Wednesday, September 21, 2016

ILLINOIS -- Deer disease CWD meetings set Oct. 18 at the Nash Recreation Center in Oregon, Illinois, and Oct. 19 at the Big Rock Park District Community Building in Big Rock

ILLINOIS -- Deer disease meetings set


Posted: Tuesday, September 20, 2016 6:43 am


LENA, Ill. (AP) — Illinois wildlife management officials have scheduled meetings to provide information on chronic wasting disease in the white-tailed deer population as hunting season nears. Illinois Department of Natural Resources meetings on CWD will be Oct. 18 at the Nash Recreation Center in Oregon, Illinois, and Oct. 19 at the Big Rock Park District Community Building in Big Rock.


Previously announced meetings will be in Elizabeth on Wednesday, Freeport on Sept. 27 and Yorkville on Sept. 28. All start at 7 p.m.



Illinois Chronic Wasting Disease Management: Part 4


Chronic Wasting Disease


Since the first case of CWD was discovered in Illinois, the Department of Natural Resources started a "targeted surveillance program" for CWD in wild deer which was first proposed by the Southeastern Cooperative Wildlife Disease Study, a diagnostic and research service which investigates wildlife diseases.


This site provides consolidated CWD information: CWD statistics shows Total Cases per Year and Total Cases per Year per County, FAQ's, a query sy...stem, test results, other CWD resources and annual reports.


A series of videos: Part 1-Introduction, Part 2-Testing CWD Samples, Part 3-Sharpshooting, Part 4-Common Questions, Research and Safe Handling of Deer.



Published on Apr 29, 2016


IDNR Biologists rely on the best science available when making wildlife management decisions. And our partners at the University of Illinois, including the Illinois Natural History Survey and Animal Science Department are instrumental in providing the research that is the underpinning of our management efforts. For answers to some common questions about CWD, let’s hear from the scientists studying the disease. This is the last in a four-part series on efforts to manage chronic wasting disease in Illinois.



Illinois Chronic Wasting Disease: 2015-2016 Surveillance and Management Report (Project Period: July 1, 2015 - June 30, 2016)


Paul Shelton and Patrick McDonald Forest Wildlife Program, Illinois Department of Natural Resources July 25, 2016


Executive Summary


First CWD positive: A suspect adult female deer from northwest Boone County was diagnosed with CWD in November 2002.


Total samples through June 30, 2016: 97,992+


Total positives through June 30, 2016: 610


Number of counties affected through June 30, 2016:


16 (Boone, DeKalb, DuPage, Grundy, JoDaviess, Kane, Kankakee, Kendall, Lake, LaSalle, Livingston, McHenry, Ogle, Stephenson, Will, Winnebago).


Distribution through June 30, 2016: Total affected area (determined by a minimum convex polygon that includes all positives) remains about 8,000 mi2. Disease is established in SE JoDaviess and SW Stephenson counties, and SE of the main CWD core area along the Illinois and Fox River watersheds (Figure 1). Recent ‘spark’ areas occur in the Vermilion, Mazon, and Kankakee River watersheds in Livingston, Grundy, Will & Kankakee counties.


Figure 1. Distribu􀆟on of all known CWD‐infected deer iden􀆟fied in Illinois through June 30, 2016.


CWD Surveillance Protocols During FY2016 (July 1, 2015‐June 30, 2016)


Tes􀆟ng: All CWD tes􀆟ng was conducted using immunohistochemistry (IHC) at Illinois Department of Agriculture’s (IDOA) Animal Disease Laboratory in Galesburg, Illinois. Samples were ini􀆟ally screened using retropharyngeal lymph nodes (RPLN), followed by confirmatory tes􀆟ng of recut RPLN 􀆟ssue and obex.


Sampling of hunter‐harvested deer: Three sources were used to provide 􀆟ssue samples from adult deer harvested by hunters: (1) mandatory firearm deer check sta􀆟ons in high‐risk coun􀆟es in northern Illinois; (2) designated voluntary drop‐off tes􀆟ng loca􀆟ons in northern Illinois; and (3) coopera􀆟ng meat lockers/taxidermists statewide who collected heads/sample 􀆟ssues for IDNR.


Surveillance by other agencies/individuals authorized by special permits: Recipients of special permits from IDNR authorizing lethal deer removals were required to collect CWD samples when working in high‐risk CWD areas or in areas needing addi􀆟onal surveillance. These permits included (1) Deer Popula􀆟on Control Permits (used by some agencies to control urban deer popula􀆟ons); (2) nuisance Deer Removal Permits (for crop depreda􀆟on, etc.); and (3) Scien􀆟fic Permits (various research projects).


Suspect (“target”) deer surveillance: Upon receiving reports from the public about sick deer, IDNR staff collected samples for CWD tes􀆟ng from deer that exhibited signs/symptoms consistent with chronic was􀆟ng disease.


Surveillance from post‐hun􀆟ng season sharpshoo􀆟ng: Sharpshoo􀆟ng was conducted from mid‐January through the end of March by trained IDNR staff. Sharpshoo􀆟ng was restricted to areas where CWD‐infected deer had been iden􀆟fied (limited to lands within a 2‐sec􀆟on buffer around known posi􀆟ve sec􀆟ons).


CWD Surveillance Results FY2016


Total number of CWD samples collected statewide: 8,544 (all whitetailed deer). Figure 2 depicts the geographic distribu􀆟on of sampling effort; Figure 3 compares annual sample numbers; Figure 4 presents a comparison of the number of deer sampled and the number of posi􀆟ves iden􀆟fied by source; and Appendix A summarizes the samples collected/posi􀆟ves iden􀆟fied by county.


Number of usable samples collected: 8,489


Number of CWD‐posi􀆟ve deer iden􀆟fied: 72. Table 1 presents a comparison of the number of posi􀆟ve deer found each year by county.


Number of coun􀆟es with posi􀆟ve deer: 13 — Boone (11), DeKalb (3), Grundy (3), JoDaviess (9), Kane (8), Kankakee (1), Kendall (6), LaSalle (5), McHenry (8), Ogle (6), Stephenson (10), Will (1), Winnebago (1). For distribu􀆟on of posi􀆟ve sec􀆟ons, see Figure 5.


Number of new CWD coun􀆟es: None.


CWD prevalence informa􀆟on for the known CWD area (16 coun􀆟es; adult deer from hun􀆟ng sources only) —


Average CWD prevalence (all adult deer): 1.09% (39/3591)


Average CWD prevalence (adult males): 1.28% (24/1881)


Average CWD prevalence (adult females): 0.88% (15/1710)


Figure 2. CWD sample distribu􀆟on across Illinois during FY2016 (all sources).


Figure 3. Number of CWD surveillance samples collected statewide each year during FY2003 through FY2016.


Figure 4. Number of CWD samples tested and number of posi􀆟ves iden􀆟fied by sampling source during FY2016.


Note: Number tested includes all samples submi􀆩ed, regardless of whether a valid test result was obtained.


Table 1. Number of CWD‐posi􀆟ve deer iden􀆟fied in each county by year.


Figure 5. Distribu􀆟on of CWD‐posi􀆟ve deer iden􀆟fied during FY2016.


CWD Management During FY2016




Appendix D. Historical distribu􀆟on of CWD in southern Wisconsin and northern Illinois as of June 30, 2016. Squares represent sec􀆟ons in which CWD has been detected.




snip...see full text 16 pages here ;


Appendix D. Historical distribu􀆟on of CWD in southern Wisconsin and northern Illinois as of June 30, 2016. Squares represent sec􀆟ons in which CWD has been detected. see page 16.



Cumulative CWD Positive Locations of Wild Deer in Wisconsin and Illinois.



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


Adam L Brandt, Amy C Kelly, Michelle L Green, Paul Shelton, Jan Novakofski & Nohra E Mateus-Pinilla To cite this article: Adam L Brandt, Amy C Kelly, Michelle L Green, Paul Shelton, Jan Novakofski & Nohra E Mateus-Pinilla (2015) Prion protein gene sequence and chronic wasting disease susceptibility in white-tailed deer (Odocoileus virginianus), Prion, 9:6, 449-462, DOI: 10.1080/19336896.2015.1115179 To link to this article:


Prion, 9:449–462, 2015 Published with license by Taylor & Francis Group, LLC ISSN: 1933-6896 print / 1933-690X online DOI: 10.1080/19336896.2015.1115179


RESEARCH PAPER Prion protein gene sequence and chronic wasting disease susceptibility in white-tailed deer (Odocoileus virginianus) Adam L Brandt1, Amy C Kelly1, Michelle L Green1,2, Paul Shelton3, Jan Novakofski2,*, and Nohra E Mateus-Pinilla1,2 1Illinois Natural History Survey; University of Illinois at Urbana-Champaign; Urbana, IL USA; 2Department of Animal Sciences; University of Illinois at Urbana-Champaign; Urbana, IL USA; 3Illinois Department of Natural Resources; Division of Wildlife Resources; Springfield, IL USA




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 noncoding 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.


Adam L Brandt, Amy C Kelly, Michelle L Green, Paul Shelton, Jan Novakofski, and Nohra E Mateus-Pinilla *Correspondence to: Jan Novakofski; Email: Received September 21, 2015; Revised October 23, 2015; Accepted October 23, 2015. Color versions of one or more of the figures in the article can be found online This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.




In this study, we find reduced susceptibility to CWD infection among white-tailed deer with haplotype C (Table 2). We still observed individual deer positive for CWD with this haplotype, demonstrating a reduced susceptibility rather than a complete genetic resistance as is seen with other TSEs (e.g., scrapie36,37). This haplotype had 2 different polymorphisms, 1 synonymous and 1 non-synonymous, both reported to be associated with decreased infection; nt286A (aa96S) and nt555T.10,26,29,30 Other haplotypes have similar mutations at nt286 and nt555 (e.g., haplotypes I, Q, and S); though, within the CWD infection area these haplotypes are not found at all (haplotype Q), occur infrequently (f < 0.01, haplotypes I and S), or are found exclusively among positive deer (haplotype I). A number of other haplotypes have the same mutations at either nt286 or nt555; again most are absent (haplotypes H, V, W and X), infrequent (f < 0.01, haplotypes N and P), or are found abundantly among positive deer (haplotype B) in the CWD infection area (Table 2). Rarity of these haplotypes prevents any meaningful association with changes in susceptibility (Table 2). The effects of mutations at nt286 and nt555 alone or in concert are unclear as other haplotypes with these polymorphisms occur infrequently and with varied susceptibility. An even larger sampling may be necessary to resolve this interaction.


Neither haplotypes with aa95H (nt285C) had a significantly reduced susceptibility to CWD (Table 2). Some previous studies reported the occurrence of this mutation among CWD negative deer only, which was interpreted as CWD resistance.26,29 In this study and in the study by Kelly et al.10 the aa95H mutation was found among deer positive for CWD; however, we find in a larger sampling (ND240) the frequency of aa95H to be lower than that found by Kelly et al.10 and not significantly associated with resistance. We cannot preclude the importance of this mutation given that a significant difference in disease susceptibility may be possible with an even larger sample size providing greater statistical power (data not shown).


The presence of aa96S has been associated with slowed disease progression, longer life span among captive deer,26,27 and does not appear to affect the rate at which prions are shed from infected individuals.38 Additionally, CWD infected mule deer have been found to excrete pathogenic prions while asymptomatic. 39 This contributes to concerns that wild deer with aa96S may be shedding infectious prions into the environment for longer periods of time than deer lacking the mutation, but are not symptomatic or detectable by immunohistochemical procedures. On the other hand, studies using epidemiological modeling suggest that deer with aa96S under certain conditions may have a selective advantage for CWD resistance over those without.40 With our data, we are unable to make accurate conclusions about detection, longevity, or increased risks of exposure to infectious prions. Nonetheless, our results do corroborate the importance of the polymorphism at G96S in reduced CWD susceptibility (Table 5).26,30


Kelly et al.10 found a negative correlation between the number of nucleotide deviations from the PRNP consensus sequence and CWD infection. The database derived consensus sequence reported is the same as the most common haplotype (haplotype A) in this study (Table 1). Haplotype C has 2 deviations from haplotype A; other haplotypes were found containing more deviations but were exceedingly rare (Table 1). These haplotypes (namely haplotypes I, N, Q, S, and X) were largely absent among CWD positive deer (only 2 positive deer were found each with a single copy of haplotype I) and their combined frequency was less than 1%. An increased number of polymorphisms may improve resistance to CWD, but the large sample size of this study (ND703) suggests that haplotypes with more than 2 nucleotide deviations are rare and would not be likely to have an appreciable effect on resistance or susceptibility within the population.


Examination of PRNP diplotypes revealed that individuals with at least one copy of haplotype C (specifically AC and BC) were less likely to test positive for CWD (Table 4). Other diplotypes containing at least one copy of haplotype C (mutations at aa96S and nt555T) had a low frequency of occurrence (<1 41="" a="" account="" additional="" address="" age="" all="" always="" analyses="" and="" animals.="" animals="" any="" are="" area.="" area="" as="" association="" at="" attempted="" available="" average="" avoid="" background.29="" basis="" be="" been="" between="" bias.="" but="" by="" c="" cases="" circumstances="" conditions="" confounding="" control="" controlled="" could="" counties="" county="" cwd.="" cwd="" decreasing="" deer43-45="" deer="" design="" determining="" diplotypes="" disease="" distances="" div="" due="" examined="" experimental="" exposed="" factor="" factors="" family="" for="" found="" free="" frequency="" frequent="" from="" genetic="" geographic="" greater="" groups="" haplotype="" harvest.="" have="" herd="" home="" hunter="" i.e.="" ideal="" identified="" illinois="" immunity="" in="" increase="" increasing="" indication="" individually="" infected="" infection="" inheritance="" is="" less="" likelihood="" likely="" locations="" low="" management="" match="" matched-case="" may="" minimize="" more="" multiple="" nature="" negative="" nonetheless="" not="" obtainable="" of="" on="" one="" or="" origin="" originating="" other="" outside="" over="" paired-case="" paired="" perfectly="" play="" population-level="" positive="" possible="" potential="" prnp="" randomly="" range="" ranging="" relatedness="" relationship="" resistance="" restricted="" results="" role="" samples="" sampling="" selected="" sequence="" sex="" significant="" similar="" spurious="" statistical="" status="" strong="" studies="" study="" studying="" suggesting="" susceptibility.="" susceptibility="" than="" that="" the="" therefore="" these="" they="" this="" though="" through="" throughout="" time="" to="" under="" use="" vital="" was="" were="" when="" whitetailed="" with="" without="">


The PRNP gene is variable within all species with some mutations affecting susceptibility to TSEs.46-48 Scrapie infection in sheep is the classic example of genetic resistance to a prion disease, where individuals with 2 copies of amino acid sequence V136, R154, Q171 are susceptible to scrapie, and those with 2 copies of the sequence A136, R154, R171 are resistant. 36,37 Changes in the protein coding sequence have been shown to affect the ability of pathogenic prions to convert normal prion proteins31; accordingly, many studies have heavily examined the amino acid variations associated with CWD. Synonymous or silent mutations are often overlooked, but may have a greater effect on protein expression and conformation than expected.49-53Other studies have found significant associations between individual synonymous mutations and CWD susceptibility. 10,28 The specific mechanisms involved between nucleotide variation (specifically synonymous mutations) and CWD are not known, but the rate at which PrPC conformations that are more favorable to PrPSC conversion are produced may be slowed by the presence of certain synonymous mutations.51 Due to the low frequency of haplotypes with similar mutations as haplotype C, we cannot accurately conclude whether or not the specific combination of mutations or any one mutation alone is responsible for reduced CWD susceptibility. Nevertheless, haplotype and diplotype analyses provide more insight in gene-disease association than those restricted to alleles and genotypes54 which are unable to detect additive effects.


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.55 Containment 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 progresses 56,57 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 14.9 Complete 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.





Tuesday, February 02, 2016


Illinois six out of 19 deer samples tested positive for CWD in the Oswego zone of Kendall County



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



Saturday, February 08, 2014


Illinois CWD confirmed in Will County deer




Since CWD testing began in Illinois, 408 deer have been confirmed with the disease in 11 years — the bulk of them in the Wisconsin border counties of Winnebago (Rockford) with 145 and Boone (Belvidere) 127. DeKalb County, south of Boone, has had 50. Adjacent to Will County, and not far west of Kankakee Sands, Grundy County has had 10 confirmed cases in the past three years, three of them last year. Kendall and DuPage counties, also adjacent to Will, each had one last year. CDW has been confirmed in a dozen northern Illinois counties, with Will, Grundy and LaSalle the farthest south.







Monday, April 08, 2013


Evaluation of a wild white-tailed deer population management program for controlling chronic wasting disease in Illinois, 2003–2008



Wednesday, January 16, 2013 Illinois


DuPage county deer found with Chronic Wasting Disease CWD



Tuesday, November 13, 2012





Friday, November 09, 2012


Chronic Wasting Disease CWD in cervidae and transmission to other species



Thursday, February 10, 2011


CWD ILLINOIS UPDATE FEBRUARY 2011 Locations of CWD-Positive Deer - Updated 2/07/2011



Thursday, January 28, 2010





Saturday, March 08, 2008


CWD UPDATE ILLINOIS Stephenson County joins CWD list



CWD Update 88


August 31, 2007


State and Provincial Updates




Paul Shelton, Illinois Department of Natural Resources provides the following: During July, IDNR identified a CWD-positive deer in LaSalle County after testing an animal showing classic signs of the illness. This was the first instance of the disease in this county. The deer was a 3 year old doe collected by a Conservation Police Officer after someone reported a sick, emaciated deer. The location was south of I-80, about 2 miles west of Grundy County, near the town of Seneca. This represents about a 25 mile distance from the previous southernmost positive in DeKalb County. Staff from the Division of Wildlife Resources are assessing the implications of the finding.


The total number of CWD-infected deer found in Illinois now numbers 189. Prior to this, the disease had been confined to Winnebago, Boone, McHenry, Ogle, and DeKalb counties. More than 28,000 deer have been tested in Illinois during the past 5 years. Illinois DNR CWD information is available at: Editor’s note: This finding in LaSalle County is a significant departure from the previously known distribution in Illinois. The new location is the first deer detected in the Illinois River basin, which winds southwest through Illinois towards St. Louis.


New Mexico:


Press Release from New Mexico Game and Fish (August 28, 2007):


LAS CRUCES: New Mexico recorded its 19th case of chronic wasting disease in deer in a sick animal found in the Bishop's Cap area of the Organ Mountains. Officer Richard McDonald investigated a report of an emaciated deer July 12. The animal was unaware of human presence, chronically thirsty, urinating often, and staying in and near a water source. Officer McDonald followed the state's protocol for disease surveillance by killing the animal and sending it to the Veterinary Diagnostic Laboratory in Albuquerque for testing. Based on the symptoms and the area from which the deer came, the laboratory was instructed that chronic wasting disease (CWD) was highly probable. Laboratory diagnostic testing confirmed presence of CWD in this deer. This is the 19th deer with confirmed CWD found since it was first detected in New Mexico in 2002. Two elk have also been found with CWD. This deer was in Game Management Unit 19, where special CWD restrictions already exist for hunters. Anyone who finds a deer or elk that appears unaware of human presence and displays symptoms including droopy ears, emaciation, chronic thirst, frequent urination, and reluctance to leave water, should report their observations to the Department of Game and Fish, Wildlife Management Division, (505) 476-8127. New Mexico Game & Fish CWD information is at: Press Release is at:





[2] Illinois Date: 23 Dec 2006 From: Terry Singeltary Source: Rockford Register Star [edited] <>


16 more CWD deer discovered




Tests for chronic wasting disease found 16 more confirmed cases in northern Illinois this fall [2006], bringing the total to 163 since the state's 1st infected deer was discovered in 2002 near Roscoe. The positive tests came from deer killed by firearm and archery hunters and a few suspicious deer taken by DNR staff. Winnebago and DeKalb counties each had 6, Boone County 4. All but one case was from deer in previously infected areas. The exception was a deer killed in southern DeKalb County, about 7 miles from the LaSalle County line. The state has included southern DeKalb in next month's [January 2007] special CWD hunt because of the new discovery. The latest positives came from about 2500 deer. Tests have not been completed on all deer sampled during the firearm seasons. Midwest states had increased firearm deer harvests this season. Illinois' total was 115 192 deer, compared with 114 209 last year [2005]. Wisconsin's harvest was 336 211, compared with 325 630 in 2005. Michigan's harvest was up about 7 percent at about 258 000. Minnesota doesn't yet have a total, but officials expect it to surpass 250 000, which would place it among the state's 5 best harvests.


[Byline: Doug Goodman ]


See Latest Map, December 2006:



Illinois Chronic Wasting Disease 2005-2006 Surveillance/Management Summary:





Terry S. Singeltary Sr.



Wednesday, August 31, 2016




 Monday, September 05, 2016

*** Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway ***

Wednesday, September 7, 2016


*** An assessment of the long-term persistence of prion infectivity in aquatic environments



Friday, September 02, 2016


*** Chronic Wasting Disease Drives Population Decline of White-Tailed Deer



Monday, August 29, 2016





Thursday, August 18, 2016





Sunday, August 28, 2016




Transmissible Spongiform Encephalopathy TSE Prion and how Politics and Greed by the Industry spread madcow type diseases from species to species and around the globe






Saturday, December 12, 2015


NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE Prion REPORT December 14, 2015



Friday, August 14, 2015


Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015



***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 CWO


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.





Saturday, May 28, 2016


*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***



Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964


How Did CWD Get Way Down In Medina County, Texas?


Confucius ponders...


Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?


Epidemiology of Scrapie in the United States 1977




Scrapie Field Trial Experiments Mission, Texas


A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.


The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ...


snip...see full text ;



Thursday, June 09, 2016


Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964


How Did CWD Get Way Down In Medina County, Texas?




Friday, April 22, 2016


*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer



Monday, July 18, 2016


Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster



Wednesday, February 10, 2016


*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***



Sunday, January 17, 2016


*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of $298,770 for 228 white-tailed deer killed on farm ***



Sunday, May 08, 2016





Friday, April 22, 2016







Monday, May 02, 2016


*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***







Saturday, April 23, 2016


*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***


Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X




Terry S. Singeltary Sr.


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