Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies 2021 Annual Report
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Research
2021 Annual Report
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CWD has been reported in the United States, Canada, South Korea, Norway, Finland, and Sweden, and the case numbers in both wild and farmed cervids are increasing rapidly. Studies indicate that lateral transmission of cervids likely occurs through the shedding of infectious prions in saliva, feces, urine, and blood into the environment. Therefore, the detection of CWD early in the incubation time is advantageous for disease management. ARS researchers in Ames, Iowa, developed a method that detects CWD using fecal samples as much as 30 months prior to the onset of clinical signs with all samples tested between 6 and 30 months post-inoculation showing RT-QuIC positivity. The combination of a highly sensitive detection tool paired with a sample type such as feces, which can be collected non-invasively allows a useful tool to support CWD surveillance in wild and captive cervids.
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4. Passing Transmissible Mink Encephalopathy (TME) prions from cattle to sheep changed the ability of the prions to infect mice. Transmissible spongiform encephalopathies (TSEs), or prion diseases, are fatal brain diseases that affect livestock species. Prion diseases have been shown to jump species as exhibited when classical bovine spongiform encephalopathy (BSE) infected cattle products were consumed by humans resulting in variant Creutzfeldt-Jakob disease. Another example of cross-species transmission results in a disease of farmed mink known as transmissible mink encephalopathy (TME), the origins of which were not previously understood; however, one possible source is L- BSE from cattle. The present study was designed to determine the effect of cross-species transmission of TSEs in livestock on the ability to infect mice expressing the cattle prion protein. We found that passing cattle adapted TME (TME that was previously passaged in cattle) to sheep changed the ability of the prions to infect bovinized mice in a laboratory inoculation. These results were compared to atypical BSE (L-BSE type) and Classical BSE in bovinized mice. Depending on the genotype of sheep used, the disease in mice appeared similar by histologic and western blot analysis to either L-BSE or C-BSE. These results indicate a shift in the disease presentation based on transmission through sheep with different genotypes. This information gives insight into origins and development of new prion strains. Because disease in one of the groups of mice resembled the L-BSE phenotype, it supports the hypothesis that TME can originate from feeding mink protein from cattle afflicted with L-BSE.
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Research
Title: Scrapie in white-tailed deer: a strain of the CWD agent that efficiently transmits to sheep?
Author item Greenlee, Justin item KOKEMULLER, ROBYN - US Department Of Agriculture (USDA) item MOORE, S - Oak Ridge Institute For Science And Education (ORISE) item WEST GREENLEE, M - Iowa State University
Submitted to: Meeting Abstract Publication Type: Abstract Only Publication Acceptance Date: 3/29/2019
Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Scrapie is a transmissible spongiform encephalopathy of sheep and goats that is associated with widespread accumulation of abnormal prion protein (PrPSc) in the central nervous and lymphoid tissues. Chronic wasting disease (CWD) is the natural prion disease of cervid species, and the tissue distribution of PrPSc in affected cervids is similar to scrapie in sheep. There are several lines of evidence that suggest that multiple strains of CWD exist, which may affect the agent’s potential to transmit to hosts of the same or different species. We inoculated white-tailed deer with the scrapie agent from ARQ/ARQ sheep, which resulted in 100% attack rates by either the intracranial or oronasal route of inoculation. When examining tissues from the brainstems or lymphoid tissues by traditional diagnostic methods such as immunohistochemistry or western blots, it is difficult to differentiate tissues from deer infected with scrapie from those infected with CWD. However, there are several important differences between tissues from scrapie-infected white-tailed deer (WTD scrapie) and those infected with CWD (WTD CWD). First, there are different patterns of PrPSc deposition in the brains of infected deer: brain tissues from deer with WTD scrapie had predominantly particulate and stellate immunoreactivity whereas those from deer with WTD-CWD had large aggregates and plaque-like staining. Secondly, the incubation periods of WTD scrapie isolates are longer than CWD isolates in mice expressing cervid prion protein. Most notably, the transmission potential of these two isolates back to sheep is distinctly different. Attempts to transmit various CWD isolates to sheep by the oral or oronasal routes have been unsuccessful despite observation periods of up to 7 years. However, WTD scrapie efficiently transmitted back to sheep by the oronasal route. Upon transmission back to sheep, the WTD scrapie isolate exhibited different phenotypic properties when compared to the sheep receiving the original sheep scrapie inoculum including different genotype susceptibilities, distinct PrPSc deposition patterns, and much more rapid incubation periods in transgenic mice expressing the ovine prion protein. The scrapie agent readily transmits between sheep and deer after oronasal exposure. This could confound the identication of CWD strains in deer and the eradication of scrapie from sheep.
SO, WHO'S UP FOR SOME MORE TSE PRION POKER, WHO'S ALL IN $$$
SO, ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS, TAKE YOUR PICK, BUT I SAID IT LONG AGO WHEN USDA OIE ET AL MADE ATYPICAL SCRAPIE A LEGAL TRADING COMMODITY, I SAID YOUR PUTTING THE CART BEFORE THE HORSE, AND THAT'S EXACTLY WHAT THEY DID, and it's called in Texas, TEXAS TSE PRION HOLDEM POKER, WHO'S ALL IN $$$
***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.
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THURSDAY, JULY 8, 2021
EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie
NOW, back to those mad mink i.e. TME. let me throw a curve ball here ;
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* and Richard A. Bessen† Emerging Infectious
Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine- passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, Htype BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profi les, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME. The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE. Transmissible mink encephalopathy (TME) is a rare prion disease in ranch-raised mink (Mustela vison) in North America and Europe (1–4). Six outbreaks have been reported from 1947 through 1985 in North America, and several have been linked to contaminated commercial feed (1). Although contamination of feed with scrapie-infected sheep parts has been proposed as the cause of TME, the origin of the disease remains elusive. The idea that scrapie in sheep may be a source of TME infection is supported by fi ndings that scrapie-infected mink have a similar distribution of vacuolar pathologic features in the brain and the same clinical signs as mink with natural and experimental TME (5). However, mink are not susceptible to scrapie infection following oral exposure for up to 4 years postinoculation, which suggests that either the scrapie agent may not be the source of natural TME infection or that only specifi c strains of the scrapie agent are able to induce TME (6,7). Epidemiologic investigations in the Stetsonville, Wisconsin, outbreak of TME in 1985 suggested a possible cattle origin, since mink were primarily fed downer or dead dairy cattle but not sheep products (8). Experimental transmission of Stetsonville TME into cattle resulted in transmissible spongiform encephalopathy (TSE) disease with an incubation period of 18.5 months. Back passage of bovine TME into mink resulted in incubation periods of 4 and 7 months after oral or intracerebral inoculation, respectively, which was similar to that found following inoculation of Stetsonville TME into mink by these same routes (8). These fi ndings indicated that cattle are susceptible to TME, and that bovine-passaged TME did not result in a reduced pathogenicity for mink. These studies raised the question as to whether an unknown TSE in cattle was the source of TME infection in the Stetsonville outbreak. Several additional TME outbreaks in the United States have been associated with mink diet that contained downer or dead cattle (9). ...
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1985
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
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The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
THURSDAY, FEBRUARY 03, 2022
Transmissible Mink Encephalopathy TME, Atypical L-Type BSE PrP, and typical C-Type BSE, which came first, the cart or the horse?
WEDNESDAY, JANUARY 12, 2022
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA, what if?
Monday, November 14, 2022
Prion Diseases in Dromedary Camels (CPD) 2022 Review
THURSDAY, NOVEMBER 10, 2022
Annual Report of the Scientific Network on BSE‐TSE 2022
SUNDAY, OCTOBER 16, 2022
USDA Transmissible Spongiform Encephalopathy TSE Prion Action Plan National Program 103 Animal Health 2022-2027
http://transmissiblespongiformencephalopathy.blogspot.com/2022/10/usda-transmissible-spongiform.html
FRIDAY, NOVEMBER 04, 2022
Texas CWD TSE Prion 409 Cases Confirmed To Date TPWD emergency rule adds two new surveillance zones located primarily in Gillespie and Limestone counties
Terry S. Singeltary Sr.
