Yes I think that studies should continue.
I doubt they test every single beef slaughtered. Ponder that undertaking for a second.
Thirdly I once read(on the interesting LOL) that part of being kosher meat was that no bones were cut and only deboned meat used. May be hogwash May be true. It did make me ponder what is natural though.
Eating a T bone that has been cut on a band saw(down the spinal column) probably would be more of a danger than a filleted loin that is boneless.
There is also the evidence of humans getting it from eating squirrel brains. Where is the worry about eating squirrels?
FOOD FOR THOUGHT.
educate yourselves, and for sure, if you can, process your own meat, and be very careful doing it. here's an example with cattle, and please remember, science to date shows, cwd compared to bse, is much more transmissible vertically and horizontally, and there is some evidence that indeed, tse prion can be infectious i.e. casual contact, and with the recent/old findings of detectable tse prion in skin, with the right strain, transmission of the tse prion via casual contact is not so out of the question...imo, if it has not happened already...please understand, to date, there has been no documented cases of _familial_ type tse prion in any animal species, only human, which brings me to my deduction to date (which is meaningless), that the science surrounding human familial type prion disease is still questionable in my opinion, and evidently, i am not the only one that has questioned this;
10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY
TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question...
''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors
First published: 17 January 2018
https://doi.org/10.2903/j.efsa.2018.5132 ;
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
snip...
The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132
also see;
This provides circumstantial evidence of an inherited susceptibility to the agent and suggests that cases of iatrogenic transmission may have occurred due to the unfortunate temporal proximity of susceptible individuals exposed to the agent.
In the close geographic group of three cases possible nodes of transmission can be suggested, either iatrogenic or through dental procedures, but these must remain conjectural. It is known, however, that the similar scrapie agent can be transmitted from the gums of animals (Adams and Edgar, 1978). Such close spatial clustering of cases is extremely unusual, being previously reported in England (Matthews, 1975a), Czechoslovakia (Mayer et al., 1977) and Hungary (Majtenyi, 1978), but not detected in the study of the epidemiology of C.J.D. in urban Paris (Cathala et al., 1978) where the incidence was found to be relatively high.
The occurrence of the disease in a patient who had contact with cases of familial C.J.D., but was not genetically related, has been described in Chile (Galvez et al., 1980) and in France (Brown et al., 1979b). In Chile the patient was related by marriage, but with no consanguinity, and had social contact with subsequently affected family members for 13 years before developing the disease. The contact case in France also married into a family in which C.J.D. was prevalent and had close contact with an affected member. In neither instance did the spouse of the non-familial case have the disease. The case described in this report was similarly related to affected family members and social contact had occurred for 20 years prior to developing C.J.D. If contact transmission had occurred, the minimum transmission period would be 11 years. Contact between sporadic cases has not been described and it is remarkable that possible contact transmissions have all been with familial cases. No method of transmission by casual social contact has been suggested.
***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent.
snip...see full text here;
http://web.archive.org/web/20050425210551/http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf
The occurrence of the disease in a patient who had contact with cases of familial C.J.D., but was not genetically related, has been described in Chile (Galvez et al., 1980) and in France (Brown et al., 1979b). In Chile the patient was related by marriage, but with no consanguinity, and had social contact with subsequently affected family members for 13 years before developing the disease. The contact case in France also married into a family in which C.J.D. was prevalent and had close contact with an affected member. In neither instance did the spouse of the non-familial case have the disease. The case described in this report was similarly related to affected family members and social contact had occurred for 20 years prior to developing C.J.D. If contact transmission had occurred, the minimum transmission period would be 11 years. Contact between sporadic cases has not been described and it is remarkable that possible contact transmissions have all been with familial cases. No method of transmission by casual social contact has been suggested.
***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent.
snip...see full text here;
http://web.archive.org/web/20050425210551/http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf
http://transmissiblespongiformencep...014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html
Wednesday, January 23, 2019
CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019
https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html
kind regards, terry
