Tuesday, August 26, 2014

Pennsylvania 'Unprecedented' level of chronic wasting disease found on Reynoldsville farm

'Unprecedented' level of chronic wasting disease found on Reynoldsville farm
By Bob Frye Monday, Aug. 25, 2014, 6:51 p.m. Updated less than a minute ago
Researchers from around the country are getting to study chronic wasting disease because of an “unprecedented” find.
Officials with the Pennsylvania Department of Agriculture announced in April that a 5-year-old captive deer on a farm in Reynoldsville, Jefferson County, tested positive for the disease. Subsequent testing of the deer on the farm found six more with CWD.
That doubled the number of cases in the state, which now stands at 14.
“This is an unprecedented level of infection in a captive deer herd,” agriculture secretary George Greig said.
Sunday, August 24, 2014
USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program Goals TSE PRION October 17 – 23, 2013
Thursday, July 31, 2014
Pennsylvania Helps State and National Researchers Combat Chronic Wasting Disease
Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.
Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?
Tuesday, July 01, 2014
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape
Wednesday, November 14, 2012
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Saturday, June 29, 2013
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania
Sunday, January 06, 2013
*** "it‘s no longer its business.”
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” ...page 26.
Saturday, February 04, 2012
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month.
*** Two of the six fawns with CWD detected were 5 to 6 months old.
All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.
Saturday, February 04, 2012
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
Infectious agent of sheep scrapie may persist in the environment for at least 16 years
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
Survival and Limited Spread of TSE Infectivity after Burial
Sunday, September 01, 2013
hunting over gut piles and CWD TSE prion disease
Sunday, April 13, 2014
Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer
Environmental Geochemistry and Health
Monday, June 18, 2012
natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red deer crossbreeds captive Korea and Experimental oral transmission to red deer (Cervus elaphus elaphus)
spreading cwd around...tss
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.
***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.
spreading cwd around...tss
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.
On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.
Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.
Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.
Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.
In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.
: Corresponding author: Dr. Hyun-Joo Sohn (+82-31-467-1867, E-mail: shonhj@korea.kr) 2011 Pre-congress Workshop: TSEs in animals and their environment 5
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
snip...see more here ;
Wednesday, July 23, 2014
After the storm? UK blood safety and the risk of variant Creutzfeldt-Jakob Disease
never say never when it comes to TSE prion disease.
85%+ of all human TSE prion disease i.e. sporadic CJD’s, have never been proven scientifically to be of any spontaneous nature. not one single case. sporadic CJDs simply mean unknown to date.
all iatrogenic CJD is, is sporadic cjd, until route and source of said iatrogenic event took place, documented, and put in the academic/public domain, and that vary rarely happens. any human TSE from any other species might just look like any of the sub-types of the sporadic CJD’s. there has already been documentation of other animals TSE prion disease related very closely to some sub-types of CJD, i.e. atypical BSE, Scrapie, and atypical Nor-98 Scrapie.
please remember what was said long ago by one of the top prion Gods ;
> In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong.
From: "Belay, Ermias"
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
MY point, if there was a horizontal lateral transmission possibility from animal to man, with the surveillance for both human and animal TSE prion disease in the USA, in my honest opinion, they would never know it, and the only few cases that have been documented, could be a direct result of horizonatl lateral transmission, or not, just a happenstance of bad luck, a chance happening. so, in my opinion, we cannot rule anything out.
the USA does not even test cats or dogs for TSE prion disease, and they have been used in pet food, along with other animal carcasses. in fact, it is still legal to take a deer from a cwd endemic area, and use it in animal feed. only thing you cannot use, is a CWD positive deer. don’t believe me, see ;
> 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.
but, when felines get a TSE prion disease, it’s Feline Spongiform Encephalopathy i.e. FSE, there is one documented case of sporadic CJD in a man and his cat. ...just saying.
Research letters Volume 352, Number 9134 3 October 1998
Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy
We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.
This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2 Taken together, our data suggest that the same agent strain of sporadic CJD was involved in the patient and in his cat.
It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source, or the chance occurrence of two sporadic forms.
Terry S. Singeltary Sr. wrote:
Greetings list members,
ODD that some FELINE in Italy seem to have this same or maybe very similar phenotype of TSE;
In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.
Case‐to‐case transmission in humans: case reports and series in which spread through everyday human contact is suggested
There are six reports in which this possible mode of transmission is considered. The most recent is that of a couple from the USA who had been married for 30 years.47 The husband died at age 53. He had no relevant family history, but had had a rotator cuff repair one year before disease onset. His wife developed symptoms four and half years after her husband's death. She was morbidly obese and had had a previous hysterectomy, hernia repair and cholecystectomy. Both occasionally ate brains in the form of ‘kizka’, a type of sausage.
Immunocytochemistry confirmed pathogenic prion protein deposition in brain tissue from both husband and wife. Full sequencing of the open reading frame of the PRNP failed to demonstrate any pathogenic mutations.
Another suspected conjugal case has recently been shown not to be CJD. The histopathological specimens did not stain for prion protein despite the microscopic appearance of spongiform change.48
Sporadic CJD has been described in two co‐workers who shared a school wing for 9 months.49 The first was a 48‐year‐old Californian‐born man of Hispanic American descent who had had a traumatic leg amputation at age 23, but was otherwise well. The second was a 48‐year‐old Chilean‐born male who had a blood transfusion 6 months before onset of symptoms, and was known to eat lambs' brains. The first patient developed symptoms 5 months after the last contact with his colleague and was confirmed to have spCJD 2 months after this. The second patient developed symptoms months later and died 9 months after the last contact with his colleague.
An English woman, who died of CJD, histologically confirmed at post mortem, was known to have contact with several affected members of a family with familial CJD and was related to them by marriage.39 She had known one of the family, who later died of CJD and had afternoon tea with her at family gatherings, twice a year, for 20 years, as well as visiting in her final illness. The woman herself died 12 years later.
There is another similar case of probable CJD, reported in a Chilean woman who died 13 years after contact with a family with familial CJD. No details of contact are given.
A third case of death from CJD in someone related in marriage to a family with familial CJD has been reported in France, in a Tunisian family. No details are given with regards to family history or contact.21
What is notable about these last three incidents of supposed infection by social contact is that all have occurred in association with familial CJD. Although these patients were not known to have been genetically related to their spouses, the possibility that they came from the same gene pool cannot be dismissed.
Simultaneous Onset of Alzheimer's Disease in a Husband and Wife in Their Mid Fifties: What do We Really Know?
NEUROLOGY 1998;50:684-688 © 1998 American Academy of Neurology
Creutzfeldt-Jakob disease in a husband and wife
A 53-year-old man died of sporadic Creutzfeldt-Jakob disease (CJD) after a 1.5-year clinical course. Four and a half years later, his then 55-year-old widow died from CJD after a 1-month illness. Both patients had typical clinical and neuropathologic features of the disease, and pathognomonic proteinase-resistant amyloid protein ("prion" protein, or PrP) was present in both brains. Neither patient had a family history of neurologic disease, and molecular genetic analysis of their PrP genes was normal. No medical, surgical, or dietary antecedent of CJD was identified; therefore, we are left with the unanswerable alternatives of human-to-human transmission or the chance occurrence of sporadic CJD in a husband and wife.
Received May 5, 1997. Accepted in final form September 10, 1997.
for anyone interested, please see ;
*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.
*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
Monday, March 26, 2012
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets? ***
Sunday, November 10, 2013
kind regards, terry




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