Been in existence for over 50 years. No one. Not flounder, not nogalis prairie, or any other chicken little can name one wild population that cwd has decimated.

Yet ehd and anthrax have each decimated many localilized wild populations over the same time period. It is impossible to take anyone seriously who ignores those two facts in an effort to promote an agenda.

But please continue. You are here specifically for my entertainment and I’m amused. Dance dog dance.

flounder posts the same [censored] on every hunting website out there...

Ive said it too, if people gave a damn about dead deer they'd go after EHD. The ONLY reason CWD is in the hot seat is because of the occurrences tied directly to breeding operations.

and now, entities like the King Ranch are stepping up to prevent this horrible tragedy form harming the deer. odd how they've never launched full blown campaigns to stop EHD?


I got a question for you flounder.... Do you hunt? do you own land? If so, how many animals have you volunteered up for CWD testing? have you gone out to a pasture that you own or lease, and just start killing deer so you can hit a certain number of tests? everyone keeps focusing on captive deer, which is odd, since they're captive. Maybe we need to test YOUR deer. For that matter, what percentage of animals has the king ranch offered up for testing? Does anyone know? have they tested 80% of postmortem deer? 10%? 10 deer?

kind regards!

Bingo!

Still trying to get an answer from you on this flounder.

Dont hold your breath

Subject: cwd genetic susceptibility

Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§

Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g

snip...

Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.

http:// http://forest.wisc.edu/files/pdfs/samuel...c%20wasting.pdf

http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1083&context=nrem_pubs

http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2017.4667/epdf

http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1115179

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/pdf/kprn-09-06-1115179.pdf

http://www.sciencedirect.com/science/article/pii/S1567134809001956?via%3Dihub

Prion protein gene sequence and chronic wasting disease susceptibility in white-tailed deer (Odocoileus virginianus)

Adam L Brandt,1 Amy C Kelly,1 Michelle L Green,1,2 Paul Shelton,3 Jan Novakofski,2,* and Nohra E Mateus-Pinilla1,2 Author information ► Article notes ► Copyright and License information ►

The sequence of the prion protein gene (PRNP) affects susceptibility to spongiform encephalopathies, or prion diseases in many species. In white-tailed deer, both coding and non-coding single nucleotide polymorphisms have been identified in this gene that correlate to chronic wasting disease (CWD) susceptibility. Previous studies examined individual nucleotide or amino acid mutations; here we examine all nucleotide polymorphisms and their combined effects on CWD. A 626 bp region of PRNP was examined from 703 free-ranging white-tailed deer. Deer were sampled between 2002 and 2010 by hunter harvest or government culling in Illinois and Wisconsin. Fourteen variable nucleotide positions were identified (4 new and 10 previously reported). We identified 68 diplotypes comprised of 24 predicted haplotypes, with the most common diplotype occurring in 123 individuals. Diplotypes that were found exclusively among positive or negative animals were rare, each occurring in less than 1% of the deer studied. Only one haplotype (C, odds ratio 0.240) and 2 diplotypes (AC and BC, odds ratios of 0.161 and 0.108 respectively) has significant associations with CWD resistance. Each contains mutations (one synonymous nucleotide 555C/T and one nonsynonymous nucleotide 286G/A) at positions reported to be significantly associated with reduced CWD susceptibility. Results suggest that deer populations with higher frequencies of haplotype C or diplotypes AC and BC might have a reduced risk for CWD infection – while populations with lower frequencies may have higher risk for infection. Understanding the genetic basis of CWD has improved our ability to assess herd susceptibility and direct management efforts within CWD infected areas.

KEYWORDS: CWD, diplotype, G96S, PRNP, prion, synonymous polymorphism, haplotype

snip...

A solid understanding of the genetics of CWD in white-tailed deer is vital to improve management of CWD on the landscape. Most TSEs are found in domestic or captive animals where management of infected individuals is feasible. For example, scrapie infected flocks can be handled through a process generally involving genetic testing, removal and destruction of infected or suspect animals, followed by decontamination of facilities and equipment.55Containment of free ranging deer in wild populations potentially infected with CWD and decontamination of the environment is not reasonably possible. The long term effects of CWD are not yet known but it is conceivable that an unmanaged infected population would be gradually extirpated as the disease progresses56,57 or at least reduced to low densities with high disease prevalence.58,59 Either outcome would have severe ecological effects (e.g., deer play a major role in affecting plant communities60 and as a prey source61,62) as well as negative economic impacts to hunting. Overall disease prevalence has remained at relatively low levels in Illinois compared to Wisconsin.11 It is important to note that at the time of sampling, CWD had been found in 6 Illinois counties and has since been detected in 14.9Complete eradication of CWD among free ranging white-tailed deer may not be possible; however, an active containment effort in Illinois appears to have prevented significant increases in prevalence.9,11,12 Further examination of PRNP haplotype and diplotype frequencies across northern Illinois and southern Wisconsin in conjunction with population structure and movement45,63,64 will be useful in identifying localities with greater or reduced susceptibility risk. Effectiveness of CWD containment efforts can be aided through genetic testing and redirecting management resources.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/

***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.

P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion

Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD

In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible.

***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.

PRION 2016 CONFERENCE TOKYO

http://prion2016.org/dl/newsletter_03.pdf

''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''

c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.

https://www.gov.uk/government/uploads/sy...ntroduction.pdf

http://chronic-wasting-disease.blogspot.com/

WHAT DO YOU PROPOSE BE DONE IN TEXAS TO DEAL WITH CWD, flounder???

Copy & paste obnoxiously long posts that use obscenely long & scientifically sounding words, all whilst carefully avoiding direct questions?

He's about to go on ignore. I read all the same carp he posts here without needing a deer hunting forum. In essence, he's doing nothing but trolling. Mr. TS, please tell us what you propose to deal with CWD in Texas. Otherwise, I'm gonna have to block you since you add NOTHING else to the forum, or the conversation on your own posts!

Dont hold your breath

i have told you time and time again, yet most ignore. i have supplied links to what i propose be done, i have supplied links to usda et al on comments to dockets pertaining to cwd explaining what i thought should be done, and posted them here. i am not getting pulled into another BS debate with ones that;

don't care

don't believe

don't want to help

i post for others that read it, and happen to care, believe, and want to help, they may not say much, but they are there.

December 14, 2017 will be 20 years trying to warn folks about the tse prion disease.

yet the ignorance still today, defies common sense, and then you have the industry and government which still fuels the BS machine, when scientist are screaming otherwise.

until you get the industry and the government out of tse prion science and policy making there from, you will never eradicate the tse prion disease.

it's not a liberal thing, or a conservative thing, it's just a thing of greed, the world thrives on it, and so do tse prion disease.

TUESDAY, DECEMBER 05, 2017

Norway 30,000 deer animals have so far been tested for Skrantesyke chronic wasting disease CWD TSE PRION DISEASE

http://chronic-wasting-disease.blogspot.com/2017/12/norway-30000-deer-animals-have-so-far.html


carry on Texas Hunters et al here, carry on. Good luck. ...


Terry S. Singeltary Sr.

Never heard of a disease thriving on greed before. Is that maybe why it's not really destroying deer herds? Because deer don't have the mental capacity to posses greed, therefore CWD can't thrive?

some of you might find interest in this. getting closer to a live cwd tse prion test. keep your fingers crossed...terry

SUNDAY, DECEMBER 10, 2017

Detection of Prions in Blood of Cervids at the Asymptomatic Stage of Chronic Wasting Disease

The results showed a sensitivity of 100% in animals with very poor body condition that were IHC-positive in both brain and lymph nodes, 96% in asymptomatic deer IHC-positive in brain and lymph nodes and 53% in animals at early stages of infection that were IHC-positive only in lymph nodes. The overall mean diagnostic sensitivity was 79.3% with 100% specificity. These findings show that PMCA might be useful as a blood test for routine, live animal diagnosis of CWD.

https://www.nature.com/articles/s41598-017-17090-x

http://chronic-wasting-disease.blogspot.com/2017/12/detection-of-prions-in-blood-of-cervids.html

Good news hopefully.

Is there a possible treatment in the future?

Much ado about some very isolated cases. IMO, a waste of time and expense.

If only somebody would continue to randomly post threads about CWD, that contain unreadable walls of texts, with lotsa words in all caps (to simulate yelling), making the wildest claims, offer no real solutions at all, & refuse to answer any direct questions concerning the topic. I think that's the best way to keep everyone informed.

CWD is not all about effect on deer populations. One difference is the possibility of CWD animals that are consumed by humans being infected with the disease. Canandian study on monkeys shows 3 of 5 who consumed CWD infected animals contracted the disease. First known transmission of the prion disease to a primate.

If it comes to light that’s even a possibility for humans - we are all in for a very rude awakening. Deer farmers, hunters, everyone. Let’s pray it doesn’t.

Carry on.....

Becareful using a study that’s Not published yet

2 where infected by intracranial injection aka straight shots to the brain.
1 was infected via being fed brain material (no amount noted)
2 infected by consumption of thier infected compadres and infected Whitetail meat(still looking for definitive consumption amount)


Should also be noted CWD infected Blood transfusions did not result in transmission of the disease, nor did it take on open wounds.


Those Monkey carry herpes B virus which is harmless to them but often fatal to humans....

i didn't yell i my post, it was short, i explained at the top of my post in short what it was about, supplied link. i thought everyone would be happy to see a potential live cwd tse prion test with some hope. well, i thought anyway. you 'maximus_flavius' and a few others i have been told, just don't want me posting anything here about cwd tse prion, and would like to censor me. if you have a problem with my post don't read them. if you have a question, ask it, i will try and answer it. i will not discuss my diet on a weekly basis, i have already said time and time again, or when my last hunt was and where. i am disabled from neck injury and don't hunt anymore. and i will not discuss what kind or how many guns i have. i am pro-hunt, pro-gun, pro-meat, just anti stupid. i don't want to eat cwd tse prions, or be exposed to them and neither should you, tse prions can kill you and yours. if you just want to complain and whine, and want me banned for speaking about cwd tse prion, then write a moderator, that's out of my control what content and how it is posted here. i have complied with what they ask. they ask me to shorten my postings i did. they told me some were concerned i would not answer questions, and that's simply just not true. what i will not do here is be insulted. and if that takes me being banned, so be it. if you can't understand English, that's not my problem either. what the real problem here is, you Sir 'maximus_flavius', and a few others, don't want to be informed, and you and a few others don't want me to inform anyone else anymore about cwd tse prion. that's all it is. so i will just leave you all with one final post for the year below and then you and others can carry on Sir...and yes, in this post, there will be a line with all caps, unlike my last post i was accused of, yet no caps were there.

To the rest of Texas Hunters, have a great hunt, stay safe and warm, and Merry Christmas to all.

kind regards, terry

p.s. these postings are self explanatory with one topic heading, for those that are interested. i do not advertise or make money from this, never have. just updated science on cwd tse prion and links there to...we must stay informed.


Subject: USA CJD, BSE, SCRAPIE, CWD, TSE PRION ANNUAL END OF YEAR REPORTS 2017


TUESDAY, DECEMBER 12, 2017

Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017

http://chronic-wasting-disease.blogspot.com/2017/12/chronic-wasting-disease-cwd-tse-prion.html

That is not what the articles providing the news on the study say. While 18 have been exposed in various ways (including injection directly to the brain all the way to just skin contact) with varying results, 3 of 5 fed meat only (the equivalent of a steak a month) contracted CWD.

That is all in the above article.

If you know something different and/or the news reports are in error, I would love to see it. I sincerely hope you are right, and not just pushing back because the results are scary.

He has answered this question: Scorched Earth. Kill all animals in the infected area and quarantine the area until there is no longer a presence of TSE Prions.

Please correct me if I'm wrong Terry.

Another long winded post. Look, I couldn't possibly care less what you post. I only offered a few ideas to help get your point across (if you have 1). Calling it "mad deer disease" puts this more in perspective to me, I'm sure this'll be just as big a deal as "mad cow disease". I can't help but recall all the media hype about that, how it ruined a lot of ranchers financially, & all over something that never happened in the US (it was fake news, before fake news was cool).

As an aside, does anyone know where the term "PMS" come from? "mad cow disease" was already taken.

"Scorched earth" won't work. Already seen. Panic does no one any good. (Neither does denial.)

There is no easy answer or solution. Best available practices for containment is about it. I hope the live testing becomes widespread soon.

Killed a doe about two weeks ago on Camp Bullis where they have a biologist that inspects all the deer that are brought in. He weighed, aged, and removed two nodules from the base of neck behind the jaw and placed them in a jar for testing for CWD.
I watched him remove the nodules and it's an easy process and they are just under the skin.
Seems like it would be something most any hunter could do, and send in the specimen to be tested.
I'm with the crowd that is asking, "where are all the big die offs" if the problem is so dire, and what about anthrax which has recorded deer die offs?