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    BSE INQUIRY EVIDENCE

    Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.
    ------------------------------------------------------------------------
    TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
    see references:
    DEER BRAIN SURVEY

    https://web.archive.org/web/20090506...1/20004001.pdf

    https://www.facebook.com/groups/1557...c_location=ufi

    i have not updated my blogspot url with all this data archived, but i will work on it...but until then, i have updated this on the above links with live urls to the actual BSE Inquiry documents...

    Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY

    Date: Fri, 18 Oct 2002 23:12:22 +0100

    From: Steve Dealler

    Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member

    To: BSE-L@ References: <3daf5023 .4080804="" wt.net="">

    Dear Terry,

    An excellent piece of review as this literature is desparately difficult to get back from Government sites.

    What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!

    Steve Dealler ===============

    https://caninespongiformencephalopat...pathy-aka.html

    Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk

    BSE Inquiry Steve Dealler

    Management In Confidence

    BSE: Private Submission of Bovine Brain Dealler

    https://web.archive.org/web/20090506...2/08003001.pdf

    reports of sheep and calf carcasses dumped...

    https://web.archive.org/web/20090505...2/07002001.pdf

    re-scrapie to cattle GAH Wells BSE Inquiry

    https://web.archive.org/web/20090506...2/09001001.pdf

    Dr. Dealler goes rogue to confirm BSE

    https://web.archive.org/web/20090506...2/14003001.pdf

    https://web.archive.org/web/20090506...2/14003001.pdf

    https://web.archive.org/web/20090505...2/17003001.pdf

    Confirmation BSE Dealler's mad cow

    https://web.archive.org/web/20090505...2/16006001.pdf

    BSE vertical transmission

    https://web.archive.org/web/20090506...2/13003001.pdf

    1993 cjd report finds relationship with eat venison and cjd increases 9 fold, let the cover up begin...tss

    https://web.archive.org/web/20090506...7/00001001.pdf

    FINDINGS

    *** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

    *** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

    *** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

    There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02)..

    The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

    snip...

    It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

    snip...

    In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

    snip...

    In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

    snip...see full report ;

    https://web.archive.org/web/20170126...8/00004001.pdf

    GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID

    BSE INQUIRY

    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.

    http://web.archive.org/web/200305110...0/00003001.pdf

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