Thursday, July 30, 2020

Ohio Deer Summary 2019 - 2020 CWD TSE Prion 24 Confirmed To Date All Captive Cervid

Ohio Deer Summary 2019 - 2020 CWD TSE Prion 24 Confirmed To Date All Captive Cervid

Ohio Deer Summary 2019 - 2020

DISEASE UPDATE

Chronic Wasting Disease

Nearly 24,000 free-ranging deer have been tested for CWD since 2002 and, to-date, none have tested positive for the disease.

Chronic Wasting Disease (CWD) is a fatal disease of the central nervous system of mule deer, white-tailed deer, elk, moose, and reindeer. CWD is caused by abnormal proteins, or prions (not a bacteria or virus), that ultimately destroy brain tissue. This type of disease is known as a transmissible spongiform encephalopathy. This family of diseases includes bovine spongiform encephalopathy (mad cow disease), scrapie in sheep, and Creutzfeldt-Jakob Disease in humans.

Since 2002 the Division of Wildlife has conducted statewide CWD surveillance, testing 23,959 deer. To date, there has yet to be a wild, free-ranging deer test positive for the disease in Ohio. In 2019, a record 3,818 deer were submitted for CWD testing. Division of Wildlife staff collected 899 road-killed deer from all 88 counties and hunters submitted (directly or via taxidermist/processor) 2,831 deer (one of which was an escaped captive deer) for CWD testing. An additional five escaped or confiscated captive cervids, 32 deer displaying abnormal behavior and/or poor physical condition, 14 found dead under suspicious circumstances, 26 removed in conflict situations, and 11 others were tested for CWD in 2019. CWD was not detected in any of these samples.

Disease Surveillance Area

In October 2014, a mature buck from a shooting preserve in Holmes County tested positive for CWD, becoming the first-ever CWD positive deer in Ohio. The shooting preserve was depopulated in April 2015, and testing revealed no additional CWD-positive animals. Subsequent testing of nearly 300 free-ranging deer in an eight-township area around the shooting preserve failed to detect any CWD positive deer as well. However, in spring of 2015, two more CWD-positive deer were reported from a captive white-tailed deer breeding pen in Holmes County. This herd was depopulated in June 2015, and 16 additional deer tested positive for the disease, bringing the total of CWD-positive animals found in Ohio to 19 (all in captive herds). In response to these findings, the Division of Wildlife conducted targeted surveillance in the immediate vicinity of the infected facility during the summer of 2015. Staff collected 18 deer, including two that had escaped from captive facilities, with none testing positive for CWD.

Additionally, the focus area in 2015 was expanded to include two townships in southern Wayne County, and the 10-township focus area was declared a Disease Surveillance Area (DSA, visit wildohio.gov for specific regulations pertaining to a DSA). The 10-township DSA in central Holmes and southern Wayne counties expired on July 31, 2018 after three seasons of intensive surveillance revealed no CWD positive animals in the wild herd. However, due to the early 2018 discovery of three additional CWD-positives in an eastern Holmes County captive facility, a new, 7-township DSA was established (Figure 10). During the 2019-20 season, 248 hunter harvested deer from DSA 2018-01 were collected at inspection stations during Ohio’s 7-day gun season. Again, CWD was not detected in any of the deer tested.

Figure 10. Disease Surveillance Area 2018-01 (DSA)

https://ohiodnr.gov/wps/wcm/connect/gov/b15f858d-17f6-4536-83c6-6548eec07372/Pub+5304_2019_final.pdf?MOD=AJPERES&CONVERT_TO=url&CACHEID=ROOTWORKSPACE.Z18_M1HGGIK0N0JO00QO9DDDDM3000-b15f858d-17f6-4536-83c6-6548eec07372-ncF2luj

Please note, to date, NO CWD TSE Prion positive WILD cervid has been detected in the great state of Ohio.

Please note, to date, 24 CASES OF CWD TSE PRION POSITIVE HAVE been detected in Captive Cervid in Ohio, with the latest being announced May 16, 2020 in Wayne County farm. ''Subsequent to that announcement, another doe tested positive on the same farm, bringing the total number of CWD+ deer (all captive) to 24''.

personal communication Michael J. Tonkovich, Ph.D. Deer Program Administrator Ohio DNR Division of Wildlife, July 30, 2020.

Sent: Sat, May 16, 2020 10:18 am

Subject: Ohio Chronic Wasting Disease Detected on Wayne County Farm

Chronic Wasting Disease Detected on Wayne County Farm

May 15, 2020 | Animal Health

Chronic Wasting Disease Detected on Wayne County Farm

REYNOLDSBURG, Ohio (May 15, 2020) – Chronic Wasting Disease (CWD) has been detected at a farm in Wayne County. CWD is a degenerative brain disease that affects elk, mule deer and white-tailed deer. Investigators with the Ohio Department of Agriculture (ODA) detected CWD in a doe in the herd. 

ODA is conducting an epidemiological investigation on the farm and developing a herd plan. ODA has applied for an indemnity plan with the United States Department of Agriculture for depopulation of the herd. This is necessary in order to stop the transmission and spread of CWD. Once approved, ODA officials will depopulate the affected herd.

CWD has occurred in Ohio in the past but has been eradicated through depopulation. It has never been found in Ohio’s wild deer herd population. 

If you have questions or concerns regarding CWD, please contact the Division of Animal Health at 614-728-6220 or by email, animal@agri.ohio.gov.


A captive white-tailed deer breeding facility in Holmes County was confirmed CWD-positive in January 2018 and depopulated in February 2018. Two of the 93 deer euthanized were CWD-positive as well. A disease surveillance area (DSA) has been established around the facility and will remain in effect for at least three years.


***> Ohio is considered free of CWD and has robust surveillance programs in captive and free-ranging deer

LOL! simply put, if you don't test enough, you will not find cwd, until it finds you, then it's too late...tss

there were 19 CONFIRMED CASES OF CWD BACK IN 2015 IN OHIO, so how in the world can a state claim to be CWD TSE Prion?

 Ohio Changes in CWD Sample Submission for IHC Testing, Ohio is considered free of CWD?

Ohio Department of Agriculture - December 2018

Changes in CWD Sample Submission for IHC Testing

Dr. Jeff Hayes, DVM, MS, ADDL Pathology Section Head 

The United States Department of Agriculture (USDA) has recently made changes in the procedures required for sample collection from cervids for chronic wasting disease (CWD) testing by immunohistochemistry. Ohio is considered free of CWD and has robust surveillance programs in captive and free-ranging deer. The Ohio ADD has tested over 8000 samples per year, for the last several years. The following changes are now required for veterinarians submitting samples to an approved laboratory for CWD testing, including submission of both fresh and formalin-fixed samples.

Formalin-fixed tissue (10:1 ratio of formalin to tissue sample): 1- OBEX: After removing the brainstem from the foramen magnum, ensure the proper obex sample (bifurcation or “V”) is preserved. Further trim the brainstem section by making a transverse cut ¾ inch in front of the “V” shape bifurcation and an equal distance behind the bifurcation. Place the trimmed obex into the formalin jar. 2- MEDIAL RETROPHARYNGEAL LYMPH NODES (MRPLNs): Remove each left and right MRPLN as done previously, now, longitudinally incise each lymph node. Place half of the left and half of the right node into the formalin jar, and the other halves into a whirl-pak bag (see below).

Fresh tissue (collect samples in one labeled whirl-pak bag): 1- BRAINSTEM: Place the rostral and distal pieces of brainstem in the labeled bag. 2- RETROPHARYNGEAL LYMPH NODES: Place the other halves of each node into the same bag. 3- ID TAGS AND SKIN: Remove the official ID with a 1”X1” piece of ear attached for each animal sampled, place it in the labeled bag and submit with other fresh tissues. DO NOT PLACE IN FORMALIN.

NOTE: If the animal is a trophy animal, submit the official ID and attach a new official ID to another piece of skin. If no official ID is present, the collector must affix one and record the information. Microchips must be in tissue.

Call the ADDL with any questions or concerns at 614-728-6220.

=====

ODNR Takes New Action to Monitor Chronic Wasting Disease in Ohio's Deer Herd 11/28/2018 Division of Wildlife COLUMBUS, OH – As of Aug. 1, portions of Holmes and Tuscarawas counties have been declared a Disease Surveillance Area (DSA) as part of the state’s ongoing efforts to monitor Chronic Wasting Disease (CWD), according to the Ohio Department of Natural Resources (ODNR). This designation was made after a deer at a captive white-tailed deer facility in Holmes County tested positive for CWD. In addition, the state has established new carcass rules for hunters who hunt wild deer, elk, caribou and moose in other states.

The new carcass rules will apply to Ohio hunters who plan to travel out of state to hunt any CWD-susceptible species (white-tailed deer, mule deer, elk, caribou or moose). No person is permitted to bring or transport high-risk carcass parts of CWD-susceptible species into Ohio from any state or Canadian province, regardless of the CWD status of the exporting jurisdiction. Additional information on carcass regulations can be found at wildohio.gov.

The newly-established DSA includes the areas within a 6-mile radius from the CWD positive samples in Holmes County and includes: Wayne and Sugar Creek townships in Tuscarawas County, and Salt Creek, Paint, Berlin, Walnut Creek and Clark townships in Holmes County. This DSA designation will remain in effect for a minimum of three years. The area will be mapped and posted on the division’s website: Diseases in Wildlife: CWD

The following regulations will apply within the DSA:

• Requires hunters to bring deer carcasses harvested within the DSA boundaries to an ODNR Division of Wildlife inspection station for sampling during the deer-gun and deer muzzleloader seasons;

• Prohibits the placement of or use of salt, mineral supplement, grain, fruit, vegetables or other feed to attract or feed deer within the DSA boundaries. Prohibits hunting of deer by the aid of salt, mineral supplement, grain, fruit, vegetables or other feed within the DSA boundaries; and

• Prohibits the removal of a deer carcass killed by a motor vehicle within the DSA boundaries unless the carcass complies with deer carcass regulations.

Normal agricultural activities including feeding of domestic animals as well as hunting deer over food plots, naturally occurring or cultivated plants and agriculture crops are not prohibited.

Hunters harvesting deer within the DSA are required to deliver their deer to a carcass inspection station. Two locations have been designated as Carcass Inspection Stations for the deer-gun seasons and the deer muzzleloader season. Both locations will be open and staffed from 10 a.m. to 8 p.m. during the deer-gun and deer muzzleloader seasons. The dates for these seasons are: Nov. 26-Dec. 2, Dec. 15-16 and Jan. 5-8, 2019.

• Sugarcreek Village Hall, 410 S Broadway St., Sugarcreek 44681.

• Walnut Creek Township Garage, 2490 Township Road 414, Dundee 44624.

Hunters will be asked to provide their confirmation number from the game check process as well as the location where the deer was killed (the address of the farm or nearest road intersection are acceptable). Tissue samples will be taken and tested for CWD. The process should take no more than 10 minutes; however, delays are likely at peak times of the day. Hunters are strongly encouraged to complete the game check process before proceeding to the inspection. Hunters that harvest a deer and wish to have it mounted will still need to bring their deer to a carcass inspection station. Samples will not be taken at the time, but staff will collect additional information so that samples can be collected later.

If hunters have questions about the carcass inspection stations or need directions to the locations, they may call 800-WILDLIFE or the Wildlife District Three office at 330-644-2293. The ODNR Division of Wildlife is responsible for protecting and managing Ohio’s fish and wildlife resources for the benefit of all Ohioans. We greatly appreciate the cooperation of hunters in helping us monitor Ohio’s deer herd. For more information about CWD, visit wildohio.gov.

The state’s first DSA, DSA 2015-01, which was established in 2015, has expired after being in place for three years with no evidence of CWD found in wild deer. The original DSA was established after CWD was first detected at a shooting preserve and breeding facility in Holmes County, and included portions of Holmes and Wayne counties.

ODNR ensures a balance between wise use and protection of our natural resources for the benefit of all. Visit the ODNR website at ohiodnr.gov.

– 30 –


***> Ohio is considered free of CWD and has robust surveillance programs in captive and free-ranging deer

LOL!

hell, there were 19 CONFIRMED CASES OF CWD BACK IN 2015 IN OHIO, so how in the world can a state claim to be CWD TSE Prion?

WEDNESDAY, AUGUST 05, 2015

Ohio confirms to me Chronic Wasting Disease 

CWD Spreads 19 confirmed cases to date Just got off the phone with Christy Clevenger of Ohio

Ohio Department of Agriculture March 2012 – Present (3 years 6 months) Reynoldsburg, Ohio CWD program

Ms. Clevenger confirmed, to date, from the Yoder debacle, 1 confirmed case of CWD from the Hunting Preserve, 2 confirmed cases from the Breeding Farm, and 16 confirmed cases of CWD from the Breeder Depopulation, with a total to date of 19 cases of CWD in Ohio...with sad regards, Terry





A captive white-tailed deer breeding facility in Holmes County was confirmed CWD-positive in January 2018 and depopulated in February 2018. Two of the 93 deer euthanized were CWD-positive as well. A disease surveillance area (DSA) has been established around the facility and will remain in effect for at least three years.


    Disease Surveillance Area (DSA) Changes
    In 2015, the ODNR Division of Wildlife declared a 10-township area in Holmes (all or portions of Ripley, Prairie, Salt Creek, Monroe, Hardy, Berlin, Killbuck, Mechanic, and Richland townships) and Wayne (Franklin and Clinton townships) counties a Disease Surveillance Area (DSA.) The area was formally declared DSA 2015-01 and was to exist for a minimum of three years. Effective July 31, 2018, that designation and all rules associated with it have expired. CWD was not detected in any of the approximately 2,000 wild deer tested that were harvested in the area over a 4-year period. 

    In response to a captive cervid facility testing positive for CWD in January 2018 in eastern Holmes County, a new DSA 2018-01 has been established. All rules associated with DSA 2018-01 are effective beginning August 1st, 2018. These rules include the following: 

    • Requires hunters to bring deer carcasses harvested within the DSA 2018-01 boundaries to an ODNR Division of Wildlife inspection station for sampling during the deer-gun and deer muzzleloader seasons;
    • Prohibits the placement of or use of salt, mineral supplement, grain, fruit, vegetables, or other feed to attract or feed deer within the DSA boundaries;
    • Prohibits hunting of deer by the aid of salt, mineral supplement, grain, fruit, vegetables, or other feed within the DSA boundaries; and
    • Prohibits the removal of a deer carcass killed by a motor vehicle within the DSA 2018-01 boundaries unless the carcass complies with deer carcass restrictions.


    Disease Surveillance Area 2018
     
    Click to enlarge


    Normal agricultural activities including feeding of domestic animals as well as hunting deer over food plots, naturally occurring or cultivated plants and agriculture crops are not prohibited. 

    Hunters harvesting deer during Ohio’s gun seasons (7-day traditional, 2-day bonus, and 4-day muzzleloader) within the DSA are required to deliver their deer to a carcass inspection station. Hunters are NOT required to present their deer for testing during the 2-day youth gun season. Two locations have been designated as Carcass Inspection Stations for the deer-gun seasons and the deer muzzleloader season. Both locations will be open and staffed from 10 a.m. to 8 p.m. during the deer-gun and deer muzzleloader seasons. 

    • Sugarcreek Village Hall (Tuscarawas County), 410 South Broadway Street, Sugarcreek, OH 44681
    • Walnut Creek Township Garage (Holmes County), 2490 Township Road 414, Dundee, OH 44624

    Hunters will be asked to provide their 18-digit confirmation number from the game check process as well as the location where the deer was killed. Tissue samples will be taken and tested for CWD. Samples can be taken from either just the head or complete carcass. Hunters that harvest a deer and wish to have it mounted must still bring their deer to an inspection station. Samples will not be taken at the time, but staff will collect additional information, so samples can be collected later. 

    Although CWD has not been detected in the wild deer herd, hunters who plan to hunt in DSA 2018-01 are encouraged to consider having their deer processed commercially to ensure high-risk carcass parts are disposed of properly. Hunters who plan to process their deer are strongly encouraged to double-bag all high-risk carcass parts and set them with household trash for pickup. There is no strong evidence that CWD affects humans; however, hunters can take some common-sense precautions, such as not harvesting deer that appear sick or otherwise abnormal and wearing rubber gloves while field dressing and processing deer. 

    White-tailed Deer Harvested in Ohio
    Irresponsible dumping of carcasses can spread disease. Hunters who process their white-tailed deer at home should properly dispose of the hide, brain and spinal cord, eyes, spleen, tonsils, bones, and head by double-bagging these parts and set them with the trash for disposal at a municipal landfill. It is unlikely that hunters would increase CWD transmission by field dressing and leaving the entrails and internal organs in the field. 

    Anyone who sees deer that appear to be sick or are displaying abnormal behavior should immediately report the occurrence to the ODNR Division of Wildlife. The person reporting the animal should describe the location of the animal, its symptoms, and behavior. Hunters should not kill or handle a deer that they believe is sick. 



    a pitiful way to report to the public, OR, how NOT to report to the public, exactly how many cases of CWD TSE Prion there are in your state.

    out of sight, out of mind, surveillance of CWD TSE Prion...tss

    SATURDAY, MAY 16, 2020 
    Ohio Chronic Wasting Disease Detected on Wayne County Farm
    TUESDAY, DECEMBER 04, 2018 

    Ohio Changes in CWD Sample Submission for IHC Testing, Ohio is considered free of CWD?


    THURSDAY, JANUARY 25, 2018 

    Ohio Chronic Wasting Disease CWD TSE Prion aka mad deer update 2016-2017 SEASON SUMMARY


    January 14, 2018

    Ohio ODA confirms CWD TSE Prion in more captive deer




    Chronic Wasting Disease Update

    Dr. Jeff Hayes, MS, DVM, ADDL Pathology Section Head

    Through November 2017, the ADDL has performed immunohistochemistry (IHC) to detect the prion agent associated with Chronic Wasting Disease (CWD) in tissues from 1,585 captive deer and from 411 wild deer this year. The majority of the wild deer were submitted by the Ohio Division of Wildlife. To date this has included the examination of 7,100 tissues. No suspect or positive animals have been detected among all deer tested in 2017, and none have been detected in Ohio since two premises were identified as having CWD-infected captive white-tailed deer in late 2014 and early 2015.


    2018 updates for trace in's and out's from this Ohio positive cwd captive? any positives there from? just wondering....terry

    SUNDAY, DECEMBER 03, 2017 

    Ohio Chronic Wasting Disease Update Through November 2017


    WEDNESDAY, NOVEMBER 15, 2017 

    Ohio ODNR Continues Plan to Monitor Ohio’s Deer Herd for Chronic Wasting Disease or do they?


    WEDNESDAY, AUGUST 16, 2017

    OHIO Chronic Wasting Disease CWD TSE Prion UPDATE?


    Ohio Deer Hunting Season 2017-2018 Today, the deer population in Ohio exceeds 750,000.


    see map;


    IT would be great if such a detailed assessment of Chronic Wasting Disease CWD TSE Prion in CAPTIVE FARMS in Ohio were available...terry

    WEDNESDAY, AUGUST 05, 2015

    Ohio confirms to me Chronic Wasting Disease 

    CWD Spreads 19 confirmed cases to date Just got off the phone with Christy Clevenger of Ohio

    Ohio Department of Agriculture March 2012 – Present (3 years 6 months) Reynoldsburg, Ohio CWD program

    Ms. Clevenger confirmed, to date, from the Yoder debacle, 1 confirmed case of CWD from the Hunting Preserve, 2 confirmed cases from the Breeding Farm, and 16 confirmed cases of CWD from the Breeder Depopulation, with a total to date of 19 cases of CWD in Ohio...with sad regards, Terry


    FRIDAY, OCTOBER 23, 2015

    Ohio Wildlife Council Passes Rule to Help Monitor CWD From: Terry S. Singeltary Sr.

    Sent: Friday, October 23, 2015 4:39 PM



    Subject: Ohio Wildlife Council Passes Rule to Help Monitor CWD


    MONDAY, AUGUST 24, 2015 

    Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests CWD


    WEDNESDAY, AUGUST 05, 2015

    Ohio confirms to me Chronic Wasting Disease 

    CWD Spreads 19 confirmed cases to date Just got off the phone with Christy Clevenger of Ohio

    Ohio Department of Agriculture March 2012 – Present (3 years 6 months) Reynoldsburg, Ohio CWD program

    Ms. Clevenger confirmed, to date, from the Yoder debacle, 1 confirmed case of CWD from the Hunting Preserve, 2 confirmed cases from the Breeding Farm, and 16 confirmed cases of CWD from the Breeder Depopulation, with a total to date of 19 cases of CWD in Ohio...with sad regards, Terry


    Thursday, April 02, 2015

    OHIO CONFIRMS SECOND POSTIVE CHRONIC WASTING DISEASE CWD on Yoder's properties near Millersburg


    Wednesday, February 11, 2015

    World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with two counts of tampering with evidence


    Thursday, October 23, 2014 

    *** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE 


    Monday, June 11, 2012

    *** OHIO Captive deer escapees and non-reporting ***


    Geographic variation in the PRNP gene and its promoter, and their relationship to chronic wasting disease in North American deer

    Robert M. Zink ,Nadje Najar,Hernán Vázquez-MirandaORCID Icon,Brittaney L. BuchananORCID Icon,Duan Loy &Bruce W. BrodersenORCID Icon

    Pages 185-192 | Received 12 May 2020, Accepted 11 Jul 2020, Published online: 26 Jul 2020


    ABSTRACT

    PRNP genotypes, number of octarepeats (PHGGGWGQ) and indels in the PRNP promoter can influence the progression of prion disease in mammals. We found no relationship between presence of promoter indels in white-tailed deer and mule deer from Nebraska and CWD presence. White-tailed deer with the 95 H allele and G20D mule deer were more likely to be CWD-free, but unlike other studies white-tailed deer with the 96S allele(s) were equally likely to be CWD-free. We provide the first information on PRNP genotypes and indels in the promoter for Key deer (all homozygous 96SS) and Coues deer (lacked 95 H and 96S alleles, but possessed a uniquely high frequency of 103 T). All deer surveyed were homozygous for three tandem octarepeats.

    KEYWORDS: Coues deer, genotype, Key deer, mule deer, octarepeats, prion, promoter indels, white-tailed deer

    snip...

    Introduction

    Chronic Wasting Disease (CWD), a transmissible spongiform encephalopathy (TSE) of cervids, has led to declines of mule deer (Odocoileus hemionus) and white-tailed deer (O. virginianus) over the last two decades [1,2]. An incomplete understanding of the disease and its genetic control has in part hampered attempts to manage outbreaks. The relationship between different genotypes at the PRNP gene and the expression of CWD in cervids was explored in several studies [3–10]. For example, Johnson et al. [8] and Race et al. [10] provided experimental evidence that white-tailed deer orally inoculated with prions from CWD-positive deer expressing 95 H surviving the longest post-inoculation. Mule deer with at least one F at position 225 lived longer than wild type deer [11]. Thus, there is evidence that an individual’s PRNP genotype can influence the rate at which an infected deer succumbs to CWD. Unlike the situation with scrapie in sheep [12], there does not appear to be a genotype that provides nearly complete resistance to CWD in deer, although Haley et al. [13] suggest there might be. Vázquez-Miranda and Zink [14] pointed out that a single mutation in the PRNP gene in white-tailed deer could yield a genotype similar to the one in sheep that provides resistance to scrapie.

    snip...

    Discussion

    Several aspects of variation in the PRNP gene and its promoter could influence progression of prion disease. Our study is the first to our knowledge to describe the relationship between PRNP genotype, indels in the promoter region, frequency of octarepeats, and the presence of CWD in white-tailed deer and mule deer. In bovines, deletions in the promoter are associated with an enhanced frequency of BSE, presumably due to an altered rate of transcription caused by loops in the promoter [18,30]. Heaton et al. [24] found that 6% of white-tailed deer and 2% of mule deer were heterozygous for an 8-base pair deletion, whereas from a considerably larger sample size, albeit from a different geographic region, our frequencies were 2.4% and 0%, respectively. We found no relationship between the presence of indels and the incidence of CWD in white-tailed deer (Table 2) from Nebraska, and indels were uncommon (~9% of sampled white-tailed deer and 0% of mule deer had an indel). The most common deletion removes a TATA box, which is important for the start of transcription, and this could explain its rarity. There was also no correlation between different PRNP genotypes and the two deletions observed in 19 white-tailed deer, which in general occurred in the most common genotypes. Thus, deletions in this promoter region do not appear to be associated with an enhanced incidence of CWD in our sample of white-tailed deer.

    The inference of reduced susceptibility to CWD in deer possessing alleles 95 H and 96S comes from relatively few deer that were kept in captivity and inoculated with unnaturally concentrated doses of prions from later-stage CWD positive deer [8,9]. Individuals with alleles 95 H and 96S (either heterozygous or homozygous) lived longer, but still perished from CWD. It is unknown whether the onset of CWD in 95 H and 96S deer was shifted later in life or developed more slowly than other genotypes, and when during the course of infection these deer shed prions in sufficient quantity to infect healthy deer. Haley et al. [13] studied PRNP genotypes and presence of CWD in captive deer herds from the US and Canada, and found that 95 HH (n = 2) and 95 HQ/96SG (4) were negative for CWD, and that seven of 28 95 HQ/96 GG individuals were CWD positive. Haley et al. [13] found that 25 of 143 (17.5%) 96SS individuals were positive for CWD. Of interest is that Haley et al. [13] found that in Canada, only two of 42 116 GG and 96SG/116 GA genotypes were CWD positive, whereas 96 GG/116 GA exhibited 40 out of 189 deer that were positive for CWD. However, we found that only one of nine 95 H individuals was CWD positive, which was significant in an odds ratio test (P = 0.051; Table 4) relative to the wild type, a result also found by other studies [13,31].

    Table 4. Likelihood and odds ratios of disease for a given genotype. Odds ratios are relative to the most common genotype (the wildtype), which is not necessarily the genotype with the highest risk for disease. An odds ratio of 1 indicates the reference genotype to which the other two are compared. Some combinations are not included because they were either not found or too rare for statistical analysis.

    CSVDisplay Table

    In contrast to other studies, we found that individuals with or without the 96S allele were equally likely to be CWD positive. Although in previous studies, deer with a least one copy of the 96S allele experienced increased longevity (or delayed onset), the ages of our deer are unknown, and it is possible that many were relatively older bucks. ELISA tests are likely incapable of detecting CWD in very early disease stages. We found that having one copy of A116 G did reduce the odds of disease, but not significantly so, constituting only equivocal support for results in Haley et al. [13]. In a captive herd of white-tailed deer from Nebraska, O’Rourke et al. [5] found 13 CWD-positive deer (out of 133) that were heterozygous for the 116 G allele, also suggesting that the allele does not provide resistance to CWD. Thus, it is possible that a population with a high frequency of H95Q, S96G or A116 G alleles might show increased longevity, perhaps even mimicking the normal mortality schedule of past CWD-free generations. Haley et al. [13] suggested that captive breeding of individuals with 96S and 95H alleles might yield a relatively CWD-resistant herd. At the least, it could shift the occurrence of the disease past the first year or two of reproduction. It is noteworthy, however, that our percentages of CWD positive 96SS and 116 GA deer differed considerably from the results of Haley et al. [13], and suggests more widespread geographic testing is needed to verify the effects of particular genotypes on CWD susceptibility.

    Our sequence data for deer outside of Nebraska came from individuals of unknown CWD status; however, CWD is not present in Florida (Key deer) or Arizona (Coues deer). Our sample of Key deer was fixed for 96S; these homozygous 96SS individuals might be relatively resistant should CWD make it to the Florida Keys. Our sample of Coues deer showed a relatively high frequency of 103 T, which has not been found in other white-tailed deer samples; this might be associated with reduced susceptibility to CWD, but this is unknown. However, we provide the first information at the PRNP locus, its promoter, and the number of octarepeats for these populations. Our widely spaced samples underscore the need for a denser sampling of deer throughout North America to document the pattern of genetic variation at the PRNP locus and its promoter as the incidence of CWD continues to increase geographically.


    TUESDAY, JULY 28, 2020 

    Geographic variation in the PRNP gene and its promoter, and their relationship to chronic wasting disease in North American deer


    SUNDAY, MARCH 29, 2020 

    Can genetic assignment tests provide insight on the influence of captive egression on the epizootiology of chronic wasting disease?

    https://chronic-wasting-disease.blogspot.com/2020/03/can-genetic-assignment-tests-provide.html

    Research Paper

    Management of chronic wasting disease in ranched elk: conclusions from a longitudinal three-year study

    N.J. Haley,D.M. Henderson,R. Donner,S. Wyckoff,K. Merrett,J Tennant,

    Pages 76-87 | Received 09 Oct 2019, Accepted 28 Jan 2020, Published online: 07 Feb 2020


    ABSTRACT

    Chronic wasting disease is a fatal, horizontally transmissible prion disease of cervid species that has been reported in free-ranging and farmed animals in North America, Scandinavia, and Korea. Like other prion diseases, CWD susceptibility is partly dependent on the sequence of the prion protein encoded by the host’s PRNP gene; it is unknown if variations in PRNP have any meaningful effects on other aspects of health. Conventional diagnosis of CWD relies on ELISA or IHC testing of samples collected post-mortem, with recent efforts focused on antemortem testing approaches. We report on the conclusions of a study evaluating the role of antemortem testing of rectal biopsies collected from over 570 elk in a privately managed herd, and the results of both an amplification assay (RT-QuIC) and conventional IHC among animals with a several PRNP genotypes. Links between PRNP genotype and potential markers of evolutionary fitness, including pregnancy rates, body condition, and annual return rates were also examined. We found that the RT-QuIC assay identified significantly more CWD positive animals than conventional IHC across the course of the study, and was less affected by factors known to influence IHC sensitivity – including follicle count and PRNP genotype. We also found that several evolutionary markers of fitness were not adversely correlated with specific PRNP genotypes. While the financial burden of the disease in this herd was ultimately unsustainable for the herd owners, our scientific findings and the hurdles encountered will assist future CWD management strategies in both wild and farmed elk and deer.

    KEYWORDS: Prion, elk, RAMALT, RT-QuIC, antemortem

    snip...

    This manuscript describes one such property, a herd of over 570 elk maintained on 3500 acres of fenced habitat in northwestern Colorado.

    snip...

    Return rate of CWD positive animals In the 2017 sampling period, 315 animals were tested for CWD antemortem. Of those, 71 tested positive by IHC, RT-QuIC, or both. Thirty-four infected animals (thirty-three cows and one bull) were euthanized and confirmed CWD positive post-mortem, with the remaining thirty-seven animals (Twenty-six bulls and eleven cows) released back onto the property. Of those animals which were released, four were harvested in the fall of 2017 and were found to be CWD positive post-mortem. Three of the remaining thirty (10%) returned for the 2018 sampling period, the remainder were lost in the field and went untested. All three were 132ML heterozygous animals, each positive again on antemortem testing in year three. In contrast, 120 of the 329 animals negative by antemortem testing were harvested in the fall of 2017, with 26 found to be CWD positive (21.7%). Of the remaining 209 animals, 141 returned for the 2018 sampling period (67.5%), with the remaining animals presumed lost in the field, untested. (Table 1 and Figure 1)

    Over the course of the entire study, four of forty-nine CWD positive 132MM animals released back onto the property (8.2%) returned for a second year of sampling. Nine of thirty-three 132ML animals positive for CWD returned for a second year of sampling (27%), a return rate that was significantly greater than that of CWD positive 132MM animals (risk ratio: 3.34, p = 0.03). The lone 132LL cow identified during the course of antemortem testing in year two did not return for sampling in year three. Cumulatively, just 13 of 82 animals identified as CWD positive and released onto the property returned the following year (15.9%). These low rates of yearly return are in stark contrast to the cumulative return rate for CWD negative animals. For animals homozygous for the 132M allele, 107/144 returned in year two, and 28/69 returned in year three (63% overall). For 132ML heterozygous animals, 170/221 returned in year two, with 62/181 returning in year three (58% overall). Twenty-five of thirty-five animals homozygous for the 132L allele returned in year two, with fifteen of thirty-five returning in year three (57% overall). Cumulatively, 60% of animals negative for CWD returned the following year – a yearly return rate nearly over 3.5 times that of CWD positive animals (risk ratio: 3.62, p < 0.001; 95% confidence interval 1.96–6.69).

    snip...

    Discussion

    While reports on the management of chronic wasting disease in wild deer and elk are many and varied [33–43], rare is the case presented for managing the disease in farmed cervids. Almost without exception, farmed cervids are immediately placed under quarantine and eventually depopulated when CWD is discovered on site [12]. This manuscript reports our efforts to manage CWD in a large elk herd, in a controlled setting with endemic CWD, through the use of annual live animal testing and targeted culling of CWD positive cows. Although the herd owners were presented with additional management directives, including culling of CWD positive bulls and those animals positive by an amplification assay (RT-QuIC), they were not implemented due to concern regarding its potential impact on hunting revenue. Ultimately, we could not completely evaluate our management practices, as the herd was slowly depopulated after the final sampling period due to the financial burden brought by the disease.

    snip...see full text;


    ***> at present, no PrPC allele conferring absolute resistance in cervids has been identified. 

    J Gen Virol. 2017 Nov; 98(11): 2882–2892.

    Published online 2017 Oct 23. doi: 10.1099/jgv.0.000952

    PMCID: PMC5845664

    PMID: 29058651

    Estimating chronic wasting disease susceptibility in cervids using real-time quaking-induced conversion

    Chronic wasting disease (CWD) resistance in cervids is often characterized as decreased prevalence and/or protracted disease progression in individuals with specific alleles; at present, no PrPC allele conferring absolute resistance in cervids has been identified. 

    snip...

    In summary, evaluating the amplification rates and efficiencies of recombinant PrPC substrates by RT-QuIC could be a useful tool for estimating the susceptibility of rare or newly discovered PRNP alleles, allowing researchers to target specific alleles for downstream evaluation in challenge studies. In the face of an ever-expanding CWD-endemic area, it is increasingly important to characterize the natural susceptibility of these alleles, as well as their geographical distribution and the evolutionary basis for their rarity. Do the QGAK, 225F and 225Y alleles represent recent, random anomalies, or are they more primitive mutations that adversely affect reproductive fitness? Perhaps they are an indication that cervids with these rare alleles were themselves once the target of a primordial prion strain. While some evidence has been presented for distinct strains of CWD, little is known about their geographical distribution or virulence in cervid hosts of diverse PRNP backgrounds. It is possible that, with the appropriate framework, RT-QuIC could allow for the discrimination of known and novel prion strains. Without further research into disease management and prevention, including resistance, the only certainty seems to be that CWD will continue its insidious spread, with further discoveries in new hosts and geographical locations.


    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.

    PRION 2016 CONFERENCE TOKYO 


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

    ''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. 


    ''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.'' 

    ADOPTED: 26 September 2019 doi: 10.2903/j.efsa.2019.5863 Update on chronic wasting disease (CWD) III

    snip...

    3.2.1.2. Non-cervid domestic species

    The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD-contaminated shared rangeland and subsequently developing a novel CWD-related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.

    For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).

    In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post-infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen-Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen-Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life-long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).

    A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low-level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low-level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.

    3.2.1.3. Other species

    Studies have demonstrated that the CWD agent(s) can be transmitted by the IC route in several species of rodents, such as voles (Subfamily Arvicolinae), deer mice (Peromyscus maniculatus), mice and hamsters (Subfamily Cricetinae). The susceptibility was, however, variable, being high in voles and deer mice but lower in mice and hamsters (Raymond et al., 2007; Heisey et al., 2010; Kurt et al., 2011; Di et al., 2013; Lee et al., 2013). Mink (subfamily Mustelinae) (Harrington et al., 2008), ferrets (Mustela putorius) (Bartz et al., 1998; Sigurdson et al., 2008) and cats (Mathiason et al., 2013) were susceptible to IC challenge with NA CWD sources, while CWD transmitted poorly to raccoons (Procyon lotor) by the IC route (Moore et al., 2019).

    3.2.2. European isolates

    The host range of CWD in Europe has been much less investigated so far, due to its recent identification. Among the cervid species involved in the CWD epidemics in North America, only some species (such as moose and reindeer) inhabit Europe; mule deer, white-tailed deer and elk/wapiti are American cervid species, although a few populations of white-tailed deer have been introduced into Europe. Others cervids that mainly inhabit Europe are red deer and roe deer. After the first detection in a reindeer in Norway in 2016 (Benestad et al., 2016), CWD has been detected in wild reindeer, moose and one red deer in Norway (Mysterud and Edmunds, 2019), in a moose in Finland in March 2018 and in three moose in Sweden in March, May and September 2019. CWD has not been detected

    Chronic Wasting Disease (CWD) III www.efsa.europa.eu/efsajournal 14 EFSA Journal 2019;17(11):5863

    so far in wild roe deer, fallow deer or white-tailed deer nor in any farmed cervid species. However, for fallow deer and white-tailed deer, the number of animals tested by the surveillance systems is still very low.

    The potential host range of European CWD strains is under investigation by bioassay experiments in a range of model species; most of these studies are ongoing and there are no published data available so far. Data from the experiments that are known to be ongoing in different laboratories have been gathered for the purposes of this Opinion. Overall, reindeer CWD, moose CWD and red deer CWD brain isolates (and LRS isolates from some selected cases) are being tested for transmissibility in mice, hamsters, bank voles and in a range of tg mouse lines expressing PrP sequences from: cervids (Q226 or E226 deer PrP variants), small ruminants (ARQ, VRQ, AHQ and ARR PrP polymorphic variants), cattle, pig, vulture and human (M129 and V129 PrP polymorphic variants) (see Section 3.3.1). Importantly, in most of these animal models, the transmissibility of European CWD isolates will be directly comparable with the outcome of similar (published or ongoing) experiments with CWD isolates from North America.

    While most of these studies are still ongoing, some experiments with CWD isolates from Europe have already produced evidence of transmission in some recipient species (Table 1). These include bank voles, conventional laboratory mice and tg mice expressing cervid PrP, sheep PrP and mouse PrP. The same rodent models are also susceptible to NA CWD isolates and will therefore allow comparative strain typing of NA and European CWD strains in due course. There is no strong evidence so far for rodent models being widely susceptible to NA isolates but not to European isolates or vice versa.

    Table 1 summarises more than 500 ongoing, published or unpublished primary transmission experiments of NA or European CWD isolates from different cervids into various rodent models, which have been gathered following the requests described in Section 2.2. The CWD isolates are grouped according to geographical origin and cervid species, with each column summarising the results obtained with one or more CWD isolates from a given species and country. Rodent models are grouped according to the PrP species expressed. Some species have polymorphic PrP sequences, so more than one PrP sequence per species has been modelled. In these cases, each row summarises the data obtained with more than one PrP variant of a given species. Therefore, conventional mice include wt mice expressing PRNPa or PRNPb mouse PrP variants; bank voles include two genetic lines with different amino acids at codon 109 (Bv109M and Bv109I); tg-cervidPrP mice include mouse lines expressing several cervid PrP variants (the deer wt Q226, the elk wt E226, the WTD variant S96, the elk variant M132); tg-sheepPrP mice include mouse lines expressing the ARQ, VRQ, AHQ or ARR small ruminant PrP variants; finally, tg-humanPrP mice include mouse lines expressing M or V at the human PrP polymorphic codon 129. Therefore, each box in the Table 1 summarises the outcome of bioassay experiments with one or more CWD isolates (from the same species and origin) in one or more recipient rodent models (expressing PrP from a single given species).

    Chronic Wasting Disease (CWD) III www.efsa.europa.eu/efsajournal 15 EFSA Journal 2019;17(11):5863

    Most of the studies conducted by molecular/biochemical methods are still ongoing. The preliminary data obtained by molecular/biochemical methods were difficult to summarise and will not be reported in the present Opinion. This was mainly due to lack of detail in the results obtained by direct PrPSc analyses (PrPres typing, conformational stability, proteinase K resistance, which are intended to investigate CWD strains) and to the different methodological approaches employed in amplification assays (PMCA and RT-QuIC). The information gathered by this activity shows that experiments aimed at modelling the species barrier for NA or European CWD isolates into different animal species, including humans, are underway in different laboratories and will be of help for understanding the potential host range of CWD strains.

    3.2.3 Impact of the PRNP gene on transmissibility

    Polymorphisms in the PRNP gene are known to influence susceptibility/resistance to prion disease in both small ruminants and humans (for recent review, see EFSA BIOHAZ Panel 2014, EFSA BIOHAZ Panel, 2017; Diack et al., 2014). Effects of host PRNP polymorphisms on CWD susceptibility/resistance have also been described in a number of cervid species (reviewed in EFSA BIOHAZ Panel, 2017, 2018).

    However, deer and elk wild-type PrP primary structures are equivalent, except at residue 226, which is glutamate in elk and glutamine in deer. The effect of this difference on CWD pathogenesis has been recently investigated using a gene-targeting approach in which the mouse PrP coding sequence was replaced with elk or deer PrP. The results obtained following experimental challenge with deer and elk CWD inocula from NA showed that the resulting GtE226 and GtQ226 mice had distinct kinetics of disease onset, with incubation times shorter in GtE226 than in GtQ226 mice, indicating that amino acid differences at PrP residue 226 dictate the selection and propagation of divergent strains in deer and elk with CWD. As prion strain properties largely dictate host range potential, these findings suggest that prion strains from elk and deer might pose distinct risks to sympatric species or humans exposed to CWD (Bian et al., 2019).

    The most common cervid species in Europe (moose, red deer, reindeer and roe deer) share the same PrP primary structure, i.e. Q226. However, red deer PrP is polymorphic at residue 226 and can therefore code for either Q226 or E226. Interestingly, CWD cases detected so far in four Norwegian moose, the first Swedish moose and one Norwegian reindeer are all homozygous for Q226 (Benestad, 2019b,c,d), but the CWD case in red deer is instead homozygous for E226 (Vikøren et al., 2019). The impact of these differences in PrP genotype on the transmissibility and strain properties of European CWD isolates is currently under investigation using GtE226 and GtQ226 mice (Bian et al., 2019). PRNP genotypes of the other reindeer from Norway and of the other moose cases in Sweden and Finland are not in the public domain.

    Data on the transmissibility of CWD in species with different PrP sequences obtained by in vivo or in vitro modelling allow the investigation of the structural basis of the transmission barriers for CWD. This in turn could provide hints for predicting, to some extent, the susceptibility of non-cervid species to CWD. Taken together, studies with CWD isolates from NA suggest that the 165–175 sequence similarity between cervid and host PrP is one important factor governing the susceptibility of different species to CWD (reviewed by Kurt et al., 2016). In particular, polymorphisms at N/S170 in the recipient species might be important for susceptibility, with species that have N170 being more susceptible than those with S170 (Kurt et al., 2016). However, this must not be seen as an absolute rule, as species having S170 in their PrP, such as squirrel monkeys, have also been reported to be susceptible to CWD. It is however pertinent to note that all livestock species and humans have PrP sequences with S170, so they should not be considered among the species with supposedly high susceptibility to NA CWD isolates. Ongoing experiments in rodent models seem to indicate a similar trend for European CWD isolates, as rodent models, apparently more susceptible to European CWD isolates such as bank voles and tg mice expressing deer PrP, are N170.

    Little information is currently known about the genetics of either wild or farmed cervid populations in Europe. A recent published study of several deer species (mostly in Great Britain) reported that red deer showed the most PRNP gene variation, with polymorphisms at codons 98, 168, 226 and 247 and marked variability in genotype frequencies in different regions. Other deer species showed less variation, with roe and fallow deer having identical PRNP gene sequences in all the animals sampled. Based on comparison with PRNP sequences of NA cervids affected by CWD and limited experimental challenge data, the authors conclude that a high proportion of wild deer in Great Britain may be susceptible to CWD (Robinson et al., 2019). A similar conclusion was reached by a previous study of 715 genotyped cervids (red deer, roe deer and chamois) from the UK and Italy (Peletto et al., 2009).

    3.2.4. Concluding remarks

    • The transmission of prions between species is limited by the ‘transmission barrier’ and the amino acid sequence of the host PrP plays a very key role in the overall susceptibility to TSE. Even for prions deriving from the same species, the host range may vary according to the prion strain, implying that different CWD strains might have different host ranges and different potential for transmitting to livestock species and to humans.

    • Whether the natural host range of CWD in NA extends beyond the family Cervidae is currently unclear and no natural infections have been reported so far in other wildlife species (e.g. predators and scavengers) with overlapping geographical ranges.

    • NA CWD has been transmitted experimentally to cattle and sheep, but with incomplete attack rates. The species barrier appears higher for pigs, although challenged animals can support low-level prion amplification.

    • Experimental transmission to tg mice and other rodent models shows some difference in the host ranges of different isolates but, particularly for the European isolates, many bioassays are still ongoing and data are not yet available.

    • The number of strains, the strain diversity, the prevalence and the potential host range of disease in both NA and Europe CWD may be underestimated. 

     snip...see full text;


    THURSDAY, JULY 09, 2020 

    Arkansas CWD TSE Prion Positives found as of June 20, 2020 844 Cases Confirmed


    FRIDAY, JANUARY 24, 2020 

    Arkansas Chronic Wasting Disease CWD TSE Prion FY2020 211 Positive Cases as of January 17, 2020


    THURSDAY, MAY 14, 2020 
    COLORADO As of February 2020, CWD has been detected in 33 of 54 deer herds, 14 of 43 elk herds, and 2 of 9 moose herds
    SATURDAY, FEBRUARY 01, 2020 

    Colorado confirmed CWD TSE Prion in 24 game management units in the state where it previously hadn’t been found

    Colorado Chronic Wasting Disease Response Plan December 2018

    I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.

    snip...

    IMPORTANT PUBLIC HEALTH MESSAGE

    Disease in humans resulting from CWD exposure has not been reported to date. However, public health officials cannot determine there is no risk from eating meat from infected animals. Consequently, officials recommend that people avoid exposure to CWD-infected animals. Please see the Colorado Department of Public Health and Environment website 
    for the most current recommendations on carcass testing and other preventive measures.

    To minimize exposure to CWD and other diseases of potential concern, Colorado Parks and Wildlife (CPW) and state public health officials advise hunters not to shoot, handle or consume any deer, elk or moose that is acting abnormally or appears to be sick. When fielddressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord (backbone). Minimize contact with brain or spinal cord tissues, eyes, spleen or lymph nodes. Always wash hands and utensils thoroughly after dressing and processing game meat. (the map on page 71, cwd marked in red, is shocking...tss)


    TUESDAY, MARCH 03, 2020 

    North Dakota Eight deer taken during the 2019 deer gun season tested positive for chronic wasting disease CWD TSE Prion

    https://chronic-wasting-disease.blogspot.com/2020/03/north-dakota-eight-deer-taken-during.html

    TUESDAY, FEBRUARY 11, 2020 

    South Dakota Chronic Wasting Disease CWD TSE Prion Detected in New Areas 

    https://chronic-wasting-disease.blogspot.com/2020/02/south-dakota-chronic-wasting-disease.html

    SUNDAY, DECEMBER 22, 2019 

    Illinois CWD TSE Prion 90 CWD-positive deer with 826 confirmed positive Total positives through June 30, 2019


    FRIDAY, OCTOBER 04, 2019 

    Indiana CWD TSE Prion Surveillance 2020, 2019 and before?



    TUESDAY, FEBRUARY 25, 2020 

    Iowa Chronic Wasting Disease CWD TSE Prion Cases Climb To 89 positive To Date in Wild Cervid


    MONDAY, FEBRUARY 10, 2020 

    Iowa CWD TSE Prion 2019/20 (confirmed or suspect) 43 cases to date Wild Cervid


    WEDNESDAY, JULY 15, 2020 

    Kansas Chronic Wasting Disease Confirmed in Captive Cervid Herd


    MARYLAND CWD TSE PRION REPORT UPDATE 2020 MIA???



    TUESDAY, MAY 28, 2019

    Maryland Chronic Wasting Disease Detected in 25 Deer


    WEDNESDAY, FEBRUARY 21, 2018

    Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties


    Michigan CWD TSE Prion Update

    Total Deer Tested and Total Positives Cases

    Deer Tested for Chronic Wasting Disease Since Detection of First Positive Free-ranging Deer (May 2015)

    Michigan CWD TSE Prion Total Suspect Positive Deer Moves Up To 189 with total deer tested 80,687 to date


    WEDNESDAY, MARCH 25, 2020 

    Michigan CWD TSE Prion Total Suspect Positive Deer Moves Up To 188 with total deer tested 80,696 to date



    THURSDAY, JANUARY 30, 2020 

    Michigan CWD TSE Prion Total Suspect Positive Deer Jumps To 181 to date


    MONDAY, JANUARY 27, 2020 

    Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?


    TUESDAY, JANUARY 14, 2020 

    Michigan MDARD has confirmed chronic wasting disease (CWD) in 3 white-tailed deer from a Newaygo County deer farm


    WEDNESDAY, APRIL 29, 2020 

    Minnesota CWD investigation spurred by Douglas County deer farm detection concludes 


    SATURDAY, MARCH 14, 2020 

    Minnesota 4 More Farmed Deer and 1 wild positive for CWD TSE Prion

    TUESDAY, JANUARY 21, 2020 

    Minnesota CWD update test results from deer harvested in the 2019 hunting season and the special hunts have returned 27 wild deer tested positive for CWD all from the southeast DMZ


    FRIDAY, JANUARY 10, 2020 

    Minnesota Investigation leads to additional CWD positive deer on Pine County farm


    TUESDAY, JANUARY 28, 2020 

    Mississippi MDWFP North MS CWD Management Zone Since October 2019, 25 CWD-positive deer have been detected from this zone


    SATURDAY, JANUARY 04, 2020 

    Mississippi CWD TOTALS JUST ABOUT DOUBLE Since October 1, 2019 To Date Statewide Total is 37 Confirmed


    WEDNESDAY, MAY 06, 2020 

    Missouri 46 new cases Chronic Wasting Disease found, total to date at 162 documented CWD


    TUESDAY, FEBRUARY 11, 2020 

    Missouri MDC 2019-2020 SAMPLING RESULTS CWD TSE PRION TO DATE 28 Positive


    SUNDAY, JANUARY 19, 2020 

    Missouri CWD TSE Prion 2019-2020 SAMPLING RESULTS TO DATE 25 Positive


    THURSDAY, JANUARY 02, 2020 

    Missouri MDC officially reports more than 20 new cases of Chronic Wasting Disease CWD TSE Prion


    TUESDAY, MAY 19, 2020 

    Montana White-tailed deer in Gallatin County suspected positive for CWD


    MONDAY, FEBRUARY 03, 2020 

    Montana Chronic Wasting Disease CWD TSE Prion in Eastern Part of State Game Farm Elk


    FRIDAY, FEBRUARY 07, 2020 

    Montana 142 animals tested positive for CWD thus far during 2019/20 sampling


    FRIDAY, JANUARY 17, 2020

    Montana Moose Tests Positive for Chronic Wasting Disease CWD TSE PRION in Libby Area

    Montana Fish, Wildlife & Parks 2019 CWD Surveillance Hunter Test Results CWD TSE PRION LOOKS LIKE 136 POSITIVE SO FAR, count them up...


    WEDNESDAY, DECEMBER 25, 2019 

    Montana 16 more deer positive for CWD first time positive hunting district 705 in southeast


    MONDAY, DECEMBER 17, 2018 

    Nebraska Confirms 131 Cases of CWD detected for first time in Valley, Keya Paha counties


    SATURDAY, MAY 16, 2020 

    Ohio Chronic Wasting Disease Detected on Wayne County Farm 


    TUESDAY, JANUARY 07, 2020 

    Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive


    MONDAY, JULY 27, 2020 

    Pennsylvania GAME COMMISSION UNVEILS NEW CWD RESPONSE PLAN


    FRIDAY, JUNE 26, 2020 

    Pennsylvania CWD TSE Prion AREAS EXPAND

    https://chronic-wasting-disease.blogspot.com/2020/06/pennsylvania-cwd-tse-prion-areas-expand.html

    WEDNESDAY, JANUARY 29, 2020 

    Pennsylvania CWD TSE Prion 2019-20 hunting seasons as of January 14, 148 of the samples had tested positive for CWD in Wild Deer


    SUNDAY, DECEMBER 22, 2019 

    Pennsylvania Steady Climb of CWD TSE Prion Confirms 250 Positive To Date In Wild Cervid As At September 12, 2019 

    Pennsylvania Captive Cervid Industry Total CWD TSE Prion ??? anyone's guess...


    SATURDAY, JANUARY 25, 2020 

    Tennessee 2019-20 deer season 462 CWD TSE Prion Confirmed To Date


    WEDNESDAY, JANUARY 29, 2020 

    Utah CWD TSE Prion Since July 1, 2019, the DWR confirmed 16 positive deer statewide Six of those, including Coal, were in the La Sal Unit, 59 test pending


    FRIDAY, FEBRUARY 28, 2020 
    Virginia DGIF say 21 new cases of CWD TSE Prion confirmed in white-tailed deer in northwest Virginia throughout 2019
    TEXAS CWD TSE PRION UPDATE

    Sent: Thu, Jul 9, 2020 10:00 am

    Subject: Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date

    Texas CWD TSE Prion Jumps To 182 Confirmed Cases

    2020-06-25 Free Range El Paso N/A Mule Deer F 5.5

    2020-06-16 Free Range El Paso N/A Mule Deer M 5.5

    2020-06-10 Breeder Release Site Medina Facility #3 White-tailed Deer F 5.5

    2020-06-10 Breeder Release Site Medina Facility #3 White-tailed Deer M 3.5

    2020-06-10 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 5.5

    2020-06-09 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 2.5

    2020-06-09 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 4.5

    2020-05-22 Free Range Hartley N/A Mule Deer M 4.5

    2020-05-22 Free Range Hartley N/A Mule Deer F 5.5

    2020-05-22 Free Range Hartley N/A Mule Deer M 4.5

    2020-05-22 Free Range Dallam N/A Mule Deer M 2.5

    2020-05-22 Free Range Hartley N/A Mule Deer M 5.5

    2020-05-22 Free Range Hartley N/A Mule Deer M 5.5


    Sent: Thu, Jul 9, 2020 10:00 am

    Subject: Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date


    SATURDAY, JULY 04, 2020 

    TAHC CHAPTER 40 CHRONIC WASTING DISEASE 406th COMMISSION MEETING AGENDA June 23, 2020 8:30 A.M.


    TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?

    OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?

    apparently, no ID though. tell me it ain't so please...

    23:00 minute mark

    ''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''


    Wyoming CWD Dr. Mary Wood

    ''first step is admitting you have a problem''

    ''Wyoming was behind the curve''

    wyoming has a problem...


    the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.


    Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...


    SATURDAY, JANUARY 19, 2019

    Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS


    FRIDAY, DECEMBER 20, 2019

    TEXAS ANIMAL HEALTH COMMISSION EXECUTIVE DIRECTOR ORDER DECLARING A CHRONIC WASTING DISEASE HIGH RISK AREA CONTAINMENT ZONE FOR PORTIONS OF VAL VERDE COUNTY


    TUESDAY, DECEMBER 31, 2019 

    In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus 

    SUNDAY, AUGUST 02, 2015  

    TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if? 


    SUNDAY, FEBRUARY 16, 2020
    ***> Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion?
    https://chronic-wasting-disease.blogspot.com/2020/02/jerking-for-dollars-are-texas.html

    TUESDAY, FEBRUARY 04, 2020 

    TEXAS REPORTS 20 NEW CWD TSE PRION CASES 3 WILD 17 BREEDER 166 POSITIVE TO DATE


    FRIDAY, MAY 22, 2020 

    TPW Commission has adopted rules establishing Chronic Wasting Disease (CWD) management zones to further detection and response efforts among WTD


    SUNDAY, MARCH 01, 2020 

    Texas As one CWD investigation continues, another launches...THE FULL MONTY!


    SATURDAY, DECEMBER 02, 2017 

    TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017 


    SUNDAY, MAY 14, 2017 

    85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play 


    SUNDAY, JANUARY 22, 2017 

    Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry 


    *** TEXAS TAHC OLD STATISTICS BELOW FOR PAST CWD TESTING ***

    CWD TEXAS TAHC OLD FILE HISTORY

    updated from some of my old files, some of the links will not work.

    *** Subject: CWD testing in Texas ***

    Date: Sun, 25 Aug 2002 19:45:14 –0500

    From: Kenneth Waldrup


    snip...see ;


    MONDAY, AUGUST 14, 2017

    *** Texas Chronic Wasting Disease CWD TSE Prion History ***


    FRIDAY, JUNE 26, 2020 

    Long-Term Incubation PrP CWD With Soils Affects Prion Recovery but Not Infectivity

    https://chronic-wasting-disease.blogspot.com/2020/06/long-term-incubation-prp-cwd-with-soils.html

    CWD WEBINAR CWD YESTERDAY! December 11, 2019

    Dr. Mckenzie and CIDRAP on CWD TSE Prion


    122: Prions and Chronic Wasting Disease with Jason Bartz


    Texas CWD Symposium: Transmission by Saliva, Feces, Urine & Blood

    the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.


    ''On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis. ''

    Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS

    See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...


    WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO


    cwd update on Wisconsin from Tammy Ryan...


    TUESDAY, JUNE 09, 2020 

    Wisconsin Trempealeau County Deer Farm Tests Positive for CWD ​Release Date: June 9, 2020


    MONDAY, JUNE 01, 2020 

    Wisconsin CWD TSE Prion Continues to Spiral Out of Control, 6585 Cases Confirmed to Date in Wild, and it's anyone's guess for captive


    WEDNESDAY, MARCH 13, 2019 

    CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood

    Subject: Prion 2019 Conference

    See full Prion 2019 Conference Abstracts


    see scientific program and follow the cwd studies here;

    Thursday, May 23, 2019 

    Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts


    THURSDAY, DECEMBER 19, 2019

    TSE surveillance statistics exotic species and domestic cats Update December 2019


    MONDAY, DECEMBER 16, 2019 

    Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update

    ***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***

    What if?


    Friday, December 14, 2012 

    DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 

    snip..... 

    In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: 

    1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and 

    2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. 

    Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. 

    The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. 

    It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. 

    Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. 

    There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products. 

    snip..... 

    36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). 

    snip..... 

    In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. 

    snip..... 

    Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. 

    snip..... 


    ***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; 

    BSE TESTING (failed terribly and proven to be a sham) 

    BSE SURVEILLANCE (failed terribly and proven to be a sham) 

    BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) 

    these are facts folks. trump et al just admitted it with the feed ban. 

    see; 

    FDA Reports on VFD Compliance 

    John Maday 

    August 30, 2019 09:46 AM VFD-Form 007 (640x427) 

    Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.


    SUNDAY, SEPTEMBER 1, 2019 

    ***> FDA Reports on VFD Compliance 


    TUESDAY, APRIL 18, 2017 

    *** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** 



    I STRENUOUSLY URGE TEXAS FDA MODIFY THESE FEED BANS ASAP!

    SEE;

    Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary

    View Attachment:View as format pdf




    cwd scrapie pigs oral routes 

    ***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** 

    >*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** 

    ***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). 

    ***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. 




    ***> In summary, our results establish aerosols as a surprisingly efficient modality of prion transmission. This novel pathway of prion transmission is not only conceptually relevant for the field of prion research, but also highlights a hitherto unappreciated risk factor for laboratory personnel and personnel of the meat processing industry. In the light of these findings, it may be appropriate to revise current prion-related biosafety guidelines and health standards in diagnostic and scientific laboratories being potentially confronted with prion infected materials. While we did not investigate whether production of prion aerosols in nature suffices to cause horizontal prion transmission, the finding of prions in biological fluids such as saliva, urine and blood suggests that it may be worth testing this possibility in future studies.



    Adriano Aguzzi ''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''

    7. TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT

    ***> PLEASE SEE HISTORY OF TEXAS TRUCKING CWD TSE PRION DISEASE AT THE BOTTOM OF MY SUBMISSION, TOO LONG TO POST HERE.

    8.CONSIDERING RECENT SCIENCE THAT CWD TSE PRION WILL TRANSMIT ORALLY TO PIGS AND ALSO SCRAPIE TO PIGS BY ORAL ROUTES, CONSIDERING CWD TRANSMIT EASILY TO CERVID BY ORAL ROUTE, CONSIDERING A NEW TSE PRION OUTBREAK IN A NEW LIVESTOCK SPECIES, THE CAMEL, CONSIDERING THE FACT THE USA THAT THE 1997 BSE feed regulation at 589.2000, which remains in effect but which applies only to feed for cattle and other ruminants, and specifically, the new section 589.2001, WAS AND STILL IS A TOTAL AND COLOSSAL FAILURE, AND PROVEN TO BE SO BY RECENT COMMENTS COMING FROM THE FDA, BUT FIRST, COMMENTS FROM DEFRA;

    In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

    Animals considered at high risk for CWD include:

    1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

    2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

    Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

    The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

    Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

    There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

    snip.....


    ***> cattle, pigs, sheep, cwd, tse, prion, oh my! 

    ***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). 

    Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. 



    FRIDAY, OCTOBER 04, 2019 

    Inactivation of chronic wasting disease prions using sodium hypochlorite

    i think some hunters that don't read this carefully are going to think this is a cure all for cwd tse contamination. IT'S NOT!

    first off, it would take a strong bleach type sodium hypochlorite, that is NOT your moms bleach she uses in her clothes, and store bought stuff.

    Concentrated bleach is an 8.25 percent solution of sodium hypochlorite, up from the “regular bleach” concentration of 5.25 percent.Nov 1, 2013 https://waterandhealth.org/disinfect/high-strength-bleach-2/

    second off, the study states plainly;

    ''We found that a five-minute treatment with a 40% dilution of household bleach was effective at inactivating CWD seeding activity from stainless-steel wires and CWD-infected brain homogenates. However, bleach was not able to inactivate CWD seeding activity from solid tissues in our studies.''

    ''We initially tested brains from two CWD-infected mice and one uninfected mouse using 40% bleach for 5 minutes. The results from these experiments showed almost no elimination of prion seeding activity (Table 4). We then increased the treatment time to 30 minutes and tested 40% and 100% bleach treatments. Again, the results were disappointing and showed less than a 10-fold decrease in CWD-seeding activity (Table 4). Clearly, bleach is not able to inactivate prions effectively from small brain pieces under the conditions tested here.''

    ''We found that both the concentration of bleach and the time of treatment are critical for inactivation of CWD prions. A 40% bleach treatment for 5 minutes successfully eliminated detectable prion seeding activity from both CWD-positive brain homogenate and stainless-steel wires bound with CWD. However, even small solid pieces of CWD-infected brain were not successfully decontaminated with the use of bleach.''

    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659

    https://chronic-wasting-disease.blogspot.com/2019/10/inactivation-of-chronic-wasting-disease.html

    i think with all the fear from recent studies, and there are many, of potential, or likelihood of zoonosis, if it has not already happened as scjd, i think this study came out to help out on some of that fear, that maybe something will help, but the study plainly states it's for sure not a cure all for exposure and contamination of the cwd tse prion on surface materials. imo...terry
    HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...
    * 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
    Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
    Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
    Laboratory of Central Nervous System Studies, National Institute of
    Neurological Disorders and Stroke, National Institutes of Health,
    Bethesda, MD 20892.
    Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
    PMID: 8006664 [PubMed - indexed for MEDLINE]
    Wednesday, September 11, 2019 
    Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion

    172. Establishment of PrPCWD extraction and detection methods in the farm soil

    Kyung Je Park, Hoo Chang Park, In Soon Roh, Hyo Jin Kim, Hae-Eun Kang and Hyun Joo Sohn
    Foreign Animal Disease Division, Animal and Plant Quarantine Agency, Gimcheon, Gyeongsangbuk-do, Korea
    ABSTRACT
    Introduction: Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2016 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and faeces of TSE-infected animals. Soil can serve as a stable reservoir for infectious prion proteins. We found that PrPCWD can be extracted and detected in CWD contaminated soil which has kept at room temperature until 4 years after 0.001 ~ 1% CWD exposure and natural CWD-affected farm soil through PBS washing and sPMCAb.
    Materials and Methods: Procedure of serial PMCAb. CWD contaminated soil which has kept at room temperature (RT) for 1 ~ 4 year after 0.001%~1% CWD brain homogenates exposure for 4 months collected 0.14 g. The soil was collected by the same method once of year until 4 year after stop CWD exposure. We had conducted the two steps. There are two kinds of 10 times washing step and one amplification step. The washing step was detached PrPSc from contaminated soil by strong vortex with maximum rpm. We harvest supernatant every time by 10 times. As the other washing step, the Washed soil was made by washing 10 times soil using slow rotator and then harvest resuspended PBS for removing large impurity material. Last step was prion amplification step for detection of PrPCWD in soil supernatant and the washed soil by sPMCAb. Normal brain homogenate (NBH) was prepared by homogenization of brains with glass dounce in 9 volumes of cold PBS with TritonX-100, 5 mM EDTA, 150 mM NaCl and 0.05% Digitonin (sigma) plus Complete mini protease inhibitors (Roche) to a final concentration of 5%(w/v) NBHs were centrifuged at 2000 g for 1 min, and supernatant removed and frozen at −70 C for use. CWD consisted of brain from natural case in Korea and was prepared as 10%(w/v) homogenate. Positive sample was diluted to a final dilution 1:1000 in NBH, with serial 3:7 dilutions in NBH. Sonication was performed with a Misonix 4000 sonicator with amplitude set to level 70, generating an average output of 160W with two teflon beads during each cycle. One round consisted of 56 cycles of 30 s of sonication followed 9 min 30 s of 37°C incubation. Western Blotting (WB) for PrPSc detection. The samples (20 µL) after each round of amplification were mixed with proteinase K (2 mg/ml) and incubated 37°C for 1 h. Samples were separated by SDS-PAGE and transferred onto PVDF membrane. After blocking, the membrane was incubated for 1 h with 1st antibody S1 anti rabbit serum (APQA, 1:3000) and developed with enhanced chemiluminescence detection system.
    Results: We excluded from first to third supernatant in view of sample contamination. It was confirmed abnormal PrP amplification in all soil supernatants from fourth to tenth. From 0.01% to 1% contaminated washed soils were identified as abnormal prions. 0.001% contaminated washed soil did not show PrP specific band (Fig 1). The soil was collected by the same method once of year until 4 year after stop CWD exposure. After sPMCAb, there were no PrPCWD band in from second to fourth year 0.001% washed soil. but It was confirmed that the abnormal prion was amplified in the washing supernatant which was not amplified in the washed soil. we have decided to use soil supernatant for soil testing (Fig. 2). After third rounds of amplification, PrPSc signals observed in three out of four sites from CWD positive farm playground. No signals were observed in all soil samples from four CWD negative farm (Fig. 3).
    Conclusions: Our studies showed that PrPCWD persist in 0.001% CWD contaminated soil for at least 4 year and natural CWD-affected farm soil. When cervid reintroduced into CWD outbreak farm, the strict decontamination procedures of the infectious agent should be performed in the environment of CWD-affected cervid habitat.
    ===

    186. Serial detection of hematogenous prions in CWD-infected deer

    Amy V. Nalls, Erin E. McNulty, Nathaniel D. Denkers, Edward A. Hoover and Candace K. Mathiason
    Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA
    CONTACT Amy V. Nalls amy.nalls@colostate.edu
    ABSTRACT
    Blood contains the infectious agent associated with prion disease affecting several mammalian species, including humans, cervids, sheep, and cattle. It has been confirmed that sufficient prion agent is present in the blood of both symptomatic and asymptomatic carriers to initiate the amyloid templating and accumulation process that results in this fatal neurodegenerative disease. Yet, to date, the ability to detect blood-borne prions by in vitro methods remains difficult.
    We have capitalized on blood samples collected from longitudinal chronic wasting disease (CWD) studies in the native white-tailed deer host to examine hematogenous prion load in blood collected minutes, days, weeks and months post exposure. Our work has focused on refinement of the amplification methods RT-QuIC and PMCA. We demonstrate enhanced in vitro detection of amyloid seeding activity (prions) in blood cell fractions harvested from deer orally-exposed to 300 ng CWD positive brain or saliva.
    These findings permit assessment of the role hematogenous prions play in the pathogenesis of CWD and provide tools to assess the same for prion diseases of other mammalian species.
    Considering the oral secretion of prions, saliva from CWD-infected deer was shown to transmit disease to other susceptible naïve deer when harvested from the animals in both the prions in the saliva and blood of deer with chronic wasting disease. 
     and preclinical stages69
     of infection, albeit within relatively large volumes of saliva (50 ml). In sheep with preclinical, natural scrapie infections, sPMCA facilitated the detection of PrPSc within buccal swabs throughout most of the incubation period of the disease with an apparent peak in prion secretion around the mid-term of disease progression.70
     The amounts of prion present in saliva are likely to be low as indicated by CWD-infected saliva producing prolonged incubation periods and incomplete attack rates within the transgenic mouse bioassay.41
    snip...
    Indeed, it has also been shown that the scrapie and CWD prions are excreted in urine, feces and saliva and are likely to be excreted from skin. While levels of prion within these excreta/secreta are very low, they are produced throughout long periods of preclinical disease as well as clinical disease. Furthermore, the levels of prion in such materials are likely to be increased by concurrent inflammatory conditions affecting the relevant secretory organ or site. Such dissemination of prion into the environment is very likely to facilitate the repeat exposure of flockmates to low levels of the disease agent, possibly over years.
    snip...
    Given the results with scrapie-contaminated milk and CWD-contaminated saliva, it seems very likely that these low levels of prion in different secreta/excreta are capable of transmitting disease upon prolonged exposure, either through direct animal-to-animal contact or through environmental reservoirs of infectivity.
    the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
    ***>>> 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

    HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...

    * 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
    Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
    Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
    Laboratory of Central Nervous System Studies, National Institute of
    Neurological Disorders and Stroke, National Institutes of Health,
    Bethesda, MD 20892.
    Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
    PMID: 8006664 [PubMed - indexed for MEDLINE]
    Wednesday, September 11, 2019 

    Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion

    SATURDAY, MARCH 16, 2019 

    Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission


    THURSDAY, SEPTEMBER 27, 2018 

    ***> Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control model


    THE tse prion aka mad cow type disease is not your normal pathogen. 

    The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. 

    you cannot cook the TSE prion disease out of meat. 

    you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. 

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

    the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

    IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. 

    you can bury it and it will not go away. 

    The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. 

    it’s not your ordinary pathogen you can just cook it out and be done with. 

    ***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

    1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

    ***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 

    Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

    Laboratory of Central Nervous System Studies, National Institute of 

    Neurological Disorders and Stroke, National Institutes of Health, 

    Bethesda, MD 20892. 

    Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 

    PMID: 8006664 [PubMed - indexed for MEDLINE] 


    2018 - 2019

    ***> This is very likely to have parallels with control efforts for CWD in cervids.

    Rapid recontamination of a farm building occurs after attempted prion removal


    Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2

    Abstract

    The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. 

    Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. 

    Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. 

    Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). 

    A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. 

    Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3. 

    The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.

    snip...

    As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.

    This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.

    Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.

    Funding This study was funded by DEFRA within project SE1865. 

    Competing interests None declared. 


    Saturday, January 5, 2019 

    Rapid recontamination of a farm building occurs after attempted prion removal 


    THURSDAY, FEBRUARY 28, 2019 

    BSE infectivity survives burial for five years with only limited spread



    ***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018

    P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer 

    Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) 

    (1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. 

    Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. 

    Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. 

    Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. 

    https://prion2018.org/


    ***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years


    ***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. 


    Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3

    Correspondence

    Gudmundur Georgsson ggeorgs@hi.is

    1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland

    2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland

    3 Bethesda, Maryland, USA

    Received 7 March 2006 Accepted 6 August 2006

    In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.

    http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A
     
     
    TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 

    https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261
     

     *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 

    http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article
     

    SEE;

    Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

    Some unofficial information from a source on the inside looking out -

    Confidential!!!!

    As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

    ---end personal email---end...tss

    http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html

    Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).

    http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf


    Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document

    https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf


    THURSDAY, FEBRUARY 28, 2019 

    BSE infectivity survives burial for five years with only limited spread


    Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. 

    Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. 

    Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

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

    ***>>> 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://transmissiblespongiformencephalopathy.blogspot.com/2013/07/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

    Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). 

    Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). 

    Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). 

    Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. 

    Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. 

    Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). 

    The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. 

    When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. 

    This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. 

    Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. 

    It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. 

    Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. 

    Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. 

    Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. 

    PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. 

    In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. 

    In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). 

    As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. 

    False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). 

    This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. 

    This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. 

    In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. 

    Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. 

    The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. 

    In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). 

    A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). 

    This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. 

    Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. 

    In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. 

    These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. 

    Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification 

    http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full

    Wednesday, December 16, 2015 

    *** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** 

    http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html

    WEDNESDAY, MARCH 13, 2019 

    CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood

    Subject: Prion 2019 Conference

    See full Prion 2019 Conference Abstracts


    see scientific program and follow the cwd studies here;

    Thursday, May 23, 2019 

    Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts


    THURSDAY, DECEMBER 19, 2019

    TSE surveillance statistics exotic species and domestic cats Update December 2019


    MONDAY, DECEMBER 16, 2019 

    Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update

    ***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***

    What if?


    > However, to date, no CWD infections have been reported in people.
    key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
    *** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
    *** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
    Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
    We hypothesize that:
    (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
    (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
    (3) Reliable essays can be established to detect CWD infection in humans; and
    (4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
    ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
    Prion 2017 Conference
    First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 
    University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 
    This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 
    Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 
    At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 
    PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 
    PRION 2018 CONFERENCE
    Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
    Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
    To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
    After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
    Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
    The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
    Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
    The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
    ***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
    READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
    P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
    Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
    SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
    states.
    AND ANOTHER STUDY;
    P172 Peripheral Neuropathy in Patients with Prion Disease
    Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
    IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
    AND
    included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
    AND
    THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
    snip…
    see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
    PRION 2019 ABSTRACTS 

    1. Interspecies transmission of the chronic wasting disease agent

    Justin Greenlee

    Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service

    ABSTRACT

    The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.

    53. Evaluation of the inter-species transmission potential of different CWD isolates

    Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa

    aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile

    ABSTRACT

    Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.

    56. Understanding chronic wasting disease spread potential for at-risk species

    Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman

    Department of Biological Sciences, University of Alberta, Edmonton AB, Canada

    CONTACT Catherine I. Cullingham cathy.cullingham@ualberta.ca

    ABSTRACT

    Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.

    KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates

    Thursday, May 23, 2019 

    Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts


    see full Prion 2019 Conference Abstracts

    THURSDAY, OCTOBER 04, 2018
    Cervid to human prion transmission 5R01NS088604-04 Update
    snip…full text;
    SATURDAY, FEBRUARY 09, 2019
    Experts: Yes, chronic wasting disease in deer is a public health issue — for people
    SATURDAY, FEBRUARY 23, 2019 

    Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019


    TUESDAY, NOVEMBER 04, 2014 

    Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011

    Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "


    Transmission Studies

    Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS

    resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.

    snip.... 


    Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ 

    Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations

    In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species. 


    Prions in Skeletal Muscles of Deer with Chronic Wasting Disease 

    Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure. 


    *** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.

    see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”

    From: TSS 

    Subject: CWD aka MAD DEER/ELK TO HUMANS ???

    Date: September 30, 2002 at 7:06 am PST

    From: "Belay, Ermias"

    To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

    Sent: Monday, September 30, 2002 9:22 AM

    Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

    Dear Sir/Madam,

    In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

    Ermias Belay, M.D. Centers for Disease Control and Prevention

    -----Original Message-----

    From: Sent: Sunday, September 29, 2002 10:15 AM


    Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

    Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS

    Thursday, April 03, 2008

    A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.

    snip...

    *** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

    snip... full text ; 


    > However, to date, no CWD infections have been reported in people. 

    sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.

    if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;



    key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

    *** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

    *** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 



    FRIDAY, JULY 26, 2019 

    Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species


    TUESDAY, JANUARY 21, 2020 

    ***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020


    ***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***

    ***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<*** 

    ***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***

    ***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<*** 

    ***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***


    FRIDAY, OCTOBER 25, 2019 

    Experts testify United States is underprepared for bioterrorism threats Transmissible Spongiform Encephalopathy TSE Prion disease 

     ***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

    Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.

    https://www.nature.com/articles/srep11573 

    O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations 
    Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France 

    Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). 

    Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. 

    *** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, 

    ***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), 

    ***is the third potentially zoonotic PD (with BSE and L-type BSE), 

    ***thus questioning the origin of human sporadic cases. 

    We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. 

    =============== 

    ***thus questioning the origin of human sporadic cases*** 

    =============== 

    ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. 

    ============== 
    https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf 

    ***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

    ***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

    ***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 
    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20 

    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 online

    Taylor & Francis

    Prion 2016 Animal Prion Disease Workshop Abstracts

    WS-01: Prion diseases in animals and zoonotic potential

    Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

    These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 
    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

    Title: Transmission of scrapie prions to primate after an extended silent incubation period) 

    *** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. 

    *** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. 

    *** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. 
    http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

    1: J Infect Dis 1980 Aug;142(2):205-8

    Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

    Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

    Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

    snip...

    The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

    PMID: 6997404


    Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"

    Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

    snip...

    76/10.12/4.6


    Nature. 1972 Mar 10;236(5341):73-4.

    Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

    Gibbs CJ Jr, Gajdusek DC.

    Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

    Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

    C. J. GIBBS jun. & D. C. GAJDUSEK

    National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

    SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).



    Wednesday, February 16, 2011

    IN CONFIDENCE

    SCRAPIE TRANSMISSION TO CHIMPANZEES

    IN CONFIDENCE


    MONDAY, JULY 27, 2020 

    BSE Inquiry DFA's a review


    Terry S. Singeltary Sr.

    posted by Terry S. Singeltary Sr. at 2:56 PM

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