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Minerals and CWD

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Let's bring back wolves, half kidding, half serious, I know that it isn't possible, but when we start talking about letting nature run its course.......
I’d bet a nickel.... most sick deer in my area (good, bad or indifferent) will get killed and eaten by a coyote. I’m filled with coyotes. They see a deer starting to act sick- they will target and kill it. Don’t know how this impacts the cwd discussion & maybe it doesn’t change a thing. Just a side note or result & what I think will happen.
 
I am just on the outskirts of the effected area in NE Iowa. I have been going back and forth on this issue for the last two weeks. Even though I know there are a million different ways that a deer can possibly get CWD I really do not want to help contribute to the passage of it around me. Yes I believe my plots and farmer's fields are also a way to acquire CWD, but no mineral is one less way to get it I feel. I know there are benefits in mineral but the negative outweighs the benefits in my mind.
 
So...the skeptics are all in on your minerals? Skip??
I actually ain’t gonna “suggest” people use minerals with cwd in question. I’m gonna stay “neutral”. This is one schmuck’s opinion on things BUT with minerals- I am just pleading the 5th or simply staying neutral. I honestly can see both sides of that & I gonna sit on sidelines for “my opinion” when it comes to those 2 topics mixing together.
 
The CWD questions seemed pretty good, but I lost a little interest when the questions on the next page had to do with how much roadkill you eat..
Ha!!!! I didn’t get that far!!!! Omg!!! Hilarious!!!
 
I think minerals would obviously aid in the spread. But one article I read suggested Copper and Magnesium help deter the prion and also once an animal is infected they slow the rate at what CWD progresses.
 
I purchased all of my mineral just prior to the positive test in Wayne and have been debating ever since. I'm curious as to what everyone else is doing with their mineral sites.?

December 2014, Volume 36, Issue 6, pp 1049–1061 | Cite as

Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer

Authors Authors and affiliations Michael J. LavelleEmail authorGregory E. PhillipsJustin W. FischerPatrick W. BurkeNathan W. SewardRandal S. StahlTracy A. NicholsBruce A. WunderKurt C. VerCauteren 1. 2. 3. 4.
Article First Online: 08 April 2014 258 Downloads 1 Citations

Abstract

Free-ranging cervids acquire most of their essential minerals through forage consumption, though occasionally seek other sources to account for seasonal mineral deficiencies. Mineral sources occur as natural geological deposits (i.e., licks) or as anthropogenic mineral supplements. In both scenarios, these sources commonly serve as focal sites for visitation. We monitored 11 licks in Rocky Mountain National Park, north-central Colorado, using trail cameras to quantify daily visitation indices (DVI) and soil consumption indices (SCI) for Rocky Mountain elk (Cervus elaphus) and mule deer (Odocoileus hemionus) during summer 2006 and documented elk, mule deer, and moose (Alces alces) visiting licks. Additionally, soil samples were collected, and mineral concentrations were compared to discern levels that explain rates of visitation. Relationships between response variables; DVI and SCI, and explanatory variables; elevation class, moisture class, period of study, and concentrations of minerals were examined. We found that DVI and SCI were greatest at two wet, low-elevation licks exhibiting relatively high concentrations of manganese and sodium. Because cervids are known to seek Na from soils, we suggest our observed association of Mn with DVI and SCI was a likely consequence of deer and elk seeking supplemental dietary Na. Additionally, highly utilized licks such as these provide an area of concentrated cervid occupation and interaction, thus increasing risk for environmental transmission of infectious pathogens such as chronic wasting disease, which has been shown to be shed in the saliva, urine, and feces of infected cervids.
Keywords Cervus elaphus Chronic wasting disease Elk Geophagy Mineral lick Mule deer Odocoileus hemionus

https://rd.springer.com/article/10.1007/s10653-014-9600-0

Elk and Deer Use of Mineral Licks: Implications for Disease Transmission

Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: kurt.c.vercauteren@aphis.usda.gov

North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents.

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

========================

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

http://www.pnas.org/content/97/7/3418.full

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf

A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract

Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals

http://transmissiblespongiformencep...07/rapid-assessment-of-bovine-spongiform.html

PPo4-4:

Survival and Limited Spread of TSE Infectivity after Burial

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

URINE

SUNDAY, JULY 16, 2017

*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***

http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html


kind regards, terry
 
As of 2017, apparently now there's been a study done where they've successfully passed cwd into monkeys by feeding them contaminated venison. Anyone have a take on this?

you can see the updated studies, and old studies, on zoonosis of cwd, and the potential there from, if it has not happened already, and been happening...too much to post all here. see;

TUESDAY, FEBRUARY 13, 2018

MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations

http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-state-department-of-health.html


kind regards, terry
 
This is a SIMPLE article (not the Flounder type studies that I've been reading)..... BASICALLY.....
ONE SOLUTION...... There seems to be a common thread in the studies that show certain genetic strains of deer are tolerant or "immune" to CWD - to differing degrees. Immunity takes time of course. So, if we dive deeper in the WY study (that I won't bore you with posting) - it pointed out "at this rate, our herd will be dead in 40 years....... BUT...... Since the genetically immune species will take the place, that logic is completely false". HMMMMM - ooooooppps, someone had to finally think through this and finally realized the truth in that study. Here's the easier read though & I realize this "ARTICLE" has some opinion and contraversial parts to it.....
http://www.deeranddeerhunting.com/a...genetically-resistant-chronic-wasting-disease

(snip...tss)FOLLOW THE LOGIC STEP BY STEP & that's the ONLY conclusion that really gets to the heart of this. CORRECT ME IF I'M WRONG YET AGAIN. :)


to date, there is no cervid that has been documented to be totally resistant to cwd tse prion.

***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/uploa...nt_data/file/209755/Part_1_-_Introduction.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/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf

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/2009%20blanchong%20et%20al%20genetic%20susceptibility%20chronic%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=ihub

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

kind regards, terry
 
I think people need to let nature run it’s course. There is already way to much influence on wildlife as it is. Going in and killing healthy deer is the wrong way to do it. Let nature cull the heard for good of the heard.
 
I think minerals would obviously aid in the spread. But one article I read suggested Copper and Magnesium help deter the prion and also once an animal is infected they slow the rate at what CWD progresses.
Ya- there’s where I personally run into to Trouble... again, I ain’t gonna be the guy that posts “ya, ur fine” BUT..... my thought line on other side of it is a “healthier deer” with a better immune system. A lot of those minerals aid in that. Why I put em out, carefully (not creating mud pits or salty standing water) for EHD (and mixed granulated garlic & sulfur for flies, midges, ticks, etc). Health, immune system, etc.
I’m on the side of letting nature take its course but I ain’t gonna tell others what to do. What I “fear” is government taking the WI approach to wipe out all the deer. Which is madness, IMO. I sure hope they don’t tell me what to do on my own farm. Doesn’t seem like they are so far. Hope it stays that way.
 
I actually ain’t gonna “suggest” people use minerals with cwd in question. I’m gonna stay “neutral”. This is one schmuck’s opinion on things BUT with minerals- I am just pleading the 5th or simply staying neutral. I honestly can see both sides of that & I gonna sit on sidelines for “my opinion” when it comes to those 2 topics mixing together.
Almost forgot about this...fair enough skip, I see where you're going with this. Also, great job on the site and good luck with it!
 
I think the best thing the government can do is by not helping. All there worried about is the political side of most things anyway.
 
I think the best thing the government can do is by not helping. All there worried about is the political side of most things anyway.
I agree 100%, but I have to believe that there has to be a financial gain to be had in all of this,?,? At least for today.....but tomorrow could be much different.
 
I agree 100%, but I have to believe that there has to be a financial gain to be had in all of this,?,? At least for today.....but tomorrow could be much different.

We could partner with TBI they exploit whitetails for profit down to a T. Oh Maybe we can find a way to only kill the small bucks and replace with high fence mutants, the only reason people deer hunt is to bring home the biggest deer anyway. We can breed them so they have 250 inches the first year, because I don’t want to have to wait or have to pass on deer when I’m hunting. Remember if it’s brown it’s down.
Sorry a little off course.. just had to rant for a minute. Plus I’m only half way thru my cup of coffee :)
 
I agree 100%, but I have to believe that there has to be a financial gain to be had in all of this,?,? At least for today.....but tomorrow could be much different.
Yes..... anytime there’s Government + a problem + research + tax dollars = $ to be made or motives SOMEWHERE. To keep it simple..... one poster child example of this is the Global Warming scenario..... that has made many companies and people multi-millionaires (heck, Gore made in $100’s of millions I believe). The Grants and government funding pay people, UNIVERSITIES & company’s for research, “possible solutions” and it employs a large amount of people.
With CWD- Then you have folks like Farm Bureau who see an avenue to support all this (kill all the deer). It really is a mess behind the scenes. Not saying certain areas or problems don’t have merit to them BUT $ & motives do exist.
 
(and mixed granulated garlic & sulfur for flies, midges, ticks, etc). Health, immune system, etc.
Sligh, where does one get this granulated garlic and sulfer in quantities for lick stations and how do you disperse it(large areas or only at licks)?
 
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