Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project and Hunkering Down in the BSE Situation Room USDA 1998

Greetings Arkansas Arkansas Game and Fish Commission, Hunters and Sportsman/woman et al,

 

I am going to run some more history by you, for those interested. please don’t shoot the messenger.

 

I know some of you are interested in the history of the Elk Restoration Project in Arkansas, and I thought I would pull up some old files from toms old site, some good old info there on CWD BSE Scrapie TSE Prion History. 

 

kind regards, terry

 

CWD in Arkansas? -- no IHC testing SCWDS Briefs newsletter. Arkansas Game & Fish Commission Little Rock, AR 72205 tel 501-223-6300

 

JASPER - Saturday, Aug. 1,1998 is when the 18 remaining elk hunting permits for 1998 will be drawn. More than 16,000 persons applied for the free elk-hunting permits. Return of the Elk by Michael E. Cartwright, Deer/Elk Program Coordinator, Arkansas Game and Fish Commission

 

Elk once numbered in the millions and occupied habitats spanning most of North America. Unfortunately, shrinking habitat and overhunting reduced populations to a few persistent herds in the mountainous West. Had the elk not been remarkably adaptable, it might now be extinct. The eastern elk (Cerrus elaphus canadensis) lived in eastern boreal and hardwood forests. This was the subspecies native to Arkansas, though historical records indicate it persisted no later than the 1840s. It is now extinct. The U.S. Forest Service introduced Rocky Mountain elk (Cersus elaphus nelsoni) in Franklin County's Black Mountain Refuge in 1933. Three bulls and eight cows from Wichita National Wildlife Refuge in Oklahoma were released. The population grew to 125 by 1948, but by then, wildlife biologists were concerned about the herd's future.

 

The herd increased to an estimated 200 by the mid 1950s and then vanished. No one knows for sure what caused these elk to disappear. Some speculate that illegal hunting, natural mortality and shrinkage of suitable range through natural ecological succession eventually resulted in their extermination.

 

In 1981, the Game & Fish Commission, in cooperation with private citizens and the National Park Service, initiated another elk restoration project in the Ozark Mountains of northwest Arkansas. Between 1981 and 1985, 112 elk from Colorado and Nebraska were released at five sites near Pruitt in Newton County.

 

All release sites were on or adjacent Buffalo National River lands. Some elk were ear-tagged and tested for diseases such as brucellosis and leptospirosis prior to release. The Game & Fish Commission and Park Service monitor elk using field observations, helicopter counts and, in recent years, thermal infrared sensing equipment. Elk have been reported in Washington, Carroll, Boone, Marion, Newton, Searcy, Stone, Conway, Pope, Van Buren and Faulkner counties, but most of the approximately 350 elk in the Arkansas herd occur along 67 miles of the upper and middle Buffalo National River corridor in Newton and Searcy counties, primarily on National Park Service land.

 

Fifty-five elk deaths were documented between 1981 and 1993. Poaching (32 percent) and disease (31 percent) are primary factors in these losses. Without suitable habitat, elk would soon disappear from Arkansas. Realizing this, state, federal and private interests have worked together to expand and improve elk habitat along the Buffalo River. Arkansas's First Elk Season Set By Game and Fish Commission

 

Arkansas Elk Hunt "Elk were once found in much of the Southeast, and there has been considerable interest in restoration of elk to their historic range. The Arkansas Game and Fish Commission, in cooperation with private citizens, began an elk restoration project in the Ozark Mountains of northwest Arkansas in 1981. From 1981 to 1985, 112 Rocky Mountain elk from Colorado and Nebraska were introduced at sites near the Buffalo National River. Since that time, the Arkansas Game and Fish Commission and the National Park Service have conducted extensive habitat improvement projects, and the population has grown to about 450 animals." "In the fall of 1998, Arkansas held its first modern-day elk hunt as part of its elk management program. SCWDS has prepared a Model Health Protocol for Importation of Wild Elk for Restoration (see SCWDS BRIEFS Vol. 13, No. 3 and Vol. 14, No. 2). The Arkansas elk hunt was an excellent opportunity to evaluate the health status of a recently established population consisting of translocated elk. " "SCWDS staff members examined and obtained samples from 17 elk. All elk examined appeared to be in good to excellent condition, and tests for diseases of major concern, i.e., chronic wasting disease, bovine tuberculosis, brucellosis, Johne's disease, and Pasteurella pneumonia, were negative. [Unfortunately, these animals were tested by histology alone, no immunohistochemistry, pers. comm Dr. Nettles 25 May 99 to webmaster]

 

Serologic evidence of exposure to bluetongue, epizootic hemorrhagic disease, and leptospirosis was detected in some animals, but clinical signs or lesions resulting from these diseases were not evident. Parasitism due to lungworms, Sarcocystis, and ectoparasites was subclinical, and there was no evidence of blood parasites such as Anaplasma. However, there was histologic evidence suggestive of previous exposure to the deer meningeal worm, Parelaphostrongylus tenuis, which suggests that many elk can overcome infection with this parasite.... "

 

Arkansas elk re-introduction: animals from high-risk states used Comment (webmaster): These elk came from high risk states at a time when CWD was first getting established in wild elk and research facilities. The state fish and game site does not disclose whether these were wild or captive elk, nor what subsequently transpired at those facilites.. The investigative pattern, as in many states, is to bow to hunters' concerns and take a look for CWD, but use the worst methods possible. In the last 6 months, Oregon and Arkansas have both opted to used methodologies from the 1970's. Yet prion monoclonals have been around for 13 years: Barry RA, Prusiner SB l. Monoclonal antibodies to the cellular and scrapie prion proteins. J Infect Dis. 1986 Sep;154(3):518-21

 

Prusiner SB et al. Acta Neuropathol (Berl) 1987;72(4):299-314 "Monoclonal antibodies to PrP 27-30, as well as antisera to PrP synthetic peptides, specifically react with both PrPC and PrPSc, establishing their relatedness."

 

Kascsak RJ, et al. Mouse polyclonal and monoclonal antibody to scrapie-associated fibril proteins. J Virol. 1987 Dec;61(12):3688-93. Affinity BioReagents in Colorado now offers: PA1-750, Polyclonal (Rabbit) Anti-Cellular Prion Protein. PA1-750 was produced by immunizing New Zealand White rabbits with a synthetic peptide (Cat. # PEP-034) corresponding to amino acid residues 90-102 of human PrP. Peptide sequence: G90 Q G G G T H N Q W N K P102 G G C. This product is for in vitro experimental use only, and is not intended for use in humans or clinical diagnosis. MA1-750, Monoclonal (Mouse) Anti-Prion Protein Monoclonal antibody F89/160.1.5 directed at ruminant prion has been licensed from USDA and is currently in the ascites production phase. They expect to have this material in IgG purification/testing by the middle of June 1999. If an evaluation at Pullman is satisfactory, it will be available at that time. At this time they are taking people's numbers so they can let them know about the antibody as soon as it's ready. {Contact: Phillip E. Schwartz, Director of Scientific Development, Affinity BioReagents, Inc.

 

Arkansas Elk Hunt Elk were once found in much of the Southeast, and there has been considerable interest in restoration of elk to their historic range.� The Arkansas Game and Fish Commission, in cooperation with private citizens, began an elk restoration project in the Ozark Mountains of northwest Arkansas in 1981.� From 1981 to 1985, 112 Rocky Mountain elk from Colorado and Nebraska were introduced at sites near the Buffalo National River.� Since that time, the Arkansas Game and Fish Commission and the National Park Service have conducted extensive habitat improvement projects, and the population has grown to about 450 animals. In the fall of 1998, Arkansas held its first modern-day elk hunt as part of its elk management program.� SCWDS has prepared a Model Health Protocol for Importation of Wild Elk for Restoration (see SCWDS BRIEFS Vol. 13, No. 3 and Vol. 14, No. 2).� The Arkansas elk hunt was an excellent opportunity to evaluate the health status of a recently established population consisting of translocated elk.�

 

SCWDS staff members examined and obtained samples from 17 elk.� All elk examined appeared to be in good to excellent condition, and tests for diseases of major concern, i.e., chronic wasting disease, bovine tuberculosis, brucellosis, Johne's disease, and Pasteurella pneumonia, were negative. {Unfortunately, these animals were tested by histology alone, pers. comm Dr. Nettles 25 May 99]� Serologic evidence of exposure to bluetongue, epizootic hemorrhagic disease, and leptospirosis was detected in some animals, but clinical signs or lesions resulting from these diseases were not evident.� Parasitism due to lungworms, Sarcocystis, and ectoparasites was subclinical, and there was no evidence of blood parasites such as Anaplasma.� However, there was histologic evidence suggestive of previous exposure to the deer meningeal worm, Parelaphostrongylus tenuis, which suggests that many elk can overcome infection with this parasite....

 

Immunohistochemistry: a superior diagnostic method Listserve. Dr.Janice Miller 28 Apr 99

 

"Veterinary Record returned the manuscript in December with reviewer comments wanting a more detailed description of the neuroanatomical PrPSc localizations. Unfortunately, we were not able to meet such a requirement because the brain samples that had been collected were not appropriate. We withdraw the paper and the senior author is now rewriting the paper for submission to a different journal." "With regard to specific information presented in the paper, it should be noted that the 17 animals examined were a selected group taken from a very large herd and the selection process was not intended to provide a valid assessment of overall CWD prevalence."

 

"The ability to detect positive brains in elk that had not yet developed clinical signs or lesions was reported several years ago using laboratory animal models of scrapie. In our 1993 and 1994 papers on the use of IHC for scrapie diagnosis in sheep, we reported finding many IHC positive brains that had been designated as only suggestive or inconclusive for scrapie by histopathological criteria. Since that time the APHIS National Veterinary Services Laboratory has been using IHC for diagnosis of TSEs."

 

"According to Drs. Linda Detwiler and Al Jenny, all brains from sheep, goats, cattle, deer, and elk with neurological disease are examined histologically and by IHC. Brains from the *downer cow* surveillance program are also examined by both tests. APHIS, with the assistance of state animal health and wildlife officials, has tested over 2,000 brain samples from free-ranging cervids in Nebraska, South Dakota, Kansas, Michigan, and New Jersey. All brains were negative for PrPSc by IHC."

 

"State diagnostic laboratories know about the availability of IHC testing at the NVSL and tissue samples from suspect cases are sent to that laboratory on a referral basis. IHC has been used routinely in the diagnostic laboratories of Colorado and Wyoming for several years so undoubtedly the 1998 prevalence report was based on that type of testing procedure."

 

Clarifications on immunohistochemical detection of preclinical CWD in captive elk Listserve. Dr.Janice Miller 13 May 99

 

The number of positive animals found (10 of 17) should not be extrapolated to represent the whole herd because it was a selected group. The full text of the article states: "Seventeen elk from a large captive herd in South Dakota were slaughtered in April, 1998. Individual members of the original herd were diagnosed with CWD in December, 1997. The owners reduced the herd in hopes of salvaging some of the animals for meat. Slaughtered elk were chosen based on young age and the likelihood that they were not yet infected. The slaughtered elk were all male, ranging in age from two to five years (9=2 years, 7=3 years, 1=5 years)."

 

"The five year old and one of the three year old elk exhibited clinical signs consistent with CWD as seen by the herdsman of the ranch. Three of the 17 elk, including the two elk with clinical signs, had histologic lesions consistent with CWD, including spongiform change of the gray matter neuropil, vacuolated neurons, and mild gliosis."

 

"Separately, a three year old aclinical animal displayed histologic lesions suggestive of CWD, including mild spongiform change in the gray matter of the medulla oblongata and cerebrum, a few vacuolated neurons, and mild gliosis in the brain stem and spinal cord. Medulla oblongata at the obex from each of the 17 elk were immunohistochemically examined for PrP-Sc according to the method of Miller and others, 1994. Tissues from 10 of the 17 elk (58.8 %) were positive."

 

This work strongly validates concerns about horizontal transmission in elk. I have heard Drs. Mike Miller and Elizabeth Williams speak many times and they always stress that the epidemiology of CWD indicates it is laterally transmitted. Dr. Williams spoke just last week here in Ames and her handout about CWD states:

 

"The mode of transmission of CWD is not known. Epidemiologic evidence strongly suggests lateral transmission occurs among deer and elk and probably from mule deer to elk and white-tailed deer. Maternal transmission may occur but does not explain many cases of CWD. Concentration of animals in captivity may facilitate transmission; however, CWD is maintained in populations of deer even at moderate to low populations densities."

 

Dr. Mike Miller's most recent publication (Epidemiology of Chronic Wasting Disease in Captive Rocky Mountain Elk, Journal of Wildlife Diseases 34:532-538, 1998), states the following:

 

"Our observations provide compelling circumstantial evidence for lateral transmission of CWD among elk. We believe the most plausible explanation for the epidemic pattern observed in this captive elk herd is animal-to-animal transmission of CWD."

 

Preclinical detection of scrapie and BSE: Papers describing detection of PrP-res in tissues without histopathologically detectable lesions: in addition to our 1993 and 1994 papers that describe this situation in sheep scrapie, there are other similar reports in the literature. One of the most thorough studies was by Bruce, et al., published in 1994 (PrP in Pathology and Pathogenesis in Scrapie-Infected Mice, Molecular Neurobiology 8:105-112). The following statement summarized the work on serial examinations of PrP accumulation:

 

"PrP changes were first seen relatively early, between a fifth and a quarter of the way through the intracerebral incubation period, depending on the model, and many weeks before the development of vacuolar degeneration. Abnormal distributions of PrP appeared at about the time that relatively protease-resistant PrP became detectable by Western blotting."

 

An earlier report by Lantos et al. also described the greater sensitivity afforded by immunohistochemistry in human prion diseases (Prion protein immunocytochemistry helps to establish the true incidence of prion diseases, Neuroscience Letters 147:67-71, 1992). The summary states:

 

"It has been reported that prion diseases may occur without the histological hallmarks of spongiform encephalopathies: vacuolation of the cerebral grey matter, neuronal loss and astrocytosis. These cases without characteristic neuropathology may go undiagnosed and consequently the true incidence of transmissible dementias is likely to have been under-estimated. Immunocytochemistry using antibodies to prion protein gives positive staining of these cases, albeit the pattern of immunostaining differs from that seen in typical forms. Accumulation of prion protein is a molecular hallmark of prion diseases, and thus a reproducible, speedy and cost-efficient immunocytochemical screening of unusual dementias may help to establish the true incidence of prion diseases."

 

A paper published last year by Wells et al. (Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update, Veterinary Record 142:103-106, 1998) describes an experiment done in the UK in which cattle were experimentally exposed orally to BSE and necropsies were conducted at periodic intervals for examination of tissues by histopathology, immunohistochemistry, and mouse bioassay. After a discussion of similar studies done earlier in sheep scrapie, the paper reports the following relative to immunohistochemistry results: "

 

Table 2 also shows the IHC and BSE fibril results from 32 months after inoculation, the time after which abnormal PrP was detected in the CNS. This change preceded the pathognomonic histopathological changes in the brain, and the onset of clinical signs, and was most consistently detected in the lumbar spinal cord." (Note: 3 cattle killed 36 months after exposure were positive by immunohistochemistry but only 1 had histopathologic lesions of BSE.)

 

On the use of immunohistochemistry by APHIS for its BSE surveillance: All *downer cow* brains collected in the collaborative study conducted by APHIS and FSIS (Food Safety and Inspection Service) are examined with this technique at the APHIS lab in Ames [note rabbit polyclonal antibody must have been used early on -- a weaker reagent] . Bovine brains from rabies suspects are submitted to state public health or animal health diagnostic laboratories and tissues from non-rabid animals are sent to Ames for the BSE examinations.

 

All veterinary pathologists should now be well aware of CWD and the need for immunohistochemistry testing. In fact, that is how the cases in captive elk in South Dakota, Nebraska, and Oklahoma were found. The last annual meeting of the American Association of Veterinary Laboratory Diagnosticians (October, 1998) featured 3 talks on CWD. Dr. Beth Williams gave an overview of the disease, Dr. D.H. Zeman described the identification of CWD in South Dakota commercial elk facilities, and Dr. Al Jenny presented results from the APHIS survey for CWD in deer (that information although it has not yet been submitted to a journal).

 

Dr. Jenny will be presenting results of the current year's survey at the next AAVLD meeting (October, 1999). These meetings are attended by representatives from every animal health diagnostic laboratory in the country, so I think it is very likely that any current and future suspect CWD cases will be referred to APHIS for immunohistochemical testing.

 

With regard to the question about whether immunohistochemistry was used in CWD surveys done in endemic areas (Colorado and Wyoming) prior to 1998, the technique has been used since 1995 (see remarks of Dr. Mike Miller in the attached USAHA report). In January of this year all of the people involved in CWD research attended a meeting in Fort Collins and Dr. Mike Miller reported on their survey results to that point in time. Everything I heard him say indicated that both the targeted and hunter-kill surveillance efforts are continuing annually in both deer and elk. The histopathology and immunohistochemistry work for these surveys is not done by Colorado Fish and Game but by Dr. Terry Spraker at the Colorado State Veterinary Diagnostic Laboratory.

 

It is true that my comments about results of the APHIS survey on wild cervids involved only deer. That is not surprising because the states where those studies were conducted do not have many (or any) elk. Dr. Jenny told me that there were a few elk brains in this year's collections from South Dakota and Nebraska and they were all negative. That data has not been tabulated and is not included in the information I cited earlier.

 

Could the immunohistochemical test to brain tissue be applied to the 12-year old cow that was in contact with CWD deer and elk at the Foothills Research Station? That would certainly be possible if paraffin blocks of the animal's brain are available. However, unless the animal showed clinical signs of a CNS problem (which apparently it didn*t) it is unlikely that brain tissue would have been collected for histopathologic examination. If such material exists, however, it could certainly be examined by Dr. Spraker at the Colorado Veterinary Diagnostic Laboratory since he is very experienced with both the histopathology of CWD and the immunohistochemistry procedure for detection of PrP.

 

Should tonsil tissue from hunters in the Fort Collins area be subjected to PrP immunohistochemical examination? Personally, I hope that clinically healthy people are not encouraged to subject themselves to a surgical procedure of that nature, because there is always a certain degree of risk involved. However, even if hunters are willing to participate in such a study, or if archived tonsillectomy samples are available, I feel it would be totally inappropriate for me to do an immunohistochemical test on a tissue and species with which I have no experience. Although I have many years of experience in applying the test to brains of ruminants, only in recent months have I begun to investigate its use on lymphoid tissues of sheep (which I find presents a much more difficult challenge with respect to interpretion of staining reactions).

 

Furthermore, we don't even know if our reagents would work on human tissue (many PrP antibodies are species specific). A laboratory that has used immunohistochemistry to detect PrP in lymphoid tissues from CJD and nvCJD patients would be more suitable.

 

TSE discussion highlights sheep and goal disease committee meeting Oct. 5, 1998 United States Animal Health Association press release

 

MINNEAPOLIS, Minn-- There is an ever-increasing focus on transmissible spongiform encephalopathies (TSEs) throughout the world -- expecially in reference to sheep and goats. Dr. Linda Detwiler with the U.S. Department of Agriculture's Animal and Plant Health Inspection Service told the USAHA committee on sheep and goats, which met here today, that one of the biggest concerns of the international sheep and goat industry is the possibility that bovine spongiform encephalopathy (BSE) exists in the native sheep and goat populations of the United Kingdom and other European countries because of exposure to BSE-contaminated meat and bone meal. BSE has been expermentally transmitted via feed to sheep, but no natural disease has been identified to date. Surveillance studies are underway in the UK to look for BSE in the sheep and goat populations there.

 

Dr. Detwiler said that because of this possibility, importation of sheep and goats into the United States has been prohibited except from Canada, Mexico, Australia and New Zealand.

 

She also said that the Organization International des Epizooties (OIE) is establishing international guidelines and standards for declaring a country free of sheep scrapie and for trade in live animals, germplasm and products with respect to this disease.

 

Dr. Diane Sutton, also with USDA-APHIS, provided the committee with an update on the scrapie program. APHIS currently addresses scrapie through two approaches: (1) a regulatory program to prevent the interstate movement of infected and high-risk animals and (2) the Voluntary Scrapie Flock Certification Program, which is designed to identify scrapie-free and reduced-risk animals. APHIS is currently drafting a proposed rule in response to a 1996 USAHA resolution and a Jan. 26, 1998, advanced notice of proposed rulemaking regarding the interstate movement of sheep and goats from states that do not quarantine scrapie-infected and source flocks.

 

APHIS is also developing a new generic data base, which is year 2000 compliant, to improve the accuracy and timeliness of information provided on the APHIS flock status web pages (www.aphis.usda.gov/vs/scrapie/).

 

Dr. Katherine O'Rourke with USDA's Agricultural Research Service told the committee that a live animal test for scrapie, described last spring, has been revised twice to improve sensitivity and specificity. She anticipates a two-year validation test involving U.S. sheep.

 

Dr. Nora Wineland with USDA-APHIS reported on a possible National Animal Health Monitoring Service national study for sheep in the year 2000. This means that a needs assessment to find the largest "information gaps" must be completed by the spring of 1999.

 

http://www.mad-cow.org/~tom/usda_downers.html#kkmm

 

 PrP genotypes of captive and free-ranging Rocky Mountain elk (Cervus elaphus nelsoni) with chronic wasting disease J Gen Virology Oct 1999 pg 2765-2769 free pdf K. I. O'Rourke, T. E. Besser, M. W. Miller, T. F. Cline, T. R. Spraker, A. L. Jenny, M. A. Wild, G. L. Zebarth and E. S. Williams

 

CWD probably arose in confined cervids as a horizontal transfer of scrapie from sheep co-housed and pastured previously at the Dept of Wildlife's Foothills Research Station in Ft. Collins, Colorado. This study looked at whether a coding polymorphism in elk (M129L) could have been responsible instead. Ironically, the polymorphism turned out to be protective. In 387 carefully sequenced elk, only this one coding polymorphism was observed. A silent change was also seen in codon 104, namely AAG to AAA. This region is not within hairpin C. (Flanking primer pairs were not used after learning a mule deer allele was not amplified; that allele is not described. ) Genotype frequencies were 0.75, 0.24, and 0.01, for met/met, met/leu, and leu/leu, ie, in approximate Hardy-Weinberg equilibrium with 12% leucine. This is not a possible frequency for a mutation that could cause disease onset in a 2 year old elk; however, it might well affect susceptibility, as seen in human CJD.

 

 

 

Met/met was signficantly over-represented in CWD-affected game farm animals at the South Dakota facility. CWD was seen in some heterozygotes (without a striking delay in onset) but not in leucine homozygotes.

 

The results are difficult to interpret. The genotype of the original infecting animal(s) is not known. Sheep of course are met/met, as are mule deer. Assuming it was met/met, then the like-like principle favors transmission to similar animals and a barrier might occur to unlike animals. This is like the situation in BSE, where met/met cows are initially infecting met/met humans instead of val/val. A leu/leu elk with CWD may eventually be found; that animal might conversely transmit better to other leu/leu animals.

 

The study did rule out "familial CWD" involving 129L viewed as a rare mutation. However, some other rare mutation, long since lost, could have initiated the epidemic. Non-coding mutations, such as upregulation alleles linked to met, could also be a factor. Other genes, such as cervid doppel, were not examined in this study.

 

The South Dakota game farm is severely impacted with 42 confirmed cases dating back to 1995, strongly suggesting horizontal efficient transmission. Leakage from this facility is of grave concern to large herds of wild elk on surrounding public and tribal lands. While no CWD was reported in pen mates or via fenceline contact in this study, a previous study has documented transfer from captive elk to wild deer across a fenceline.

 

When no CWD is detected, one always has to wonder if the incubation period was too short or whether the methods were not sensitive enough. This study used good methods for their day, but not the ultra-sensitive methods that would be used now. For that reason, negative results must be revisited and for now regarded with caution. The vastly improved detection method of the companion paper was not used: sequential tissue treatment by formic acid, protease K, hydrated autoclaving, followed by immunohistochemical staining with monoclonal antibody F89/160.1.5.

 

The Montana facility is also reported negative. Since the paper was submitted, a second elk shipped to Oklahoma was confirmed positive. The Montana Wildlife Federation has also strongly questioned testing procedures at the farm; an elk with a missing head was found.

 

The politics of CWD is explosive: it is bad enough to have the disease endemic in Rocky Mtn National Park -- to have it escape from already-controversial game farms into huge elk populations at Yellowstone NP and the Black Hill, not to mention cattle and sheep on public and private lands, is almost unthinkable.

 

Two of the authors of this paper draw their salaries primarily through the sale of Colorado elk hunting tags and a third is an employee of the game farm industry. Indeed, it is impossible to obtain necessary CWD samples without the cooperation of their host institutions. This paper however appears scientifically sound and does not exhibit much by way of overt bias.

 

http://www.mad-cow.org/oct99_sci_news.html#ddd

 

http://www.mad-cow.org/99feb_cwd_special.html#ddd

 

http://www.mad-cow.org/99feb_cwd_special.html

 

http://www.mad-cow.org/99feb_cwd_special.html#bbb

 

http://www.mad-cow.org/00/dec00_cwd.html

 

http://www.mad-cow.org/elk_cwd.html#xxx

 

Hunkering down in the APHIS BSE Situation Room 15 May 99 USDA FOIA response document, listserve discussion, webmaster opinion

 

A bizarre internal USDA publication dated October 1998 describes a James bond-type US effort to control media should the long-anticipated first case of BSE in the US be admitted. The document has become available as pdfat APHIS, making it invisible to Internet search engines. Players on the 27 member BSE Response Team are to be flown in from all over the country to a BSE Headquarters 'situation room, ' apparently an underground bunker (Unilt 41) in Riverdale, Maryland under the command of the Assistant Secretary of Marketing and Regulation, one of many "line officers" on the Team.

 

Authentic-looking press releases are already prepared and ready to go out after a few specifics have been filled in such as the name of the cow. They are spelled out in a separate document, the BSE Red Book, aka BSE Emergency Disease Guidelines, which is not available online.

 

Aphis' National Veterinary Services Laboratories (NVSL) is given the mission of activating team assembly. From the time a bovine brain sample is submitted, it takes 14-18 days to confirm a diagnosis of BSE. In the first 10-13 days, NVSL have enough information to determine the need for additional tests. If a provisional BSE diagnosis is made, the sample is 'hand-carried' (are they going to tell the airline and customs?) to the Central Veterinary Laboratory in England for confirmation, where they are expecting a 24 to 96 hour turn-around.

 

Does this mean we can get the white tiger brain analyzed by Friday despite the 22 year delay to date. Maybe we could throw in a few cougar brains from NE Colorado too.

 

A Team Member is designated to silently monitor the Internet -- for what, it doesn't say. The Freedom of Information Act request from the East Coast consumer group turned up numerous "top-secret" USDA downloads from this site and Dr. Dealler's.

 

After 24 hours of secret briefings for 'select industry and trading partners' (to allow them to take positions on the commodities markets opposite the 'non-select' industry and trading partners?), a press conference will be held the following day.

 

There are plans to trace the cow, its lineage, its herdmates, the renderer, traceout of product, buyout of herd, farm of origin, to get the state involved to quarantine the herd (pre-arranged for all 50 states), expectations for trade bans, notification of OIE within 24 hours, media 800 numbers, spokespersons and backups, notify CDC, FDA, NIH, and many other commendable activities. In short, that cow is going to be toast by the time the public first hears about it.

 

The Flow Chart is a sight to behold:

 

http://www.mad-cow.org/~tom/usda_downers.html#ccc

 

Hunkering down in the APHIS BSE Situation Room

 

FLASHBACK

 

1999

 

BSE Response Team

 

The BSE Response Team will complete the informational memorandum for the Secretary. The Team will prepare the letter to the Office of International Epizootics (OIE), the international animal health organization, for signature by the APHIS, VS Deputy Administrator. OIE requires that all countries submit official notification within 24 hours of confirming a diagnosis of BSE. The BSE Response Team and the office of the APHIS, VS Deputy Administrator would coordinate a teleconference to inform all APHIS regional directors and AVIC'S. The BSE Response Team and the office of the FSIS, OPHS Deputy Administrator would coordinate a teleconference to inform all regional and field FSIS offices. The BSE Response Team would coordinate a teleconference to notify other Federal agencies. The BSE Response Team would coordinate a teleconference to notify key industry/consumer representatives. The BSE Response Team and APHIS International Services would notify foreign embassies. The BSE Response Team would establish a toll-free 800 telephone line for industry representatives, reporters, and the public. The BSE Response Team would coordinate with APHIS Legislative and Public Affairs and USDA office of Communications to issue a press release the day the diagnosis is confirmed. The press release would announce a press conference to be held the morning after the diagnosis is confirmed......

 

THE END

 

From: Terry S. Singeltary Sr. (216-119-138-126.ipset18.wt.net)

 

Subject: Hunkering down in the APHIS BSE Situation Room...

 

Date: February 14, 2000 at 9:04 am PST

 

Subject: hunkering down in the APHIS BSE Situation Room

 

Date: Wed, 12 May 1999 01:55:54 –0800

 

From: tom

 

Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de

 

i am looking now a bizarre Oct 98 internal USDA publication describing a james bond-type US effort to control media should the long-anticipated first case of BSE in the US be admitted.

 

'Players' on the 27 member BSE Response Team are to be flown in from all over the country to a BSE Headquarters 'situation room' apparently an underground bunker in Riverdale, Maryland under the command of the Assistant Secretary of Marketing.

 

Authentic press releases are already prepared and ready to go out after a few specifics have been filled in. They are spelled out in a separate document, the BSE Red Book, aka BSE Emergency Disease Guidelines.

 

Aphis' National Veterinary Services Laboratories (NVSL) activates team assembly. From the time a bovine brain sample is submitted, it takes 14-18 days to confirm a diagnosis of BSE. In the first 10-13 days, NVSL have enough information to determine the need for additional tests. If a provisional BSE diagnosis is made, the sample is 'hand-carried' (are they going to tell the airline and customs?) to the Central Veterinary Laboratory in England for confirmation, where they are expecting a 24 to 96 hour turn-around.

 

I guess that means we can get the white tiger brain analyzed by Friday despite the 22 year delay to date. Maybe we could throw in a few cougar brains from NE Colorado too.

 

A Team Member is designated to silently monitor this listserve and www.mad-cow.org (among others) -- for what, it doesn't say. The Freedom of Information Act request from the East Coast consumer group turned up numerous top-secret USDA downloads from that site and Dealler's.

 

After 24 hours of secret briefings for 'select industry and trading partners' (to allow them to take positions on the commodities markets opposite the 'non-select' industry and trading partners?), a press conference will be held the next day.

 

There are plans to trace the cow, its lineage, its herdmates, the renderer, traceout of product, buyout of herd, farm of origin, to get the state involved to quarantine the herd (pre-arranged for all 50 states), expectations for trade bans, notification of OIE within 24 hours, media 800 numbers, spokespersons and backups, notify CDC, FDA, NIH, and many other commendable activities. The Flow Chart is a sight to behold, I will try to scan it in tomorrow.

 

In short, that cow is going to be toast by the time the public first hears about it.

 

The Plan does not speak to the scenario in which the CVL says, yes, this is bovine spongiform encephalopathy all right but it is one of your strains, not ours. Invoking their Absence of Evidence is Evidence of Absence principle, there may be no perceived need for public disclosure in this case.

 

USDA is caught completely unprepared if BSE first turns up in a US zoo animal. These animals could easily be diagnosed outside the "system" and be the subject of a publicity-seeking lab press release. I think this is a more likely scenario because the US has likely imported many thousands of zoo animals with advanced infections from Britain and France and there has been zero monitoring. Unlike with downer cows, anyone with the right colleagues can get ahold of a fallen zoo animal. Zoo animals enter the food chain in some cases after being rendered.

 

Another scenario would be some stock market speculator obtaining the Red Book and issuing a flurry of bogus but authentic-looking press releases that included bogus 800 and hacked USDA web links. The press here is so lazy and so accustomed to putting out public relation handouts as news that the objectives would be accomplished for a few hour (or days, depending on the Response Team's paralysis vis-a-vis off-flow chart events). Some people think a practise run for this happened in the Indiana case a year or two back.

 

The first case of nvCJD in an American will also be a public relations fiasco. In the dim bulb of the public mind, any American with mad cow disease would have gotten it from eating meat here. USDA has no way to prove that the victim acquired it on a three week trip to England in 1987. This will sound lame even to the press. All CJD is synonymous with mad cow disease in the public perception; the more often the different kinds are explained, the more their suspicions are aroused. The first case of nvCJD in an American will simply validate what they already know and just be viewed as an overdue admission from the government.

 

tom

 

___________________________________________________________

 

From: Terry S. Singeltary Sr. (216-119-130-102.ipset10.wt.net)

 

Subject: When a case of B.S.E. is found in the U.S/Response to Disease outbreak...'redbook'

 

Date: March 13, 2000 at 10:13 am PST

 

BSE Red Book 2.1-26

 

snip...see full text ;

 

http://www.mad-cow.org/~tom/usda_downers.html#ccc

 

http://bseusa.blogspot.com/2008/08/qualitative-analysis-of-bse-risk.html

 

>>>RE-1999-In short, that cow is going to be toast by the time the public first hears about it. <<<

 

Texas BSE Investigation Final Epidemiology Report August 2005

 

http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/bse_final_epi_report8-05.pdf

 

State-Federal Team Responds to Texas BSE Case

 

JUNE 30, 2005

 

(please note 7+ month delay in final confirmation so the BSE MRR policy could be set in stone first. $$$...tss)

 

http://www.tahc.state.tx.us/news/pr/2005/2005Jun30_BSE_Positive_Results.pdf

 

https://www.cidrap.umn.edu/cidrap/content/other/bse/news/june3005bse.html

 

SEE ATTEMPTED COVER-UP BEFORE THE END AROUND BY FONG ET AL OF THE O.I.G

 

The U.S. Department of Agriculture confirmed June 29 that genetic testing had verified bovine spongiform encephalopathy (mad cow disease) in a 12-year-old cow that was born and raised in a Texas beef cattle herd.

 

Subsequent epidemiological investigations resulted in the culling and testing of 67 adult animals from the index herd. Bio-Rad tests for BSE were conducted on all 67 animals by the National Veterinary Services Laboratory (NVSL) in Ames, Iowa. All tests were negative.

 

On July 12, Texas officials lifted the quarantine on the source herd. At press time, USDA's Animal and Plant Health Inspection Service was tracing animals of the same age that had left the ranch.

 

Timeline

 

The BSE-positive animal was a Brahman-cross cow born and raised in a single Texas herd. The location of the ranch was not disclosed.

 

On Nov. 11, 2004, the 12-year-old cow was taken to a Texas auction market. Because of its condition, the cow was sent to Champion Pet Foods in Waco, Texas. The company produces several blends of dog food, primarily for the greyhound industry.

 

On Nov. 15, the animal arrived dead at Champion. Under procedures established by USDA's intensive surveillance program, a sample was sent to the USDA-approved Texas Veterinary Medical Diagnostic Testing Laboratory (TVMDL) at Texas A&M University.

 

Between June 1, 2004, and June 1, 2005, TVMDL tested nearly 34,000 samples from Texas, New Mexico, Arkansas and Louisiana. They tested the sample from Champion on Nov. 19 using a Bio-Rad ELISA rapid test for BSE. Initial results were inconclusive.

 

Because of the inconclusive results, a representative from USDA took the entire carcass to TVMDL where it was incinerated. USDA's Animal and Plant Health Inspection Service (APHIS) began tracing the animal and herd.

 

The sample was then sent to the National Veterinary Services Laboratory for further testing. Two Immunohistochemistry (IHC) tests were conducted and both were negative for BSE. At that point APHIS stopped their trace.

 

USDA scientists also ran an additional, experimental IHC "rapid" tissue fixation test for academic purposes. This test has not been approved internationally.

 

Some abnormalities were noted in the experimental test, but because the two approved tests came back negative, the results were not reported beyond the laboratory.

 

Monitoring by OIG

 

USDA's Office of Inspector General (OIG) has been monitoring implementation of the BSE expanded surveillance program and evaluating the following:

 

* Effectiveness of the surveillance program;

 

* Performance of BSE laboratories in complying with policies and procedures for conducting tests and reporting results;

 

* Enforcement of the ban on specified risk materials in meat products;

 

* Controls to prevent central nervous system tissue in advanced meat recovery products;

 

* Ante mortem condemnation procedures; and

 

* Procedures for obtaining brain tissue samples from condemned cattle.

 

While reviewing voluminous records, OIG auditors noticed conflicting test results on one sample-rapid inconclusive, IHC negative, experimental reactive.

 

Sample retested

 

At the recommendation of the Inspector General, the sample was retested during the week of June 5 with a second confirmatory test, the Western Blot. The results were reactive.

 

USDA scientists then conducted an additional IHC confirmatory test, using different antibodies from the November 2004 test. On Friday, June 10, Secretary of Agriculture Mike Johanns publicly announced the results as a "weak positive."

 

On June 16 an official with USDA's National Veterinary Services Laboratory hand-carried samples for further testing to the Veterinary Laboratory Agency (VLA) in Weybridge, England. Since 1991, the VLA has been a BSE reference laboratory for the World Organization for Animal Health (OIE).

 

Experts from the Weybridge lab confirmed the accuracy of the results of USDA's November confirmatory IHC test, concurring that the case could not have been confirmed on the basis of this sample. They also examined the November experimental IHC test and interpreted the results to be positive.

 

Weybridge also conducted additional tests, including IHC, OIE-prescribed Western Blot, NaTTA Western Blot and Prionics Western Blot tests.

 

To better understand the conflicting results, USDA also conducted Bio-Rad and IDEXX rapid screening tests, IHC and OIE-prescribed Western Blot. USDA also used DNA sequencing to determine the prion protein gene sequence of the animal.

 

http://findarticles.com/p/articles/mi_qa5420/is_200508/ai_n21377094

 

Texas even had a 'secret' test that showed that mad cow positive; experimental IHC test results, because the test was not a validated procedure, and because the two approved IHC tests came back negative, the results were not considered to be of regulatory significance and therefore were not reported beyond the laboratory. . A Western blot test conducted the week of June 5, 2005, returned positive for BSE.

 

http://www.usda.gov/documents/vs_bse_ihctestvar.pdf

 

48 hr BSE confirmation turnaround took 7+ months to confirm this case, so the BSE MRR policy could be put into place. ...TSS

 

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

 

Subject: re-USDA's surveillance plan for BSE aka mad cow disease

 

Date: Mon, 02 May 2005 16:59:07 -0500

 

From: "Terry S. Singeltary Sr."

 

To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us

 

Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............

 

snip...

 

There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...

 

Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx

 

Date: June 14, 2005 at 1:46 pm PST

 

In Reply to:

 

Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results

 

posted by TSS on June 13, 2005 at 7:33 pm:

 

Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS

 

MAD COW IN TEXAS NOVEMBER 2004. ...TSS

 

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

 

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

Date: Mon, 22 Nov 2004 17:12:15 -0600

 

From: "Terry S. Singeltary Sr."

 

To: Carla EverettReferences: [log in to unmask]; [log in to unmask] ;

 

Greetings Carla, still hear a rumor;

 

Texas single beef cow not born in Canada no beef entered the food chain?

 

and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update?

 

I HAVE NO ACTUAL CONFIRMATION YET...

 

can you confirm??? terry

 

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

 

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

 

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

Date: Fri, 19 Nov 2004 11:38:21 -0600

 

From: Carla Everett

 

To: "Terry S. Singeltary Sr."References;[log in to unmask];

 

The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas.

 

Carla

 

At 09:44 AM 11/19/2004, you wrote:

 

Greetings Carla,

 

i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from

 

TEXAS. can you comment on this either way please?

 

thank you,

 

Terry S. Singeltary Sr

 

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

 

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

 

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

Date: Mon, 22 Nov 2004 18:33:20 -0600

 

From: Carla Everett

 

To: "Terry S. Singeltary Sr."References: <[log in to unmask]><[log in to unmask] us><[log in to unmask]> <[log in to unmask]us> <[log in to unmask]>

 

our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.

 

At 06:05 PM 11/22/2004,

 

you wrote:

 

why was the announcement on your TAHC site removed?

 

Bovine Spongiform Encephalopathy:

 

November 22: Press Release title here

 

star image More BSE information

 

terry

 

Carla Everett wrote:

 

no confirmation on the U.S.'inconclusive test...

 

no confirmation on location of animal. ;

 

FROM HERE, IT TOOK 7 MONTHS TO CONFIRM THIS MAD COW, while the BSE MRR policy was being bought and sold...(in my opinion...tss)

 

http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html

 

http://madcowtesting.blogspot.com/

 

Saturday, August 16, 2008

 

Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)

 

http://bseusa.blogspot.com/2008/08/qualitative-analysis-of-bse-risk.html

 

TEXAS OFFICIALS DEAD WRONG ON AMOUNT OF INFECTIVITY TO CAUSE A TSE PRION DISEASE ;

 

"FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds."

 

5.5 GRAMS OF INFECTIOUS PROHIBITED MAD COW FEED FOR EACH OF THE 1,222 ANIMALS (5.5 GRAMS X 1,222 ANIMALS) IS ENOUGH INFECTIOUS MAD COW FEED TO KILL A SMALL HERD OF COWS...TSS

 

U.S. Food and Drug Administration FDA News | Today the Food and Drug Administ…U.S. Food and Drug Administration FDA News

 

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle — a violation of FDA’s 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

 

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams – approximately a quarter ounce — of prohibited material. These animals weigh approximately 600 pounds.

 

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

 

According to Dr. Bernard Schwetz, FDA’s Acting Principal Deputy Commissioner, “The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture’s (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE.”

 

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

 

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

 

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

 

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

 

http://www.usmef.org/news-statistics/press-releases/us-food-and-drug-administration-fda-news-today-the-food-and-drug-administ-13375/

 

FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

 

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT

 

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

 

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

 

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

 

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

 

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

 

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

 

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

 

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

 

http://www.fda.gov/bbs/topics/news/2001/new00752.html

 

PRION 2009 CONGRESS BOOK OF ABSTRACTS

 

O.4.3

 

Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission

 

Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany

 

Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).

 

Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.

 

Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.

 

Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.

 

Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.

 

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf

 

P04.27

 

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

 

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

 

Background:

 

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

 

Aims:

 

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

 

Methods:

 

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

 

Results:

 

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

 

Conclusions:

 

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.

 

The work referenced was performed in partial fulfillment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

 

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

 

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.

 

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

 

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

 

Risk of oral infection with bovine spongiform encephalopathy agent in primates

 

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

 

snip...

 

BSE bovine brain inoculum

 

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

 

Primate (oral route)* 1/2 (50%)

 

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

 

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

 

PrPres biochemical detection

 

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

 

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

 

bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

 

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

 

Published online January 27, 2005

 

http://www.thelancet.com/journal/journal.isa

 

Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........

 

http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose

 

It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.

 

http://web.archive.org/web/20061003022720/http://www.bseinquiry.gov.uk/files/ws/s145d.pdf

 

6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.

 

http://web.archive.org/web/20061003022724/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf

 

SEE FULL TEXT OF ALL THIS HERE ;

 

2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

 

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html

 

Thursday, October 22, 2015

 

*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened ***

 

http://madcowusda.blogspot.com/2015/10/former-ag-secretary-ann-veneman-talks.html

 

Tuesday, April 19, 2016

 

Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in focal area With 82 Confirmed to Date

 

http://chronic-wasting-disease.blogspot.com/2016/04/arkansas-first-phase-of-cwd-sampling.html

 

 Friday, April 08, 2016

 

Arkansas AGFC Chronic Wasting Disease CWD TSE Prion Confirms 23 Additional Cases Total At 79 To Date

 

http://chronic-wasting-disease.blogspot.com/2016/04/arkansas-agfc-chronic-wasting-disease.html

 

Friday, April 01, 2016

 

ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION CASES EXPLODE BY 27 NEW CASES WITH 50 CASES TOTAL TO DATE

 

http://chronic-wasting-disease.blogspot.com/2016/04/arkansas-chronic-wasting-disease-cwd.html

 

Tuesday, April 12, 2016

 

The first detection of Chronic Wasting Disease (CWD) in Europe

 

http://chronic-wasting-disease.blogspot.com/2016/04/the-first-detection-of-chronic-wasting.html

 

Friday, April 22, 2016

 

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

 

http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html

 

Thursday, March 31, 2016

 

*** Chronic Wasting Disease CWD TSE Prion Roundup USA 2016 ***

 

http://chronic-wasting-disease.blogspot.com/2016/03/chronic-wasting-disease-cwd-tse-prion.html

 

Tuesday, April 19, 2016

 

Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission

 

http://madcowfeed.blogspot.com/2016/04/docket-no-fda-2013-n-0764-for-animal.html

 

Saturday, April 16, 2016

 

APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission

 

http://animalhealthreportpriontse.blogspot.com/2016/04/aphis-docket-no-aphis-2016-0029.html

 

Sunday, March 20, 2016

 

*** UPDATED MARCH 2016 URGENT Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission

 

http://chronic-wasting-disease.blogspot.com/2016/03/docket-no-fda-2003-d-0432-formerly-03d.html

 

Monday, April 11, 2016

 

*** DECLARATION OF EXTRAORDINARY EMERGENCY DUE TO A FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA ?

 

http://chronic-wasting-disease.blogspot.com/2016/04/declaration-of-extraordinary-emergency.html

 

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

 

22

 

Visits to Colorado State University, College of Veterinary Medicine and the Wyoming Game and Fish Department, Sybille Wildlife Research and Conservation Education Unit.

 

The main objective here was to obtain some understanding of CWD. A visit was made to the University of wyoming Game and Fish Department, Sybille wildlife Research and Conservation Education Unit where most of the cases of CWD have occurred. The Sybille Wildlife facility is situated some 50 miles northeast of Laramie, Wyoming through the Laramie Mountains. Here most of the hoofed big game species of North America; Hule Deer (odocoileus hemionus), Whitetail Deer (Odocoileus virginianus), Elk (Cervis canadensis) Mountain Goat (Oreamnos americana), Bighorn Sheep (0vis canadensis} and Pronghorn (Antilocapra americana) and some other wildlife species are kept in small numbers for experimental use in the investigation of wildlife diseases.

 

A colony of the blackfooted ferret (Hustela nigripes) has been established because of its imminent extinction. At present there are only 35 but it is proposed to breed up to 200 and then, probably in 1991, re-introduce them into the wild in a nation wide operation. Blackfooted ferret diet is mainly Prairie Dog (Cynoms spp.) and it is thought that the elimination of this species from large areas by poisoning campaigns in the past has been responsible for the precipitous ferret decline.

 

The buildings and pens at the facility are entirely of wooden/log construction with heavy duty wire mesh fences. Pen floors are bare earth. A long race connecting many different areas within the facility enables movement of deer and antelope between pens when necessary. There is provision for holding deer of different sizes in a custom built crush for bleeding and treatments.

 

23

 

The educational role of the unit includes school visits to provide instruction in the work of the department and to promote conservation. I was accompanied on this visit by Stuart Young and Beth Williams. on arrival I was introduced to Hughie Dawson who has managed the facility for some 20 years.

 

CWD occurred principally in two locations, this one at Sybille and in a similar facility at Fort Collins, Colorado, some 120 miles southwest. It was estimated that in total probably 60-10 cases of CWD have occurred.

 

It was difficult to gain a clear account of incidence and temporal sequence of events ( - this presumably is data awaiting publication - see below) but during the period 1981-84, 10-15 cases occurred at the Sybille facility. Recollections as to the relative total numbers of cases at each facility were confusing. Beth Williams recalled that more cases had occurred in the Colorado facility.

 

The morbidity amongst mule deer in the facilities ie. those of the natural potentially exposed group has been about 90% with 100% mortality. the age distribution of affected deer was very similar to that in ESE. The clinical duration of cases was 6-8 weeks. Mortality in CWD cases was greatest in winter months which can be very cold.

 

When the problem was fully appreciated both the Sybille and the Colorado facilities were depopulated. All cervids were culled but Pronghorn, Bighorn Sheep and Mountain goat, where present simultaneously in the facility, were retained. There have been no cases of CWD in these non cervid species.

 

A few cases continue to occur at Sybille, the last was 4 months ago.

 

24

 

An account of the occurrence of CWD at the Colorado facility was obtained from Terry spraker, Diagnostic Laboratory, CSU College of Veterinary Medicine, Fort Collins. He examined tissues from cases of CWD at the Colorado facility some time prior to Beth Williams's involvement and examination of brains which resulted in the initial diagnosis. The deer holding facilities in Colorado comprise the Colorado Division of Wildlife Research Pen, established 10 years ago and some older deer pens at the Foot Hills Campus of CSU, close to Fort Collins. Originally there were just 1-2 cases CWD/year and a total of 24 over several years. In contrast to Beth Williams recollection Terry Spraker thought more cases had‘ occurred at Sybille than in Colorado. The cull at the Colorado facility involved 20-30 clinically normal deer. Early lesions in dorsal nucleus of the vagus and olfactory cortex were found in (some) of these deer. At the time of the cull here Pronghorn was the only other hoofed species present. Bighorn sheep and Mountain Goat were introduced only one year after the cull and occupied ground where CWD had occurred. Immediately after depopulation the ground was ploughed and disinfection was carried out using ?1% NaOH. The buildings/pens were not changed. There has been no recurrence of disease at the Colorado facility since the cull.

 

25

 

Transmission Studies

 

Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases (‘’first passage by this route’’ MARKED OUT...TSS) resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. one control animal became affected, it is J believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in all of these species with the shortest incubation period in the ferret.

 

Mouse and hamster transmissions were attempted at Wyoming State Diagnostic Laboratory, Laramie and at CSU Fort Collins but were unsuccessful.

 

Also at the Wyoming State Diagnostic Laboratory, Laramie, transmission to goats was attempted. In 1984 three goats were inoculated intracerebrally with a 10% CWD brain suspension. one goat, untreated, was placed in contact with the CWD inoculated goats and three controls, housed separately, received saline intracerebrally. To date these animals remain healthy.

 

Epidemiology of CWD

 

Descriptive epidemiological data has been collected from the two wildlife facilities and a publication is in preparation.

 

The occurrence of CWD must be viewed against the context of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA viewed it as a wildlife problem and consequently not their province! Thus

 

26

 

there have been no specific epidemiological studies, other than information gained from noting the occurrence of cases. Because of the relatively short term nature of the programmed research at the facilities it has not been possible to keep Mule Deer under the appropriate experimental circumstances or for sufficient periods to establish horizontal or maternal transmission. Beth Williams is of the view that the occurrence of CWD at Sybille is entirely related to propagative spread by contagion. Investigations have failed to identify any common source of infection and the incident has presented a protracted time course with sporadic cases throughout. There is no evidence that wild born deer were responsible for introduction of the disease to the facility.

 

I asked Hughie Dawson about the nutritional aspects of the deer kept at Sybille. Mule Deer calves are reared on condensed milk and homogenised or pasteurised domestic cow's milk from birth to 1 month or to 6 months. some would be given "Lamb milk replacer" which has a higher butter fat content than either of the former products, but is derived also from domestic cow's milk. It was thought that at the Colorado facility calves would receive only "evaporated milk". Calves are weaned on to a pelletted feed containing corn, wheat bran and linseed meal with no crude mineral suppliment. Salt licks ("sulphur blocks") which have a specific mineral composition are supplied.

 

CWD has occurred or is suspected to have occurred in establishments supplied with Mule Deer from the Colorado facility. In some cases evidence for this is tenuous. For example, it is understood that Denver zoo state that "they have not had cases of CWD" and yet they have had cases of Mule Deer succumbing to a chronic wasting disorder which was not diagnosed. A case of CWD occurred in a Mule Deer in Toronto zoo in 1976. The animal in

 

27

 

question came from Denver zoo but was originally from the Colorado wildlife facility.

 

Pathology of CWD

 

A paper (Williams et al) is in preparation on the distribution of brain lesions in CWD. Vacuolar changes occur predominantly in the dorsal nucleus of the vagus nerve (this nucleus is invariably affected), the hypothalamus and the olfactory cortex with occasional vacuolation of the olfactory tract white matter.

 

Cerebellar lesions are sometimes present but there are very few changes in the spinal cord which probably accounts for the rarity of ataxia clinically. As in sheep scrapie the hypothalamic lesions correlate with the common clinical occurrence of polydipsia. Beth Williams is aware of occasional neuronal vacuoles occurring in the red nucleus of clinically normal deer! Spraker has added that he has experienced vacuoles in neurons of Gasserian ganglia and at the level of the obex in normal deer.

 

It has never been reported but Pat Merz carried out SAF detection on CWD brain material. Work may be undertaken with NIH on the immunohistological demonstration of PrP in sections but to date there has been no PrP work.

 

Does CWD occur in free-living cervids?

 

There is some, mostly circumstantial, evidence that CWD occurs in free-living cervids but to what extent, if at all, this represents an established reservoir of infection in the wild is not known.

 

At Sybille two Mule Deer orphans (wild caught) and a White—tail Deer (Odocoileus virginianus) hybrid developed clinical signs when only 2 1/2 years of age.

 

28

 

An Elk (Cervus canadensis) wild caught as an adult, presumed 2 years old, developed signs when 3-4 years old.

 

Another group of elk, wild caught 400 miles from the facility, with an age range 2-8 years, old subsequently developed the disease in the facility (?period of captivity). The location of capture relative to the facility did not apparently rule out that they may have at some time had fence-line nose contact with animals in the facility!

 

Cases have also occurred in Mule Deer that were obtained from the wild within one hour of birth but these were never kept completely isolated through to maturity.

 

Also at Sybille there has been one case of CWD diagnosed in a free ranging Elk. It was killed in Sybille Canyon 3 miles from the facility. It could have had fence-line contact with captive Mule Deer in the facility.

 

Similar incidents had occurred in Colorado. In 1985 a free-ranging affected Elk was caught in the Rocky Mountain National Park within a 2 mile radius of the Colorado Division of Wildlife Research Pen. In 1986 and again in 1987 a single affected Mule Deer on each occasion was caught within a 5 mile radius of the Pen. These latter cases occurred within 2 years of the -cervid cull at the Pen (?1985). Brain tissue from the free—ranging Elk brain was inoculated into mice but for some reason these were kept for only 6 months and then the experiment was abandoned.

 

A specific exercise has been carried out by Beth Williams with the Wyoming State Diagnostic Laboratory and Fish Department to sample the brains of healthy wild Mule Deer for histological examination. On two separate occasions the first in 1985 and again in 1987 a total of 150 Mule Deer

 

29

 

brains were collected from areas of, and ajacent to, Sybille Canyon. These deer would have been shot under a game permit by local hunters. As they were brought down from the hills to the Game station for the mandatory registration of the kill the heads were removed and ages estimated. Most were 2-5 year old with a few 6 year old. For obvious reasons hunters were reluctant to give up stag heads. Thus, but for 15-20 brains from stags, examinations were on brains from females. No evidence of CWD lesions was found in any of these brains. However, it was considered that sporadic cases of CWD, should they occur in the wild population, would soon become separated from the herd and fall prey to coyotes (Canis latrans).

 

The possibility of any reservoir of infection in wild cervids originating from scrapie in domestic sheep flocks seems remote. Scrapie has been recorded in only three flocks in Wyoming since 1947 and Beth Williams could recall only one previous occurrence in 1966. This had involved a Suffolk flock close to the border with Nebraska. However, there has been one new confirmed and a suspected affected flock this year in Wyoming. In the latter a ewe bought—in from an Illinois flock is incriminated.

 

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 about 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. Whether they were scrapie infected sheep or not is unclear. There were domestic sheep and goats present in the facility also in the 1960's but there is no evidence that these animals developed scrapie. During the 60's hybridization studies between the Bighorn and domestic sheep were carried

 

30

 

out, again, without evidence of scrapie. Domestic goats were also kept at Sybille in the 1960's.

 

Spraker considers that the nasal route is responsible for transmission of CWD through nose to nose contact, which may well occur also between captive and free—living individuals.

 

In domestic cattle of which about 15-20 adults were necropsied per year at the Diagnostic Laboratory, CSU., Spraker had not encountered any lesions suggesting BSE. Polioencephalomalacia (PEM) and Encephalic Listeriosis were the most common morphologic neuropathological diagnoses. No bovine rabies was seen.

 

31

 

Appendix I

 

VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE

 

Dr Clark lately of the Scrapie Research Unit, Mission Texas has I successfully transmitted ovine and caprine Scrapie to cattle. The experimental results have not been published but there are plans to do this. This work was initiated in 1978. A summary of it is:-

 

Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a 2nd Suffolk scrapie passage:- i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.

 

1/6 went down after 48 months with a scrapie/BS2-like disease.

 

Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus 2/6 went down similarly after 36 months.

 

Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.

 

Diagnosis in A, B, C was by histopath. No reports on SAF were given.

 

2. Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally— (and naturally) infected sheep by ET. He had found difficulty in obtaining embryos from naturally infected sheep (cf SPA).

 

3. Prof. A Robertson gave a brief accout of BSE. The us approach was to

 

32

 

accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in USA.

 

4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.

 

5. Scrapie agent was reported to have been isolated from a solitary fetus.

 

6. A western blotting diagnostic technique (? on PrP) shows some promise.

 

7. Results of a questionnaire sent to 33 states on" the subject of the national sheep scrapie programme survey indicated

 

17/33 wished to drop it

 

6/33 wished to develop it

 

8/33 had few sheep and were neutral

 

Information obtained from Dr Wrathall‘s notes of a meeting of the U.S. Animal Health Association at Little Rock, Arkansas Nov. 1988.

 

33

 

snip...see full text ;

 

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

 

3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...

 

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

 

PL1

 

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

 

Claudio Soto

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

see ;

 

with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion. see ;

 

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

 

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

 

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

 

see ;

 

http://www.tandfonline.com/doi/pdf/10.4161/pri.28467

 

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.

 

https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson%20et%20al%20prions%20in%20soil.pdf

 

tse prion soil

 

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf

 

http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217

 

http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4

 

Wednesday, December 16, 2015

 

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

 

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

 

The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf

 

>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<

 

Fate of Prions in Soil: A Review

 

Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*

 

Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160281/

 

P.161: Prion soil binding may explain efficient horizontal CWD transmission

 

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

 

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

 

Wednesday, December 16, 2015

 

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

 

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

 

Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1

 

1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK

 

Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.

 

snip...

 

Discussion

 

Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).

 

Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.

 

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.

 

PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.

 

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.

 

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

 

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

 

Wednesday, December 16, 2015

 

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

 

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

 

Circulation of prions within dust on a scrapie affected farm

 

Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben C Maddison2*

 

Abstract

 

Prion diseases are fatal neurological disorders that affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk are contagious prion diseases where environmental reservoirs have a direct link to the transmission of disease. Using protein misfolding cyclic amplification we demonstrate that scrapie PrPSc can be detected within circulating dusts that are present on a farm that is naturally contaminated with sheep scrapie. The presence of infectious scrapie within airborne dusts may represent a possible route of infection and illustrates the difficulties that may be associated with the effective decontamination of such scrapie affected premises.

 

snip...

 

Discussion

 

We present biochemical data illustrating the airborne movement of scrapie containing material within a contaminated farm environment. We were able to detect scrapie PrPSc within extracts from dusts collected over a 70 day period, in the absence of any sheep activity. We were also able to detect scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m distance away from the scrapie contaminated buildings, suggesting that the chance of contamination of pasture by scrapie contaminated dusts decreases with distance from contaminated farm buildings. PrPSc amplification by sPMCA has been shown to correlate with infectivity and amplified products have been shown to be infectious [14,15]. These experiments illustrate the potential for low dose scrapie infectivity to be present within such samples. We estimate low ng levels of scrapie positive brain equivalent were deposited per m2 over 70 days, in a barn previously occupied by sheep affected with scrapie. This movement of dusts and the accumulation of low levels of scrapie infectivity within this environment may in part explain previous observations where despite stringent pen decontamination regimens healthy lambs still became scrapie infected after apparent exposure from their environment alone [16]. The presence of sPMCA seeding activity and by inference, infectious prions within dusts, and their potential for airborne dissemination is highly novel and may have implications for the spread of scrapie within infected premises. The low level circulation and accumulation of scrapie prion containing dust material within the farm environment will likely impede the efficient decontamination of such scrapie contaminated buildings unless all possible reservoirs of dust are removed. Scrapie containing dusts could possibly infect animals during feeding and drinking, and respiratory and conjunctival routes may also be involved. It has been demonstrated that scrapie can be efficiently transmitted via the nasal route in sheep [17], as is also the case for CWD in both murine models and in white tailed deer [18-20].

 

The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf

 

Saturday, April 16, 2016

 

APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission

 

http://animalhealthreportpriontse.blogspot.com/2016/04/aphis-docket-no-aphis-2016-0029.html

 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations 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.

 

======

 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

31 Jan 2015 at 20:14 GMT

 

see Singeltary comment ;

 

http://www.plosone.org/annotation/listThread.action?root=85351

 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 

http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143

 

*** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.

 

*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

 

*** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

see page 176 of 201 pages...tss

 

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf

 

Saturday, April 16, 2016

 

APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission

 

http://animalhealthreportpriontse.blogspot.com/2016/04/aphis-docket-no-aphis-2016-0029.html

 

Sunday, May 1, 2016

 

Center for Biologics Evaluation and Research 25th Meeting of: The Transmissible Spongiform Encephalopathies Advisory Committee June 1, 2015 Transcript

 

AND DRUG ADMINISTRATION

 

http://tseac.blogspot.com/2016/05/center-for-biologics-evaluation-and.html

 

Saturday, April 23, 2016

 

v-CJD prion distribution in the tissues of patients at preclinical and clinical stage of the disease PRION 2016 TOKYO

 

http://vcjd.blogspot.com/2016/04/v-cjd-prion-distribution-in-tissues-of.html

 

Saturday, April 23, 2016

 

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

 

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

 

http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html

 

Monday, May 02, 2016

 

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

 

http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html

 

Sunday, May 1, 2016

 

Center for Biologics Evaluation and Research 25th Meeting of: The Transmissible Spongiform Encephalopathies Advisory Committee June 1, 2015 Transcript

 

AND DRUG ADMINISTRATION

 

http://tseac.blogspot.com/2016/05/center-for-biologics-evaluation-and.html

 

*** 2001 FDA CJD TSE Prion Singeltary Submission ***

 

http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf

 

I asked someone recently, what sort of hunting legacy do you want to leave your children, did you want to have where all you have are blind, slobbering, drooling, stumbling, or maybe even healthy looking subclinical cwd infected cervid, to go on and expose who knows what (cause cwd is spreading, it has mutated, and nobody can stop it so far), but is this what we want to leave our children? the only answer I ever seem to get from anyone in the industry, is just let cwd take care of itself. well hell, how is that working for us so far?

 

this cwd tse prion must be stopped. the vertical and lateral transmission of this cwd tse prion agent amongst cervids, if cwd jumps species (if it has not already), and transmits the same ways vertical and lateral in other species, and the other species are as susceptible from so many different routes and sources, simply put, we’re screwed. just saying. I am not trying to scare anyone, I am simply presenting the facts, you must make your own decision or not. we have ignored these tse prion disease way too long.

 

these blogs are for educational use. I do not advertise or make money from them.

 

MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget, and never let them forget...

 

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