Does CWD (wasting disease) in Deer fit that descrpition too (not transmissible to people)? If so, it’d give me a relief.
This is silly.
There is hardly any waste at all from meat processing plants (the old saying was ‘they use every part of the pig except the squeal’). And they certainly do not haul what waste there is out into the forests to dump where deer can find it.
Stop reading propaganda from PETA and other humaniacs. Or at least, stop believing it so credulously.
When I say “waste” I am talking about manure. (I should have said waste from feedyards and factory farms, not the processing plants.)
You mean valuable organic fertilizer. That’s not ‘waste’. It is sold, for a good price.
Well, even so, it gets into the groundwater all the same. I’m not trying to be dogmatic or pigheaded here - what I am saying is that it seems to me that prions will wind up in the groundwater.
Are you suggesting that prions are excreted in shit? Do you have any basis for this suggestion at all?
No I don’t. Can it be? Has anyone done research into it?
Everything I’ve ever read indicates that prions remain in the central nervous system tissue. But you just tried to say that deer might have developed CWD from consuming manure from feedlots. I’m confused at this point about how you think this might work.
Here’s my line of thinking:
Cows with BSE who have not been detected as such and disposed of might enter the food chain. This means that they could end up as feed for cows (or pigs.) Either through being eaten by people and then scraps of table waste making their way into feed, or by having their carcasses rendered into feed. Yes, the prions are in the central nervous tissue of these animals. But once they are consumed (by other cows) in the form of feed, the prions could pass through those cows’ digestive system and wind up in the manure and ultimately in the groundwater. How is this not making sense?
Prions are proteins. This is a crucial point. They are not some super material that resists all attack. What they do resist is conventional sterilisation techniques that are directed at the puny mechanisms of living cells or viral DNA. In particular they are resistant to the quick sterilisation techniques we are used to using. (Lets face it, when we use boiling water or other heat, we are simply cooking any organisms to about the same extent we cook an egg. Many proteins survive this, which is partly why cooking does not destroy our food.) But this does not mean that prions are resistant to the same degradation mechanisms that other proteins are subject to. In the environment they will be degraded just as any other random protein is. Prions getting into the groundwater unscathed is about as likely as proteins from a raw egg broken on the ground contaminating the groundwater. Bacteria will mop the prions up just as fast as any other protein.
OTOH, proteins do survive the gut, especially in ruminants. The creation of feed supplements for farm animals can contain some pretty appalling components by human standards. Chicken shit can be used for instance. This can lead to all sorts of other disease issues of a more conventional nature. Eating fresh dung might expose you to prions if the animal had eaten contaminated food, but the normal degradation processes that break down feaces is going to break down any prions.
If prions could easily be found in the feces, then they would have worked to create an ante-mortem diagnostic test based on a fecal sample, which I haven’t read them been able to do. That said, prions are not detected everywhere in the animals affected, they’re detected in the central nervous system, and some prion diseases may also be found in some nerves and lymph nodes. And even in those places, in many cases it seems to be there only for some time and not throughout the infection.
As to the connection of if CWD is transmissible to people, I’m not sure they’ve been able to completely rule it out. This is why it is a big research interest in it, from deer farms to cattle living next to wild deer. IIRC, different strains of CWD are transmissible amongst deer.
My point was that you keep harping on those diseases as if all of them are exactly the same as BSE, and I keep telling you that there are other diseases that are not transmitted to humans (scrapies) and again, are natural (ie, not from feeding of animal parts to another herbivore).
Again, Argent, doing what you described has been illegal for quite a while. Could someone illegally do it? Yes, but it is more likely that the one who does it is a relatively small, unknown company and not a big company that does not want to deal with that issue.
Also, IIRC, they’ve cut down (it may be illegal, but I’m not 100%) on the selling of cow brain tissue for human consumption.
The short answer is that vCJD incidence is now very low indeed, even in britain, and there are plenty of better candidates for one’s hypochondria 
It still gets plenty of study however as for another spongiform encephalopathy, kuru, there was found to be a very long incubation period.
But it seems unlikely that incidence would peak, flatten to virtually zero and then peak again.
Another reason for studying the disease is that there are still some unknowns about the mechanism. We know it’s caused by prions, but the exact details of under what circumstances prions form aggregations is debated. It seems more complex than a virus-like spread.
It’s been illegal to use such feed for a couple decades. I suppose illicit use of animal proteins in cattle feed might still occur on a small scale, but feed plants are inspected in sufficient numbers that we know it’s not a widespread thing.
Can I just add that prions really aren’t still in the realm of mysterious things we don’t understand. There are a lot of people working very hard on them, and we’ve learned a lot. There’s a guy in my own department here that researches them.
Ok, after devoting part of my afternoon to reading various recent (within last year) articles on prion diseases, this is what I found, some of which is a repeat of what I said before, some of it which is new (I didn’t know):
-CWD and scrapies are both infectious. Meaning other deer or sheep around the infected animals can get the disease. Scrapies is not known to cause human disease (and has been known for centuries). Both can be found in other areas of the body, like the lymph nodes (mentioned earlier), saliva, and, most recently, feces. It was not completely known, yet, if the prion proteins found in the deer would be enough to infect another deer. It just shows that fecal transmission is possible. Transmission through the olfactory bulb is also plausible.
-In contrast, classical BSE and vCJD are considered more “food-borne” diseases. The animals have to ingest infected organs. Cow to cow transmission has not been observed. And for the most part, the majority of prions are found in the central nervous system, in contrast with scrapies and CWD.
I’ll be honest and say I won’t read every single article (there are quite a few recent ones within the last year). The above is just an overview of the main reviews from the main journals. It is possible newer detection methods can be developed in the coming years.
I want to repeat a point I made earlier, that even though the disease is not in the news, does not mean it is not being researched and surveillance is not done. Of course it is researched, they want to know how else to prevent it, and in the case of CWD, control it. Also, surveillance (both active and passive) is done for various prion diseases. This is how they have gained more information about the diseases, this is how they have found rare, sporadic cases of other prion diseases.
First, it is accepted that prions are difficult to remove from metal surfaces, and that even autoclaving may not provide sufficient cleaning. Tonsillectomies in the UK require the use of a single-use kit, because the prions accumulate in the tonsils of vCJD sufferers. (Welsh NHS site). If a surgical patient develops vCJD, a notification process occurs to identify other patients operated on later with the same equipment (cite). Those patients then cannot give blood and require special measures if they have surgery. They will also be monitored to see if they do develop vCJD.
It is also proposed that there may be a genetically mandated response to prion infection. One genetic subtype (MM) develops vCJD very rapidly (those that have suffered vCJD from the BSE outbreak and subsequent person-to-person infection). Other genetic subtypes (MV, VV) develop much more slowly. Some type MV cases have developed vCJD. Late developing Kuru is also associated with type MV. An unanswered question is whether slow-developing VV sufferers will ever actually develop vCJD within their lifetime. (BBC article with info on genetic influence on vCJD development). This genetic mix (25% MM, 50% MV, 25% VV) could give a double or triple wave of vCJD cases. However, in the UK this may only lead to an additional 350 cases (among MV) and maybe another very late group of about 170 (VV, similar to the number of MM patients).
So the numbers are small (for the UK), and it could take a long time to find out what is really going to happen.
Si
Denny Crane!
Headcheese is still produced, and considered quite a delicacy by many.
I thought that is made from pork, not beef?
Person-to-person? I didn’t think that was possible.