Cwd ????
08-31-2015, 06:12 PM
#71
Nontypical Buck
Join Date: Feb 2015
Location: Illinois
Posts: 3,695
And that gives you more insight how? I've peed in a cup and handed it to a lab tech and filled out the paper work. That doesn't mean I'm a lab specialist! I've pulled splinters out of my dogs paws but that doesn't make me a vet! I've raised cattle and horses and gave them their shots and treated them for pinkeye but that also doesn't make me a vet! Just because you have yanked some nodes and brains out and filled out the paperwork for the EXPERTS to do the RESEARCH doesn't make you anything more than a farmer still.
08-31-2015, 06:18 PM
#72
Spike
Join Date: Aug 2015
Posts: 62
Uhhh yes! If the prions are found IN the deer ANYWHERE then it is infected. They just haven't reached the brain yet. If it's only in the nodes then they haven't progressed to the brain. They wouldn't be showing signs. Pretty simplistic to understand even for a remedial reader. You were suggesting that the deer found to only be carrying in the nodes were just carriers and that it was genetically based. Which is 100% incorrect. Keep backpeddeling there BigTime1. The educated are watching and having a good laugh from your ignorance 
08-31-2015, 06:22 PM
#73
Nontypical Buck
Join Date: Oct 2009
Location: WI
Posts: 1,089
08-31-2015, 06:27 PM
#74
Nontypical Buck
Join Date: Feb 2015
Location: Illinois
Posts: 3,695
LMAO@ this guy. You seriously need to get some Google time and look up your subject matter fella. Cancer and CWD couldn't be MORE different. As I stated in the previous post, there is NO genetic proclivity for or against the CWD prion. There is no genetic barrier at this point and time in the evolution of the whitetail species. Maybe over time mother nature will allow one to be erected but for now. Nadda. Cancer on the other hand is a whole different ball game. It's a CELLULAR disease not an invasive prion. There is a cancer gene as most anyone knows, there isn't a prion gene because it's not a GENETIC DISEASE like cancer. Reading is fundamental BigTime1. Give it a try and quit trying to blow so much smoke up peoples rears and you might just learn a thing or two! Have a nice night, wife and I are catching up on the History show "Vikings" so that should give you a little while to bone up. Maybe you can actually bring something other than a pea shooter to this gunfight
08-31-2015, 07:30 PM
#75
Spike
Join Date: Aug 2015
Posts: 62
LMAO@ this guy. You seriously need to get some Google time and look up your subject matter fella. Cancer and CWD couldn't be MORE different. As I stated in the previous post, there is NO genetic proclivity for or against the CWD prion. There is no genetic barrier at this point and time in the evolution of the whitetail species. Maybe over time mother nature will allow one to be erected but for now. Nadda. Cancer on the other hand is a whole different ball game. It's a CELLULAR disease not an invasive prion. There is a cancer gene as most anyone knows, there isn't a prion gene because it's not a GENETIC DISEASE like cancer. Reading is fundamental BigTime1. Give it a try and quit trying to blow so much smoke up peoples rears and you might just learn a thing or two! Have a nice night, wife and I are catching up on the History show "Vikings" so that should give you a little while to bone up. Maybe you can actually bring something other than a pea shooter to this gunfight
Hmmm. No Gene he says...
The prion gene
At some point the gene that codes for the prion protein was found. Where? In the host. That is, the prion gene -- the gene for the prion protein -- is a normal host gene. When a sheep gets a prion disease (scrapie),Deer,(Chronic Wasting Disease) the animal's own gene for the prion protein codes for any new prion protein that is produced.
A direct test showing the importance of the host prion gene for the prion disease came with mice, where it is "easy" to delete a specific gene. Mice lacking the gene for the prion protein cannot be infected with prions. (The method used to make such a "knockout mouse" is discussed briefly on the BITN page Agricultural biotechnology (GM foods) and Gene therapy - Introduction.)
Finding the prion gene solves one problem in the prion mystery. The protein does not truly self-replicate. It is coded for by a gene, a normal gene -- in fact, by a host gene. Thus the feature of the prion model which most seriously challenged our common understanding of genes and proteins is no longer a problem. Attention now turns to the question of how this host protein turns "toxic", and how its toxic form can be infectious?
08-31-2015, 08:02 PM
#76
Nontypical Buck
Join Date: Feb 2015
Location: Illinois
Posts: 3,695
So you are saying you can show that a deer is CWD clinically positive by only testing positive in the lymph nodes. 100% cwd positive? If this is what you are trying to make us believe feel free to show that research. !00% nodes only positive!
Hmmm. No Gene he says...
The prion gene
At some point the gene that codes for the prion protein was found. Where? In the host. That is, the prion gene -- the gene for the prion protein -- is a normal host gene. When a sheep gets a prion disease (scrapie),Deer,(Chronic Wasting Disease) the animal's own gene for the prion protein codes for any new prion protein that is produced.
A direct test showing the importance of the host prion gene for the prion disease came with mice, where it is "easy" to delete a specific gene. Mice lacking the gene for the prion protein cannot be infected with prions. (The method used to make such a "knockout mouse" is discussed briefly on the BITN page Agricultural biotechnology (GM foods) and Gene therapy - Introduction.)
Finding the prion gene solves one problem in the prion mystery. The protein does not truly self-replicate. It is coded for by a gene, a normal gene -- in fact, by a host gene. Thus the feature of the prion model which most seriously challenged our common understanding of genes and proteins is no longer a problem. Attention now turns to the question of how this host protein turns "toxic", and how its toxic form can be infectious?
Hmmm. No Gene he says...
The prion gene
At some point the gene that codes for the prion protein was found. Where? In the host. That is, the prion gene -- the gene for the prion protein -- is a normal host gene. When a sheep gets a prion disease (scrapie),Deer,(Chronic Wasting Disease) the animal's own gene for the prion protein codes for any new prion protein that is produced.
A direct test showing the importance of the host prion gene for the prion disease came with mice, where it is "easy" to delete a specific gene. Mice lacking the gene for the prion protein cannot be infected with prions. (The method used to make such a "knockout mouse" is discussed briefly on the BITN page Agricultural biotechnology (GM foods) and Gene therapy - Introduction.)
Finding the prion gene solves one problem in the prion mystery. The protein does not truly self-replicate. It is coded for by a gene, a normal gene -- in fact, by a host gene. Thus the feature of the prion model which most seriously challenged our common understanding of genes and proteins is no longer a problem. Attention now turns to the question of how this host protein turns "toxic", and how its toxic form can be infectious?
Excerpt from same :
Abstract
Prions are self-propagating proteinaceous infectious agents capable of transmitting disease in the absence of nucleic acids. The nature of the infectious agent in prion diseases has been at the center of passionate debate for the past 30 years. However, recent reports on the in vitro generation of prions have settled all doubts that the misfolded prion protein (PrPSc) is the key component in propagating infectivity. However, we still do not understand completely the mechanism of prion replication and whether or not other cellular factors besides PrPSc are required for infectivity. In this article, we discuss these recent reports under the context of the protein-only hypothesis and their implications.
Key words: prions, infectivity, protein-only hypothesis, protein misfolding cyclic amplification, synthetic prion
Prions, Bizarre Infectious Agents, Unique Diseases
Prions are self-propagating particles of proteinaceous origin which share the ability to transmit disease with typical infectious organisms such as viruses and bacteria, but in contrast to them, prions do not have genetic material. Prion diseases have been found in humans and other mammals, including cattle, sheep, cervids, felines and rodents. In addition to transmission by infection, the disease can have inherited and sporadic origins. In the transmissible cases, infection of the host is preceded by a variable incubation period and followed by the appearance of clinical symptoms. Prion diseases are 100% fatal and after a long pre-symptomatic period in which the agent is slowly replicating, the clinical phase is often very rapid, progressive and severe.3
Although the exact molecular nature of prions is not completely clear, it is widely accepted in the field that the prion protein (denoted PrP) in its infectious conformation (PrPSc) is the main, or perhaps only, component of the infectious agent.2,3 Having a misfolded protein as an infectious agent makes prions very unconventional. Even if some co-factors are proven to be required, the minimal infectious agent should be much less complex than a virus or any other form of conventional micro-organism. Given the heretical nature of prions, the “protein-only” hypothesis has remained controversial for decades.4,5 Recent reports demonstrating the formation of highly infectious prions completely in vitro have provided the strongest proof for the prion hypothesis and have taken the field to an entirely new position.6–9 In this article, we summarize these findings and critically discuss their contribution to understand the molecular nature of prions and their unique mechanism of propagation
Abstract
Prions are self-propagating proteinaceous infectious agents capable of transmitting disease in the absence of nucleic acids. The nature of the infectious agent in prion diseases has been at the center of passionate debate for the past 30 years. However, recent reports on the in vitro generation of prions have settled all doubts that the misfolded prion protein (PrPSc) is the key component in propagating infectivity. However, we still do not understand completely the mechanism of prion replication and whether or not other cellular factors besides PrPSc are required for infectivity. In this article, we discuss these recent reports under the context of the protein-only hypothesis and their implications.
Key words: prions, infectivity, protein-only hypothesis, protein misfolding cyclic amplification, synthetic prion
Prions, Bizarre Infectious Agents, Unique Diseases
Prions are self-propagating particles of proteinaceous origin which share the ability to transmit disease with typical infectious organisms such as viruses and bacteria, but in contrast to them, prions do not have genetic material. Prion diseases have been found in humans and other mammals, including cattle, sheep, cervids, felines and rodents. In addition to transmission by infection, the disease can have inherited and sporadic origins. In the transmissible cases, infection of the host is preceded by a variable incubation period and followed by the appearance of clinical symptoms. Prion diseases are 100% fatal and after a long pre-symptomatic period in which the agent is slowly replicating, the clinical phase is often very rapid, progressive and severe.3
Although the exact molecular nature of prions is not completely clear, it is widely accepted in the field that the prion protein (denoted PrP) in its infectious conformation (PrPSc) is the main, or perhaps only, component of the infectious agent.2,3 Having a misfolded protein as an infectious agent makes prions very unconventional. Even if some co-factors are proven to be required, the minimal infectious agent should be much less complex than a virus or any other form of conventional micro-organism. Given the heretical nature of prions, the “protein-only” hypothesis has remained controversial for decades.4,5 Recent reports demonstrating the formation of highly infectious prions completely in vitro have provided the strongest proof for the prion hypothesis and have taken the field to an entirely new position.6–9 In this article, we summarize these findings and critically discuss their contribution to understand the molecular nature of prions and their unique mechanism of propagation
You may click the link to read more on that PROVEN testing as I have provided a link which BigTime1 seems to fail to do with ANYTHING he says. Took me a little while to find that little excerpt he put up AND EDITED severely. Nice try again, have a nice night
08-31-2015, 08:12 PM
#77
Spike
Join Date: Aug 2015
Posts: 62
Again more copy and paste to add your own crap to the mix.....Now here is a post from your buddy with his...They sky is falling scare tactics and then a post from the real world true hunter....CWD is a joke and has done no harm anywhere. Thats real world!
Join Date: Feb 2012
Location: Texas
Posts: 1,015
Exclamation Illinois Loosing Ground to CWD 71 confirmed in 2015 and 538 confirmed cases to date
Monday, August 31, 2015
Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date
http://chronic-wasting-disease.blogs...o-chronic.html
Terry S. Singeltary Sr.
Funny how this state has all this WILD CWD yet there has NEVER been a case on a farm in this state. Typical........
Join Date: Mar 2008
Location: NE Wisconsin
Posts: 2,606
Default
Just got back from an antelope hunt in WY in the center of the cwd epidemic. Talking with the guides. Sounded like those I know in cwd areas in WI
Blame the DNR for over blowing it. Believe it's always been there. Elk are thriving. Residents get 3 elk tags
Thats the truth and real story of CWD from state to state.....Only the agenda pushers blow smoke and push CWD as a killer or even a disease that is doing anything any harm!
Join Date: Feb 2012
Location: Texas
Posts: 1,015
Exclamation Illinois Loosing Ground to CWD 71 confirmed in 2015 and 538 confirmed cases to date
Monday, August 31, 2015
Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date
http://chronic-wasting-disease.blogs...o-chronic.html
Terry S. Singeltary Sr.
Funny how this state has all this WILD CWD yet there has NEVER been a case on a farm in this state. Typical........
Join Date: Mar 2008
Location: NE Wisconsin
Posts: 2,606
Default
Just got back from an antelope hunt in WY in the center of the cwd epidemic. Talking with the guides. Sounded like those I know in cwd areas in WI
Blame the DNR for over blowing it. Believe it's always been there. Elk are thriving. Residents get 3 elk tags
Thats the truth and real story of CWD from state to state.....Only the agenda pushers blow smoke and push CWD as a killer or even a disease that is doing anything any harm!
08-31-2015, 10:26 PM
#78
Nontypical Buck
Join Date: Feb 2015
Location: Illinois
Posts: 3,695
There you go getting circular in your smoke blowing BigTime1. So which is it, No cases of CWD found in the wild or so many it's ridiculous?
I don't believe a singe person in either of these discussions has said that the SOLE reason for CWD outbreaks are because of deer farms. I certainly haven't! What I HAVE said, and several times, is that it is most prevalent in deer farms as well as more easily detected because the deer are behind a fence as well as more testing can be done on them. There's no telling HOW CWD got into Illinois. Just like there is no telling how the disease got started in the first place. It's a misfiring protein with a longevity from hell. One that is slow in action and relatively impossible to pin down in the wild. Some deer have a genetic structure that allow them to slow the process of the prions (most commonly the deer found with it only in their nodes) while others it acts much faster but is STILL a slow killer. It's ALWAYS fatal. Period. Deer will always succumb to it eventually. Some faster, some much slower but if something else doesn't drop them first, it will get them eventually. Unlike on a deer farm, wild deer aren't nose to nose at feeder stations transmitting it to each other like a cold goes through the snot nosed kids at school. ANY disease that happens to be communicable will be more prevalent in a captive situation. In the wild, you will have a deer here, a deer there in most places anyway, there are some where you will see many deer in a small area but in general a disease such as this will be slower spreading because of the way it is transmitted. Whereas EHD is transmitted through other means not requiring the close proximity of the hosts. The problem is, the more deer that become hosts to CWD, then by natural law, the more it is spread. A young buck that has become host to the disease is run off by a dominant, it roams around till it finds a herd of doe without a dominant in close proximity to run it off, bam, new hosts!
You say this disease is doing no harm, yet it is being seen more and more in the wilds. Funny how that works isn't it. It's "doing no harm" yet it's being seen much more nowadays. Not just on deer farms. You ask how did it get into Illinois without deer farms? Well, you can't tell me that people around the Golden Triangle counties didn't purchase some stock to boost their gene lines around there. Business was dropping off a few years ago. Not saying it WAS that but it's a definite possibility. It could have been infected feed. It could have been infected urine. Hell, Michigan and Wisconsin border Illinois, could have been an escapee from one of those farms that had tons of infected deer get loose. Don't try to tell me that whitetail wont travel far either. They TYPICALLY don't but they do at times.
CWD, as stated, is a slow disease and has been around for many many years, but it is a little bit fishy that it wasn't commonly seen in the wild until deer farming became "big business" as you put it. Once the escapes started getting worse, the disease was found in the wild more. Coincidence? COuld be. May not be. Who knows, who really cares. Pointing fingers at who started it isn't going to help a damn thing. Getting a handle on the disease before it really starts to kill off herds is what matters.
I don't believe a singe person in either of these discussions has said that the SOLE reason for CWD outbreaks are because of deer farms. I certainly haven't! What I HAVE said, and several times, is that it is most prevalent in deer farms as well as more easily detected because the deer are behind a fence as well as more testing can be done on them. There's no telling HOW CWD got into Illinois. Just like there is no telling how the disease got started in the first place. It's a misfiring protein with a longevity from hell. One that is slow in action and relatively impossible to pin down in the wild. Some deer have a genetic structure that allow them to slow the process of the prions (most commonly the deer found with it only in their nodes) while others it acts much faster but is STILL a slow killer. It's ALWAYS fatal. Period. Deer will always succumb to it eventually. Some faster, some much slower but if something else doesn't drop them first, it will get them eventually. Unlike on a deer farm, wild deer aren't nose to nose at feeder stations transmitting it to each other like a cold goes through the snot nosed kids at school. ANY disease that happens to be communicable will be more prevalent in a captive situation. In the wild, you will have a deer here, a deer there in most places anyway, there are some where you will see many deer in a small area but in general a disease such as this will be slower spreading because of the way it is transmitted. Whereas EHD is transmitted through other means not requiring the close proximity of the hosts. The problem is, the more deer that become hosts to CWD, then by natural law, the more it is spread. A young buck that has become host to the disease is run off by a dominant, it roams around till it finds a herd of doe without a dominant in close proximity to run it off, bam, new hosts!
You say this disease is doing no harm, yet it is being seen more and more in the wilds. Funny how that works isn't it. It's "doing no harm" yet it's being seen much more nowadays. Not just on deer farms. You ask how did it get into Illinois without deer farms? Well, you can't tell me that people around the Golden Triangle counties didn't purchase some stock to boost their gene lines around there. Business was dropping off a few years ago. Not saying it WAS that but it's a definite possibility. It could have been infected feed. It could have been infected urine. Hell, Michigan and Wisconsin border Illinois, could have been an escapee from one of those farms that had tons of infected deer get loose. Don't try to tell me that whitetail wont travel far either. They TYPICALLY don't but they do at times.
CWD, as stated, is a slow disease and has been around for many many years, but it is a little bit fishy that it wasn't commonly seen in the wild until deer farming became "big business" as you put it. Once the escapes started getting worse, the disease was found in the wild more. Coincidence? COuld be. May not be. Who knows, who really cares. Pointing fingers at who started it isn't going to help a damn thing. Getting a handle on the disease before it really starts to kill off herds is what matters.
09-01-2015, 03:25 AM
#79
Spike
Join Date: Aug 2015
Posts: 62
There you go getting circular in your smoke blowing BigTime1. So which is it, No cases of CWD found in the wild or so many it's ridiculous?
I don't believe a singe person in either of these discussions has said that the SOLE reason for CWD outbreaks are because of deer farms. I certainly haven't! What I HAVE said, and several times, is that it is most prevalent in deer farms as well as more easily detected because the deer are behind a fence as well as more testing can be done on them. There's no telling HOW CWD got into Illinois. Just like there is no telling how the disease got started in the first place. It's a misfiring protein with a longevity from hell. One that is slow in action and relatively impossible to pin down in the wild. Some deer have a genetic structure that allow them to slow the process of the prions (most commonly the deer found with it only in their nodes) while others it acts much faster but is STILL a slow killer. It's ALWAYS fatal. Period. Deer will always succumb to it eventually. Some faster, some much slower but if something else doesn't drop them first, it will get them eventually. Unlike on a deer farm, wild deer aren't nose to nose at feeder stations transmitting it to each other like a cold goes through the snot nosed kids at school. ANY disease that happens to be communicable will be more prevalent in a captive situation. In the wild, you will have a deer here, a deer there in most places anyway, there are some where you will see many deer in a small area but in general a disease such as this will be slower spreading because of the way it is transmitted. Whereas EHD is transmitted through other means not requiring the close proximity of the hosts. The problem is, the more deer that become hosts to CWD, then by natural law, the more it is spread. A young buck that has become host to the disease is run off by a dominant, it roams around till it finds a herd of doe without a dominant in close proximity to run it off, bam, new hosts!
You say this disease is doing no harm, yet it is being seen more and more in the wilds. Funny how that works isn't it. It's "doing no harm" yet it's being seen much more nowadays. Not just on deer farms. You ask how did it get into Illinois without deer farms? Well, you can't tell me that people around the Golden Triangle counties didn't purchase some stock to boost their gene lines around there. Business was dropping off a few years ago. Not saying it WAS that but it's a definite possibility. It could have been infected feed. It could have been infected urine. Hell, Michigan and Wisconsin border Illinois, could have been an escapee from one of those farms that had tons of infected deer get loose. Don't try to tell me that whitetail wont travel far either. They TYPICALLY don't but they do at times.
CWD, as stated, is a slow disease and has been around for many many years, but it is a little bit fishy that it wasn't commonly seen in the wild until deer farming became "big business" as you put it. Once the escapes started getting worse, the disease was found in the wild more. Coincidence? COuld be. May not be. Who knows, who really cares. Pointing fingers at who started it isn't going to help a damn thing. Getting a handle on the disease before it really starts to kill off herds is what matters.
I don't believe a singe person in either of these discussions has said that the SOLE reason for CWD outbreaks are because of deer farms. I certainly haven't! What I HAVE said, and several times, is that it is most prevalent in deer farms as well as more easily detected because the deer are behind a fence as well as more testing can be done on them. There's no telling HOW CWD got into Illinois. Just like there is no telling how the disease got started in the first place. It's a misfiring protein with a longevity from hell. One that is slow in action and relatively impossible to pin down in the wild. Some deer have a genetic structure that allow them to slow the process of the prions (most commonly the deer found with it only in their nodes) while others it acts much faster but is STILL a slow killer. It's ALWAYS fatal. Period. Deer will always succumb to it eventually. Some faster, some much slower but if something else doesn't drop them first, it will get them eventually. Unlike on a deer farm, wild deer aren't nose to nose at feeder stations transmitting it to each other like a cold goes through the snot nosed kids at school. ANY disease that happens to be communicable will be more prevalent in a captive situation. In the wild, you will have a deer here, a deer there in most places anyway, there are some where you will see many deer in a small area but in general a disease such as this will be slower spreading because of the way it is transmitted. Whereas EHD is transmitted through other means not requiring the close proximity of the hosts. The problem is, the more deer that become hosts to CWD, then by natural law, the more it is spread. A young buck that has become host to the disease is run off by a dominant, it roams around till it finds a herd of doe without a dominant in close proximity to run it off, bam, new hosts!
You say this disease is doing no harm, yet it is being seen more and more in the wilds. Funny how that works isn't it. It's "doing no harm" yet it's being seen much more nowadays. Not just on deer farms. You ask how did it get into Illinois without deer farms? Well, you can't tell me that people around the Golden Triangle counties didn't purchase some stock to boost their gene lines around there. Business was dropping off a few years ago. Not saying it WAS that but it's a definite possibility. It could have been infected feed. It could have been infected urine. Hell, Michigan and Wisconsin border Illinois, could have been an escapee from one of those farms that had tons of infected deer get loose. Don't try to tell me that whitetail wont travel far either. They TYPICALLY don't but they do at times.
CWD, as stated, is a slow disease and has been around for many many years, but it is a little bit fishy that it wasn't commonly seen in the wild until deer farming became "big business" as you put it. Once the escapes started getting worse, the disease was found in the wild more. Coincidence? COuld be. May not be. Who knows, who really cares. Pointing fingers at who started it isn't going to help a damn thing. Getting a handle on the disease before it really starts to kill off herds is what matters.
You also fail to accept the fact that yes there are a FEW cases when it comes to total number of whitetails in the states BUT these deer are not dead to a disease!!! This deer are dead to every other way a deer can die and then test positive. Who cares if a deer COULD die at 4-5-6 years of age and then die when 90% of whitetails never live past their second birthday.
This disease is doing nothing to any cervid herds anywhere to cause any kind of hurt of the total herds. Period. As is shown and proven in every state CWD is in. Most positive states are over populated with deer or the total other spectrum is shown by having no whitetails because of mis-management and wolves or EHD....Not CWD!
You either stop all vectors of a disease or you dont worry about the disease but for you and a few others to only pick out deer farms and the products they sell to shut down only shows what your agenda is.
But we have known that from the start, have we not!
09-01-2015, 03:55 AM
#80
Giant Nontypical
Join Date: Oct 2013
Posts: 9,230
I find it laughable that 2 "members", both of whom are deer pimps and both of whom just happened to come to the forum during the same year are the only ones endorsing captive deer hunting! What a HNI Rule 1 Violation edited by JW Languagejoke! Killing livestock behind an escape proof fence IS NOT HUNTING!
Last edited by JW; 09-01-2015 at 05:44 AM. Reason: language HNI rule 1