Saturday, September 30, 2017

Norway, CWD TSE Prion, Humans, Zoonosis, Fortsatt lite sannsynlig at mennesker kan smittes av skrantesyke?

Hygiene og smittestoffer

Fortsatt lite sannsynlig at mennesker kan smittes av skrantesyke

Rapportnr: 2017: 26

Bestilt: 10.07.2017

Publisert: 29.09.2017

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Det er fortsatt liten sannsynlighet for at mennesker kan bli smittet av skrantesyke hos hjortedyr.

Det stadfester Vitenskapskomiteen for mattrygghet (VKM) i en ny uttalelse om skrantesyke, som er gjort på oppdrag fra Mattilsynet og Miljødirektoratet.

Ifølge to rapporter publisert av VKM i 2016 og 2017, er det aldri påvist sykdom forårsaket av skrantesyke (CWD, Chronic Wasting Diease) hos mennesker. Begge vurderingene konkluderer med at det er svært liten sannsynlighet for at smittestoffet som finnes i skrantesyke kan overføres til mennesker.

Etter at VKM publiserte sin andre rapport i mars 2017, la flere kanadiske og amerikanske nettsider ut informasjon om resultater av et forskningsprosjekt om skrantesyke hos aper. Mattilsynet og Miljødirektoratet ønsket en uttalelse fra VKM om disse eller eventuelt andre nye opplysninger endrer noen av konklusjonene i tidligere risikovurderingene fra VKM.

En prosjektgruppe i VKM har vurdert ny informasjon og stadfestet at den ikke endrer konklusjoner i våre tidligere risikovurderinger av skrantesyke. 


Main message: There is still little likelihood that humans may be infected with scurvy in deer animals.

It will convene the Scientific Committee on Food Safety (VKM) in a new statement on blunt disease, commissioned by the Norwegian Food Safety Authority and the Environment Directorate.

According to two reports published by VKM in 2016 and 2017, there has never been a disease of CWD, Chronic Wasting Diease in humans. Both assessments conclude that there is very little likelihood that the infectious agent found in scratch sickness can be transmitted to humans.

After VKM published its second report in March 2017, several Canadian and U.S. web sites published information about the results of a research project on scanty disease in monkeys. The Norwegian Food Safety Authority and the Norwegian Environmental Protection Agency requested a statement from VKM if these or any other new information changes some of the conclusions in previous risk assessments from VKM.

A project group in VKM has reviewed new information and confirmed that it does not change the conclusions of our previous risk assessments of scratch sickness.


Background and terms of reference as provided by the Norwegian Food Safety Authority/ Norwegian Environment Agency

Regarding the risk assessments on CWD (Phase1 and Phase2).

Canadian and American websites have published information about the results of a research project on experimental transmission of CWD to macaques. Links as follows:

The Norwegian Food Safety Authority and the Norwegian Environment Agency want a statement from VKM whether these or any other new information changes any of the conclusions in the risk assessments from VKM. 

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VKM Report 2017: 26 6

Literature and new data

Articles referring to the new studies were provided byt the Norwegian Food Safety Authority and the Norwegian Environment Agency and are listed in the references. A phone conference between Stefanie Czub, head of the virology department at the Canadian Food Inspection Agency (CFIA) and Michael Tranulis was held 28th August to further clarify the results of the study presented earlier this year (Czub, 2017). Findings in new studies

At the international prion conference held in Edinburgh, Scotland May 23-26, 2017, Dr. Stefanie Czub, head of the virology department at the Canadian Food Inspection Agency (CFIA), presented a progress report from a study initiated in 2009 (Czub, 2017). Although preliminary, the data reported were of great significance, since for the first time it was shown that CWD prions could, after experimental transmission, give rise to prion disease in Cynomolgus macaques (Macaca fascicularis), which is the closest relative to humans allowed for such transmission studies.

The study included 21 female macaques, 2.5 years old when recruited. All animals were of Mauritian origin and wild-type PRNP genotype, homozygous for Met at codon 129. Cynomolgus macaques from Mauritius are prone to development of type 2 diabetes (T2D), which particularly affects females. This feature of the animals was not taken into account when the present study was designed (Personal communication, Stefanie Czub). Several of the animals in the study have developed T2D of varying severity. Importantly, some of the features of this disease, such as weight loss is difficult to discriminate from the wasting seen in clinical CWD. Related to this, is the question of whether T2D could increase the susceptibility to CWD. Dysregulation of insulin signaling can increase neuronal vulnerability to different stressors. The putative importance of this for the results of this study is unknown and mentioned here for background purposes.

The principal objective of the study was to investigate the zoonotic potential of CWD. In order to achieve this, 18 animals were challenged with infectious material by four different routes: intracranial inoculation (8), oral (5), skin scarification (2) and through intravenous blood transfusion (3). Three animals were inoculated with non-infected material, serving as mock-infected controls.

Infectious material (inocula) were derived from two principal sources, namely CWD-positive brain or muscle tissue from preclinical white tailed deer (Odocoileus virginianus) and a brainpool from three cases of clinical CWD in wapiti (Cervus Canadensis). Infectious material for blood transfusion was derived from non-clinical CWD infected macaques. 

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VKM Report 2017: 26 7

By the time the preliminary data were presented 11 animals had been sacrificed, one of which was a mock-inoculated control. Of the other 10 sacrificed animals, six were infected intracranially and four by the oral route. From this group of 10 animals, analyses were sufficiently complete for five animals: two from the intracranial group and three from the orally infected group. During presentation of the data, the focus was on these five animals. For the remaining five animals, the analyses are in progress (Personal communication, Stefanie Czub).

All five animals had prion specific histopathological changes, with accumulation of PrPSc deposits and/or amyloid seeding activity (RT-QuIC positive) in samples from brain and/or spinal cord. Thus, there could be no doubt that the animals had developed or were in the process of developing prion disease.

One of the animals (ID AU389) had been inoculated intracranially with CWD-positive brain tissue from wapiti and developed ataxia, anxiety, tremor and a wasting syndrome. This animal was sacrificed 4.5 years after inoculation due to the clinical symptoms. It tested positive on all diagnostic tests for prion disease (IHC and RT-QuIC). It was also shown that this animal suffered from T2D. The second animal in the intracranially infected group (AU519) was sacrificed according to experimental plan, 5.2 years after inoculation and was clinically healthy. This animal had been inoculated with CWD-positive brain material from white tailed deer and it tested positive for prion disease on all tests.

Two of the animals that were orally infected (AU501, AU385) developed ataxia, tremor, apathy and wasting to varying degrees and initially very subtle. These two animals had been fed raw (?) meat from white tailed deer that were in the preclinical stage of CWD. These animals were from a flock of farmed deer that was stamped out due to occurrence of CWD. A total dose of 5 kg meat was given to the animals over a period of two years, with approximate doses of 200 gram per month. They were sacrificed 5.4 (AU501) and 6.3 (AU385) years after their primary inoculation. Both animals tested positive on all tests for prion disease. One of the animals (AU385) suffered from T2D.

The last animal (AU467) had been orally infected with brain material from white tailed deer and this animal died during anesthesia, 5.9 years after inoculation, without previous display of clinical symptoms. It tested positive on all tests for prion disease.

The presented results are remarkable for the following reasons:

1. For the first time it is shown that Macaque monkeys are susceptible to CWD, through both the intracranial and oral route of inoculation.

2. CWD inocula were from different species (white tailed deer and wapiti) and analysis of these indicated the presence of different CWD strains/types. The brain pool derived from three cases of CWD in wapiti was shown to be the CWD2 strain. The brain inoculum derived from the clinical case of CWD in white tailed deer was shown to the be heterogenic, consisting of two distinct CWD strains, demonstrating the co-

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VKM Report 2017: 26 8

occurrence of CWD strains in a single diseased animal, as has previously been observed also in sheep scrapie (Masujin et al 2009, Arch Virol).

3. Incubation periods were relatively short. For comparison: Intracerebral inoculation of classical scrapie (see below) resulted in disease in a macaque after a 10-year incubation period (Comoy et al., 2015). A single oral dose of 5 grams of BSE infected material results in 100 % attack rate in macaques with a median incubation period of 4.7 years (Holznagel et al., 2013).

4. Oral challenge of two macaques with meat derived from CWD positive but preclinical white tailed deer, resulted in prion disease with only marginally longer incubation period than intracranial injection. This experiment was specifically designed to mimic a real-life human exposure to CWD through intake of venison.

It will take several years for the study to be finalized with all downstream analyses. Another investigation (Race et al., 2014) observed that cynomolgus macaques did not develop CWD after intracranial (six animals) or oral (eight animals) inoculation. Animals were observed for more than 10 years after inoculations. The reasons for the discrepancies between this that study and the ongoing study discussed above are incompletely clarified and re-analysis of some of the materials derived from the study by Race et al is ongoing (Personal communication Stefanie Czub). For instance, the spinal cord must be carefully investigated and analysis of “prion converting activity” as assessed by RT-QuIC or equivalent would increase the sensitivity of analysis. The outcome of these studies will be published in due course.

Update on Norwegian situation

By 20. September 2017, a total of 4200 wild reindeer have been examined for CWD. Six of those (0,14%) tested positive, of which only one showed clinical symptoms of CWD. In three cases, the CWD agent was detected both in brain tissue and in lymphatic samples. Interestingly, brain samples from the other three animals (all tested in 2017) were negative, whereas lymphatic tissues were positive. This is not unexpected, as classical CWD is characterized by a prolonged asymptomatic incubation period, during which the agent may be detected in peripheral tissues including lymph nodes, and even in blood, prior to its detection in the CNS. It is important to realize that meat from such animals, as well as from their counterparts with clinical CWD, may represent a source for human exposure. In our previous opinion (VKM, 2017), we emphasized that “absence of clinical illness does not preclude human exposure, since cervids may harbour and shed the CWD agent for several months prior to onset of their symptoms”. Thus, the findings in 2017 does not alter our conclusions. 

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VKM Report 2017: 26 9

Data from the ongoing surveillance of Norwegian cervids are frequently updated on the webpages of the Norwegian Veterinary Institute;

Uncertainties/data gaps

A growing body of scientific literature critically assessing the validity of animal experimentation generally, raises important concerns about the reliability and predictive value for human outcomes (Akhtar, 2015). Although the oral challenge experiments described above were specifically designed to resemble a real-life human exposure to CWD through intake of venison, there are considerable difficulties of reproducing the complexity of human diseases in animal models.

It is notable that the macaques were fed raw venison, while human consumption is restricted to cooked meat, although rare or medium steaks are preferred by many consumer. This, however, does not alter the conclusion since the prions retain their infectivity after exposure to the temperatures normally used in food preparation (Rutala, Weber, & Society for Healthcare Epidemiology of, 2010).

It needs to be underlined, that the results obtained from the experiments conducted by Czub et al. are preliminary data presented as a progress report from an ongoing study that will require several years to complete, including a number of additional analyses. The results have not yet been peer-reviewed and published.

It is also worth mentioning that a previous study failed to infect macaques orally after being observed for more than ten years post-inoculation (Race et al., 2014). As stated in the preceding section, some of the materials derived from that stydu are now subject to reanalysis using more sensitive techniques.

Moreover, in North America, human exposure to the agent via consumption of venison in the enzootic areas is well documented (Sigurdson, 2008). Data accrued to date provide no evidence of CWD causing disease in humans, despite a substantial consumption of meat from CWD-infected deer over several decades, and the large number of hunters being exposed to the agent through contact with infected deer. This, however, does not preclude that cases of human CWD may appear, given a sufficient incubation period and exposure frequency. Hence, the importance of reinforced surveillance and vigilance regarding Creutzfeldt-Jakob disease (CJD) suspect cases should be emphasized, including characterization of CJD subtypes using analyses enabling identification of CWD. It is important to realize that the clinical presentation of human CWD is unknown and may differ from CJD as well as from classical CWD in cervids. 

16-105 final VKM Report 2017: 26 10


The progress report by Czub and collaborators underlines that in prion diseases, the species barrier for disease transmission is rarely, if ever, absolute. Comoy and co-workers also showed this, when demonstrating that a case of natural classical scrapie in sheep could be transmitted to cynomolgus macaques by intra-cranial inoculation, after a 10-year incubation period (Comoy et al., 2015). This observation has not led to reassessment of the zoonotic risk of classical scrapie in sheep.

The uncertainty related to incomplete species barriers was carefully assessed in two previous VKM opinions, which concluded that the zoonotic potential is considered very low (VKM, 2016, 2017). The term “very low” was defined as “very rare but cannot be excluded. Furthermore, the released data illustrate another aspect of CWD that was also discussed by VKM namely that infected animals can harbor significant levels of infectious prions in musculature while still appearing clinically healthy. According to Czub (Personal communication), this is particularly prominent in white tailed deer CWD and less so in wapiti CWD, in which levels of infectivity in peripheral organs seems somewhat lower. The data emerging from Norwegian cases of CWD in reindeer, although limited, indicate that this CWD strain is lymphotrophic, with significant involvement of peripheral lymphoid organs during the preclinical phase of disease. This is based on the observation of cases in reindeer with positive findings in lymph nodes while still negative/or very weak signals in the brain. These findings are in line with data from CWD in white tailed deer. Therefore, until investigated with sensitive methods, it should be considered likely that CWD infectivity is present also in reindeer musculature even at the preclinical stage of disease. Consequently, removal of the head and/or spinal cord may be a less effective measure for reducing human exposure for CWD prions than for other prion diseases.

The susceptibility of macaques to CWD after oral challenge with meat derived from CWDpositive, preclinical, white-tailed deer reinforces the need for precautionary and pro-active measure to reduce human exposure. At the present stage of knowledge, it cannot be excluded that CWD prions may cause human disease, but the risk appears very low. In conclusion, the zoonotic risk of CWD is still considered to be very low, in accordance with our previous assessments. 


Greetings Norway et al,

not so fast here, i believe Norway is now risking the Norwegian human population by playing down the zoonosis zoonotic risk factors of CWD Chronic Wasting Disease Skrantesyke to humans. by continuing to ignore these risk factors from the sound science to date, will only continue to load up the environment, and hospitals and surgical units all around that nation with the TSE prion. this statement is very foolish in my opinion, and by consumption, further risks by exposure there from, every hospital, surgical unit, donated tissue, blood, dental, via the iatrogenic, pass it forward mode of transmission of the TSE prion disease...very risky and foolish imo!

Terry S. Singeltary Sr.

once exposed to the cwd tse prion agent, once exposed, then there is a risk of friendly fire, second hand transmission via the iatrogenic, medical, surgical, dental, blood, tissue mode of transmission. 


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

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

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

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

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

PMID: 8006664 [PubMed - indexed for MEDLINE] 


*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017 ***


Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017


Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 

Chronic Wasting Disease (CWD) 


If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people. 

Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat. 

Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD. 

To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD: 

Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD. 

Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP) 

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

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


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

Molecular Barriers to Zoonotic Transmission of Prions 

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein. 

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


CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 

Subject: Prion 2017 Conference Abstracts CWD


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

Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 

University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 

This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 

Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 

At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 





 TUESDAY, JUNE 13, 2017


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

TUESDAY, JULY 04, 2017


TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD

Wednesday, May 24, 2017 

PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1 

SATURDAY, JULY 29, 2017 

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


*** Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis

(see origin of cwd in Colorado debate and evidence there from...tss)


Norway Nordfjella 2 out of apprx 150 animals shot now suspect for Chronic Wasting Disease CWD Skrantesjuke





In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.


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


What is the risk of chronic wasting disease being introduced into Great Britain? A Qualitative Risk Assessment October 2012

Thursday, April 07, 2016

What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016

Subject: DEFRA What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016

Friday, September 30, 2016

DEFRA What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016

Scientific Opinion

Chronic wasting disease (CWD) in cervids


EFSA Panel on Biological Hazards (BIOHAZ),

First published: 18 January 2017Full publication history DOI: 10.2903/j.efsa.2017.4667View/save citation

TUESDAY, JUNE 20, 2017 

Norway Confirms 6th Case of Skrantesjuke CWD TSE Prion Disease

Tuesday, December 13, 2016

Norway Chronic Wasting Disease CWD TSE Prion disease Skrantesjuke December 2016 Update

Thursday, September 22, 2016


Saturday, September 03, 2016

NORWAY Regulation concerning temporary measures to reduce the spread of Chronic Wasting Disease (CWD) as 4th case of skrantesjuke confirmed in Sogn og Fjordane

Wednesday, August 31, 2016


Wednesday, August 31, 2016


Tuesday, August 02, 2016

Chronic wasting disease of deer – is the battle to keep Europe free already lost?

Tuesday, June 14, 2016

*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag Norway ***

Thursday, July 07, 2016

Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd Norwegian moose

14/06/2016 - Norway reports a third case

Tuesday, April 12, 2016

The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging reindeer from the Nordfjella population in South-Norway.

Saturday, April 9, 2016

The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer (Rangifer tarandus tarandus)

Department for Environment, Food and Rural Affairs

Terry S. Singeltary Sr.


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