CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
CHRONIC WASTING DISEASE CWD, SCRAPIE, BSE, TSE PRION REPORT UNITED STATES
DECEMBER 2015 TEXAS CWD
Monday, November 16, 2015
*** TEXAS PARKS AND WILDLIFE DEPARTMENT EXECUTIVE DIRECTOR ORDER NO.
015-006 Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer
and mule deer resources of Texas
Saturday, November 14, 2015
TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DETECTED
Wednesday, March 18, 2015
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
Wednesday, March 25, 2015
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, November 26, 2015
TEXAS CWD TSE PRION REPORTING TURKEY OF THE YEAR AWARD GOES TO SHANNON
TOMPKINS OF THE HOUSTON CHRONICLE
Sunday, August 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super
ovulation, and the potential TSE Prion connection, what if?
*** CENSORED, RAW, UNCUT...
Sunday, July 26, 2015
*** TEXAS IN MELT DOWN MODE OVER CAPTIVE CWD AND THEY ARE PUTTING LIPSTICK
ON THAT PIG AND TAKING HER TO THE DANCE LIKE MAD COW DISEASE ***
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Wednesday, July 01, 2015
*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
WYOMING CWD
Tuesday, December 15, 2015
Wednesday, December 16, 2015
Wyoming Game and Fish finds CWD in new elk hunt area in southeast
Tuesday, December 15, 2015
Chronic Wasting Disease will cause a Wyoming deer herd to go virtually
extinct in 41 years, a five-year study predicts
Study: Chronic Wasting Disease kills 19% of deer herd annually
Thursday, December 10, 2015
Wyoming Game and Fish seeks public comment on draft of updated CWD plan
Tuesday, December 08, 2015
Wyoming Game and Fish finds CWD in new elk hunt area in Johnson County
Friday, November 27, 2015
Wyoming Game and Fish finds CWD in new Deer Hunt Area near Sheridan
Monday, November 16, 2015
*** Wyoming Latest round of testing CWD surveillance program has found the
disease in three new hunt areas
Wyoming WGF Commission Meeting 11/6/2015 Afternoon Edition Vidoe
CWD starts at minute 58:51 of first hour of meeting discussion of previous
models predicting extinction of deer population and elk population.
please mark hour 1:02 where remarks were made about potential resistant
genes and prolonged survival, however a recent study (I posted directly next
after youtube link) where it states ;
‘’Our study also demonstrates that mice expressing the deer S96-PRNP
allele, previously shown to be resistant to various cervid prions, are
susceptible to H95+ CWD prions. The potential for the generation of novel
strains raises the possibility of an expanded host range for CWD. ‘’
hour minute mark 1:03
captive Elk study
39 femail elk calves captured on National Elk Refuge In Jackson, WY
Transported to WGFD Thorne-Williams Wildlife Research Unit (Sybille,
TWWRU)
Worst-case scenario for prion exposure
Genotypes
-27 M/M132 (69.2%)
-11 M/L132 (28.2%)
-1 L/L132 (2.6%)
38 of 39 elk died over 10-year study
1 remaining elk was L/L132
still alive and remained negative for PrPCWD by rectal biopsy
Appears healthy, weighs 242kg, and bore healthy calf in May, 2012
CWD infection rate in this study ???
> During the analysis, 37 of 39 elk died, all of which were positive for
CWD.
*** Our study also demonstrates that mice expressing the deer S96-PRNP
allele, previously shown to be resistant to various cervid prions, are
susceptible to H95+ CWD prions. ***
*** The potential for the generation of novel strains raises the
possibility of an expanded host range for CWD. ***
Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic
Wasting Disease Strains
Camilo Duque Velásqueza,b, Chiye Kima,c, Allen Herbsta,b, Nathalie
Daudea,d, Maria Carmen Garzaa,e, Holger Willea,e, Judd Aikena,b and Debbie
McKenziea,c aCentre for Prions and Protein Folding Diseases, University of
Alberta, Edmonton, Alberta, Canada bDepartment of Agricultural, Food and
Nutritional Science, University of Alberta, Edmonton, Alberta, Canada
cDepartment of Biological Sciences, University of Alberta, Edmonton, Alberta,
Canada dDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada
eDepartment of Biochemistry, University of Alberta, Edmonton, Alberta, Canada
B. Caughey, Editor
+ Author Affiliations
ABSTRACT
Transmission of chronic wasting disease (CWD) between cervids is influenced
by the primary structure of the host cellular prion protein (PrPC). In
white-tailed deer, PRNP alleles encode the polymorphisms Q95 G96 (wild type
[wt]), Q95 S96 (referred to as the S96 allele), and H95 G96 (referred to as the
H95 allele), which differentially impact CWD progression. We hypothesize that
the transmission of CWD prions between deer expressing different allotypes of
PrPC modifies the contagious agent affecting disease spread. To evaluate the
transmission properties of CWD prions derived experimentally from deer of four
PRNP genotypes (wt/wt, S96/wt, H95/wt, or H95/S96), transgenic (tg) mice
expressing the wt allele (tg33) or S96 allele (tg60) were challenged with these
prion agents. Passage of deer CWD prions into tg33 mice resulted in 100% attack
rates, with the CWD H95/S96 prions having significantly longer incubation
periods. The disease signs and neuropathological and protease-resistant prion
protein (PrP-res) profiles in infected tg33 mice were similar between groups,
indicating that a prion strain (Wisc-1) common to all CWD inocula was amplified.
In contrast, tg60 mice developed prion disease only when inoculated with the
H95/wt and H95/S96 CWD allotypes. Serial passage in tg60 mice resulted in
adaptation of a novel CWD strain (H95+) with distinct biological properties.
Transmission of first-passage tg60CWD-H95+ isolates into tg33 mice, however,
elicited two prion disease presentations consistent with a mixture of strains
associated with different PrP-res glycotypes. Our data indicate that H95-PRNP
heterozygous deer accumulated two CWD strains whose emergence was dictated by
the PrPC primary structure of the recipient host. These findings suggest that
CWD transmission between cervids expressing distinct PrPC molecules results in
the generation of novel CWD strains.
IMPORTANCE CWD prions are contagious among wild and captive cervids in
North America and in South Korea. We present data linking the amino acid variant
Q95H in white-tailed deer cellular prion protein (PrPC) to the emergence of a
novel CWD strain (H95+). We show that, upon infection, deer expressing H95-PrPC
molecules accumulated a mixture of CWD strains that selectively propagated
depending on the PRNP genotype of the host in which they were passaged. Our
study also demonstrates that mice expressing the deer S96-PRNP allele,
previously shown to be resistant to various cervid prions, are susceptible to
H95+ CWD prions. The potential for the generation of novel strains raises the
possibility of an expanded host range for CWD.
*** Our study also demonstrates that mice expressing the deer S96-PRNP
allele, previously shown to be resistant to various cervid prions, are
susceptible to H95+ CWD prions. ***
*** The potential for the generation of novel strains raises the
possibility of an expanded host range for CWD. ***
UPDATE CWD VACCINE ELK minute mark 1:22:00
VACCINE
RECOMBINANT PROTEIN FUSION VACCINE
Hedlin, PD et al ‘’Design and delivery of a cryptic PrP c epitope for
induction of Prp Sc-specific antibody responses.’’ Vaccine 28.4 (2010)
981-988.
PAN-PROVINCIAL VACCINE ENTERPRISES (PREVENT)
Dose: 2ml IM CWD VACCINE UPDATE IS A FAILURE, I REPEAT, A NEGATIVE RESULTS
FOR CWD VACCINE. .tss
MICHIGAN CWD
Tuesday, December 01, 2015
MICHIGAN 4TH WILD CHRONIC WASTING DISEASE CWD SUSPECT CONFIRMED
Friday, November 13, 2015
*** Michigan Suspected CWD found in DeWitt Township deer tests are
indicating that the deer could be the fourth case
Thursday, August 06, 2015
Michigan DNR confirms third deer positive for CWD; hunter participation is
critical this fall
Friday, July 17, 2015
Michigan confirms CWD in second free-ranging white-tailed deer
Tuesday, May 26, 2015
Michigan confirms state's first case of chronic wasting disease in
free-ranging white-tailed deer
Monday, August 25, 2008
CWD FIRST DOCUMENTED IN MICHIGAN Michigan's First Case of Chronic Wasting
Disease Detected at Kent County Deer Breeding Facility
Contact: Bridget Patrick (MDA) or Mary Dettloff (DNR) 517-241-2669 or
517-335-3014 Agency: Natural Resources
August 25, 2008 LANSING - The Michigan departments of Agriculture (MDA) and
Natural Resources (DNR) today confirmed the state's first case of Chronic
Wasting Disease (CWD) in a three-year old white-tailed deer from a privately
owned cervid (POC) facility in Kent County.
PENNSYLVANIA CWD
Saturday, November 07, 2015
PENNSYLVANIA CHRONIC WASTING DISEASE CWD TSE PRION RULES EXPAND
Saturday, November 07, 2015
Pennsylvania 2015 September Minutes CWD Urine Scents
Tuesday, October 21, 2014
*** Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer
Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
Tuesday, May 05, 2015
Pennsylvania CWD DETECTED IN SIX MORE FREE-RANGING DEER Disease Management
Area 2 again expanded due to new cases Release #030-15
Sunday, October 18, 2015
*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans
Singeltary 2002 from speaking A smelly situation UPDATED 2015
OHIO CWD
Friday, November 20, 2015
ODNR Takes Action to Monitor Chronic Wasting Disease in Ohio's Deer
Herd
Friday, October 23, 2015
Ohio Wildlife Council Passes Rule to Help Monitor CWD
Monday, August 24, 2015
Ohio wildlife officials ramp up fight against fatal deer brain disease
after 17 more positive tests CWD
Wednesday, August 05, 2015
Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases
to date
Thursday, October 23, 2014
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Wednesday, February 11, 2015
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with
two counts of tampering with evidence
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
Monday, June 11, 2012
*** OHIO Captive deer escapees and non-reporting ***
ILLINOIS CWD
Monday, August 31, 2015
*** Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting
with 71 confirmed in 2015 and 538 confirmed cases to date ***
MISSOURI CWD
Thursday, December 03, 2015
Missouri MDC reports CWD found in Franklin County
Saturday, September 05, 2015
Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for
Money, while mad deer and elk disease silently spreads
Tuesday, June 16, 2015
Missouri MDC changes deer hunting regs to help slow CWD
Wednesday, March 11, 2015
MDC reports 11 new cases of Chronic Wasting Disease CWD in Missouri deer
Monday, January 26, 2015
Missouri MDC reports two new cases of CWD found in Adair and Macon counties
KANSAS CWD
Wednesday, July 15, 2015
Kansas Ten Deer Test Positive for CWD in 2014-2015 7-16-15 News
Thursday, April 02, 2015
Kansas Chronic Wasting Disease CWD Spreads 9 Confirmed Positive including
first-time cases in six southwest counties
IOWA CWD
DNR to continue Surveillance for Chronic Wasting Disease
The Iowa DNR’s wildlife staff will be collecting tissue samples during
Iowa’s shotgun deer seasons to test for the presence of Chronic Wasting Disease
(CWD) in Iowa’s wild deer herd.
The effort will concentrate in Allamakee County after four wild deer tested
positive for CWD, and on portions of northeast and eastern Iowa near Wisconsin
and Illinois, south-central Iowa near Missouri, as well as in Pottawattamie,
Cerro Gordo and Buchanan counties, following positive tests in the past from
captive facilities and wild deer in or near those counties.
Most of the 4,500 samples the DNR hopes to collect will be taken during the
first half of December, as more than 120,000 hunters take part in Iowa’s shotgun
deer seasons. Sampling involves removing and testing the brain stem and lymph
nodes of mature deer.
Many hunters voluntarily contribute samples of their harvested deer for
these testing efforts. Most samples are obtained by wildlife staff, checking
with hunters in the field or at home processing points.
Hunters willing to provide samples may contact the DNR regionally to
arrange collection. In Allamakee, Clayton and Winneshiek counties, call
563-380-3422; in Dubuque, Jackson, Clinton, Scott and Delaware counties, call
563-357-2035; in Davis, Wapello, Van Buren and Jefferson counties, call
641-799-0793; in Wayne, Appanoose and Monroe counties, call 641-203-6185; in
Pottawattamie County, call 712-350-0147; in Cerro Gordo County, call
641-425-2814; and in Buchanan County, call 319-213-2815.
Since 2002, more than 51,000 wild deer in Iowa have been tested, with four
positive CWD results in the wild herd detected in Allamakee County, the first in
2013.
Iowa DNR’s website provides information about CWD and other information on
infectious disease at:
Wednesday, October 07, 2015
Iowa DNR Meeting to Discuss Chronic Wasting Disease in Deer Set for Oct
13th in Bloomfield
Tuesday, January 20, 2015
Iowa Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee
County
Wednesday, April 09, 2014
Iowa : Chronic Wasting Disease Detected for First Time in Wild Iowa Deer
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED
79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD). The owners of the
quarantined herd have entered into a fence maintenance agreement with the Iowa
Department of Agriculture and Land Stewardship, which requires the owners to
maintain the 8’ foot perimeter fence around the herd premises for five years
after the depopulation was complete and the premises had been cleaned and
disinfected CWD is a progressive, fatal, degenerative neurological disease of
farmed and free-ranging deer, elk, and moose. There is no known treatment or
vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS)
National Veterinary Services Lab in Ames, IA confirmed that a male white tail
deer harvested from a hunting preserve in southeast IA was positive for CWD. An
investigation revealed that this animal had just been introduced into the
hunting preserve from the above-referenced captive deer herd in north-central
Iowa. The captive deer herd was immediately quarantined to prevent the spread of
CWD. The herd has remained in quarantine until its depopulation on August 25 to
27, 2014. The Iowa Department of Agriculture and Land Stewardship participated
in a joint operation to depopulate the infected herd with USDA Veterinary
Services, which was the lead agency, and USDA Wildlife Services. Federal
indemnity funding became available in 2014. USDA APHIS appraised the captive
deer herd of 376 animals at that time, which was before depopulation and
testing, at $1,354,250. At that time a herd plan was developed with the owners
and officials from USDA and the Iowa Department of Agriculture and Land
Stewardship. Once the depopulation was complete and the premises had been
cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will
be paid to the owners as compensation for the 356 captive deer depopulated. The
Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD
program for farms that sell live animals. Currently 145 Iowa farms participate
in the voluntary program. The above-referenced captive deer facility left the
voluntary CWD program prior to the discovery of the disease as they had stopped
selling live animals. All deer harvested in a hunting preserve must be tested
for CWD.
-30-
INFORM: Cervid Health and States Indemnity FY 2015 USDA Animal and Plant
Health Inspection Service sent this bulletin at 09/19/2014 05:22 PM EDT Animal
and Plant Health Inspection Service (APHIS), Veterinary Services (VS) received a
total of $3 million in appropriated funding to support cervid health activities
in fiscal year (FY) 2014, and made approximately $1.0 million of this funding
available for indemnity of chronic wasting disease (CWD) positive, suspect, and
exposed farmed cervids. All of the available FY2014 indemnity funding was used
to depopulate three CWD-infected herds. However, several States have asked about
the availability of Federal indemnity funds for CWD-exposed animals in the
future. VS plans to offer Federal indemnity for CWD-exposed cervids beginning in
FY2015. Briefly, we will prioritize the highest risk CWD-exposed animals for
indemnity based on the availability of funding. Any newly reported CWD-positive
herds will be considered for indemnity as they are identified, based first on
funding availability and secondly on the risk presented by the herd. We will
reassess our fiscal year funding on a quarterly basis so that providing
indemnity for exposed animals does not exhaust available funding early in the
fiscal year. By taking this fiscally cautious approach, we hope to provide
indemnity for positive herds identified later in the fiscal year while removing
high-risk animals from the landscape as soon as possible to minimize the risk
for disease spread. Further, removal and testing of these exposed animals will
provide a better understanding of the disease risk presented by these
animals/herds. VS plans to work with our State and industry stakeholders on the
criteria to assess the risk and on the process through which States can request
this indemnity. These will be finalized in a VS Guidance Document in the near
future. We look forward to working with you to implement this process in the
coming year.
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
see history of this CWD blunder here ;
MARYLAND CWD
Tuesday, January 20, 2015
Four Maryland Deer Test Positive for Chronic Wasting Disease
WISCONSIN CWD
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
Wednesday, December 16, 2015
Wisconsin Chronic wasting disease confirmed in Crawford County buck
harvested on private land
Friday, December 04, 2015
Wisconsin CWD-positive white-tailed deer found on Oneida County hunting
preserve December 3, 2015
Thursday, November 19, 2015
Wisconsin Eau Claire Co. deer herd two day round of depopulation CWD
testing shows 23 positive
Tuesday, August 11, 2015
Wisconsin doing what it does best, procrastinating about CWD yet again
thanks to Governor Walker
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
Tuesday, October 07, 2014
*** Wisconsin white-tailed deer tested positive for CWD on a Richland
County breeding farm, and a case of CWD has been discovered on a Marathon County
hunting preserve
Thursday, June 25, 2015
Wisconsin CWD-positive white-tailed deer found on Eau Claire County farm
Tuesday, July 14, 2015
TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin CWD
postive farm Yellow ear tag
NORTH DAKOTA CWD
Monday, March 23, 2015
North Dakota Documents Two More Cases of Chronic Wasting Disease CWD TSE
Prion
VIRGINIA CWD
Wednesday, July 01, 2015
DRAFT Virginia Deer Management Plan 2015-2024 (bans urine scents do to CWD
2015)
Wednesday, February 12, 2014
VIRGINIA VDGIF Reports Two New CWD Positives in Frederick County
*** PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS ***
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Additionally, human rPrP was competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
1984
*** The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT
THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
snip...
85%+ of all human tse prion disease is sporadic CJD.
see what the NIH prion Gods say themselves ;
‘’In the Archives of Neurology you quoted (the abstract of which was
attached to your email), we did not say CWD in humans will present like variant
CJD. That assumption would be wrong.’’
‘’Also, we do not claim that "no-one has ever been infected with prion
disease from eating venison." Our conclusion stating that we found no strong
evidence of CWD transmission to humans in the article you quoted or in any other
forum is limited to the patients we investigated.’’
*** 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).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
*** 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).***
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases...TSS
===============
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
***Title: Transmission of chronic wasting disease to sentinel reindeer
(Rangifer tarandus tarandus)
Authors
item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt,
Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring,
fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer
tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has
not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed
reindeer. 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; CWD-wtd), mule deer
(Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) 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 CWD-wtd, CWD-md, or CWD-elk. Two years
after challenge of inoculated reindeer, non-inoculated control reindeer were
introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a
pen adjacent to the CWD-md inoculated reindeer (n=2). 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 (PrP-CWD). Intracranially challenged
reindeer developed clinical disease from 21 months post-inoculation (MPI).
PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed
clinical disease during the study period (<57 div="" mpi="">
***We have shown that reindeer are susceptible to CWD from various cervid
sources and can transmit CWD to naive reindeer both directly and indirectly.
Last Modified: 12/3/2015
***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6
developed clinical disease during the study period (<57 div="" mpi="">
***We have shown that reindeer are susceptible to CWD from various cervid
sources and can transmit CWD to naive reindeer both directly and indirectly.
Tuesday, September 29, 2015
*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer
tarandus tarandus) can transmit CWD to naive reindeer both directly and
indirectly
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
CWD, spreading it around...
for the game farm industry, and their constituents, to continue to believe
that they are _NOT_, and or insinuate that they have _NEVER_ been part of the
problem, will only continue to help spread cwd. the game farming industry, from
the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet
mills, shooting pens, to large ranches, are not the only problem, but it is
painfully obvious that they have been part of the problem for decades and
decades, just spreading it around, as with transportation and or exportation and
or importation of cervids from game farming industry, and have been proven to
spread cwd. no one need to look any further than South Korea blunder ;
===========================================
spreading cwd around...
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
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.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al.,
2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
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.
snip...
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.
snip...
98 | Veterinary Record | January 24, 2015
EDITORIAL
Scrapie: a particularly persistent pathogen
Cristina Acín
Resistant prions in the environment have been the sword of Damocles for
scrapie control and eradication. Attempts to establish which physical and
chemical agents could be applied to inactivate or moderate scrapie infectivity
were initiated in the 1960s and 1970s,with the first study of this type focusing
on the effect of heat treatment in reducing prion infectivity (Hunter and
Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate
the prion protein are based on the method developed by Kimberlin and
collaborators (1983). This procedure consists of treatment with 20,000 parts per
million free chlorine solution, for a minimum of one hour, of all surfaces that
need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so
on). Despite this, veterinarians and farmers may still ask a range of questions,
such as ‘Is there an official procedure published somewhere?’ and ‘Is there an
international organisation which recommends and defines the exact method of
scrapie decontamination that must be applied?’
From a European perspective, it is difficult to find a treatment that could
be applied, especially in relation to the disinfection of surfaces in lambing
pens of affected flocks. A 999/2001 EU regulation on controlling spongiform
encephalopathies (European Parliament and Council 2001) did not specify a
particular decontamination measure to be used when an outbreak of scrapie is
diagnosed. There is only a brief recommendation in Annex VII concerning the
control and eradication of transmissible spongiform encephalopathies (TSE
s).
Chapter B of the regulation explains the measures that must be applied if
new caprine animals are to be introduced to a holding where a scrapie outbreak
has previously been diagnosed. In that case, the statement indicates that
caprine animals can be introduced ‘provided that a cleaning and disinfection of
all animal housing on the premises has been carried out following
destocking’.
Issues around cleaning and disinfection are common in prion prevention
recommendations, but relevant authorities, veterinarians and farmers may have
difficulties in finding the specific protocol which applies. The European Food
and Safety Authority (EFSA ) published a detailed report about the efficacy of
certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and
even a formulation of copper or iron metal ions in combination with hydrogen
peroxide, against prions (EFSA 2009). The report was based on scientific
evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006,
Solassol and others 2006) but unfortunately the decontamination measures were
not assessed under outbreak conditions.
The EFSA Panel on Biological Hazards recently published its conclusions on
the scrapie situation in the EU after 10 years of monitoring and control of the
disease in sheep and goats (EFSA 2014), and one of the most interesting findings
was the Icelandic experience regarding the effect of disinfection in scrapie
control. The Icelandic plan consisted of: culling scrapie-affected sheep or the
whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of
stables, sheds, barns and equipment with high pressure washing followed by
cleaning with 500 parts per million of hypochlorite; drying and treatment with
300 ppm of iodophor; and restocking was not permitted for at least two years.
Even when all of these measures were implemented, scrapie recurred on several
farms, indicating that the infectious agent survived for years in the
environment, even as many as 16 years after restocking (Georgsson and others
2006).
In the rest of the countries considered in the EFSA (2014) report,
recommendations for disinfection measures were not specifically defined at the
government level. In the report, the only recommendation that is made for sheep
is repopulation with sheep with scrapie-resistant genotypes. This reduces the
risk of scrapie recurrence but it is difficult to know its effect on the
infection.
Until the EFSA was established (in May 2003), scientific opinions about TSE
s were provided by the Scientific Steering Committee (SSC) of the EC, whose
advice regarding inactivation procedures focused on treating animal waste at
high temperatures (150°C for three hours) and high pressure alkaline hydrolysis
(SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory
Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe
working and the prevention of TSE infection. Annex C of the ACDP report
established that sodium hypochlorite was considered to be effective, but only if
20,000 ppm of available chlorine was present for at least one hour, which has
practical limitations such as the release of chlorine gas, corrosion,
incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its
active chemicals and the stability of dilutions (ACDP 2009).
In an international context, the World Organisation for Animal Health (OIE)
does not recommend a specific disinfection protocol for prion agents in its
Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General
recommendations on disinfection and disinsection (OIE 2014), focuses on
foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on
prion disinfection. Nevertheless, the last update published by the OIE on bovine
spongiform encephalopathy (OIE 2012) indicates that few effective
decontamination techniques are available to inactivate the agent on surfaces,
and recommends the removal of all organic material and the use of sodium
hydroxide, or a sodium hypochlorite solution containing 2 per cent available
chlorine, for more than one hour at 20ºC.
The World Health Organization outlines guidelines for the control of TSE s,
and also emphasises the importance of mechanically cleaning surfaces before
disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO
1999).
Finally, the relevant agencies in both Canada and the USA suggest that the
best treatments for surfaces potentially contaminated with prions are sodium
hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution,
while most commercial household bleaches contain 5.25 per cent sodium
hypochlorite. It is therefore recommended to dilute one part 5.25 per cent
bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency
2013).
So what should we do about disinfection against prions? First, it is
suggested that a single protocol be created by international authorities to
homogenise inactivation procedures and enable their application in all
scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available
chlorine seems to be the procedure used in most countries, as noted in a paper
summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015).
But are we totally sure of its effectiveness as a preventive measure in a
scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease
be needed?
What we can conclude is that, if we want to fight prion diseases, and
specifically classical scrapie, we must focus on the accuracy of diagnosis,
monitoring and surveillance; appropriate animal identification and control of
movements; and, in the end, have homogeneous and suitable protocols to
decontaminate and disinfect lambing barns, sheds and equipment available to
veterinarians and farmers. Finally, further investigations into the resistance
of prion proteins in the diversity of environmental surfaces are required.
References
snip...
98 | Veterinary Record | January 24, 2015
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc
MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C.
Maddison, BSc, PhD3 + Author Affiliations
1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey
KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of
Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS
UK, School of Veterinary Medicine and Science, The University of Nottingham,
Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for
correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and
chronic wasting disease of deer/elk are contagious prion diseases where
environmental reservoirs are directly implicated in the transmission of disease.
In this study, the effectiveness of recommended scrapie farm decontamination
regimens was evaluated by a sheep bioassay using buildings naturally
contaminated with scrapie. Pens within a farm building were treated with either
20,000 parts per million free chorine solution for one hour or were treated with
the same but were followed by painting and full re-galvanisation or replacement
of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype
VRQ/VRQ were reared within these pens and their scrapie status was monitored by
recto-anal mucosa-associated lymphoid tissue. All animals became infected over
an 18-month period, even in the pen that had been subject to the most stringent
decontamination process. These data suggest that recommended current guidelines
for the decontamination of farm buildings following outbreaks of scrapie do
little to reduce the titre of infectious scrapie material and that environmental
recontamination could also be an issue associated with these premises.
SNIP...
Discussion
Thorough pressure washing of a pen had no effect on the amount of
bioavailable scrapie infectivity (pen B). The routine removal of prions from
surfaces within a laboratory setting is treatment for a minimum of one hour with
20,000 ppm free chlorine, a method originally based on the use of brain
macerates from infected rodents to evaluate the effectiveness of decontamination
(Kimberlin and others 1983). Further studies have also investigated the
effectiveness of hypochlorite disinfection of metal surfaces to simulate the
decontamination of surgical devices within a hospital setting. Such treatments
with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower
than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous
treatment of the pen surfaces did not effectively remove the levels of scrapie
infectivity over that of the control pens, indicating that this method of
decontamination is not effective within a farm setting. This may be due to the
high level of biological matrix that is present upon surfaces within the farm
environment, which may reduce the amount of free chlorine available to
inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had
also became scrapie positive within nine months, with all animals in this pen
being RAMALT positive by 18 months of age. Pen D was no further away from the
control pen (pen A) than any of the other pens within this barn. Localised hot
spots of infectivity may be present within scrapie-contaminated environments,
but it is unlikely that pen D area had an amount of scrapie contamination that
was significantly different than the other areas within this building.
Similarly, there were no differences in how the biosecurity of pen D was
maintained, or how this pen was ventilated compared with the other pens. This
observation, perhaps, indicates the slower kinetics of disease uptake within
this pen and is consistent with a more thorough prion removal and
recontamination. These observations may also account for the presence of
inadvertent scrapie cases within other studies, where despite stringent
biosecurity, control animals have become scrapie positive during challenge
studies using barns that also housed scrapie-affected animals (Ryder and others
2009). The bioassay data indicate that the exposure of the sheep to a farm
environment after decontamination efforts thought to be effective in removing
scrapie is sufficient for the animals to become infected with scrapie. The main
exposure routes within this scenario are likely to be via the oral route, during
feeding and drinking, and respiratory and conjunctival routes. It has been
demonstrated that scrapie infectivity can be efficiently transmitted via the
nasal route in sheep (Hamir and others 2008), as is the case for CWD in both
murine models and in white-tailed deer (Denkers and others 2010, 2013).
Recently, it has also been demonstrated that CWD prions presented as dust when
bound to the soil mineral montmorillonite can be infectious via the nasal route
(Nichols and others 2013). When considering pens C and D, the actual source of
the infectious agent in the pens is not known, it is possible that biologically
relevant levels of prion survive on surfaces during the decontamination regimen
(pen C). With the use of galvanising and painting (pen D) covering and sealing
the surface of the pen, it is possible that scrapie material recontaminated the
pens by the movement of infectious prions contained within dusts originating
from other parts of the barn that were not decontaminated or from other areas of
the farm.
Given that scrapie prions are widespread on the surfaces of affected farms
(Maddison and others 2010a), irrespective of the source of the infectious prions
in the pens, this study clearly highlights the difficulties that are faced with
the effective removal of environmentally associated scrapie infectivity. This is
likely to be paralleled in CWD which shows strong similarities to scrapie in
terms of both the dissemination of prions into the environment and the facile
mode of disease transmission. These data further contribute to the understanding
that prion diseases can be highly transmissible between susceptible individuals
not just by direct contact but through highly stable environmental reservoirs
that are refractory to decontamination.
The presence of these environmentally associated prions in farm buildings
make the control of these diseases a considerable challenge, especially in
animal species such as goats where there is lack of genetic resistance to
scrapie and, therefore, no scope to re-stock farms with animals that are
resistant to scrapie.
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE)
Accepted October 12, 2014. Published Online First 31 October 2014
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
Willingham, Erin McNulty, Kelly Anderson, Jeanette Hayes-Klug, Amy Nalls,
and Candace Mathiason Colorado State University; Fort Collins, CO USA
Chronic wasting disease (CWD) is the transmissible spongiform
encephalopathy (TSE), of free-ranging and captive cervids (deer, elk and moose).
The presence of infectious prions in the tissues, bodily fluids and
environments of clinical and preclinical CWD-infected animals is thought to
account for its high transmission efficiency. Recently it has been recognized
that mother to offspring transmission may contribute to the facile transmission
of some TSEs. Although the mechanism behind maternal transmission is not yet
known, the extended asymptomatic TSE carrier phase (lasting years to decades)
suggests that it may have implications in the spread of prions.
Placental trafficking and/or secretion in milk are 2 means by which
maternal prion transmission may occur. In these studies we explore these avenues
during early and late infection using a transgenic mouse model expressing cervid
prion protein. Na€ıve and CWD-infected dams were bred at both timepoints, and
were allowed to bear and raise their offspring. Milk was collected from the dams
for prion analysis, and the offspring were observed for TSE disease progression.
Terminal tissues harvested from both dams and offspring were analyzed for
prions.
We have demonstrated that
(1) CWDinfected TgCerPRP females successfully breed and bear offspring, and
(2) the presence of PrPCWD in reproductive and mammary tissue from
CWD-infected dams.
We are currently analyzing terminal tissue harvested from offspring born to
CWD-infected dams for the detection of PrPCWD and amplification competent
prions. These studies will provide insight into the potential mechanisms and
biological significance associated with mother to offspring transmission of
TSEs.
==============
P.157: Uptake of prions into plants
Christopher Johnson1, Christina Carlson1, Matthew Keating1,2, Nicole
Gibbs1, Haeyoon Chang1, Jamie Wiepz1, and Joel Pedersen1 1USGS National Wildlife
Health Center; Madison, WI USA; 2University of Wisconsin - Madison; Madison, WI
USA
Soil may preserve chronic wasting disease (CWD) and scrapie infectivity in
the environment, making consumption or inhalation of soil particles a plausible
mechanism whereby na€ıve animals can be exposed to prions. Plants are known to
absorb a variety of substances from soil, including whole proteins, yet the
potential for plants to take up abnormal prion protein (PrPTSE) and preserve
prion infectivity is not known. In this study, we assessed PrPTSE uptake into
roots using laser scanning confocal microscopy with fluorescently tagged PrPTSE
and we used serial protein misfolding cyclic amplification (sPMCA) and detect
and quantify PrPTSE levels in plant aerial tissues. Fluorescence was identified
in the root hairs of the model plant Arabidopsis thaliana, as well as the crop
plants alfalfa (Medicago sativa), barley (Hordeum vulgare) and tomato (Solanum
lycopersicum) upon exposure to tagged PrPTSE but not a tagged control
preparation. Using sPMCA, we found evidence of PrPTSE in aerial tissues of A.
thaliana, alfalfa and maize (Zea mays) grown in hydroponic cultures in which
only roots were exposed to PrPTSE. Levels of PrPTSE in plant aerial tissues
ranged from approximately 4 £ 10 ¡10 to 1 £ 10 ¡9 g PrPTSE g ¡1 plant dry weight
or 2 £ 105 to 7 £ 106 intracerebral ID50 units g ¡1 plant dry weight. Both stems
and leaves of A. thaliana grown in culture media containing prions are
infectious when intracerebrally-injected into mice. ***Our results suggest that
prions can be taken up by plants and that contaminated plants may represent a
previously unrecognized risk of human, domestic species and wildlife exposure to
prions.
===========
***Our results suggest that prions can be taken up by plants and that
contaminated plants may represent a previously unrecognized risk of human,
domestic species and wildlife exposure to prions.***
SEE ;
Friday, May 15, 2015
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
Report
============
P.19: Characterization of chronic wasting disease isolates from freeranging
deer (Odocoileus sp) in Alberta and Saskatchewan, Canada
Camilo Duque Velasquez1, Chiye Kim1, Nathalie Daude1, Jacques van der
Merwe1, Allen Herbst1, Trent Bollinger2, Judd Aiken1, and Debbie McKenzie1
1Centre for Prions and Protein Folding Diseases; University of Alberta;
Edmonton, Canada; 2Western College of Veterinary Medicine; University of
Saskatchewan; Saskatoon, Canada
Chronic wasting disease (CWD) is an emerging prion disease of free ranging
and captive species of Cervidae. In North America, CWD is enzootic in some wild
cervid populations and can circulate among different deer species. The
contagious nature of CWD prions and the variation of cervid PRNP alleles, which
influence host susceptibility, can result in the emergence and adaptation of
different CWD strains. These strains may impact transmission host range, disease
diagnosis, spread dynamics and efficacy of potential vaccines. We are
characterizing different CWD agents by biochemical analysis of the PrPCWD
conformers, propagation in vitro cell assays1 and by comparing transmission
properties and neuropathology in Tg33 (Q95G96) and Tg60 (Q95S96) mice.2 Although
Tg60 mice expressing S96- PrPC have been shown resistant to CWD infectivity from
various cervid species,2,3
***these transgenic mice are susceptible to H95 C CWD, a CWD strain derived
from experimental infection of deer expressing H95G96-PrPC. The diversity of
strains present in free-ranging mule deer (Odocoileus hemionus) and white-tailed
deer (Odocoileus virginianus) from Alberta and Saskatchewan is being determined
and will allow us to delineate the properties of CWD agents circulating in CWD
enzootic cervid populations of Canada.
References
1. van der Merwe J, Aiken J, Westaway D, McKenzie D. The standard scrapie
cell assay: Development, utility and prospects. Viruses 2015; 7(1):180–198;
PMID:25602372; http://dx.doi.org/10.3390/v7010180
2. Meade-White K, Race B, Trifilo M, Bossers A, Favara C, Lacasse R, Miller
M, Williams E, Oldstone M, Race R, Chesebro B. Resistance to chronic wasting
disease in transgenic mice expressing a naturally occurring allelic variant of
deer prion protein. J Virol 2007; 81(9):4533–4539; PMID: 17314157; http://dx. doi.org/10.1128/JVI.02762-06
3. Race B, Meade-White K, Miller MW, Fox KA, Chesebro B. In vivo comparison
of chronic wasting disease infectivity from deer with variation at prion protein
residue 96. J Virol 2011; 85(17):9235–9238; PMID: 21697479; http://dx.doi.org/10.1128/JVI.00790-11
=========
***these transgenic mice are susceptible to H95 C CWD, a CWD strain derived
from experimental infection of deer expressing H95G96-PrPC.
==========
P.136: Mother to offspring transmission of CWD—Detection in fawn tissues
using the QuIC assay
Amy Nalls, Erin McNulty, Clare Hoover, Jeanette Hayes-Klug, Kelly Anderson,
Edward Hoover, and Candace Mathiason Colorado State University; Fort Collins, CO
USA
To investigate the role mother to offspring transmission plays in chronic
wasting disease (CWD), we have employed a small, polyestrous breeding, indoor
maintainable cervid model, the Reeves’ muntjac deer. Muntjac doe were inoculated
with CWD and tested positive by lymphoid biopsy at 4 months post inoculation.
From these CWD-infected doe, we obtained 3 viable fawns. These fawns tested
IHC-positive for CWD by lymphoid biopsy as early as 40 d post birth, and all
have been euthanized due to clinical disease at 31, 34 and 59 months post birth.
The QuIC assay demonstrates sensitivity and specificity in the detection of
conversion competent prions in peripheral IHC-positive tissues including tonsil,
mandibular, partotid, retropharyngeal, and prescapular lymph nodes, adrenal
gland, spleen and liver. In summary, using the muntjac deer model, we have
demonstrated CWD clinical disease in offspring born to CWD-infected doe and
found that the QuIC assay is an effective tool in the detection of prions in
peripheral tissues. ***Our findings demonstrate that transmission of prions from
mother to offspring can occur, and may be underestimated for all prion
diseases.
===============
***Our findings demonstrate that transmission of prions from mother to
offspring can occur, and may be underestimated for all prion diseases.
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, ***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
================
P.97: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and
Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State
University; Ames, IA USA
The purpose of this work was to determine susceptibility of white-tailed
deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to
that of the original inoculum and chronic wasting disease (CWD). We inoculated
WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5)
with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues at preclinical time points,
and deer necropsied after 28 months post-inoculation had clinical signs,
spongiform encephalopathy, and widespread distribution of PrPSc in neural and
lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular
profiles. WB on cerebral cortex had a profile similar to the original scrapie
inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc
with a higher profile resembling CWD. Homogenates with the 2 distinct profiles
from WTD with clinical scrapie were further passaged to mice expressing cervid
prion protein and intranasally to sheep and WTD. In cervidized mice, the 2
inocula have distinct incubation times. Sheep inoculated intranasally with WTD
derived scrapie developed disease, but only after inoculation with the inoculum
that had a scrapie-like profile. The WTD study is ongoing, but deer in both
inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary,
this work demonstrates that WTD are susceptible to the agent of scrapie, 2
distinct molecular profiles of PrPSc are present in the tissues of affected
deer, and inoculum of either profile readily passes to deer.
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
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.
snip...
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.
snip...
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
Monday, October 26, 2015
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Sunday, October 25, 2015
USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE
LIVESTOCK CWD SCRAPIE TSE PRION
http://chronic-wasting-disease.blogspot.com/2015/10/usaha-detailed-events-schedule-119th.html
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation ***
Saturday, September 12, 2015
In utero transmission and tissue distribution of chronic wasting
disease-associated prions in free-ranging Rocky Mountain elk
>>>Interestingly, five of fifteen sPMCA positive dams showed no
evidence of PrPCWD in either CNS or LRS, sites typically assessed in diagnosing
CWD. Analysis of fetal tissues harvested from the fifteen sPMCA positive dams
revealed PrPCWD in 80% of fetuses (12/15), regardless of gestational stage.
These findings demonstrate that PrPCWD is more abundant in peripheral tissues of
CWD exposed elk than current diagnostic methods suggest, and that transmission
of prions from mother to offspring may contribute to the efficient transmission
of the CWD in naturally exposed cervid populations.<<<
***S P O N T A N E O U S***S P O R A D I C***
spontaneous atypical BSE ???
if that's the case, then France is having one hell of an epidemic of
atypical BSE, probably why they stopped testing for BSE, problem solved
$$$
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
so 20 cases of atypical BSE in France, compared to the remaining 40 cases
in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+
cases per country, besides Frances 20 cases. you cannot explain this away with
any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
*** spontaneous TSE prion, that's wishful thinking. on the other hand, if
spontaneous did ever happen (never once documented in the field), it would be
our worst nightmare, due to feed. just saying.
*** We describe the transmission of spongiform encephalopathy in a
non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie.
Because of this extended incubation period in a facility in which other prion
diseases are under study, we are obliged to consider two alternative
possibilities that might explain its occurrence. We first considered the
possibility of a sporadic origin (like CJD in humans). Such an event is
extremely improbable because the inoculated animal was 14 years old when the
clinical signs appeared, i.e. about 40% through the expected natural lifetime of
this species, compared to a peak age incidence of 60–65 years in human sporadic
CJD, or about 80% through their expected lifetimes. ***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.***
***>>> 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.
<<<***
2015
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
*** Title: Transmission of scrapie prions to primate after an extended
silent incubation period Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573. Interpretive Summary: The
transmissible spongiform encephalopathies (also called prion diseases) are fatal
neurodegenerative diseases that affect animals and humans. The agent of prion
diseases is a misfolded form of the prion protein that is resistant to breakdown
by the host cells. Since all mammals express prion protein on the surface of
various cells such as neurons, all mammals are, in theory, capable of
replicating prion diseases. One example of a prion disease, bovine spongiform
encephalopathy (BSE; also called mad cow disease), has been shown to infect
cattle, sheep, exotic undulates, cats, non-human primates, and humans when the
new host is exposed to feeds or foods contaminated with the disease agent.
***The purpose of this study was to test whether non-human primates
(cynomologous macaque) are susceptible to the agent of sheep scrapie. After an
incubation period of approximately 10 years a macaque developed progressive
clinical signs suggestive of neurologic disease. Upon postmortem examination and
microscopic examination of tissues, there was a widespread distribution of
lesions consistent with a transmissible spongiform encephalopathy.
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is
an animal prion disease that also causes variant Creutzfeldt-Jakob disease in
humans. Over the past decades, c-BSE's zoonotic potential has been the driving
force in establishing extensive protective measures for animal and human health.
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.
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
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Transmission of the agent of
sheep scrapie to deer results in PrPSc with two distinct molecular profiles
Authors
item Greenlee, Justin item Moore, Sarah - item Smith, Jodi item West
Greenlee, Mary - item Kunkle, Robert
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance
Date: March 31, 2015 Publication Date: May 25, 2015 Citation: Greenlee, J.,
Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015.
Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum. Prion 2015. p. S62. Technical Abstract: The purpose of this
work was to determine susceptibility of white-tailed deer (WTD) to the agent of
sheep scrapie and to compare the resultant PrPSc to that of the original
inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route
of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie
isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc
was detected in lymphoid tissues at preclinical time points, and deer necropsied
after 28 months post-inoculation had clinical signs, spongiform encephalopathy,
and widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes reveal PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile type readily passes to deer.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Scrapie transmits to
white-tailed deer by the oral route and has a molecular profile similar to
chronic wasting disease Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A
Technical Abstract: The purpose of this work was to determine
susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to
compare the resultant PrPSc to that of the original inoculum and chronic wasting
disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral
and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer
had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at
preclinical time points, and deer necropsied after 28 months post-inoculation
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with
2 distinct molecular profiles. WB on cerebral cortex had a profile similar to
the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph
nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the
2 distinct profiles from WTD with clinical scrapie were further passaged to mice
expressing cervid prion protein and intranasally to sheep and WTD. In cervidized
mice, the two inocula have distinct incubation times. Sheep inoculated
intranasally with WTD derived scrapie developed disease, but only after
inoculation with the inoculum that had a scrapie-like profile. The WTD study is
ongoing, but deer in both inoculation groups are positive for PrPSc by rectal
mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to
the agent of scrapie, two distinct molecular profiles of PrPSc are present in
the tissues of affected deer, and inoculum of either profile readily passes to
deer.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
Monday, October 26, 2015
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Wednesday, October 07, 2015
Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic
Wasting Disease Strains
Tuesday, February 26, 2013
*** Planned elk drive from Wind Cave National Park raises question about
spread of disease
yes, it did take place, I called to confirm. insanity at it’s
finest...tss
Saturday, May 25, 2013
Wyoming Game and Fish Commission Alkali Creek Feedground #39126 Singeltary
comment submission
Friday, November 16, 2012
Yellowstone elk herds feeding grounds, or future killing grounds from CWD
Tuesday, March 05, 2013
Chronic Wasting Disease Management Plan/Environmental Impact Statement,
Shenandoah National Park Virginia
Friday, August 14, 2015
*** Susceptibility of cattle to the agent of chronic wasting disease from
elk after intracranial inoculation
Friday, August 14, 2015
Carcass Management During a Mass Animal Health Emergency Draft Programmatic
Environmental Impact Statement—August 2015
Tuesday, September 22, 2015
*** Host Determinants of Prion Strain Diversity Independent of Prion
Protein Genotype
Friday, August 28, 2015
*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical
infection
Sunday, October 25, 2015
*** USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE
LIVESTOCK CWD SCRAPIE TSE PRION ***
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Monday, October 26, 2015
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
Sunday, October 25, 2015
*** USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE
LIVESTOCK CWD SCRAPIE TSE PRION ***
Sunday, December 28, 2014
CHRONIC WASTING DISEASE CWD TSE PRION DISEASE AKA MAD DEER DISIEASE USDA
USAHA INC DECEMBER 28, 2014
Sunday, October 18, 2015
*** World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research ***
FLASHBACK
1999
BSE Response Team
The BSE Response Team will complete the informational memorandum for the
Secretary. The Team will prepare the letter to the Office of International
Epizootics (OIE), the international animal health organization, for signature by
the APHIS, VS Deputy Administrator. OIE requires that all countries submit
official notification within 24 hours of confirming a diagnosis of BSE. The BSE
Response Team and the office of the APHIS, VS Deputy Administrator would
coordinate a teleconference to inform all APHIS regional directors and AVIC'S.
The BSE Response Team and the office of the FSIS, OPHS Deputy Administrator
would coordinate a teleconference to inform all regional and field FSIS offices.
The BSE Response Team would coordinate a teleconference to notify other Federal
agencies. The BSE Response Team would coordinate a teleconference to notify key
industry/consumer representatives. The BSE Response Team and APHIS International
Services would notify foreign embassies. The BSE Response Team would establish a
toll-free 800 telephone line for industry representatives, reporters, and the
public. The BSE Response Team would coordinate with APHIS Legislative and Public
Affairs and USDA office of Communications to issue a press release the day the
diagnosis is confirmed. The press release would announce a press conference to
be held the morning after the diagnosis is confirmed......
THE END
From: Terry S. Singeltary Sr. (216-119-138-126.ipset18.wt.net)
Subject: Hunkering down in the APHIS BSE Situation Room...
Date: February 14, 2000 at 9:04 am PST
Subject: hunkering down in the APHIS BSE Situation Room
Date: Wed, 12 May 1999 01:55:54 –0800
From: tom
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
i am looking now a bizarre Oct 98 internal USDA publication describing a
james bond-type US effort to control media should the long-anticipated first
case of BSE in the US be admitted.
'Players' on the 27 member BSE Response Team are to be flown in from all
over the country to a BSE Headquarters 'situation room' apparently an
underground bunker in Riverdale, Maryland under the command of the Assistant
Secretary of Marketing.
Authentic press releases are already prepared and ready to go out after a
few specifics have been filled in. They are spelled out in a separate document,
the BSE Red Book, aka BSE Emergency Disease Guidelines.
Aphis' National Veterinary Services Laboratories (NVSL) activates team
assembly. From the time a bovine brain sample is submitted, it takes 14-18 days
to confirm a diagnosis of BSE. In the first 10-13 days, NVSL have enough
information to determine the need for additional tests. If a provisional BSE
diagnosis is made, the sample is 'hand-carried' (are they going to tell the
airline and customs?) to the Central Veterinary Laboratory in England for
confirmation, where they are expecting a 24 to 96 hour turn-around.
I guess that means we can get the white tiger brain analyzed by Friday
despite the 22 year delay to date. Maybe we could throw in a few cougar brains
from NE Colorado too.
A Team Member is designated to silently monitor this listserve and
www.mad-cow.org (among others) -- for what, it doesn't say. The Freedom of
Information Act request from the East Coast consumer group turned up numerous
top-secret USDA downloads from that site and Dealler's.
After 24 hours of secret briefings for 'select industry and trading
partners' (to allow them to take positions on the commodities markets opposite
the 'non-select' industry and trading partners?), a press conference will be
held the next day.
There are plans to trace the cow, its lineage, its herdmates, the renderer,
traceout of product, buyout of herd, farm of origin, to get the state involved
to quarantine the herd (pre-arranged for all 50 states), expectations for trade
bans, notification of OIE within 24 hours, media 800 numbers, spokespersons and
backups, notify CDC, FDA, NIH, and many other commendable activities. The Flow
Chart is a sight to behold, I will try to scan it in tomorrow.
In short, that cow is going to be toast by the time the public first hears
about it.
The Plan does not speak to the scenario in which the CVL says, yes, this is
bovine spongiform encephalopathy all right but it is one of your strains, not
ours. Invoking their Absence of Evidence is Evidence of Absence principle, there
may be no perceived need for public disclosure in this case.
USDA is caught completely unprepared if BSE first turns up in a US zoo
animal. These animals could easily be diagnosed outside the "system" and be the
subject of a publicity-seeking lab press release. I think this is a more likely
scenario because the US has likely imported many thousands of zoo animals with
advanced infections from Britain and France and there has been zero monitoring.
Unlike with downer cows, anyone with the right colleagues can get ahold of a
fallen zoo animal. Zoo animals enter the food chain in some cases after being
rendered.
Another scenario would be some stock market speculator obtaining the Red
Book and issuing a flurry of bogus but authentic-looking press releases that
included bogus 800 and hacked USDA web links. The press here is so lazy and so
accustomed to putting out public relation handouts as news that the objectives
would be accomplished for a few hour (or days, depending on the Response Team's
paralysis vis-a-vis off-flow chart events). Some people think a practise run for
this happened in the Indiana case a year or two back.
The first case of nvCJD in an American will also be a public relations
fiasco. In the dim bulb of the public mind, any American with mad cow disease
would have gotten it from eating meat here. USDA has no way to prove that the
victim acquired it on a three week trip to England in 1987. This will sound lame
even to the press. All CJD is synonymous with mad cow disease in the public
perception; the more often the different kinds are explained, the more their
suspicions are aroused. The first case of nvCJD in an American will simply
validate what they already know and just be viewed as an overdue admission from
the government.
tom
___________________________________________________________
From: Terry S. Singeltary Sr. (216-119-130-102.ipset10.wt.net)
Subject: When a case of B.S.E. is found in the U.S/Response to Disease
outbreak...'redbook'
Date: March 13, 2000 at 10:13 am PST
BSE Red Book 2.1-26
snip...see full text ;
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened ***
Friday, May 29, 2015
GAO FEDERAL VETERINARIANS US Federal Government Is Unprepared for a
Large-Scale Animal Disease Outbreak
Monday, June 23, 2014
PRION 2014 CHRONIC WASTING DISEASE CWD
Saturday, December 12, 2015
*** NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015 ***
http://transmissiblespongiformencephalopathy.blogspot.com/2015/12/notice-environmental-impact-statement.html
Saturday, December 12, 2015
Saturday, December 12, 2015
*** CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
RIP mom December 14, 1997 confirmed hvCJD
I asked someone recently, what sort of hunting legacy do you want to leave
your children, did you want to have where all you have are blind, slobbering,
drooling, stumbling, or maybe even healthy looking subclinical cwd infected
cervid, to go on and expose who knows what (cause cwd is spreading, it has
mutated, and nobody can stop it so far), but is this what we want to leave our
children? the only answer I ever seem to get from anyone in the industry, is
just let cwd take care of itself. well hell, how is that working for us so
far?
this cwd tse prion must be stopped. the vertical and lateral transmission
of this cwd tse prion agent amongst cervids, if cwd jumps species (if it has not
already), and transmits the same ways vertical and lateral in other species, and
the other species are as susceptible from so many different routes and sources,
simply put, we’re screwed. just saying. I am not trying to scare anyone, I am
simply presenting the facts, you must make your own decision or not. we have
ignored these tse prion disease way too long.
these blogs are for educational use. I do not advertise or make money from
them.
MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget,
and never let them forget...
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
8:40 PM
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