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Mad cow

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loneranger

Well-Known Member
Just read story of a father of 31 yrs. died of the mad cow strain. Lasted a year. Article said some 350 people die from it a year. No answer to how he contracted it? Heck I have cattle all around me here in Iowa. Now deer a threat too.
 
Supposedly contact of the brain or spinal tissue from cows for mad cow as in deer. So mass produced store meat and ground beef,,,stay away from it. But how about saliva. Deer spread by saliva and mucus. Cattle slobber all over everything. Strange how humans contact this.
 
loneranger said:
Just read story of a father of 31 yrs. died of the mad cow strain. Lasted a year. Article said some 350 people die from it a year. No answer to how he contracted it? Heck I have cattle all around me here in Iowa. Now deer a threat too.
Click to expand...

In the US?
 
Tony Gibson. 33 yrs old. Nashville Tennessee. Look it up. Did he get it from store meat? Cold sandwich meat with who knows what in it? Kissing a cow? Howd he get it??
 
No one has addressed this though. Infected deer have it in their saliva correct? Deer eat in crops here in Iowa. Deer saliva gets into soil. Prions in soil come up in plants. Prions come up in crops. Crops used in many ways. An avenue to humans.
 
I read an article on it. It isn’t clear to me. Are they saying this game from transmission due to mad cow or was this sporadic CJD?


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Not worried. Ive had a good long life Dont think its a laughing matter however. If one disease dont get you another will. Know a friend. Young guy in his 40s. Just diagnosed with Parkinsons. Another brain disease.
 
not sure if this case you speak of has been confirmed by the cdc et al yet or not as nvcjd...doesn't really matter, science has shown now that sporadic cjd has been linked to typical c-BSE and the atypical BSE h and l, and also, sporadic cjd has now been linked to both atypical and typical scrapie, and sadly, cwd has been linked to sporadic cjd. i have posted it all here before, and i can link source references from the studies again if anyone wishes.....
 
flounder9 said:
not sure if this case you speak of has been confirmed by the cdc et al yet or not as nvcjd...doesn't really matter, science has shown now that sporadic cjd has been linked to typical c-BSE and the atypical BSE h and l, and also, sporadic cjd has now been linked to both atypical and typical scrapie, and sadly, cwd has been linked to sporadic cjd. i have posted it all here before, and i can link source references from the studies again if anyone wishes.....
Click to expand...


If you could put all the studies into language we all understand, that would help profoundly. You could just summarize the studies for us would be great.
 
Bottom line,,,,Humans can get Mad Cow type killing disease. Father of 4 ,,33 yrs old died from it. How he got it a question?
 
I read a brief (New England Journal of Medicine, I think- a good few years ago when I was a chemist) where two guys went to Dr with symptoms that ended up LOOKING like Mad Cow. They tested inconclusively positive for a disease that humans “can’t get”. A few observation days later in the hospital, the symptoms cleared and the proteins and/or enzymes disappeared from their systems. They were sent home.

Several months later, one of the two was back with the same. (Long story short) this time they did more extensive background and discovered that squirrel brains can contain similar proteins that manifest in cows when they have the disease. The condition is not fatal in squirrels. But because, in some places, fried squirrel brains with scrambled eggs is a great delicacy, these guys were eating enough squirrel brain that the protein was giving them mad-cow-like symptoms until their systems had purged the offending chemical.


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Tim Hull said:
If you could put all the studies into language we all understand, that would help profoundly. You could just summarize the studies for us would be great.
Click to expand...

you can't have it both ways. i put it in short terms because folks bitch about my posting the actual studies, so which is it?
 
flounder9 said:
you can't have it both ways. i put it in short terms because folks bitch about my posting the actual studies, so which is it?
Click to expand...

sorry, i am just tired. after 21 years of trying to warn the world, i get a bit testy...

WEDNESDAY, SEPTEMBER 26, 2018

JAVMA In Short Update USDA announces detection of atypical BSE

http://bovineprp.blogspot.com/2018/09/javma-in-short-update-usda-announces.html

ZOONOSIS OF SCRAPIE TSE PRION

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).

Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

***is the third potentially zoonotic PD (with BSE and L-type BSE),

***thus questioning the origin of human sporadic cases.

We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.

***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.

Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

***> why do we not want to do TSE transmission studies on chimpanzees $

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man.

***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough.

***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...

R. BRADLEY

https://web.archive.org/web/2017012...einquiry.gov.uk/files/yb/1990/09/23001001.pdf


kind regards, terry
 
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.

https://assets.publishing.service.g...3407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf

http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html

cwd scrapie pigs oral routes

***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***

>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***

***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).

***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period.
This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.

https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091

https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017

https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105


TUESDAY, APRIL 18, 2017

*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***

http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.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

hay, straw, grains...and cwd tse prion

***> NORWAY CWD UPDATE December 2018 Report from the Norwegian Scientific Committee for Food and Environment (VKM) 2018: 16

Factors that can contribute to spread of CWD – an update on the situation in Nordfjella, Norway
Opinion of Panel on biological hazards of the Norwegian Scientific Committee for Food and Environment 13.12.2018 ISBN: 978-82-8259-316-8 ISSN: 2535-4019 Norwegian Scientific Committee for Food and Environment (VKM) Po 222 Skøyen 0213 Oslo Norway FRIDAY, DECEMBER 14, 2018 Norway, Nordfjella VKM 2018 16
Factors that can contribute to spread of CWD TSE Prion UPDATE December 14, 2018

https://vkm.no/download/18.696229a71677d983532c0c11/1544792739325/CWD factors for spread 2018.pdf
https://chronic-wasting-disease.blogspot.com/2018/12/norway-nordfjella-vkm-2018-16-factors.html

THURSDAY, OCTOBER 25, 2018

***> Norway New additional requirements for imports of hay and straw for animal feed from countries outside the EEA due to CWD TSE Prion

https://www.mattilsynet.no/dyr_og_d...v_ved_import_av_hoy_og_halm_til_dyrefor.32299

https://chronic-wasting-disease.blogspot.com/2018/10/norway-new-additional-requirements-for.html

THURSDAY, FEBRUARY 14, 2019

Norway Eradication of Chronic Wasting Disease is not completed

https://chronic-wasting-disease.blogspot.com/2019/02/norway-eradication-of-chronic-wasting.html


real-estate property values will be next...tse prion survives in the soil for from 16 to 21 years...a tainted wasteland...


kind regards, terry
 
WTF, it's starting so sound like doom and gloom all over!

Guess I'll move my stands and blinds to creeks, streams and ponds to arrow some fish and start eating fish everyday. The worse it could be is Mercury poisoning....
 
flounder 9, IN your opinion do you think it is just a matter of time before it is transmitted to humans or do you think it has already happened?
 
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