“That would be the end of our industry”

From a purist perspective, the agricultural practices are creating higher deer population and density. The guy dumping a bail of alfalfa is creating seasonally greater density but not necessarily population. I think I just talked myself into banning farming.

But if frequency is a more important factor than density...with of course the problems to frequency that density can contribute...oh hell, my head is starting to hurt.
 
What it really means is that the scientists and medical experts still don't know jack sheet about CWD :giggle:

While I think there is still a lot more to learn, and I hope a lot more is learned, there does seem to be a pretty sold knowledge base on TSEs in general, and a lot of that knowledge obviously applies in a general sense to CWD.
 
But if frequency is a more important factor than density...with of course the problems to frequency that density can contribute...oh hell, my head is starting to hurt.
It makes no sense to me that frequency dependence is an issue here and density is not. No sense at all. If anyone has a simple explanation of it, I would be interested in listening to it.
 
It makes no sense to me that frequency dependence is an issue here and density is not. No sense at all. If anyone has a simple explanation of it, I would be interested in listening to it.

It was mentioned on a podcast that I wasn't closely listening to, so I searched it, and that confused me more, but what I think I get out of it is that the frequency of the occurrence of infection is more impactful to the spread than the density of the population. Although it would make sense to me, that frequency in a dense population would be more impactful than in a dispersed population...but again, I guess that depends a lot on population and deer behavior dynamics.

Hopefully someone smarter than me will come along and correct all I've screwed up.
 
Sometimes I think there are outfitters and hunters that would shoot the last deer in the forest and then shrug it off and go duck hunting.....

I think you are exactly right and it makes me sick to my stomach.
 
RockinU, that only makes sense to me if the disease is highly contagious such that one animal saturates the environment with enough prions that the spread is not limited by prion availability. But from what little I know, prions are not especially contagious, so it would take a lot of exposures (high density, not frequency) for most transmissions to occur. I'm curious where the original statements are made in the literature. Too easy to err here on something like a podcast. But I admit, they may be quite correct. Just doesn't add up for me.
 
RockinU, that only makes sense to me if the disease is highly contagious such that one animal saturates the environment with enough prions that the spread is not limited by prion availability. But from what little I know, prions are not especially contagious, so it would take a lot of exposures (high density, not frequency) for most transmissions to occur. I'm curious where the original statements are made in the literature. Too easy to err here on something like a podcast. But I admit, they may be quite correct. Just doesn't add up for me.

I get your point, but I think the frequency possibly wouldn't contribute to environmental transmission, but rather to individual to individual transmission due to the gregarious nature of deer.

I would try to find the literature and give it to you here, but I've already messed around to the point of being late. I searched "CWD frequency vs density distribution" and I believe the first entry was from esajournals. You have to go pretty deep to find the pertinent info, and to be honest I really just skimmed it, so you may be able to correct me if you dive into it.
 
I don't find your reply to be entirely accurate but I am not a biologist or medical expert that is qualified to argue those points. The research is there to postulate that it fits the classic definition of an organism:

"Prion proteins can act as infectious agents, spreading disease when transmitted to another organism"

"The concept that transmissible spongiform encephalopathies (TSEs) are caused only by proteins has changed the traditional paradigm that disease transmission is due solely to an agent that carries genetic information. The central hypothesis for prion diseases proposes that the conversion of a cellular prion protein (PrPC) into a misfolded, β-sheet-rich isoform (PrPSc) accounts for the development of (TSE). There is substantial evidence that the infectious material consists chiefly of a protein, PrPSc, with no genomic coding material, unlike a virus particle, which has both. However, prions seem to have other partners that chaperone their activities in converting the PrPC into the disease-causing isoform. Nucleic acids (NAs) and glycosaminoglycans (GAGs) are the most probable accomplices of prion conversion. Here, we review the recent experimental approaches that have been employed to characterize the interaction of prion proteins with nucleic acids and glycosaminoglycans. A PrP recognizes many nucleic acids and GAGs with high affinities, and this seems to be related to a pathophysiological role for this interaction. A PrP binds nucleic acids and GAGs with structural selectivity, and some PrP:NA complexes can become proteinase K-resistant, undergoing amyloid oligomerization and conversion to a β-sheet-rich structure. These results are consistent with the hypothesis that endogenous polyanions (such as NAs and GAGs) may accelerate the rate of prion disease progression by acting as scaffolds or lattices that mediate the interaction between PrPC and PrPSc molecules. In addition to a still-possible hypothesis that nucleic acids and GAGs, especially those from the host, may modulate the conversion, the recent structural characterization of the complexes has raised the possibility of developing new diagnostic and therapeutic strategies."


Thank you for the link!

So I just skimmed the article, but it appears what they are discussing in that paper has nothing to do with disease transmission from animal to animal. They are trying to figure out the mechanism by which the abnormal protein triggers the refolding of a normal protein into an abnormal protein. They think small bits of DNA might facilitate the binding of abnormal prions to normal proteins, and lower the energy required to make refolding occur. They act as a catalyst to help make that process easier.

The basic explanation I still use from way back in my Bio101 classes “Cells make up organs, organs make up organisms”. 🙂

@RockingU - You’ve hit on the confounding issue when it comes to CWD. When the environment itself is serving as a reservoir of infection, how much transmission is environmental vs deer to deer? How much can population manipulation affect transmission? Is the disease density dependent? I’m not aware that anyone has answers to those yet. I certainly don’t. I’ve heard some heated arguments about density dependence and CWD though.

I believe the article you mentioned is this one. I haven’t read it yet.

https://esajournals.onlinelibrary.wiley.com/doi/pdf/10.1890/ES12-00141.1
 
No I dont think any baiting is ok with the exception of bears maybe, but I dont bear hunt. Were not cavemen who rely on the meat for survival. In life or death situations like that anything goes. But were not in life or death situations it's a hobby and a tradition for 99% of us so it should be fair chase. I dont believe baiting is fair chase. Especially paying someone to bait for you and guide you so you can harvest a trophy. That's ego driven not passion driven.
But to each their own just cause others do it doesn't mean I have to do it or support it. Their adults and can make their own decisions without my help. 😉 but like I said no sympathy coming from my end.
My views on fair chase are very similar to yours. Hunting Saskat giants is a unique hunting opportunity though. I would like to see our grand children have that opportunity should they choose to hunt there. I am a DIY guy on public lands. Scouting is a very pleasurable and important part of my hunt. But if using an outfitter is the only way to hunt those whitetails; the industry needs to be healthy otherwise that hunting opportunity is lost to us forever.
 
Thank you for the link!

So I just skimmed the article, but it appears what they are discussing in that paper has nothing to do with disease transmission from animal to animal. They are trying to figure out the mechanism by which the abnormal protein triggers the refolding of a normal protein into an abnormal protein. They think small bits of DNA might facilitate the binding of abnormal prions to normal proteins, and lower the energy required to make refolding occur. They act as a catalyst to help make that process easier.

The basic explanation I still use from way back in my Bio101 classes “Cells make up organs, organs make up organisms”. 🙂

@RockingU - You’ve hit on the confounding issue when it comes to CWD. When the environment itself is serving as a reservoir of infection, how much transmission is environmental vs deer to deer? How much can population manipulation affect transmission? Is the disease density dependent? I’m not aware that anyone has answers to those yet. I certainly don’t. I’ve heard some heated arguments about density dependence and CWD though.

I believe the article you mentioned is this one. I haven’t read it yet.

https://esajournals.onlinelibrary.wiley.com/doi/pdf/10.1890/ES12-00141.1
The transmission I was referring to was from a CWD prion to a normal protein. Could be DNA or RNA that the prion binds to. There is a more conclusive study done with chimps but I have to go look for it. Did you have a problem classifying an amoeba? :)
 
@RockingU - You’ve hit on the confounding issue when it comes to CWD. When the environment itself is serving as a reservoir of infection, how much transmission is environmental vs deer to deer? How much can population manipulation affect transmission? Is the disease density dependent? I’m not aware that anyone has answers to those yet. I certainly don’t. I’ve heard some heated arguments about density dependence and CWD though.

I believe the article you mentioned is this one. I haven’t read it yet.

https://esajournals.onlinelibrary.wiley.com/doi/pdf/10.1890/ES12-00141.1

I do not feel it is right to call the environment a reservoir for CWD. True, prions can linger long in the soil like a seed in the "seed bank" and then move to infecting an animal, but true reservoirs for diseases require that the disease can multiply in the reservoir - in perpetuity if you will. Serengeti carnivores are the reservoir for rabies in African domestic dogs, for instance. Does this nuance matter? I think it does as prions can only be lost in the environment, they cannot increase there, just as seeds in seed banks can only decline in number, albeit very slowly in some instances. That is an important part of the dynamics of those plants.

In skimming quickly through that article, it does seem that there is some effect of both density and frequency in their "intermediate model".
 
I do not feel it is right to call the environment a reservoir for CWD. True, prions can linger long in the soil like a seed in the "seed bank" and then move to infecting an animal, but true reservoirs for diseases require that the disease can multiply in the reservoir - in perpetuity if you will. Serengeti carnivores are the reservoir for rabies in African domestic dogs, for instance. Does this nuance matter? I think it does as prions can only be lost in the environment, they cannot increase there, just as seeds in seed banks can only decline in number, albeit very slowly in some instances. That is an important part of the dynamics of those plants.

In skimming quickly through that article, it does seem that there is some effect of both density and frequency in their "intermediate model".

Reservoir may not be the right word, but it does need to be noted that prions in the environment are a different thing altogether from most disease agents in the environment. They persist for a very long time, need no host, certain environmental conditions make them more infectious, and while they do not reproduce, their ability to persist without regard to conditions means that with the presence of animals actively shedding prions, they will tend to accumulate in areas with prevalence.
 
Listened to a podcast with Rinella and QDMA this week that mentioned baiting. I like the QDMA policy on the matter:

They won't seek to approve new baiting laws.

They do not recommend ending old baiting laws.

The reasons:

The ethics of the region have been defined. That is how that culture hunts. Changing those rules is unpredictable to the practices that may occur, and the biological repercussions of shifting baiting laws cannot easily be understood. Nor can the consequences of overhunting, or loss of hunters.

Bottom line: unless compelling evidence suggests tremendous harm is occuring under a current policy...don't change it. Changes always have unforeseen consequences and new incentives: people always respond to incentives, often in unpredictable ways.
 
I understand the vastness...my point is how hard is it to wake up at 5AM and look at the map and pick what bait pile to go sit by? That's not real tough. It's not like these guides are understanding the terrain and finding hidden funnels or saddles or dried up creek beds or depressions that the deer are using to travel from place to place. They just throw out bails of alfalfa in areas where deer are and go sit by them. Here is my $2000 sign me up and after I harvest one here is a $500 tip for great guide work.
It's also incredibly tough hunting whitetail deer in the adirondacks of NY but nobody is baiting over there, but guys and gals are still getting it done.
Try $5500. My brother in law was wanting to go to Saskatchewan to shoot a bigger buck than we get in the south. Most of them seemed to run about $5500 per 6-7 day hunt.
 
It’s always interesting to see what people consider fair chase and what they don’t. I’ve known guys here in the south that had absolutely no problem with baiting whatsoever but wouldn’t shoot a bedded animal. Had to let it stand up first because it wasn’t fair to kill it in it’s bed.
 
Nope...a single celled organism made up of organelles, which themselves are made up of the building blocks of life (carbohydrates, lipids, proteins and nucleic acids). It’s a generic yet scalable model 😂
My usage of organism was incorrect. Thank you for showing me that. They tend to label the prions with abnormal proteins as "particles". They also tend to label viruses as particles.
 

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