North Iceland reporting more cases of Scrapie (Rida)
North Iceland reporting more cases of Scrapie (Rida)
Case of Scrapie in North Iceland
By Vala Hafstad Society about 5 hours ago
Icelandic sheep
Photo: Zoë Robert.
A case of scrapie has been confirmed at a farm in Skagafjörður. Scrapie is
a fatal, degenerative disease, which affects the nervous systems of sheep and
goats. This is the fourth confirmed case of scrapie in Northwest Iceland since
February of 2015. That year, no case had been reported since 2010. Mast, the
Icelandic Food and Veterinary Authority, is currently collecting data and
preparing a course of action.
Last week, the farmer of Brautarholt in Skagafjörður suspected a case of
scrapie and contacted the district’s veterinarian. The sheep was slaughtered and
a specimen sent to the University of Iceland’s Institute for Experimental
Pathology at Keldur, which confirmed that the animal had been affected with
scrapie. Cases of the disease have come up on eleven farms in Skagafjörður in
the past two decades. Sheep had to be slaughtered at the farm Brautarholt in
1987, due to scrapie. The farm currently has 290 sheep.
Until 2010, cases of scrapie were confirmed on a few farms in the country
every year, but no cases were reported 2011-2014. Mast stresses that even though
such cases are rare, we must constantly be on guard against the disease. Every
year, samples are collected from about 3,000 sheep at slaughterhouses. Farmers
have also been encouraged to send the heads of sheep killed by accident or
disease to Keldur for examination.
Tags
Nature and Travel | Iceland Monitor | Wed 11 Mar 2015 | 10.55 GMT |
Modified at 11.11
Scrapie outbreak
Three cases of scrapie have been identified in Iceland in the last
month.
Scrapie is a fatal, degenerative disease affecting the central nervous
system of sheep. Two of the confirmed cases are in Skagafjörður and the third,
in Vatnsnes, both in Northern Iceland.
Cases not connected
The Icelandic Food and Veterinary Authority (IFVA) is currently gathering
data and preparing further action, but so far there is not considered to be any
link between the cases at the two sites. In the IFVA’s view, the current spate
of cases may be attributable to greater care and attention exercised by farmers
in the light of the first reported cases.
Líffræðifélag Íslands Líffræðiráðstefnan 2015
Erindi/veggspjald / Talk/poster V101
Scrapie control in Iceland – past and present Stefanía Þorgeirsdóttir (1)
og Auður L. Arnþórsdóttir (2)
1. Tilraunastöð Háskóla Íslands í meinafræði að Keldum, 2.
Matvælastofnun
Kynnir / Presenter: Stefanía Þorgeirsdóttir
Tengiliður / Corresponding author: Stefanía Þorgeirsdóttir (stef@hi.is)
Scrapie in sheep has been endemic in Iceland for over 130 years and has in
the past caused considerable losses to sheep farming. In 1978 a rigorous scrapie
control program was established and since 1986 the strategy has been to cull all
scrapie flocks in order to eradicate the disease. In 1993 further enhancements
of the program were made, mainly in the practical aspects of handling scrapie
cases. After disinfection of premises and a three-year waiting period, farmers
can restock with healthy sheep from scrapie-free zones. That plan is still in
effect for classical scrapie, but in 2012 different measures for atypical/Nor98
cases were adapted. In the past the fight against other diseases in sheep has
affected the control of scrapie in Iceland. In the 1930´s the country was
divided into 36 movement restriction zones, in an effort to stop the spread of
the so called Karakul diseases (maedi/visna and paratuberculosis). A few of
these zones, marked by man-made fences or natural boundaries such as rivers and
glaciers, are still scrapie-free. Marketing with live sheep is very limited,
mostly from zones considered free of scrapie and import of live sheep from
abroad has been banned since the middle of last century. Active surveillance for
scrapie has been in practice since 1978, but no cases were detected among
healthy slaughter until 2004, when rapid testing was implemented. Most classical
scrapie cases in Iceland are still detected through passive surveillance, but
majority of atypical cases have been detected through active surveillance. The
goal of complete eradication has not yet been reached, but yearly incidence has
lowered considerably and is down to a few cases per year. This is a drastic
decrease from over one hundred infected farms at the height of the epidemic a
few decades ago. On many farms scrapie has been detected in a repeated manner,
i.e. the disease is reoccurring despite extensive cleanup and restocking.
Archives of Virology
April 2008, Volume 153, Issue 4, pp 637–644
High incidence of subclinical infection of lymphoid tissues in
scrapie-affected sheep flocks
Authors Authors and affiliations Gudmundur GeorgssonEmail author Jona
Adalheidur Adolfsdottir Astridur Palsdottir Einar Jorundsson Sigurdur
Sigurdarson Stefania Thorgeirsdottir Gudmundur Georgsson 1 Email author Jona
Adalheidur Adolfsdottir 1 Astridur Palsdottir 1 Einar Jorundsson 1 3 Sigurdur
Sigurdarson 2 4 Stefania Thorgeirsdottir 1 1.Institute for Experimental
PathologyUniversity of IcelandReykjavíkIceland 2.Laboratory of Chief Veterinary
Officer, KeldurReykjavíkIceland 3.Ministry of Education, Science and
CultureReykjavíkIceland 4.Agricultural Authority of IcelandSelfossIceland
Original Article First Online: 29 January 2008 Received: 12 November 2007
Accepted: 27 December 2007 DOI: 10.1007/s00705-008-0035-8
Cite this article as: Georgsson, G., Adolfsdottir, J.A., Palsdottir, A. et
al. Arch Virol (2008) 153: 637. doi:10.1007/s00705-008-0035-8
Abstract Prion diseases are characterized by a long incubation period. In
scrapie, sheep may incubate and spread the infection for several years before
clinical signs evolve. We have previously studied the occurrence of subclincal
infection in the brain. Now, we have studied the occurrence of subclinical
infection in the brain and several lymphoid tissues in two scrapie-affected
Icelandic sheep flocks by immunohistochemistry for PrPSc, a molecular marker for
infectivity, and correlated this with results of PrP genotyping. At culling, one
flock had one confirmed scrapie case, while the other flock had two. Analysis of
106 asymptomatic sheep by immunostaining for PrPSc revealed that the incidence
of subclinical infection was 58.3% in one flock and 42.5% in the other. PrPSc
was only detected in lymphoid tissues. The youngest positive sheep were 4 months
old. PrP genotyping showed that over 90% of the sheep were of a genotype which
is moderately sensitive to infection and may delay neuroinvasion. Our results
show that asymptomatic sheep may spread the infection during the long incubation
period of several years, which constitutes an important obstacle in the
eradication of scrapie. Our findings indicate that contamination of the
environment plays an important part in sustaining the infection.
References
Epidemiology of scrapie in Iceland and experience with control measures.
Author(s) : Sigurdarson, S.
Author Affiliation : Institute for Experimental Pathology, University of
Iceland, Keidur, Reykjavik, Iceland.
Editors : Bradley, R.; Savey, M.; Marchant, B.
Conference paper : Sub-acute spongiform encephalopathies. Proceedings of a
seminar in the CEC Agricultural Research Programme, held in Brussels, 12-14
November 1990. 1991 pp.233-242
Conference Title : Sub-acute spongiform encephalopathies. Proceedings of a
seminar in the CEC Agricultural Research Programme, held in Brussels, 12-14
November 1990.
ISBN : 0792314581
Record Number : 19922268331
Abstract : Scrapie or "rida" has been known in Iceland for more than 100
years. In 1978 a new plan was adopted in cooperation with farmers, first to
reduce the losses from scrapie and prevent spreading to new areas and secondly
to eradicate the disease from new places on the border of the endemic area. The
final aim of the plan was full eradication of scrapie from Iceland. Earlier
experiments indicated that the only possible method to accomplish this was
stamping out all scrapie flocks as soon as possible after they were discovered.
Restocking was supposed to take place after 2 years, only with lambs from
isolated areas far away from all scrapie infected flocks. Through cleaning and
disinfection of the premises was carried out one year before restocking. The
result is promising. New stock has been kept for > 5 years on 76 farms and
for > 4 years on 102 other farms without reappearance of the disease. Some of
the restocked farms have already kept new stock for > 11 years without
reappearance of scrapie. Altogether 716 flocks have been slaughtered and 397 of
these have been restocked. By the end of 1990 all sheep flocks where scrapie was
confirmed after 1982 will have been slaughtered. Every year since 1978 there has
been an inspection of 10-15 000 brain samples of sheep possibly exposed to the
infection from farms where scrapie had never been confirmed. The samples were
taken in abattoirs. 15 infected farms have been identified by this method.
Comments… Cancel Save Annotate Rem
Publisher : Kluwer Academic Publishers
Location of publication : 3300 AA Dordrecht
Country of publication : Netherlands
Language of text : English
Language of summary : English
From: TSS (216-119-130-116.ipset10.wt.net)
Subject: ICELAND'S FIGHT AGAINST SHEEP DISEASES...
Date: December 9, 2000 at 3:08 pm PST
ICELAND'S FIGHT AGAINST SHEEP DISEASES.
By Stefanía Sveinbjarnardóttir-Dignum
Copyright 1991
In the last few years much has been heard about outbreaks of old and new
diseases in animals in may countries around the world. TB in buffalo,
Brucellosis in elk, Mad Cow disease, OPP and Scrapie in sheep and so on. One
wonders if this is due to increased knowledge of diseases that have been around
for a long time or if diseases are actually on the increase. All this got me
looking back to my Icelandic origins and made me think about how Icelanders have
responded to threats to their sheep farming, and in some cases to their very
survival on this remote island, due to diseases that have hit the sheep
population.
After the settlement of Iceland, which took place between 800AD and
1100AD, there was no further importation of livestock for a long time. However,
in the eighteen century the government became interested in improving the native
sheep and in 1756 tem British rams were imported for crossbreeding. That
experiment was so successful that four years later a few Merino sheep were
imported from Spain. These sheep brought with them Psoroptes Ovis which are
mites that live on blood and cause ill thrift and often death. These mites
spread around the south and west of the island and caused severe losses. There
was no cure and the only way to get rid of this pest was drastic culling of
infected sheep flocks. It was made mandatory and caused incredible losses, but a
victory was won. To make matters worse, in 1783 one of the biggest volcanic
eruptions in recorded world history started in Iceland. The resulting poisonous
gases and volcanic ash took a tremendous toll in lives of both people and
animals. It is recorded that in 1760 the population of sheep in Iceland was
357,000 head and in 1784, after the eruption, it had dropped to 50,000 head,
drop of over 70%. But with it the mites disappeared. This was a rather drastic
way to eliminate a problem, but effective.
During the next 90 years or so few importations occurred, in most cases
involving only two or three animals . Crossing these seems to have been
successful. In 1855 three Merino sheep and four English lambs were imported and
with the English lambs the same mites as before. Again, the parasite spread and
massive culling was undertaken with considerable loss, both in bloodlines and
money. My great-grandfather was one of those ordered to cull his sheep in that
episode. Dipping of sheep was also used in this fight with reasonably good
results. After this catastrophe laws were passed in 1882 whereby all importation
of sheep was forbidden. The ban lasted for fifty years.
Around 1930 interest in experiments with crossbreeding surfaced again. In
1931 the Parliament passed laws allowing importation of 26 yearling from
Britain. These sheep were kept for about 15 weeks in quarantine and then sent to
a farm where they were bred and the offsprings sold for F-1 crossing. Under the
same laws permission was given for importation of 20 Karakul sheep from Germany
in 1933 for the purpose of producing crossbred lambskins. Those sheep were kept
for only two months in quarantine and then released to farms around the country.
The next year a strange disease, that had never before been seen in Iceland,
began to appear in and around the farms where the Karakul sheep had been placed.
In only one instance had the receiving farmer put his new ram into a further on
farm quarantine. He did not like how the ram developed and culled it. he took
the carcass a few miles out to sea and sank it there. By doing so he saved the
best part of the Northwest peninsula from the worst sheep epidemic Iceland has
ever experienced.
By the late thirties it was clear that once again a disaster had struck
the Icelandic sheep population. At that time the cause of the diseases was not
known, but three different diseases had obviously come with the Karakul and were
thereafter called collectively "the Karakul diseases". The first to be
recognized was called Wet Mæði (pulmonary adenomatosis), and by the time this
one seemed to be in remission another one appeared which got the name Dry Mæði
(Maedi/Visna. OPP). Later, but only in limited area, Visna showed up. The names
of these diseases were derived from the symptoms, Mæði meaning shortage of
breath and Visna wasting. The third disease was Johne's.
Even though these diseases had been found in other countries the causative
agent was not known. By the end of the third decade it was obvious that drastic
measures were needed and the old method of culling seemed to be the only
possible approach. By this time the disease had spread over much of the country.
The culling had to be done in an organized manner to stop the spreading of the
disease and spread the unavoidable losses over time. The whole country was
divided into districts by fencing or by natural barriers where possible. Some
1250 miles of fences were erected by the government and were , and still are
kept up by people specifically employed for that purpose. When the barriers had
be completed the culling started. All sheep in district after district were
culled. After a complete eradication the area was restocked with sheep from a
clean district. Most of the northwestern peninsula (areas 11 - 14) had escaped
the disease as well as the isolated southeastern region between the Vatnajokull
glacier and the Atlantic Ocean (area 26). The new stock came from there. In most
cases the restocking was successful. The few unsuccessful cases were traced to
carelessness in allowing some old sheep to escape slaughter or to infection of
the new sheep en route.
By 1952 the systematic slaughtering was completed. Approximately 650,000
sheep were culled during this period. Occasional outbreaks recurred up to the
early sixties. It can happen, for example, that sheep are not found in the
annual roundup and these can survive the winter in the mountains. Those could
have been the source of infection. The last outbreak occurred in 1965 and since
then Maedi/Visna (OPP) has not been found in Iceland. For decades afterwards
monitoring was kept up, both on farms and in slaughterhouses but no new cases
have ever been found. Iceland is now officially and in fact free of Maedi/Visna
(OPP).
The culling was not the only attack made on the disease. Another, and
possibly more important one was the work done by Icelandic scientists. A
dedicated team, headed by Dr. Björn Sigurðsson, kept looking for the causative
agent and based on that work, Dr. Sigurðsson put forth his theory of ASlow
Progressing Viral Diseases@ which at that time was a new concept in diseases. He
and his team succeeded in isolating the Maedi virus and also proved that the
same virus caused Visna. He and his colleagues, among whom were Dr. P. A.
Pálsson, Dr. M. Guðnadóttir, and Dr. H. Thormar laid the base upon which AIDS
research was later built, since the AIDS virus and the Maedi/Visna (OPP) virus
are closely related. Dr. Sigurðsson died in 1959, only 46 years old, but his
colleagues kept on the Maedi /Visna research and also studied Scrapie, another
disease in some Icelandic sheep. Dr. Sigurðsson and his co-workers also studied
Johne´s disease and were successful in producing a vaccine. By using that
vaccine Johne´s disease has been put under control in Iceland.
One might think that after all these sacrifices and losses that Icelanders
were through with drastic measures; but, no. In 1878, before the van on
importation in the last century, an Oxford Down ram was imported to a farm in
the North of Iceland. From that farm a new disease spread through the district
by selling of sons of the Oxford ram. The disease was named "riða" (tremble), we
know this as Scrapie. It was confined to this area up till the early fifties
when it started to spread slowly but with increasing speed as the years went by.
It was not considered a serious threat at that time and it was hoped that in the
Maedi/Visna culling it would disappear. It did not. The causative agent for this
disease was much more resilient that the Maedi/Visna virus. After Maedi/Visna
had been eradicated Scrapie was still around. In the next four years the disease
appeared on 30 farms all of which and been Scrapie farms before the complete
Maedi/Visna culling. Some of these farms had been out of sheep for three years.
The Scrapie agent had somehow survived without sheep being on these farms. By
1978 it seemed obvious that Scrapie would overflow the whole country unless
drastic measures were taken. It was decided to start a new battle against the
disease, firstly by stopping the spread of it by culling all flocks where new
cases appeared, on the borders of epidemic areas. Secondly, by culling all sheep
in the epidemic areas. This was done with full co-operation between farmers, and
the government. In addition to mandatory culling of all sheep on farms where
Scrapie was confirmed or suspected, conditions for permission to restock were
made stricter and minimum of two years of sheeplessness was demanded. However
before full consensus was reached there was some dissent among farmers. some
even suggested the losses from Scrapie were so low that they could live with it.
However, culling according to the new rules was begun in 1978 and restocking
from areas where Scrapie had never been found or suspected was allowed after the
minimum time lapse. In most cases that was two years, ion some cases three years
and in one experimental case, one year. In order to be permitted to restock, the
following conditions have to be met: One year before restocking, all buildings,
machinery and manure storage have to be washed and disinfected. This involves
complete emptying of all buildings, scraping all floors and walls, opening all
walls and ducts and all places where insects or mites could be hidden. Then the
areas have to be sprayed with a jet sprayer using hypochlorite solution or some
thing similar. After this has dried, the area has to be sprayed with iodine with
a regular garden sprayer. After inspection by a government approved inspector
the buildings are sealed until the new animals arrive. All woodwork that cannot
be properly disinfected has to be burned or buried. worn tools and tools that
are used to treat the animals, such as hoof clippers, marking tongs, reusable
needles, etc. are to be disposed of. All areas where sheep commonly gathered
have to be scraped and the soil buried. Then a minimum of four inches of gravel
has to be put on these places. Manure can be spread on fields that are well
fenced but not on any place where water runoff is likely. The hay taken from
fields of farms where culling has taken place cannot be used for sheep feed.
Hay, sod, manure etc., is not permitted to move from farm to farm. All surfaces
that cannot be perfectly disinfected have to be sealed with durable paint on
metal and concrete and creosote on wood. All this work has to be inspected and
approved by government inspector. Restocking is not permitted without previous
disinfection. Farmers do get financial assistance with cleaning and compensation
while out of business due to Scrapie culling.
Between 1978 and 1987 all sheep on several farms were culled and the new
rules applied. Restocking was done from Scrapie-free areas. The results were
promising. These were in districts where the incidence of Scrapie was just a few
cases and culling was undertaken before any sign of serious spreading of the
disease occurred. The disease was most widespread and serious in the eastern and
northern part of the island. In the fall of 1987 the biggest onslaught was
undertaken when 26,000 sheep from 130 farms were culled. In 1988 a further
20,000 sheep were culled from 100 farms. That culling left the eastern part of
the country with any sheep. Last fall, in 1990 restocking in these areas began.
since 1988 all confirmed and suspected cases have been culled. In some instances
flocks from farms where no cases have been found have been culled on the grounds
that Scrapie has been found on neighbouring farms. At present (March 1991), no
cases of Scrapie are known to exist in Iceland but it is expected that some will
surface in the next few years. In that case, culling of the flock, where Scrapie
has been found, will be immediately undertaken. Some 280 farms have been
restocked since the new regulations took effect, that is in the last 11 years,
and in only two cases has Scrapie reappeared. In one case the cause could be
traced o carelessness, in the other case the new stack was bought farm a farm
nearby where Scrapie was later found.
The veterinarians are not the only ones to report suspected cases. Farmer
themselves do so also. Search is furthermore conducted in the slaughterhouses
during the slaughtering season, in sheep brain samples. It seems to be that
again Icelanders have gotten together to fight a disease in their sheep.
Compensation to farmers is reasonable and peer pressure is very strong. Any one
flock that harbors Scrapie is a threat to the whole district. Recently, the
Chief Veterinarian for sheep disease control in Iceland, Dr. Sigurður
Sigurðarson told me that they were pleasantly surprised over how well the fight
was going. He stated that even though no known cases exist at present the
battler is far from over. No country has undertaken eradication on such a large
and thorough scale before. Countries such as Australia, New Zealand, Kenya and
south Africa have found Scrapie and eradicated it, but in all these countries
the disease has been found in recently imported animals and has been stopped
before spreading into the native sheep populations. Scrapie has been known in
Iceland for over 100 years and if eradication is successful, as appears to be
happening, many countries may benefit from the lesson that is being learned in
Iceland today.
Note: I want to express my gratitude to Dr. Sigurður Sigurðarson who
kindly edited this article for accuracy, as well as making available to me his
paper AEpidemiology of Scrapie
P.S.-something else interesting. i have heard from several sources that the
sheep research station associated with the Neuropathogenesis Unit in Edinburgh,
Scotland around 1992-3 has done long studies conducted on small pastures
containing scrapie infected sheep. After leaving the pastures free and replacing
the topsoil completely at least 2 feet of thickness each year for SEVEN
years.... and then when very clean (proven scrapie free) sheep were placed on
these small pastures.... the new sheep also came down with scrapie and passed it
to their offspring.
a very horrifying thought, especially in light of the increase of scrapie
over the years in the U.S.A., and the fact that they use scrapie for a research
tool for CJD and other human/animal TSE's...
P.S. The U.S.A. has recently declared DECLARATIONS OF EMERGENCY'S for the
following;
SCRAPIE regular=over 20 different strains to date
also
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION
DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E (PRION
DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [2]
snip...end...tss
2015
update on that DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN
ATYPICAL T.S.E (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES ;
MAD SHEEP OF MAD RIVER VALLEY THE HISTORY AND TRUE STORY
A FALSE FLAG OPERATION BY THE USDA FEDERAL GOVERNMENT
Friday, February 20, 2015
***APHIS Freedom of Information Act (FOIA) Appeal Mouse Bio-Assays
2007-00030-A Sheep Imported From Belgium and the Presence of TSE Prion Disease
Kevin Shea to Singeltary 2015
Thursday, September 22, 2016
*** NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION
Skrantesjuke ***
Title: Pathological features of chronic wasting disease in reindeer and
demonstration of horizontal transmission
Author
item Moore, Sarah item Kunkle, Robert item West greenlee, Mary item
Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item
Greenlee, Justin
Submitted to: Emerging Infectious Diseases Publication Type: Peer reviewed
journal Publication Acceptance Date: 8/29/2016 Publication Date: N/A Citation:
Interpretive Summary: Chronic wasting disease (CWD) is a fatal
neurodegenerative disease that occurs in farmed and wild cervids (deer and elk)
of North America and was recently diagnosed in a single free-ranging reindeer
(Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform
encephalopathy (TSE) that is caused by infectious proteins called prions that
are resistant to various methods of decontamination and environmental
degradation. Little is known about the susceptibility of or potential for
transmission amongst reindeer. In this experiment, we tested the susceptibility
of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer)
after intracranial inoculation and tested the potential for infected reindeer to
transmit to non-inoculated animals by co-housing or housing in adjacent pens.
Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer
sources after experimental inoculation. Most importantly, non-inoculated
reindeer that were co-housed with infected reindeer or housed in pens adjacent
to infected reindeer but without the potential for nose-to-nose contact also
developed evidence of CWD infection. This is a major new finding that may have a
great impact on the recently diagnosed case of CWD in the only remaining
free-ranging reindeer population in Europe as our findings imply that horizontal
transmission to other reindeer within that herd has already occurred. Further,
this information will help regulatory and wildlife officials developing plans to
reduce or eliminate CWD and cervid farmers that want to ensure that their herd
remains CWD-free, but were previously unsure of the potential for reindeer to
transmit CWD.
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring,
fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are
susceptible to CWD following oral challenge, and CWD was recently reported in a
free-ranging reindeer of Norway. Potential contact between CWD-affected cervids
and Rangifer species that are free-ranging or co-housed on farms presents a
potential risk of CWD transmission. The aims of this study were to 1)
investigate the transmission of CWD from white-tailed deer (Odocoileus
virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus
elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to
assess for direct and indirect horizontal transmission to non-inoculated
sentinels. Three groups of 5 reindeer fawns were challenged intracranially with
CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer,
non-inoculated negative control reindeer were introduced into the same pen as
the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to
the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated
reindeer were allowed to develop clinical disease. At death/euthanasia a
complete necropsy examination was performed, including immunohistochemical
testing of tissues for disease-associated CWD prion protein (PrPcwd).
Intracranially challenged reindeer developed clinical disease from 21 months
post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel
reindeer although only 2 out of 6 developed clinical disease during the study
period (< 57 months PI). We have shown that reindeer are susceptible to CWD
from various cervid sources and can transmit CWD to naïve reindeer both directly
and indirectly.
Monday, September 05, 2016
*** Pathological features of chronic wasting disease in reindeer and
demonstration of horizontal transmission Major Findings for Norway ***
Monday, September 05, 2016
Pathological features of chronic wasting disease in reindeer and
demonstration of horizontal transmission Major Findings for Norway
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
SCRAPIE AND CWD ZOONOSIS
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Monday, September 19, 2016
Evidence of scrapie transmission to sheep via goat milk
Monday, September 19, 2016
Identification of the first case of atypical scrapie in Japan
atypical scrapie NOR-98
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier
Andréoletti1, Affiliations Contributions Corresponding author Journal name:
Nature Communications Volume: 5, Article number: 5821 DOI:
doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014
Published 16 December 2014 Article tools Citation Reprints Rights &
permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
SCRAPIE AND CWD ZOONOSIS
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Transmission of scrapie prions to primate after an extended silent
incubation period
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
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.
see ;
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable
neurological diseases likely caused by a misfolded form of the prion protein.
TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’
disease) in cattle, chronic wasting disease in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are
unique among TSEs because they can be transmitted between animals, and the
disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
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.
>>>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.
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.
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
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
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
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.
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Confucius ponders...
Could the Scrapie experiments back around 1964 at Moore Air Force near
Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides
the CWD cases that have waltzed across the Texas, New Mexico border near WSMR
Trans Pecos region since around 2001)?
Epidemiology of Scrapie in the United States 1977
snip...
Scrapie Field Trial Experiments Mission, Texas
A Scrapie Field Trial was developed at Mission, Texas, to provide
additional information for the eradication program on the epidemiology of
natural scrapie. The Mission Field Trial Station is located on 450 acres of
pastureland, part of the former Moore Air Force Base, near Mission, Texas. It
was designed to bring previously exposed, and later also unexposed, sheep or
goats to the Station and maintain and breed them under close observation for
extended periods to determine which animals would develop scrapie and define
more closely the natural spread and other epidemiological aspects of the
disease.
The 547 previously exposed sheep brought to the Mission Station beginning
in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were
purchased as field outbreaks occurred, and represented 21 bloodlines in which
scrapie had been diagnosed. Upon arrival at the Station, the sheep were
maintained on pasture, with supplemental feeding as necessary. The station was
divided into 2 areas: (1) a series of pastures and-pens occupied by male animals
only, and (2) a series of pastures and pens occupied by females and young
progeny of both sexes. ...
snip...see full text ;
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie TSE Prion Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
SCRAPIE AND CWD ZOONOSIS
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Thursday, August 04, 2016
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
snip...
1979
SILENCE ON CJD AND SCRAPIE
1980
SILENCE ON CJD AND SCRAPIE
*** 1981 NOVEMBER
snip...see full text ;
Thursday, August 04, 2016
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
*** Calling Canadian beef unsafe is like calling your twin sister ugly,"
Dopp said.
Thursday, August 25, 2016
*** FSIS Green Bay Dressed Beef Recalls Beef Products Due To Possible
Specified Risk Materials Contamination the most high risk materials for BSE TSE
PRION AKA MAD COW TYPE DISEASE ***
Tuesday, August 9, 2016
*** Concurrence with OIE Risk Designations for Bovine Spongiform
Encephalopathy [Docket No. APHIS-2015-0055]
Saturday, July 23, 2016
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING,
AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY
2016
Saturday, July 16, 2016
*** Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened those mad cows in Texas ***
Monday, June 20, 2016
*** Specified Risk Materials SRMs BSE TSE Prion Program ***
Tuesday, September 06, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. | 3:31 PM
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