Wednesday, October 03, 2018

Texas Reports 13 more cases of Chronic Wasting Disease CWD TSE Prion in Breeder Deer state total jumps to 130 Confirmed to date

Texas Reports 13 more cases of Chronic Wasting Disease CWD TSE Prion in Breeder Deer state total jumps to 130 Confirmed to date

CWD Positive

Year Confirmed CWD Positive

Confirmation Date Free Range/Captive County Source Species Sex Age

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 4

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 2

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 5

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 8

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 4

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 2

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 4

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 9

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 10

2018 9/17/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 10

2018 8/30/2018 Breeder Deer Uvalde Facility #3 white-tailed deer M 6

2018 8/30/2018 Breeder Deer Uvalde Facility #3 white-tailed deer M 2

2018 8/30/2018 Breeder Deer Uvalde Facility #3 white-tailed deer M 3

https://tpwd.texas.gov/huntwild/wild/diseases/cwd/tracking/


Sent: Wed, Aug 22, 2018 12:05 pm

Subject: TEXAS CWD TSE PRION 16 MORE CASES DETECTED TOTAL TO DATE 117 CONFIRMED NEW 14 BREEDERS 2 FREE RANGE

TEXAS CWD TSE PRION 16 MORE CASES DETECTED TOTAL TO DATE 117 CONFIRMED NEW 14 BREEDERS 2 FREE RANGE


2018 8/2/2018 Free Range El Paso Mule Deer M 3

2018 7/3/2018 Free Range Hartley white-tailed deer M 2.5

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer M 3

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer M 3

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer M 3

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer M 3

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 9

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 5

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 4

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 3

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 6

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 4

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 2

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F 4

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F <1 font="">

2018 6/13/2018 Breeder Deer Uvalde Facility #3 white-tailed deer F <1 font="">



THERE IS TWO PAGES FULL, SEE TOTALS ;



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. 




=====


ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ???

here is the latest;

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




ALSO, I FIND THIS VERY DISTURBING...SEE;


***> Prion 2018 P74 High Prevalence of CWD prions in male reproductive samples 

Carlos Kramm (1,2), Ruben Gomez-Gutierrez (1,3), Tracy Nichols (4), Claudio Soto (1) and Rodrigo Morales (1) 


READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT Protein Misfolding Cyclic Amplification PMCA results showed positive CWD prion detection in testes, epididymis and seminal fluid samples. seems also the scientists are worried about any potential mechanisms of CWD spreading and they want to decrease putative interindividual transmission associated to insemination using CWD contaminated specimens, if that might occur under natural conditions. i have been concerned about this for some time with BSE super-ovulation and since;

 PrPSc detection and infectivity in semen from scrapie-infected sheep




PITUITARY EXTRACT

This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...







MANAGEMENT IN CONFIDENCE

CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS


Tuesday, February 8, 2011

U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001


HAVE YOU BEEN THUNDERSTRUCK? 

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?

Court papers state that in February 2007, Favero acquired 184 straws of whitetail deer semen valued at about $92,000 from a buck named “Diablo'” that he knew had been illegally taken out of Texas, and again in January 2008 took another 110 straws of semen from a buck named “Thunderstruck.” (Read more in the court paper posted at the bottom of this entry.)


SUNDAY, AUGUST 19, 2018 

Texas Deer Farms, Growing Freakish Antlers, and CWD TSE Prion aka mad deer disease


Ryan, i don't care what folks eat, i am pro hunting, pro gun, i am a meat eater. BUT, when what you eat, or do, starts to have a fatal potential to do harm to my family, me, my friends, neighbors, your children, from ignorance of an industry that is full of greed (and i paint this with a very wide brush), then i get concerned. friendly fire, from second hand exposure is a very real and proven scientific fact, and as these TSE Prion strains mutate, they can become very dangerous. iatrogenic TSE Prion disease should concern all. you consume a cervid that is cwd postive, and you become exposed, then years later go on to have some sort of medical surgical procedure, then you have the potential to expose that complete surgical arena...

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] 



CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION PrP aka mad cow type disease in cervid
SATURDAY, MARCH 31, 2018

***> TEXAS DETECTS IT'S 101 CASE of CWD TSE PRION Breeder White-tailed Deer with no end in sight <***

2018 03/27/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5



THURSDAY, MARCH 22, 2018 

TEXAS CWD TSE PRION JUMP TO 100 POSITIVE, NEW CASES 17 BREEDER, 1 BREEDER RELEASE, AND 1 WILD SINCE JAN 31, 2018



SUNDAY, JUNE 10, 2018 

TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018



THURSDAY, JANUARY 26, 2017

Texas CWD Discovered Free-Ranging Whitetail DEER Houston Chronicle Shannon Tompkins PLEASE, CAN YOU HEAR ME NOW?


Saturday, October 03, 2015

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015

here is a great article by Shannon Tomkins and the Houston Chronicle on 

Chronic Wasting Disease CWD TSE prion aka mad deer disease 

Thursday, March 14, 2002 

"Ten years ago, elk and deer (imported into Texas) were not regulated at all," said Dr. Ken Waldrup, an epidemiologist with the Texas Animal Health Commission and one of the agency's point men on CWD. "If Texas doesn't already have CWD, then I say that proves that God is a Texan. "For everyone's sake, I sure hope He is." 

======================== 

Tompkins: There are a lot of reasons to be concerned about CWD 

Houston Chronicle Published 5:30 a.m., Thursday, March 14, 2002



16 years later, the silence is deafening...terry


Texas Chronic Wasting Disease CWD TSE Prion History

*** 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


Subject: CWD SURVEILLANCE STATISTICS TEXAS (total testing figures less than 50 in two years) Date: Sun, 25 Aug 2002 21:06:49 –0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

######## Bovine Spongiform Encephalopathy #########

snip...

IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.

AS i said before;

 > SADLY, they have not tested enough from the total population to

> know if CWD is in Texas or not.

 BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...

snip...end...TSS

=============================== snip...end...tss



FRIDAY, AUGUST 17, 2018 

Wisconsin Deer farm looks to educate the community about the business


TSE prions knows no borders, no walls, and especially no politics! republican, democrat, left, right, conservative, liberal, red, blue, it DOES NOT MATTER. 

where and when does it end???

***> PLEASE WATCH THIS VIDEO, AND BE SURE TO SEE AROUND THE 8 MINUTE MARK, VERY, VERY, DISTURBING...terry

https://www.youtube.com/watch?v=nrzPAMfSp1U

***> LISTEN TO THIS CWD BLUES DIDDY ABOUT WISCONSIN CWD TSE PRION...terry

https://www.youtube.com/watch?v=6DHindrC1x0

FRIDAY, APRIL 20, 2018 

***> Scrapie Transmits To Pigs By Oral Route

what about the terribly flawed USA tse prion feed ban? 

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies

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


speaking of Bambi ???


TUESDAY, APRIL 17, 2018 

***> Chronic wasting disease: Bambi vs. the prion <***

Research Project: Immunodiagnostics to Detect Prions and Other Important Animal Pathogens 

Location: Produce Safety and Microbiology Research

http://chronic-wasting-disease.blogspot.com/2018/04/chronic-wasting-disease-bambi-vs-prion.html



TSE PRION UPDATE

MICHIGAN TOTAL POSITIVE/SUSPECT POSITIVE DEER 60

WEDNESDAY, AUGUST 08, 2018 

Michigan Chronic Wasting Disease CWD TSE Prion Jumps to 60 cases MICHIGAN TOTAL POSITIVE/SUSPECT POSITIVE DEER 60



see cwd positive map




TUESDAY, AUGUST 07, 2018 

Cervid Health Operational Plan Fiscal Year 2018 Animal and Plant Health Inspection Services Veterinary Services


TUESDAY, AUGUST 07, 2018 

Passage of scrapie to deer results in a new phenotype upon return passage to sheep



TUESDAY, JULY 03, 2018 
 
Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news
 
http://chronic-wasting-disease.blogspot.com/2018/07/chronic-wasting-disease-cwd-tse-prion.html

SUNDAY, APRIL 8, 2018 

Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018


***> NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES <***

NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES

Subject: Prion Disease in Dromedary Camels, Algeria

Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.



Wednesday, May 30, 2018 

Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago


***> IMPORTS AND EXPORTS <***

SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN




WEDNESDAY, JULY 11, 2018 

CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000

http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html

TUESDAY, JULY 10, 2018
 
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS
 
*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''
 
CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS
 



FRIDAY, AUGUST 10, 2018 

From Gate to Plate, BSE aka mad cow disease, USDA, NAIS, AND TRACEABILITY



TUESDAY, AUGUST 7, 2018 

Unexpected prion phenotypes in experimentally transfused animals: predictive models for humans?

http://transmissiblespongiformencephalopathy.blogspot.com/2018/08/unexpected-prion-phenotypes-in.html


TUESDAY, JULY 31, 2018 

***> USA CJD TSE Tables of Cases Examined National Prion Disease Pathology Surveillance Center Cases Examined May 1, 2018 <***


WEDNESDAY, JULY 04, 2018 

CREUTZFELDT-JAKOB DISEASE: GUIDELINES FOR SOCIAL WORKERS IN ENGLAND June 2018


MONDAY, JUNE 18, 2018 

Ecuador Six Case series of Creutzfeldt-Jakob disease in a third-level hospital in Quito


TSE prions knows no borders, no walls, and especially no politics! republican, democrat, left, right, conservative, liberal, red, blue, it DOES NOT MATTER. 

SATURDAY, JANUARY 17, 2015 

Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease


March 10, 2016

Maryland Gov. Larry Hogan plans to leave the state Thursday evening to attend his sister's funeral in North Carolina. 

The governor's older and only sister Mary Theresa Lazarus died last Saturday at 66 from a rare degenerative brain disorder. Her funeral will be held Saturday near her home outside Charlotte, Hogan spokesman Douglass Mayer said.

Lazarus was moved into hospice care less than a week before she died from what Hogan aides said was Creutzfeldt-Jakob disease, a condition that effects about one in 1 million people worldwide. 



***> 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. <***


ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ???

here is the latest;

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.


Prion 2017 

Conference Abstracts CWD 2017 PRION 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 

Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO 

PRION 2017 

CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS 

*** PRION 2017 CONFERENCE VIDEO 



TUESDAY, JUNE 13, 2017 

PRION 2017 CONFERENCE ABSTRACT 

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 



SATURDAY, JULY 29, 2017 

Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC 

 
just out CDC...see;

Research

Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions

Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)

M. A. Barria et al.

ABSTRACT

Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted. 


Molecular Barriers to Zoonotic Transmission of Prions 

Marcelo A. Barria, Aru Balachandran, Masanori Morita, Tetsuyuki Kitamoto, Rona Barron, Jean Manson, Richard Knight, James W. Ironside, and Mark W. Headcorresponding author 

snip... 

The conversion of human PrPC by CWD brain homogenate in PMCA reactions was less efficient when the amino acid at position 129 was valine rather than methionine. 

***Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype. 

snip... 

However, we can say with confidence that under the conditions used here, none of the animal isolates tested were as efficient as C-type BSE in converting human PrPC, which is reassuring. 

***Less reassuring is the finding that there is no absolute barrier to the conversion of human PrPC by CWD prions in a protocol using a single round of PMCA and an entirely human substrate prepared from the target organ of prion diseases, the brain. 


***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders


CDC CWD 2018 TRANSMISSION 


*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. 



Volume 15, Number 5—May 2009 

Research 

Chronic Wasting Disease Prions in Elk Antler Velvet

***> Humans who consume antler velvet as a nutritional supplement are at risk for exposure to prions. 

https://wwwnc.cdc.gov/eid/article/15/5/08-1458_article

http://chronic-wasting-disease.blogspot.com/2012/02/new-supplement-from-deer-antler-velvet.html

***> Prion 2018 P74 High Prevalence of CWD prions in male reproductive samples 

Carlos Kramm (1,2), Ruben Gomez-Gutierrez (1,3), Tracy Nichols (4), Claudio Soto (1) and Rodrigo Morales (1) 


READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT Protein Misfolding Cyclic Amplification PMCA results showed positive CWD prion detection in testes, epididymis and seminal fluid samples. seems also the scientists are worried about any potential mechanisms of CWD spreading and they want to decrease putative interindividual transmission associated to insemination using CWD contaminated specimens, if that might occur under natural conditions. i have been concerned about this for some time with BSE super-ovulation and since;

 PrPSc detection and infectivity in semen from scrapie-infected sheep




PITUITARY EXTRACT

This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...







MANAGEMENT IN CONFIDENCE

CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS


Tuesday, February 8, 2011

U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001


HAVE YOU BEEN THUNDERSTRUCK? 

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?

Court papers state that in February 2007, Favero acquired 184 straws of whitetail deer semen valued at about $92,000 from a buck named “Diablo'” that he knew had been illegally taken out of Texas, and again in January 2008 took another 110 straws of semen from a buck named “Thunderstruck.” (Read more in the court paper posted at the bottom of this entry.)


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] 



TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 



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


 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

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.

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

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 



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. 


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


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


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


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


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 


PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 



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 

 
Wednesday, December 16, 2015 

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


161: Prion soil binding may explain efficient horizontal CWD transmission 

Nathaniel Denkers1, Davin Henderson1, Shannon Bartelt-Hunt2, Jason Bartz3 and Edward Hoover1

1Colorado State University; Fort Collins, Colorado USA

2University of Nebraska-Lincoln; Omaha, Nebraska USA

3Creighton University; Omaha, Nebraska USA

Background Chronic wasting disease (CWD) is unique due to the facile spread in nature. The interaction of excreted CWD prions and soil is a hypothesized contributor in environmental transmission. The present study examines whether and to what degree CWD prions bind to silty clay loam (SCL) using an adapted version of real-time quaking-induced conversion (RT-QuIC) methodology.

Materials and Methods Varying amounts (50–3.12 mg) of SCL were incubated with 1 mL-serial dilutions of CWD (+), CWD (−), or no brain homogenate (BH). Samples were centrifuged, washed, diluted 1:10 in 0.1% SDS, and 2.5 uL seeded in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Multiple well replicates of sample and supernatant fractions were assayed for positive seeding activity (recorded as thioflavin T fluorescence emission; 480 nm). Samples were considered positive if they crossed a threshold of 25,000. Reaction rates (RR) were calculated, averaged, and expressed as 1/RR.

Results Positive seeding activity was detected for most SCL samples incubated with CWD (+) BH dilutions. Higher SCL concentrations (50 mg) produced low fluorescent readings due to optical interference. Lower SCL concentrations (6.25 mg) produced minimal optical interference and removed the vast majority of seeding activity from CWD+ BH in a concentration-dependent manner; determined by seeding activity in residual BH supernatants. Control SCL and supernatants produced minimal false-positive reactions (8 of 240 replicates; 3.3%). We estimated the prion binding capacity of SCL to be 0.16 ng/mg.

Conclusion Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.


TSE Scrapie, CWD, BSE, Prion, Soil

Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois

Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla

Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x

Download Citation

Ecological epidemiology Ecological modelling Infectious diseases Prions

Received: 21 August 2017

Accepted: 08 December 2017

Published online: 22 December 2017

Abstract

Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.


Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles

Author Summary

Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.


tse prion soil





cwd tse prion and soil, see more ;


MONDAY, JUNE 12, 2017

Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?


WEDNESDAY, MAY 17, 2017

*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***


MONDAY, MARCH 05, 2018 

TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES


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

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

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

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

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

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

PRION 2016 CONFERENCE TOKYO 

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

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

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

https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf

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

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

https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf

Subject: cwd genetic susceptibility 

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

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

snip...

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

http:// http://forest.wisc.edu/files/pdfs/samuel/2009%20blanchong%20et%20al%20genetic%20susceptibility%20chronic%20wasting.pdf

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

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

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

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

http://www.sciencedirect.com/science/article/pii/S1567134809001956?via=ihub 

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

MONDAY, NOVEMBER 20, 2017 

*** What ever happened to 'LUCKY' the Wapiti cow elk thought to be immune from CWD with LL genotype MIA? ***


Mineral licks as environmental reservoirs of chronic wasting disease prions
Ian H. Plummer,Chad J. Johnson,Alexandra R. Chesney,Joel A. Pedersen ,Michael D. Samuel 
Abstract 
Chronic wasting disease (CWD) is a fatal neurodegenerative disease of deer, elk, moose, and reindeer (cervids) caused by misfolded prion proteins. The disease has been reported across North America and recently discovered in northern Europe. Transmission of CWD in wild cervid populations can occur through environmental routes, but limited ability to detect prions in environmental samples has prevented the identification of potential transmission “hot spots”. We establish widespread CWD prion contamination of mineral licks used by free-ranging cervids in an enzootic area in Wisconsin, USA. We show mineral licks can serve as reservoirs of CWD prions and thus facilitate disease transmission. Furthermore, mineral licks attract livestock and other wildlife that also obtain mineral nutrients via soil and water consumption. Exposure to CWD prions at mineral licks provides potential for cross-species transmission to wildlife, domestic animals, and humans. Managing deer use of mineral licks warrants further consideration to help control outbreaks of CWD.
Snip...
DISCUSSION
Our results demonstrate that CWD-infected white-tailed deer deposit prions at mineral licks they visit. Although the mechanism of prion deposition is unknown, we suspect deposition of saliva by infected deer during ingestion of soil and water at mineral licks has the highest potential to facilitate indirect transmission to susceptible deer. Saliva from white-tailed deer infected with CWD contains on the order of 1–5 infectious doses (ID50) per 10 mL as quantified by real-time quaking-induced conversion, where an ID50 is the dose of CWD prions capable of infecting half of the transgenic mice expressing cervid prion protein [48]. Frequent visitation by infected cervids could allow mineral licks to become potential “hot spots” for indirect transmission of CWD [49]. Currently, little is known about the relative importance of direct contact and environmental routes of CWD transmission in free-ranging cervids [10]. Thus, how artificial and natural mineral licks contribute to current and future CWD infection in cervids and whether licks should be managed to control cervid use are important questions for further research.
Despite the relatively recent detection of CWD in Wisconsin (2001) and the moderate incidence of infection (6–19% prevalence in adult deer in the area sampled at the time of sample collection), our results suggest contamination of mineral licks in the CWD outbreak zone is widespread. This finding suggests that mineral licks may serve as reservoirs of CWD prions that contribute to disease transmission to susceptible animals. Although the levels of CWD prions in the samples analyzed appears low, we note that the association of prions with clay minerals often present at mineral licks can dramatically enhance disease transmission via the oral route of exposure [30–31]. For hamster-adapted scrapie prions binding to montmorillonite clay particles enhanced transmission by a factor of 680, however, an upper bound on the enhancement factor could not be assigned [30–31]. At present, the degree to which binding to clay mineral particles enhances CWD transmission to deer via the oral (or nasal) route of exposure is not known. Furthermore, repeated oral exposure to prions is associated with increased likelihood of disease transmission [50]. Differences in the sialyation status of N-linked glycans between brain-derived and secreted/excreted PrPCWD may impact oral infectivity [51]. Cervid species that avoid interspecific contact make use of the same mineral lick sites [49], potentially leading to interspecies transmission. Mineral licks also attract livestock and other wildlife that supplement mineral intake via soil and water consumption, exposing these animals to CWD prions. Exposure of predators and scavengers to CWD prions via consumption of infected tissue has been previously documented [23]; our results suggest that environmental exposure of non-cervid animal groups can also occur via environmental routes.
We also detected CWD prions in fecal samples collected in proximity to a mineral lick, indicating that fecal excretion represents a route of CWD deposition into the environment with potential transmission to susceptible cervids [19]. Deposition of fecal pellets by white-tailed deer near bait sites increases with higher deer visitation [52] and similar patterns probably occur at mineral licks. Thus, increased local fecal deposition by CWD-infected deer likely contributes to increased environmental concentrations of prions in and around mineral licks. Deer generally avoid consumption of feces [52]; however, the apparent long-term duration of prion infectivity in the environment [27–29], the enhanced disease transmission by soil-bound prions combined with the repeated visitation, long-term existence of and multi-generational use of mineral licks suggest the impact of concentrated environmental contamination on the dynamics of disease transmission warrants further investigation. Recent laboratory research indicates plants grown in prion-contaminated soil can accumulate prions [53]. Our data suggest that plants growing near contaminated mineral licks may warrant investigation as a source of prions for foraging animals. Areas where cervids congregate for mineral consumption, feeding and baiting sites, winter yarding, wallows [54] or other activities where CWD prions are deposited in the environment may also provide potential long-term reservoirs for transmission to cervid and non-cervid species. 
CONCLUSIONS
We used mb-PMCA to detect CWD in soil and water from mineral licks naturally contaminated with prions and used by free-ranging deer, livestock, and non-cervid wildlife species. Detection of prions in environmental reservoirs represents an important first step in understanding the contribution of environmental transmission to CWD epizootics and potential for cross-species transmission. The present study characterized an environmental prion reservoir by (1) identifying an apparent “hot spot” of deposition and potential exposure to both cervid and non-cervid species; (2) indicating CWD prions shed by free-ranging cervids are present in areas of frequent use leading to environmental contamination and potentially plant uptake; and (3) motivating investigation of the exposure and susceptibility of non-cervid species to CWD contaminated soil, water, and plant materials. Future research should be directed at quantifying CWD prion concentrations at mineral licks and other areas where cervids congregate, determining the persistence of prion infectivity at these sites, delineating spatial-temporal patterns of environmental prion deposition and accumulation, and assessing consumption by susceptible animals. Identifying additional environmental reservoirs of CWD prions and determining the contributions of direct and indirect transmission over the course of CWD outbreaks represent key aims in advancing understanding of long-term CWD infection dynamics.
Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission

MARIAFERNANDAMEJIA-SALAZAR,1,CHERYLL. WALDNER,2 YEENTENHWANG,1,3 AND TRENTK. BOLLINGER1,41 Department of Veterinary Pathology, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4 Canada2 Department of Large Animal Clinical Sciences, University of Saskatchewan, 52 Campus Drive, Saskatoon,Saskatchewan S7N 5B4 Canada3 Fish and Wildlife Branch, Saskatchewan Ministry of Environment, Regina, Saskatchewan S4S 5W6 Canada4 Canadian Wildlife Health Cooperative (CWHC), 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4 Canada Citation:Mejıa-Salazar, M. F., C. L. Waldner, Y. T. Hwang, and T. K. Bollinger. 2018. 

Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission. 

Ecosphere 9(1):e02055.10.1002/ecs2.2055

Abstract.

Prions that cause chronic wasting disease (CWD) in cervids can remain infective for years out-side the host. Infectious cervids shed prions for a long time, consequently depositing prions in frequently used areas. These environmental prions are important in CWD epidemiology. Unfortunately, effective tools for quantifying CWD prions in soil, water, and other environmental sources are not currently available. Our goal was to investigate relative differences in visits by mule deer (Odocoileus hemionus hemionus) to various environmental site types as an indicator of the relative risk of prion contamination and disease transmission.For this, we deployed a system of triggered-by-movement cameras at eight site types in a CWD-endemic area in Saskatchewan, Canada. We first assessed whether the relative differences among site types in the frequency of visits by mule deer of any sex-and-age class, males, and females varied by season and site type.We then assessed whether the rate of behaviors with a high risk of environmental prion transmission (either contamination or acquisition) differed by season and site type. Finally, we assessed whether the intensity of visitation, based on the number of animals per picture, differed by season and site type. We found that grain sources and beds were key attractants for mule deer: 

(1) The greatest number of pictures with mule deer per camera-day occurred at grain sources across all seasons, except in fawning, when beds were the most visited sites; 

(2) during pre-rut and early gestation, mule deer visited grain sources at least twice as often as most other sites; 

(3) females were more likely to visit beds and grain sources, but there was no significant site preferences for males after accounting for season; 

(4) mule deer were most likely to be pictured contacting the environment at grain sources in early gestation; and 

(5) beds and grain sources were the most intensively visited sites. We also found that environmental contacts at waterholes were more frequent during spring. 

We discuss the potential importance of various sites in the transmission of CWD and how their modification could potentially reduce the risk of prion environmental exposure among mule deer.

snip...

CONCLUSIONS

In CWD-endemic areas, prion accumulation is most likely at environmental sites that are used frequently by large numbers of deer (Miller et al. 2004, Georgsson et al. 2006, Mathiason et al. 2009, Gough and Maddison 2010). The potential for CWD transmission both from prions in the environment and directly from infected deer is, therefore, also relatively higher at these locations. We demonstrated that mule deer in our study area preferentially and more intensively visited grain sources, particularly during pre-rut and early gestation, and that contacts with the environment occurred more commonly at such sites, especially during early gestation. Our findings suggest that grain sources could play a central role in the potential for CWD transmission and control. Based on these findings, limiting access to grain spills and other artificial feed sites during winter (mid-December to the end of March) is likely to help reduce CWD transmission in wild cervid populations in areas with similar characteristics to our study site. Similar recommendations have been made for management of tuberculosis in wild cervids (Miller et al. 2003).Moreover, as previously noted by Potapov et al.(2013) and Habib et al. (2011), the applicability of CWD dynamic models can be greatly improved by expanding these models by considering both the non-random social interactions between individuals (Mejıa-Salazar et al. 2017a) and the environmental dynamics of prion transmission. Until such time that analytical techniques are developed to detect concentrations of CWD prions in the environment, our results can be immediately used to rank the relative importance of various environmental sources of CWD prions in future epidemic models for this region. Without formal initiatives to address the unintentional creation of concentrated and localized attractive feeding sources for deer, such as grain spills, CWD will most likely be perpetuated, and the success of other suggested control efforts targeting population density or size (Uehlinger et al. 2016) will most likely be jeopardized.

Key words:artificial feeding; bed sites; carcass; chronic wasting disease; disease management; environmental prion contamination; frequency of visitation; grain; intensity of visitation; mule deer; prion; remote photography.Received14 September 2017; accepted 17 November 2017. Corresponding Editor: Andrew W. Park.Copyright:©2018 Mejıa-Salazar et al. This is an open access article under the terms of the Creative Commons AttributionLicense, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.E-mail:mihicoltia@gmail.com


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

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

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

Abstract 

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

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

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

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

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

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

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

Sunday, January 06, 2013

USDA TO PGC ONCE CAPTIVES ESCAPE

*** "it‘s no longer its business.”

http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html

COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. 

IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989

http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;

''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.

https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. 

https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. 

IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989

http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

Subject: CWD TSE PRION 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

Saturday, February 04, 2012

Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised


also see;

Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.



specific susceptibility? 194. It is probable, based on age-class specific prevalence data from wild cervids and epidemiological evidence from captive cervids in affected research centres, that both adults and fawns may become infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000). 198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed deer which had become enclosed by an elk farm fence, in Sioux County, northwestern Nebraska, four fawns only eight months old were among the 50% of CWD-positive animals; these fawns were not showing any clinical signs of CWD (Davidson, 2002).


SCWDS BRIEFS

Volume 17 January 2002 Number 4

CWD News from Nebraska and Kansas

Infection with the chronic wasting disease (CWD) agent recently was found in 28 of 58 formerly wild white-tailed deer in a high-fenced enclosure adjacent to a pen containing CWDaffected captive elk in northern Sioux County, Nebraska.

***Four of the positive deer were fawns approximately 8 months old, which is unusually young for animals testing positive for CWD.



CWD in adult deer and fawns

***Five of the CWD-positive deer were fawns, less than 1 year of age.

Early CWD (PrPd detected in the tonsil or retropharyngeal node but not brain) was diagnosed in 14 deer (12 adults ranging from 1?5 to more than 5 years of age and two fawns). Late CWD (PrPd detectable in brain as well as lymphoid tissues) was diagnosed in 53 deer (50 adults ranging in age from 1?5 to 7 years of age and three fawns). None of the CWD-positive deer showed clinical signs of the disease (weight loss, hypersalivation, disorientation) or gross changes consistent with CWD (serous atrophy of fat) at necropsy.


Illinois CWD, see where there 2003 sampling showed 2. % of fawns tested had CWD i.e. 1 positive out of 51 samples.

2003

Boone-Winnebago Unit Fawn 51 1 2.0%


2011 FAWN CWD POSITIVE ILLINOIS

1/26/11 WINNEBAGO 344N 2E S36 F FAWN SHARPSHOOTING

2/10/11 OGLE 341N 1E S7 F FAWN SHARPSHOOTING

3/9/11 OGLE 341N 1E S7 M FAWN SHARPSHOOTING


For example, in 2008 a fawn tested positive and in 2010 an infected yearling buck was detected in Smith County



P172 Multigenerational transmission of CWD prions from mother to offspring

Erin Mcnulty1, MS Amy Nalls1, Dr Clare Hoover1, Dr Jenny Powers2, Dr Edward Hoover1, Dr Candace Mathiason1 1Colorado State University, Fort Collins, United States, 2National Park Services, Fort Collins, United States

Aims: Chronic wasting disease (CWD) continues to demonstrate geographic expansion, now found in captive and/or free-range cervid populations in North America, South Korea and Norway. While horizontal transmission is credited for much of the spread of CWD, few studies have monitored the transmission of this disease from mother-to-offspring.

CWD-infected muntjac dams are able to become pregnant, carry, deliver and rear offspring during the long asymptomatic phase of prion infection. We have demonstrated that CWD prions can be transmitted from mother to first-generation offspring leading to prion infection and subsequent development of TSE disease, and that transmission occurs during gestation (Nalls 2013). We have also observed fecundity in first-generation offspring. In fact, one first-generation female muntjac gave birth to two nonviable second-generation offspring. Tissues harvested from these nonviable second-generation offspring harbor protein misfolding cyclic amplification (PMCA) competent prions.

Recently we revealed PrPC seeding activity and infectious prions within the reproductive milieu (uterus, ovaries, placentomes, amniotic fluid) of CWD-infected Reeve’s muntjac dams by PMCA, real time quaking-induced conversion (RT-QuIC) and bioassay. The presence of CWD prions in the pregnancy microenvironment begs the question: Is it possible CWD is transmitted from one generation to the next via intrauterine or germline exposure to infectious prions?

Methods: To begin to address this question we assessed tissues harvested from full-term second-generation nonviable muntjac offspring for infectivity by mouse bioassay. Transgenic mice expressing the cervid prion protein, Tg(CerPrP-E226)5037+/- (n=6/cohort), were IP-inoculated with PMCA-amplified lung, mammary gland, kidney or uterus from nonviable 2nd generation muntjac offspring (n=2) born to a first generation dam (n=1), or PMCA-amplified age and tissue-matched negative control second-generation offspring (n=2). Mice from all cohorts were examined for prions by western blot and RTQuIC.

Results: All mice (n=20) inoculated with PMCA-amplified tissue from “gestational CWD-exposed” second-generation offspring developed signs consistent with TSE disease, including severe ataxia and weight loss between 209-373 days pi, and were confirmed CWD positive by western blot and RT-QuIC. Negative control mice (n=9) receiving PMCA-amplified negative age and tissue-matched homogenates remained healthy and TSE-free for the same duration. Studies have been initiated to further assess the relationship between prions in ovaries and CWD transmission.

Conclusions: Our data indicates that: (1) multigenerational transmission of infectious CWD prions from mother-to-offspring may be possible and (2) early and persistent exposure of the developing embryo to infectious CWD prions in the uterine microenvironment may help explain the facile transmission of CWD in the native host.

=====

P176 Infectious CWD prions at the fetal-maternal interface

Ms. Amy Nalls1, Ms. Erin McNulty1, Ms. Laura Pulscher1, Dr. Clare Hoover1, Dr. Edward Hoover1, Dr. Candace Mathiason1 1Colorado State University, Fort Collins, United States

Aims: Ample evidence exists for the trafficking of infectious agents across the placenta, often with grave outcomes to the developing fetus (i.e. zika, brucella, cytomegalovirus). While less studied, pregnancy-related transmissible spongiform encephalopathies (TSEs) have been implicated in several species, including humans.

Our previous work demonstrated that prions can be transferred from mother-to-offspring resulting in the development of clinical TSE disease in offspring born to CWD-infected muntjac dams (Nalls 2013). We also revealed PMCA-prion seeding activity in maternal and fetal tissues harvested in utero from muntjac dams at various stages of pregnancy and CWD infection. What remained unknown was whether the prions detected at the fetal-maternal interface were infectious. In addition, we were interested to determine if the ultrasensitive RT-QuIC methodology may enhance our ability to detect prion seeding activity within the pregnancy microenvironment.

We undertook this study to assess CWD infectivity and RT-QuIC PrPc seeding activity in in utero harvested— (1) female reproductive tissues and fluids associated with the pregnancy microenvironment; the ovary, uterus and birthing fluids, and (2) the semipermeable interface between cervid mother and fetus throughout pregnancy; the placentome.

Methods: RT-QuIC: A total of 12 replicates/sample of ovary (n=6), uterus (n=6), placentome (n=5-6 placentomes each from n=2 pregnancies) and birthing fluids (n=4) were analyzed. Bioassay: Transgenic mice expressing the cervid prion protein, Tg(CerPrP-E226)5037+/- (n=9/cohort), were IC-inoculated with 30μl 10% homogenate of uterus (n=2), placentome (n=2) or 5-fold concentrated birthing fluids (n=3).

Results: RT-QuIC: PrPC seeding activity was consistently detected in 5/6 ovary, 6/6 uterus, 9/11 placentomes, 2/2 amniotic and 0/2 allantoic fluids. Bioassay: Clinical TSE disease (ataxia, weight loss and stiff tail) was observed in mice inoculated with uterus, placentome and amniotic fluid, but not allantoic fluid between 180-343 day pi while negative control cohorts remained healthy. Bioassay mice were confirmed TSE positive: brain (uterus 7/8, placentome 8/8, amniotic fluid 1/9, allantoic fluid 0/9) and spleen (uterus 7/8, placentome 7/8, amniotic fluid 2/9, allantoic fluid 0/0) by western blot and RT-QuIC.

Conclusions: Here, using a native CWD susceptible host, we have— for the first time— demonstrated infectious prions in the cervid pregnancy microenvironment and placental structure at the fetal-maternal interface. These findings reveal a source of infectious prions that the developing fetus is exposed to long before the birthing process, maternal grooming, or encounter with contaminated environments. Thus suggesting that CWD mother-to-offspring transmission may contribute to the facile transmission of CWD and be underappreciated for all TSEs.


FRIDAY, MARCH 30, 2018 

Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018

Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon..net 

Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary View Attachment:View as format pdf 



https://www.regulations.gov/docketBrowser?rpp=25&so=DESC&sb=commentDueDate&po=0&dct=PS&D=APHIS-2018-0011


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...


TUESDAY, APRIL 18, 2017 

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


TUESDAY, JANUARY 17, 2017 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION


THIS April, 4, 2017 violation of the mad cow 21 CFR 589.2000 OAI is very serious for the great state of Michigan, some 20 years post FDA mad cow feed of August 1997. if would most likely take a FOIA request and a decade of wrangling to find out more. 

TUESDAY, JANUARY 17, 2017

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION 

I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$

NAI = NO ACTION INDICATED

OAI = OFFICIAL ACTION INDICATED

VAI = VOLUNTARY ACTION INDICATED

RTS = REFERRED TO STATE

OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions. 

2016


ONE more thing, please remember, the label does not have to say ''deer ration'' for cervid to be pumped up with. you can get the same ''high protein'' from many sources of high protein feed for animals other than cattle, and feed them to cervid...

Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009


Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009


WEDNESDAY, JULY 11, 2018 

CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000

http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html

TUESDAY, JULY 10, 2018
 
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS
 
*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''
 
CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS
 
SUNDAY, AUGUST 19, 2018 

Texas Deer Farms, Growing Freakish Antlers, and CWD TSE Prion aka mad deer disease



TUESDAY, AUGUST 7, 2018 

Unexpected prion phenotypes in experimentally transfused animals: predictive models for humans?


TUESDAY, JULY 31, 2018 

USA CJD TSE Tables of Cases Examined National Prion Disease Pathology Surveillance Center Cases Examined May 1, 2018


BSE, USDA, NAIS, AND TRACEABILITY 

Let's look at how the USDA et al trace BSE aka mad cow cases, birth, and index herd cattle in the past (or rather how they could not trace them).

TEXAS MAD COW (h-BSE), that was finally tested and documented 7+ months after an act of Congress, and Scientist from all over the Globe questioning the testing methods and negative findings of this Texas mad cow. ...

TEXAS h-BSE MAD COW CASE THAT WAS FINALLY DOCUMENTED

***> The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.

this seemed to be the excuse of the day on countless trace efforts of this madcow outbreak in Texas...terry see;





PRION 2018 CONFERENCE ABSTRACT;

READING OVER THE Prion 2018 Book of Absracts, seems they found that;

O10 Zoonotic potential of atypical BSE prions: a systematic evaluation 

Marín-Moreno A (1), Espinosa JC (1), Douet JY (2), Aguilar-Calvo P (1), Píquer J (1), Lorenzo P (1), Lacroux C (2), Huor A (2), Lugan S (2), Tillier C (2), Andreoletti O (2) and Juan María Torres (1) 

Our results confirm that L-BSE transmits to TgMet129 even better than epidemic BSE. However, atypical L-BSE agent was unable to infect TgVal129 or TgMet/Val129 mice, even after passage in TgMet129. No transmission was observed with H-BSE in any mice model inoculated, irrespectively of the 129 polymorphism. 

***>After passage in sheep PrP expressing host, the properties of both H and LBSE including their capacity to cross the human species barrier were dramatically affected, emerging prion strains features that resemble those of sporadic Creutzfeldt-Jakob disease (sCJD). To date, this is the more extensive and complete analysis of the zoonotic potential of atypical BSE prions. 

***>These results advise not to ignore the zoonotic potential of these agents.

also, another study;

P77 In vitro approach to estimate the human transmission risk of prions

Iwamaru Y (1) Imamura M (2) Matsuura Y (1) Kohtaro Miyazawa (1) Takashi Yokoyama (3) (1 ) National Institute of Animal Health, Prion Disease Unit, Ibaraki, Japan (2) University of Miyazaki, Division of Microbiology, Miyazaki, Japan (3) National Institute of Animal Health, Department of Planning and General Administration, Ibaraki, Japan.

snip...

In attempt to develop the more time- and cost-saving method for assessment of the human transmission risk of prions, we performed experiments using protein misfolding cyclic amplification (PMCA) technique to investigate whether PMCA can be compatible with bioassay. Using brain homogenates of Tg expressing bovine PrP as the PrP substrate, we optimized the versatile PMCA condition that could amplify PrPSc from cattle affected with C-, H- or L-BSE. 

***>We measured the 50% PMCA seeding activity dose and the 50% lethal dose in 1 g equivalent of C-, H- or L-BSE cattle brain tissue by using PMCA or bioassay, respectively, and assessed the correlations between these doses.

and also this study;

P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge

Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2)

This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.


Sunday, February 25, 2018

PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW



***> 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. <***


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

Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation

Abstract 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

SNIP...

Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. 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.

The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.

We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.

Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.

The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.

Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.

Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.

Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.

Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. 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.



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. 
 
============== 
 
 
 ***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. 
 
 
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
 
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
 
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
 
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
 
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
 
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
 
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
 
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. 
 
 
 why do we not want to do TSE transmission studies on chimpanzees $
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
snip...
 
R. BRADLEY
 
 
 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. 
 


***> MAD COW DISEASE TEXAS, LET ME COUNT THE WAYS <***

WEDNESDAY, AUGUST 15, 2018 

The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge


SUNDAY, JUNE 3, 2018 

Clinical, pathological, and molecular features of classical and L-type atypical-BSE in goats


FRIDAY, AUGUST 10, 2018 

From Gate to Plate, BSE aka mad cow disease, USDA, NAIS, AND TRACEABILITY



WEDNESDAY, SEPTEMBER 26, 2018 J

AVMA In Short Update USDA announces detection of atypical BSE


WEDNESDAY, SEPTEMBER 5, 2018 

APHIS Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0012]


Sunday, September 16, 2018 

Mother to Offspring Transmission of TSE PRION DISEASE and risk factors there from


TUESDAY, AUGUST 07, 2018 

Passage of scrapie to deer results in a new phenotype upon return passage to sheep


THURSDAY, SEPTEMBER 27, 2018 

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


TUESDAY, SEPTEMBER 4, 2018 

USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018


WEDNESDAY, SEPTEMBER 05, 2018 

Edmonton woman one of the youngest diagnosed with CJD at 35 years old and pregnant



WEDNESDAY, SEPTEMBER 26, 2018 

A new variant of Creutzfeldt-Jakob disease in the UK 1995 revisited 2018 a review of science



i know you can't print any of this, so what the hell, may as well put my tin foil cap on and pass this along as well;


as i have also said for two decades, friendly fire, sporadic, what if?


PRION Conference 2018


P132 Aged cattle brain displays Alzheimer’s-like pathology that can be propagated in a prionlike manner 

Ines Moreno-Gonzalez (1), George Edwards III (1), Rodrigo Morales (1), Claudia Duran-Aniotz (1), Mercedes Marquez (2), Marti Pumarola (2), Claudio Soto (1) 

(1) Mitchel Center for Alzheimer´s Disease and Related Brain Disorders, Department of Neurology, University of Texas Health Science Center at Houston, Houston, TX, USA (2) Animal Tissue Bank of Catalunya (BTAC), Department of Animal Medicine and Surgery, Veterinary Faculty, Universitat Autónoma de Barcelona, Bellaterra (Cerdanyola del Valles), Barcelona, Spain. 

Amyloid beta (Ab) and hyperphosphorylated tau (ptau) are the proteins undergoing misfolding in Alzheimer‘s disease (AD). Recent studies have shown that brain homogenates rich in amyloid aggregates are able to seed the misfolding and aggregation of amyloidogenic proteins inducing an earlier onset of the disease in mouse models of AD. This seeding behavior is analogous to the disease transmission by propagation of prion protein misfolding observed in prion diseases. Prion diseases can be transmitted across species by inoculation of the misfolded prion protein from one specie into an appropriate host. For example, material from cattle affected by bovine spongiform encephalopathy can be propagate in humans inducing variant Creutzfeldt-Jakob disease. In this study, we analyzed the presence of AD-related protein aggregates in the brain of old cows and investigated whether these aggregates are capable to induce pathology in animal models of AD. We observed that many of the typical hallmarks detected in human AD brains, including Ab aggregates and tangles, were present in cow brains. When cattle tissue containing Ab aggregates or ptau were intracerebrally inoculated into APP/PS1 or P301S mice, we observed an acceleration of brain misfolded protein deposition and faster cognitive impairment compared to controls. However, when the material was orally inoculated, no effect was observed. These results may contribute to uncover a previously unsuspected etiology surrounding some cases of sporadic AD. However, the early and controversial stage of the field of prion-like transmission in non-prion diseases added to the artificial nature of the animal models utilized for these studies, indicate that extrapolation of the results to humans should not be done without further experiments.  
 

=====prion 2018===


P75 Determining transmissibility and proteome changes associated with abnormal bovine prionopathy 

Dudas S (1,2), Seuberlich T (3), Czub S (1,2) 

1. Canadian Food Inspection Agency, NCAD Lethbridge Laboratory, Canada 2. University of Calgary, Canada 3. University of Bern, Switzerland. 

In prion diseases, it is believed that altered protein conformation encodes for different pathogenic strains. Currently 3 different strains of bovine spongiform encephalopathy (BSE) are confirmed. Diagnostic tests for BSE are able to identify animals infected with all 3 strains, however, several diagnostic laboratories have reported samples with inconclusive results which are challenging to classify. It was suggested that these may be novel strains of BSE; to determine transmissibility, brain material from index cases were inoculated into cattle. 

In the first passage, cattle were intra-cranially challenged with brain homogenate from 2 Swiss animals with abnormal prionopathy. The challenged cattle incubated for 3 years and were euthanized with no clinical signs of neurologic disease. Animals were negative when tested on validated diagnostic tests but several research methods demonstrated changes in the prion conformation in these cattle, including density gradient centrifugation and immunohistochemistry. Currently, samples from the P1 animals are being tested for changes in protein levels using 2-D Fluorescence Difference Gel Electrophoresis (2D DIGE) and mass spectrometry. It is anticipated that, if a prionopathy is present, this approach should identify pathways and targets to decipher the source of altered protein conformation. In addition, a second set of cattle have been challenged with brain material from the first passage. Ideally, these cattle will be given a sufficient incubation period to provide a definitive answer to the question of transmissibility. 


=====prion 2018===

END...TSS


Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy 

>>> The only tenable public line will be that "more research is required’’ <<< 

>>> possibility on a transmissible prion remains open<<< 

O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ? 

Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy 

Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015) 

snip...see full Singeltary Nature comment here; 

Alzheimer's disease

let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease... 

Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy





Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease 

*** Singeltary comment PLoS *** 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? 

Posted by flounder on 05 Nov 2014 at 21:27 GMT 


IN CONFIDENCE

5 NOVEMBER 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. 

There are also results to be made available shortly 

(1) concerning a farmer with CJD who had BSE animals, 

(2) on the possible transmissibility of Alzheimer’s and 

(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]





***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.

***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***

Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT



layperson, no doctor, no PhDs, no president and ceo of nothing...just made a promise to mom, never forget, never let them forget, before we all do...we must remove politics, industry, and lobbyist out of the scientific policy making decisions, this is why we are at, where we are today, imo...


THURSDAY, MAY 17, 2018 

Texas TAHC CWD TSE Prion Pay to Play Federal Indemnity Program, or what i call, ENTITLEMENT PROGRAM for Game Farm Industry


Terry S. Singeltary Sr.
Bacliff, Texas USA
Galveston Bay, on the bottom.

wasted days and wasted nights...Freddy Fender

WEDNESDAY, AUGUST 22, 2018 

TEXAS CWD TSE PRION 16 MORE CASES DETECTED TOTAL TO DATE 117 CONFIRMED NEW 14 BREEDERS 2 FREE RANGE


SATURDAY, MARCH 31, 2018

***> TEXAS DETECTS IT'S 101 CASE of CWD TSE PRION Breeder White-tailed Deer with no end in sight <***

2018 03/27/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5



THURSDAY, MARCH 22, 2018 

TEXAS CWD TSE PRION JUMP TO 100 POSITIVE, NEW CASES 17 BREEDER, 1 BREEDER RELEASE, AND 1 WILD SINCE JAN 31, 2018


SUNDAY, JUNE 10, 2018 

TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018



THURSDAY, JANUARY 26, 2017

Texas CWD Discovered Free-Ranging Whitetail DEER Houston Chronicle Shannon Tompkins PLEASE, CAN YOU HEAR ME NOW?


Saturday, October 03, 2015

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015

here is a great article by Shannon Tomkins and the Houston Chronicle on 

Chronic Wasting Disease CWD TSE prion aka mad deer disease 

Thursday, March 14, 2002 

"Ten years ago, elk and deer (imported into Texas) were not regulated at all," said Dr. Ken Waldrup, an epidemiologist with the Texas Animal Health Commission and one of the agency's point men on CWD. "If Texas doesn't already have CWD, then I say that proves that God is a Texan. "For everyone's sake, I sure hope He is." 

======================== 

Tompkins: There are a lot of reasons to be concerned about CWD 

Houston Chronicle Published 5:30 a.m., Thursday, March 14, 2002



16 years later, the silence is deafening...terry


Texas Chronic Wasting Disease CWD TSE Prion History

*** 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


Subject: CWD SURVEILLANCE STATISTICS TEXAS (total testing figures less than 50 in two years) Date: Sun, 25 Aug 2002 21:06:49 –0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

######## Bovine Spongiform Encephalopathy #########

snip...

IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.

AS i said before;

 > SADLY, they have not tested enough from the total population to

> know if CWD is in Texas or not.

 BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...

snip...end...TSS

=============================== snip...end...tss



From: Terry Singeltary <flounder9@verizon.net>
To: cruz_press <cruz_press@cruz.senate.gov>
Cc: stephen_reynolds <stephen_reynolds@cornyn.senate.gov>
Sent: Wed, Aug 22, 2018 11:18 am
Subject: Texas Deer Industry To Bring Concerns Over Chronic Wasting Disease To Legislature

Greetings Honorable Senator Cornyn (please get this to Senator Cornyn Stephen), and Honorable Senator Cruz, 

i am writing you about something of dire straights for Texas, the USA, North America, and the Globe. 

chronic wasting disease cwd tse prion aka mad deer disease, or mad cow disease and or scrapie and or both, in cervid.

Senator Cornyn helped me long ago when the NIH et al were threatening to destroy our loved ones brains we had donated for researched, Senator Cornyn helped us stop that, and we graciously thank him for that. see;




JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305 April 26,2005

Mr. Terry Singeltary

P.O. Box 

Bacliff, Texas 77518

Dear Mr. Singeltary:

In response to your recent request for my assistance, I have contacted the National Institutes ofHealth. I will write you again as soon as I receive a reply. I appreciate having the opportunity to represent you in the United States Senate and to be ofservice in this matter.

Sincerely,

JOHN CORNYN United States Senator JC:djl


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


JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305

May 18,2005

Mr. Terry Singeltary

P.O. Box 

Bacliff, Texas 77518

Dear Mr. Singeltary:

Enclosed is the reply I received from the Department of Health and Human Services in response to my earlier inquiry on your behalf. I hope this will be useful to you. I appreciate having the opportunity to represent you in the United States Senate. Thank you for taking time to contact me. Sincerely,

JOHN CORNYN United States Senate JC:djl Enclosure

DEPARTMENT OF HEALTH & HUMAN SERVICES National Institutes of HealthNational Institute of NeurologicalDisorders and Stroke NINDS Building 31, Room 8A52 31 Center Dr., MSC 2540 Bethesda, Maryland 20892-2540 Phone: 301-496-9746 Fax: 301-496-0296 Email: [log in to unmask]

May 10, 2005

The Honorable John CornynUnited States SenatorOccidental Tower5005 LBJ Freeway, Suite 1150Dallas, Texas 75244-6199

Dear Senator Cornyn:

Your letter to the National Institutes of Health (NIH) forwarding correspondence from Mr. Terry S. Singeltary, Sr., has been forwarded to me for reply. Mr. Singeltary is concerned about thepreservation of Creutzfeldt-Jakob disease (CJD) brain samples that have been maintained by theNational Institute of Neurological Disorders and Stroke (NINDS) Intramural Research programfor many years. I am sorry to learn that Mr. Singeltary's mother died of CJD and can certainly understand hisdesire that any tissues that could help investigators unravel the puzzle of this deadly disease arepreserved. I hope he will be pleased to learn that all the brains and other tissues with potential tohelp scientists learn about CJD are, and will continue to be, conserved. (The tissues that arediscarded are those that have either decayed to an extent that renders them no longer appropriatefor research or those for which we do not have sufficient identification.) The purpose of gathering these brains and tissues is to help scientists learn about CJD. To that end, some of the NINDS-held samples are distributed to investigators who can demonstrate thatthey have a compelling research or public health need for such materials. For example, sampleshave been transferred to NIH grantee Dr. Pierluigi Gambetti, who heads the National PrionDiseases Pathology Surveillance Center at Case Western Reserve University in Ohio and workswith the Centers for Disease Control and Prevention to monitor all cases of CJD in the UnitedStates. Dr. Gambetti studies the tissues to learn about the formation, physical and chemicalproperties, and pathogenic mechanisms of prion proteins, which are believed to be involved inthe cause of CJD. Samples have also been transferred to Dr. David Asher, at the U.S. Food andDrug Administration, for use in assessing a potential diagnostic test for CJD.

Page 2 - The Honorable John Cornyn

in closing, we know that donating organs and tissue from loved ones is a very difficult andpersonal choice that must often be made at the most stressful of times. We at the NINDS aregrateful to those stalwart family members who make this choice in the selfless hope that it willhelp others afflicted with CJD. We also know the invaluable contribution such donations maketo the advancement of medical science, and we are dedicated to the preservation of all of thetissue samples that can help in our efforts to overcome CJD.

I hope this information is helpful to you in responding to Mr. Singeltary. Sincerely,

Story C. Landis, Ph.D. Director, National Institute ofNeurological Disorders and Stroke


==================================...end...tss


i hope Senator Cornyn and Senator Cruz can help us stop the junk science and regulations there from, that the cervid game farming industry is trying to shove down the throat of every politician out there, and that goes along with those free canned hunts that some politicians get for favors down the road, or paying to play and legislation there from...

Texas Deer Industry To Bring Concerns Over Chronic Wasting Disease To Legislature 

By RYAN POPPE • 17 HOURS AGO

Texas Deer Industry To Bring Concerns Over Chronic Wasting Disease To Legislature

By RYAN POPPE • 17 HOURS AGO

Vendors at the Texas Deer Association's annual convention and auction at the JW Marriott-Hill Country Resort.

RYAN POPPE / 2018

For some Texans, there’s big money in deer. Breeding and raising whitetail deer, running deer hunts on ranches, it’s all part of a multibillion-dollar industry. But since 2015, deer breeders and the state have been locked in an old-fashioned standoff.

Texas Parks and Wildlife Commission has restricted the movement of this deer population in an effort to contain chronic wasting disease. Meanwhile, the Texas deer industry says this hurts its livelihood, and it plans to push lawmakers to make changes during the 2019 legislative session.

Listen Listening...4:31

Every August, the Texas Deer Association hosts its annual convention and deer auction in San Antonio.

All 120,000 square feet of the convention hall is lined with mounted trophy bucks, and kiosks with vendors advertising everything from hunting excursions to the latest in deer feeders, deer stands and hunting gear.

Patrick Tarleton is the association’s executive director and calls the expo “the greatest deer show on Earth. This is the largest deer industry convention in the country — in the world. We’ll have over 3,000 people walking through the doors.” 

An auction card displaying the pedigree of a deer. CREDIT RYAN POPPE / TEXAS PUBLIC RADIO

Across from the exhibit hall, an auctioneer sifts through a PowerPoint presentation of the pedigreed deer up for sale.

Ranchers who purchase these animals will use them to breed bigger bucks with more majestic antlers.

For those who don’t want to buy a whole deer, you can even buy “material” for artificial insemination. That’s what Tom Crews, of HC Whitetails near Alice, is here for.

“They sell semen from deer and they are really good genetics and people ‘AI’ them. It’s a really good deal,” Crews said.

Each deer’s auction card describes the animal lineage and is labeled with a very important statement: “This animal is free of chronic wasting disease — or CWD — and is eligible for transport in Texas and Mexico.”

That’s important for ranchers who want to avoid introducing CWD into their herds, said Dr. Brodie Miller, a veterinarian with the Texas Animal Health Commission.

“In simple words, chronic wasting disease is a progressive, degenerative and ultimately fatal neurological disease found in deer, elk, moose and other members of the deer family,” Miller said.

He said CWD attacks a deer’s brain stem, causing the animal to stop eating and drinking, and eventually die.

Miller said the disease is spread through abnormal proteins in the animal’s skin, saliva, urine and feces.

“These abnormal proteins called prions are shed from infected animals which ultimately can infect the environment where other deer and cervids live,” Miller said.

Chronic wasting disease in Texas is primarily found in captive whitetail deer.

CREDIT RYAN E. POPPE / TEXAS PUBLIC RADIO

When comes to whitetail deer in Texas, CWD has only shown up in whitetail deer bred in captivity. That’s why the Texas Parks and Wildlife commission imposed rules restricting ranchers from moving these animals if they haven’t been tested, or if any deer in their facility have tested positive for CWD or come in contact with a deer testing positive for CWD.

Many Texas deer breeders feel the state’s rules unfairly target their industry. They’d like to see rules that are less restrictive for the relocation of these deer.

Marty Berry owns Berry Whitetails Ranch, which sits right on the waterfront of Nueces Bay near Corpus Christi and called the state’s rules a waste of public resources.

“We have pens of deer that have been together since birth and you have two in the pen with it and the rest of them don’t have it. Why is it two of them have the disease and rest don’t get it, that’s pretty phenomenal, what a waste of money,” Berry said.

Carter Smith, executive director for the Texas Parks and Wildlife Department, disagrees.

“Animal science, disease management 101, tells us there is a higher probability for disease transmission risks for animals that are concentrated or are in high numbers or moved from place to place,” Smith said.

Every Aug. 23, the Texas Parks and Wildlife Commission holds an annual public hearing so that anyone can voice their concerns about the management of Texas wildlife, including deer.

But back at the convention and auction, Patrick Tarleton, with the Texas Deer Association, felt commissioners have not addressed their concerns about what they label as overregulation, so they won’t be attending the public hearing this year.

Vendor booths inside the exhibit hall at the Texas Deer Association's convention and auction in San Antonio.

CREDIT RYAN E. POPPE / TEXAS PUBLIC RADIO

“The disease caught our regulatory agency off-guard, and what we found out is there wasn’t any emergency in most of our facilities. They’ve now found four, five facilities with CWD, and it has no effect on our population here in Texas,” Tarleton said.

Officials with Texas Parks and Wildlife disagree and said the disease has the potential to infect Texas’ total 3.6 million whitetail deer population if left unmanaged.

So, Tarleton and others are taking their concerns to state lawmakers to address during the 2019 legislative session, asking that they create regulations that better suit their industry.



Hello Ryan AND Greetings Texas Public Radio et al, 

i thought i might write you and share with you some findings on chronic wasting disease cwd tse prion that you may not be aware of. i read with interest your article today 'Texas Deer Industry To Bring Concerns Over Chronic Wasting Disease To Legislature', and thought since i have failed every day for 20 years now, trying to warn about cwd tse prion in Texas, i thought maybe since you are a reporter, i could send this science to you and what better to have than sound science to present to said legislatures...LOL! i'm sorry, but i have been trying to get something down about this since the very first madcow TAHC did succeed in covering up, and they almost got away with the second madcow, but for me and many scientist around the world writing to the Honorable Phyllis Fong of the OIG, and some 7 months later, on a 48 turn around (their regs), and much political wrangling, that madcow was finally confirmed (this all documented). i tell you this because all this cwd is, is madcow disease in cervid. i have seen it, my mother died from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, confirmed, and she did everything Linda Blair did in that movie the exorcist, except spin her head 360 degrees. it took 3 grown adults to hold her down she would jerk so bad, all the while she was screaming, 'why am i doing this, why can't i stop'. yep, about that time i was watching the Oprah Show with cattlemen mad as hell, all saying it's not here, and i was looking write at it. NOW, indeed, i have been proven correct, mad cows, mad deer, mad sheep, and mad cow dead people, all right here in TEXAS, and YES, now science has linked sporadic CJD to atypical and typical BSE, Scrapie, and now the macaque studies of CWD, positive by oral routes, a very frightening revelation. NOW, i send this all to you for your files, PLUS, something that has not been put out yet, and i promised not too, because that seemed to be the only way i could get access (FOR THE FIRST DAMN TIME EVER), to the Congressional Abstracts of Prion 2018 Congress, but that is another long story i don't plan on going into now, but i am getting the data at a small bit at a time, but i will send you this full abstract anyway, much too important, it will be the first item up below, followed by the rest of this nightmare in a blog and email news i send out to different tse prion lists. i blog this science as soon as i get it, i do not advertise, or make money from these tse prion blogs, they are for educational use, i just made a promise to mom, never forget, and never let them forget. it was 2002 i first started warning the TAHC about CWD waltzing into Texas from the White Sands Missile Range NM, around the Trans Pecos region, yes, about 2002, and i was laughed at. well, the rest is history, 10 years later or so the first cases of cwd were detected right where i had been trying to tell them...yada, yada, yada....i'm tired...kind regards, terry

***> TSE PRION UPDATE OCTOBER 2018

MONDAY, OCTOBER 01, 2018 


Update on Classical and Atypical Scrapie in Sheep and Goats: Review 2018


http://scrapie-usa.blogspot.com/2018/10/update-on-classical-and-atypical.html


THURSDAY, SEPTEMBER 27, 2018 


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




SATURDAY, SEPTEMBER 29, 2018

This Map Spells Trouble for the Future of Deer Hunting CWD TSE Prion Consumption, Exposure, and Zoonosis Potential


MONDAY, OCTOBER 01, 2018

Minnesota Deer tests positive for CWD in disease management zone


Michigan adds another CWD TSE Prion case, total at 62 to date

Total Deer Tested and Total Positives Cases 62




WEDNESDAY, SEPTEMBER 26, 2018 


Michigan adds another CWD TSE Prion case, total at 62 to date




TUESDAY, SEPTEMBER 25, 2018 

Wisconsin CWD TSE PRION PLAN preferred option disposal in a landfill OR public land is acceptable to leave the carcass in the spot of the kill



WEDNESDAY, SEPTEMBER 26, 2018 

JAVMA In Short Update USDA announces detection of atypical BSE

WEDNESDAY, SEPTEMBER 5, 2018 

APHIS Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0012]



Sunday, September 16, 2018 

Mother to Offspring Transmission of TSE PRION DISEASE and risk factors there from



TUESDAY, AUGUST 07, 2018 

Passage of scrapie to deer results in a new phenotype upon return passage to sheep



THURSDAY, SEPTEMBER 27, 2018 

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



TUESDAY, SEPTEMBER 4, 2018 

USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018



WEDNESDAY, SEPTEMBER 05, 2018 

Edmonton woman one of the youngest diagnosed with CJD at 35 years old and pregnant



WEDNESDAY, SEPTEMBER 26, 2018 

A new variant of Creutzfeldt-Jakob disease in the UK 1995 revisited 2018 a review of science



SATURDAY, SEPTEMBER 22, 2018

Emerging Diseases, Infection Control & California Dental Practice Act




Terry S. Singeltary Sr.

posted by Terry S. Singeltary Sr. at 10:19 AM

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