Thursday, May 31, 2012
MDC open house on CWD next steps June 2 in Macon County
News from the Central and Northeast regions
Published on: May. 25, 2012
Posted by Joe Jerek
JEFFERSON CITY Mo. – The Missouri Department of Conservation (MDC) will
hold an informational open house on Chronic Wasting Disease (CWD) in Macon
County on June 2 at New Cambria High School, 501 S. Main St. The public is
invited to stop by 1-4 p.m.
MDC staff will provide information on five recently found cases of CWD in
free-ranging deer in northwest Macon County, explain disease management actions
the Department is taking, answer questions and provide information on managing
private land for deer.
MDC’s disease-management steps to help contain the spread of CWD include
two regulation changes to the Wildlife Code of Missouri, recommendations on
transportation and disposal of deer carcasses and continuing CWD sampling of
deer harvested in the area where CWD has been found.
Restriction on Feeding
The Conservation Commission approved a regulation change at its May 25
meeting that places a restriction on activities that are likely to unnaturally
concentrate white-tailed deer and promote the spread of CWD. The ban on the
placement of grain, salt products, minerals and other consumable natural or
manufactured products is limited to the area where CWD has been found in Macon
County and is comprised of Adair, Chariton, Linn, Macon, Randolph and Sullivan
counties.
The regulation includes exceptions for backyard feeding of birds and other
wildlife within 100 feet of any residence or occupied building, or if feed is
placed in such a manner to reasonably exclude access by deer. The regulation
also includes exceptions for normal agricultural, forest management, crop and
wildlife food production practices.
According to MDC Deer Biologist Jason Sumners, the reason for the
regulation change is that activities such as feeding and placement of
minerals/salts that artificially concentrate deer greatly increase the
likelihood of disease transmission from animal to animal or from soil to animal.
Removal of Antler-Point Restriction
The Conservation Commission also approved a regulation change at its May 25
meeting for a special harvest provision that rescinds the antler-point
restriction (four-point rule) in Adair, Chariton, Linn, Macon, Randolph and
Sullivan counties.
According to Sumners, the reason for the regulation change is that
management strategies such as antler-point restrictions, which protect yearling
males and promote older bucks, have been found to increase prevalence rates and
further spread the disease.
Sumners explained that yearling and adult male deer have been found to
exhibit CWD at much higher rates than yearling and adult females so a reduction
in the number of male deer can help reduce the spread of CWD. He added that the
movement of young male deer from their birth range in search of territory and
mates is also a way of expanding the distribution of CWD.
Don’t Remove Carcasses from Area
MDC also encourages hunters who harvest deer in Adair, Chariton, Linn,
Macon, Randolph, and Sullivan counties not to take whole deer carcasses or
carcass parts out of the area where CWD has been found. Exceptions to this
include meat that is cut and wrapped, meat that has been boned out, quarters or
other portions of meat with no part of the spinal column or head attached, hides
or capes from which all excess tissue has been removed, antlers, antlers
attached to skull plates or skulls cleaned of all muscle and brain tissue, upper
canine teeth and finished taxidermy products.
According to Sumners, the reason for this recommendation is that CWD can be
transmitted from the environment to deer through soil and water that contain
infected waste and/or infected carcasses. Deer can be infected with CWD but have
no visible signs or symptoms. Moving harvested deer that still have parts known
to concentrate CWD (brain, spinal cord, eyes, spleen, and lymph nodes) from the
area known to have CWD can introduce the disease to other parts of the state
through the improper disposal of carcasses.
He explained that hunters should make every attempt to avoid moving the
head and spinal cord from the area and properly dispose of potentially infected
deer carcasses, including bones and trimmings, to minimize the risk of exposure
to uninfected deer. MDC advises hunters to double-bag carcass parts and take
them directly to a landfill, or place them in trash cans for pick-up. Burying
carcass waste deep enough to prevent scavengers from digging it up is another
acceptable option. As a last resort, and only on their own land, hunters can put
carcass waste back on the landscape. Carcasses should be put as close as
possible to where the deer was harvested so as to not spread CWD-causing prions
to new locations. If possible, put the carcass in a location where it will be
inaccessible to scavengers and other deer.
Fall Harvest CWD Sampling
Sumners added that MDC will also continue to work with hunters who harvest
deer this fall in Adair, Chariton, Linn, Macon, Randolph and Sullivan counties
to collect samples for CWD testing. Details on these efforts are being developed
and will be shared before the 2012 fall deer hunting season.
For more information on the open house, contact MDC Public Involvement
Coordinator Michele Baumer at 573-522-4115, ext. 3350, or
Michele.Baumer@mdc.mo.gov.
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Tuesday, January 24, 2012
CWD found in two free-ranging deer from Macon County Missouri
Friday, October 21, 2011
Chronic Wasting Disease Found in Captive Deer Missouri
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Tuesday, December 20, 2011
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.
snip...see full text and much more here ;
PRODUCT
Product is custom made deer feed packaged in 100 lb. poly bags. The product
has no labeling. Recall # V-003-5.
CODE
The product has no lot code. All custom made feed purchased between June
24, 2004 and September 8, 2004.
RECALLING FIRM/MANUFACTURER
Farmers Elevator Co, Houston, OH, by telephone and letter dated September
27, 2004. Firm initiated recall is ongoing.
REASON
Feed may contain protein derived from mammalian tissues which is prohibited
in ruminant feed.
VOLUME OF PRODUCT IN COMMERCE
Approximately 6 tons.
DISTRIBUTION
OH.
END OF ENFORCEMENT REPORT FOR October 20, 2004
################# BSE-L-subscribe-request@uni-karlsruhe.de
#################
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37
–0500
From: "Terry S. Singeltary Sr."
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html
CANADA PLANS TO IMPRISON ANYONE SPEAKING
ABOUT MAD COW or ANY OTHER DISEASE OUTBREAK, CENSORSHIP IS A TERRIBLE
THING
TSS
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
PO-031: Aerosol transmission of chronic wasting disease to white-tailed
deer
Nathaniel Denkers,1 Jeanette Hayes-Klug,1 Kelly Anderson,1 Sally Dahmes,2
David Osborn,3 Karl Miller,3 Robert Warren,3 Candace Mathiason,1 Edward Hoover1
1Colorado State University; Fort Collins, CO USA; 2WASCO Inc.; Monroe, GA
USA; 3Warnell School of Forestry and Natural Resources, University of Georgia;
Athens, GA USA
Purpose. A signature feature of chronic wasting disease (CWD) is its
efficient lateral transmission in nature, almost surely by mucosal exposure. Our
previous studies employing Tg(cerPrP) mice determined that CWD can be
transmitted to a susceptible host by aerosol exposure, a route with relatively
little investigation. The present study was designed to determine whether CWD is
transmissible by aerosol to a native cervid host, white-tailed deer.
Materials and Methods. Nine white-tailed deer were exposed to two (2)
aerosol doses of a 5% w/v CWD+ (n = 6) or CWD- (n = 3) brain homogenate,
delivered via the nasal passages using a customized aerosol apparatus. At
3-month intervals post inoculation (mpi), tonsil and recto-anal
mucosa-associated lymphoid tissue (RAMALT) biopsies were collected and assayed
for CWD infection by protein misfolding cyclic amplification (PMCA), western
blotting (WB), and immunohistochemistry (IHC).
Results. At 3 mpi and 6 mpi, tonsil and RAMALT biopsies were collected
from 5 of the 6 CWD + aerosol-exposed deer. Three of the 5 (60%) tested positive
for CWD by PMCA but not IHC or western blot analysis at 3 mpi. By 6 mpi, 5 of 5
(100%) were tonsil and/or RAMALT biopsy positive by at least two of the three
assays. Biopsies were collected from all CWD+ aerosol-exposed deer at 9 mpi,
with 6 of 6 (100%) tonsil and/ or RAMALT positive by western blot or IHC. At 10
mpi 3 of the 6 prion-exposed deer have developed early clinical signs of CWD
infection (hyperphagia, polydypsia, wide leg stance and head/neck
dorsi-flexion). All sham-inoculated deer are showing no clinical signs and have
remained CWD negative as assessed by all three assays. Interestingly, the prion
dose delivered to the deer by aerosol-exposure is estimated to be 20-fold lower
than the historical oral dose that has resulted in detectable CWD infection at 6
or 12 mpi.
Conclusions. This study documents the first aerosol transmission of CWD in
deer. These results further infer that aerosolized prions facilitate CWD
transmission with greater efficiency than does oral exposure to a larger prion
dose. Thus exposure via the respiratory mucosa may be significant in the facile
spread of CWD in deer and perhaps in prion transmission overall.
PO-073: Multiple routes of prion transepithelial transport in the nasal
cavity following inhalation
Anthony Kincaid, Shawn Feilmann, Melissa Clouse, Albert Lorenzo, Jason
Bartz Creighton University; Omaha, NE USA
Introduction. Inhalation of either prion-infected brain homogenate or
aerosolized prions has been shown to cause disease, and in the case of
inhalation of infected brain homogenate, the nasal route of infection has been
shown to be 10–100 times more efficient than the oral route. The cell types
involved in the in vivo transport of prions across the nasal cavity epithelium
have not been determined. M cells in the follicular associated epithelium have
been shown to mediate transcellular transport of prions in vitro and in the gut
of experimentally infected mice. We tested the hypothesis that M-cell mediated
transport was responsible for prion entry across nasal cavity epithelium
following inhalation.
Materials and Methods. Hamsters were inoculated extranasally with 50 or
100ul of infected (n = 31) or mock-infected (n = 13) brain homogenate. Control
animals were inoculated with buffer (n = 4) or were untreated (n = 5). Following
survival periods ranging from 15 to 180 min, animals were perfused, skulls were
decalcified and nasal cavities were embedded in paraffin. Tissue sections were
cut and processed immunohistochemically for glial fibrillary acidic protein to
identify brain homogenate, or for the disease-associated form of the prion
protein. Tissue sections not further than 112 um apart through the entire extent
of the nasal cavity were analyzed using light microscopy; photomicrographs were
obtained wherever inoculum was observed on the surface of, within, or deep to
the nasal mucosa for each animal.
Results. Infected or uninfected brain homogenate was identified within the
nasal cavities of animals at all time points and was seen crossing the nasal
cavity epithelium within minutes of inoculation; the transepithelial transport
of brain homogenate continued for up to 3 h after inoculation. Infected or
uninfected brain homogenate was seen adhering to, or located within, M cells at
all time points. However, larger volumes of infected or uninfected brain
homogenate were identified crossing between cells of the olfactory and
respiratory epithelia in multiple locations. In addition, infected or uninfected
brain homogenate was identified within the lumen of lymphatic vessels in the
lamina propria beneath the nasal mucosa at all time points.
Conclusion. Transepithelial transport of prions across nasal cavity mucosa
begins within minutes of inhalation and can continue for up to 3 h. While M
cells appear to transport prions across the follicular associated epithelium,
larger amounts of prions are transported between the cells of the respiratory
and olfactory epithelia, where they immediately enter the lymphatic vessels in
the lamina propria. Thus, inhaled prions can be spread via lymph draining the
nasal cavity and have access to somatic and autonomic nerves in the lamina
propria of the nasal cavity. The increased efficiency of the nasal cavity route
of infection compared with the oral route may be due to the rapid and prolonged
transport of prions between cells of the respiratory and olfactory
epithelia.
PO-033: Replication efficiency of soil-bound prions varies with soil type
Shannon Bartelt-Hunt,1 Samuel Saunders,1 Ronald Shikiya,2 Katie
Langenfeld,2 Jason Bartz2 1University of Nebraska-Lincoln; Omaha, NE USA;
2Creighton University; Omaha, NE USA
Prion sorption to soil is thought to play an important role in the
transmission of scrapie and chronic wasting disease (CWD) via the environment.
Sorption of PrP to soil and soil minerals is influenced by the strain and
species of PrPSc and by soil characteristics. However, the ability of soil-bound
prions to convert PrPc to PrPSc under these wide-ranging conditions remains
poorly understood. We developed a semiquantitative protein misfolding cyclic
amplification (PMCA) protocol to evaluate replication efficiency of soil-bound
prions. Binding of the hyper (HY) strain of transmissible mink encephalopathy
(TME) (hamster) prions to a silty clay loam soil yielded a greater-than-1-log
decrease in PMCA replication efficiency with a corresponding 1.3-log reduction
in titer. The increased binding of PrPSc to soil over time corresponded with a
decrease in PMCA replication efficiency. The PMCA efficiency of bound prions
varied with soil type, where prions bound to clay and organic surfaces exhibited
significantly lower replication efficiencies while prions bound to sand
exhibited no apparent difference in replication efficiency compared to unbound
controls. PMCA results from hamster and CWD agent-infected elk prions yielded
similar findings. Given that PrPSc adsorption affinity varies with soil type,
the overall balance between prion adsorption affinity and replication efficiency
for the dominant soil types of an area may be a significant determinant in the
environmental transmission of prion diseases.
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
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate.
All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep
with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the
intracranial route had evidence of PrPSc accumulation. PrPSc was detected in
lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer
that was necropsied at 15.6 months had widespread distribution of PrPSc
highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues
prior to the onset of clinical signs. IC inoculated deer necropsied after 20
months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread
distribution of PrPSc in neural and lymphoid tissues.
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.
PO-041: Susceptibility of domestic cats to CWD infection
Amy Nalls, Jeanette Hayes-Klug, Kelly Anderson, Davis Seelig, Kevin
Carnes, Susan Kraft, Edward Hoover, Candace Mathiason
Colorado State University; Fort Collins, CO USA
Domestic and non-domestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE); very likely due to consumption of bovine
spongiform encephalopathy (BSE) contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were
inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer
brain homogenate.
Between 40 and 43 months two IC-inoculated cats developed slowly
progressive symptoms including weight loss, anorexia, polydipsia, patterned
motor behaviors, and ataxia”’ultimately mandating euthanasia. PrPCWD was
detected in the brains of these animals by western blot, immunohistochemistry
(IHC), and quaking-induced conversion (RT-QuIC) assays. No clinical signs of TSE
were detected in the remaining primary passage cats at 86 months pi.
Feline-adapted CWD (FelCWD) was sub-passaged into groups (n = 4 or 5) of cats by
IC, PO, and IP/SQ routes.
All 5 IC inoculated cats developed symptoms of disease 20–24 months pi
(approximately half the incubation period of primary passage). Additional
symptoms in these animals included increasing aggressiveness and hyper
responsiveness. FelCWD was demonstrated in the brains of all the affected cats
by western blot and IHC. Currently, 3 of 4 IP/SQ, and 1 of 4 PO inoculated cats
have developed abnormal behavior patterns consistent with the early stage of
feline CWD. Magnetic resonance imaging (MRI) has been performed on 11 cats (6
clinically ill, 2 asymptomatic, and 3 age-matched negative controls).
Abnormalities were detected in 4 of 6 clinically ill cats and included
multifocal signal changes consistent with inflammation, ventricular size
increases, more prominent sulci, and white matter tract cavitation.
These results demonstrate that CWD can be transmitted and adapted to the
domestic cat, and raise the potential for cervid-to-feline transmission in
nature.
PO-055: Transgenetic modeling of the CWD species barrier to humans
Eri Saijo,1 Sehun Kim,2 Claudio Soto,3 Glenn Telling2 1University of
Kentucky College of Medicine; Fort Collins, CO USA; 2Department of Microbiology,
Immunology and Pathology; Colorado State University; Fort Collins, CO USA ;
3Department of Neurology; University of Texas Houston Medical School; Houston,
TX USA
Our recent studies raise significant concerns about the zoonotic potential
of CWD. First, we showed that tissues consumed by humans derived from deer or
elk with CWD, including skeletal muscle and antler velvet, harbor infectious
prions. In other studies, cervid PrPSc converted human PrPC after CWD prions
were stabilized by successive passages in vitro or in vivo.
We also identified at least two distinct strains of CWD, referred to as
CWD1 and CWD2, the host-range properties of which are currently undefined. Other
studies showed that codon 129, and the corresponding 132 residue in elk,
significantly influenced the transmission of BSE and CWD prions respectively in
transgenic (Tg) mouse models.
We inoculated Tg mice expressing human PrP encoding either methionine (M)
or valine (V) at codon 129 with deer or elk CWD prions that previously produced
disease in Tg mice expressing deer PrP with characteristics typical of CWD1 and
CWD2 strains, as well as CWD prions that had been passaged multiple times in Tg
mice expressing deer PrP.
While most Tg mice remained free of signs of prion disease for >260
days, small numbers of inoculated mice developed multiple, progressive
neurological signs, that were consistent with prion disease. However,
examination of brain materials from diseased mice failed to confirm the presence
of protease-resistant human PrP. These preliminary results are consistent with a
significant species barrier in humans to these CWD strains, and indicate that
the 129 polymorphism does not modulate susceptibility.
PO-056: PrPCWD profiling of white-tailed deer (Odocoileus virginianus)
with different Prnp genotypes following experimental oral infection
Camilo Duque Velasquez,1 Allen Herbst,1 Chad Johnson,2 Judd Aiken,1 Debbie
McKenzie1 1Centre for Prions and Protein Folding Diseases; University of
Alberta; Edmonton, AB Canada; 2Department of Soil Science; University of
Wisconsin; Madison, WI USA
Chronic wasting disease (CWD) affects captive and free-ranging cervid
populations in North America and farmed cervids of South Korea. CWD and scrapie
are the only prion diseases in which the transmission occurs horizontally. The
cervid Prnp gene is polymorphic at various positions. The effect of these
changes on infection is influenced by the sequence and structure compatibility
between the host and the infectious source. Prion strains have been described
virtually in every prion disease and strongly impact disease characteristics
(clinical symptoms, neuropathological profiles, incubation periods, species
tropism as well as biochemical and biophysical properties of the abnormally
folded prion protein). Prion protein sequence differences can result, upon
subsequent infection, in the generation of novel strains as documented in sheep
scrapie. We have previously shown that Prnp polymorphisms influence
susceptibility to CWD in free-ranging white-tailed deer. In CWD-positive deer
populations, alleles Q95G96 (wt) were over-represented compared to the H95G96
and Q95S96 alleles. Experimental oral infection of white-tailed deer with known
Prnp genotypes (with inoculum from CWDpositive wt/wt deer) confirmed the link
between prion protein primary sequence and the progression of disease.
Heterozygous interference occurred in varying degrees as evidenced by the
difference in the extension of the incubation period as an effect of alleles
Q95S96 and H95G96. Interestingly, the biochemical profiles of the wt/Q95S96 and
wt/H95G96 isolates resemble the wt/wt, differing only in the amount of protease
resistant PrPCWD present suggesting that the wt allele is preferentially
converted. PrPCWD profiling revealed differences between deer with at least one
wt allele and the H95G96/Q95S96 deer suggesting that this PrPCWD is unique
compared to the PrPCWD from wt/wt animals.
PO-057: Host factors influence prion strain adaptation
Crystal Meyerett Reid, Mark Zabel Colorado State University; Fort Collins,
CO USA
Background. Chronic Wasting disease (CWD) is one of many prion-mediated
diseases known as transmissible spongiform encephalopathies (TSEs). There is
ever-increasing biological and biochemical evidence that prion pathogenesis is
caused by the conversion of the normal host protein (PrPC) into an abnormal
disease causing conformation (PrPRES). How prions encipher heritable strain
properties without nucleic acid remains unclear. Previously we have shown that
host factors have contributed to the adaptation of an original deer CWD prion
strain to transgenic mice.
Materials and Methods. We assessed strain differences using biological and
biochemical assays and found that amplified cervid prions and serial-passaged
cervid prions were significantly different than that of the original cervid
strain. It is possible that prion mutation and adaptation can broaden the host
range. Previous reports, however, indicate that there is a strict species
barrier preventing CWD infection in wildtype mice.
Results. Here we show the generation of a mouse-adapted strain of CWD upon
serial passage into transgenic cervidized mice and then subsequent passage into
wildtype mice. All wildtype mice remained non-clinical upon first passage but
became completely susceptible after second passage with similar incubation times
to those of mice terminally ill from a mouse adapted scrapie strain. Inoculation
of our mouse adapted CWD strain back into cervidized mice delayed progression to
terminal disease.
Conclusion. We conclude that prion strain adaptation and mutation is
highly dependent upon host factors and host encoded PrPC primary sequence. Upon
serial passage the adapted prion strain shares more characteristics with prion
strains from the new host rather than the original species.
OR-12: Chronic wasting disease transmission and pathogenesis in cervid and
non-cervid Species
Edward A. Hoover, Candace K. Mathiason, Nicholas J. Haley, Timothy D. Kurt,
Davis M. Seelig, Nathaniel D. Denkers, Amy V. Nalls, Mark D. Zabel, and Glenn C.
Telling
Prion Research Program, Department of Microbiology, Immunology, and
Pathology; Colorado State University; Fort Collins, CO USA
Since its recognition as a TSE in the late 1970s, chronic wasting disease
(CWD) of cervids has been distinguished by its facile spread and is now
recognized in 18 states, 2 Canadian provinces, and South Korea. The efficient
horizontal spread of CWD reflects a prion/host relationship that facilitates
efficient mucosal uptake, peripheral lymphoid amplification, and dissemination
by exploiting excretory tissues and their products, helping to establish
indirect/environmental and well as direct (e.g., salivary) transmission. Recent
studies from our group also support the likelihood of early life mother to
offspring and aerosol CWD prion transmission. Studies of cervid CWD exposure by
natural routes indicate that incubation period for detection of overt infection,
while still uncertain, may be much longer than originally thought.
Several non-cervid species can be infected by CWD experimentally (e.g.,
ferrets, voles, cats) with consequent species-specific disease phenotypes. The
species-adapted prions so generated can be transmitted by mucosal, i.e., more
natural, routes. Whether non-cervid species sympatric with deer/elk can be
infected in nature, however, remains unknown. In vitro CWD prion amplification
studies, in particular sPMCA, can foreshadow in vivo susceptibility and suggest
the importance of the PrPC rigid loop region in species barrier permissiveness.
Trans-species CWD amplification appears to broaden the host range/strain
characteristics of the resultant prions. The origins of CWD remain unknown,
however, the existence of multiple CWD prion strains/ quasi-species, the
mechanisms of prion shedding/dissemination, and the relationship between sheep
scrapie and CWD merit further investigation.
PO-060: Transmission of chronic wasting disease from mother to offspring
Candace Mathiason, Amy Nalls, Stephenie Fullaway, Kelly Anderson, Jeanette
Hayes-Klug, Nicholas Haley, Edward Hoover
Colorado State University; Fort Collins, CO USA
To investigate the role mother to offspring transmission plays in chronic
wasting disease (CWD) we have developed a cervid model employing the Reeve’s
muntjac deer (Muntiacus reevesi). Eight muntjac doe were orally inoculated with
CWD and tested PrPCWD lymphoid positive by 4 mo post infection. Twelve fawns
were born to these eight CWD-infected doe, 3 were born viable, 6 were born
non-viable, and 3 were harvested as fetuses (1 each from first, second or third
trimester of pregnancy) from CWDinfected doe euthanized at end-stage disease.
The viable fawns have been monitored for CWD infection by immunohistochemistry
(IHC) performed on serial tonsil and rectal lymphoid tissue biopsies. One fawn
that was IHC PrPCWD positive at 40 d of age is now, at 28 mo of age, showing
early clinical signs associated with CWD infection. Moreover, CWD prions have
been detected by sPMCA in placenta, brain, spleen and mesenteric lymphoid tissue
harvested from 5 full-term non-viable fawns, and in fetal placenta and brain
tissue harvested in utero from the second and third trimester fetuses.
Additional tissues and pregnancy related fluids from doe and offspring are being
analyzed for CWD prions. In summary, using the muntjac deer model we have
demonstrated CWD clinical disease in an offspring born to a CWD-infected doe,
and in utero transmission of CWD from mother to offspring. These studies provide
basis to further investigate the mechanisms of maternal transfer of prions.
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
Davis Seelig, Amy Nalls, Maryanne Flasik, Victoria Frank, Candace
Mathiason, Edward Hoover Colorado State University; Fort Collins, CO USA
Background and Introduction. Chronic wasting disease (CWD) is an
efficiently transmitted prion disease of cervids with an as yet to be fully
defined host range. Moreover, the risk that CWD poses to feline predators and
scavangers, through crossspecies consumption and subsequent transmission, is
unknown. Previous and ongoing studies in our laboratory evaluating the
susceptibility of domestic cats (Felis catus) to CWD (Mathiason et. al.,
NeuroPrion 2011, Nalls et. al., NeuroPrion 2012) have documented the
susceptibility of domestic cats to CWD following intracerebral (IC) inoculation.
However, many of the pathologic features of feline-adapted CWD, including the
neural and systemic patterns of PrPCWD accumulation and neuropathology, remain
unknown.
The chief objectives of this work were:
(1) to design a sensitive, enhanced immunohistochemical (E-IHC) protocol
for the detection of CWD prions (PrPCWD) in feline tissues;
(2) to document the systemic distribution of PrPCWD in CWD-infected cats
through E-IHC;
(3) to utilize single and multiple-label immunostaining and laser scanning
confocal microscopy (LSCM) to provide insights into the subcellular patterns of
PrPCWD accumulation and neuropathologic features of CWD-infected cats; and
(4) to compare feline CWD to the other known feline TSE Materials and
Methods. Periodate-lysine-paraformaldehyde (PLP)-fixed, paraffin-embedded
(PLP-PE) from terminal, IC-inoculated (n = 9) and sham-inoculated (n = 2), 1st
and 2nd passage, CWD-infected cats were examined by E-IHC for the presence of
PrPCWD and its association with markers of cell phenotype and organelles.
Results. The most sensitive E-IHC technique for the detection of PrPCWD in
feline tissues incorporated a combination of slide pretreatment with
proteinase-K (PK) in concert with tyramide signal amplification (TSA). With this
protocol, we identified PrPCWD deposits throughout the CNS, which, in the 1st
passage cats was primarily restricted to the obex, but increased in distribution
and severity upon 2nd passage to include a number of midbrain nuclei, cortical
gray matter, the thalamus and hypothalamus, and the hippocampus. Peripheral
PrPCWD deposits were detected only in the 2nd passage cats, and included the
enteric nervous system, the Peyer’s patches, and the retropharyngeal and
mesenteric lymph nodes. PrPCWD was not detected in the sham-inoculated cats.
Moreover, using multi-label analysis, intracellular PrPCWD aggregates were
seen in association with neurofilament heavy chain (NFH)-positive neurons and
GFAP-positive astrocytes. In addition, large aggregates of intracellular PrPCWD
were identified within LAMP1-positive lysosomes.
Conclusions. Feline PrPCWD is present in CNS neurons, astrocytes and
LAMP-1-positive lysosomes. The morphologic overlap between the PrPCWD deposits
in feline CWD and BSE-origin feline spongiform encephalopathy (FSE), implicates
the importance of the host as a key determinant in the development of prion
neuropathology and suggest a signature for detection of potential spontaneous
feline prion disease.
PO-099: Estimating the risk of CWD transmission to humans—An interim report
of a comprehensive study in non-human primates
Ann-Christin Schmaedicke DPZ; Goettingen, Germany
Chronic Wasting Disease (CWD) is a transmissible prion disease that occurs
primarily among North American cervid species. CWD has emerged as a prion
disease in captive as well as freeranging cervids with rising incidence.
Continuous consumption of cervid-derived products in conjunction with increasing
CWD prevalence suggests a risk for human exposure to CWD prions.
Although surveillance data collected in the North American population did
not provide epidemiological evidence for CWD transmissions to humans it remains
unclear whether a biological risk for such transmissions exists or can be
excluded. In order to gauge the potential transmissibility of CWD to humans, a
comprehensive CWD risk assessment in cynomolgus macaques has been initiated. To
test for the CWD interspecies transmission to humans, we used a primate species
previously shown to mimic the BSE susceptibility of humans. In addition, this
species is phylogenetically close to humans with a homologous amino acid
sequence of the prion protein. When we assessed the genotype of macaque PrP, the
homozygosity for methionine at codon 129 was confirmed in all animals.
The zoonotic potential of CWD is evaluated by challenging groups of
animals via different inoculation routes. General transmissibility of CWD to
macaques is tested by intracerebral (i.c.) inoculation of brain homogenate from
CWD-infected white-tailed deer (WTD) and elk. This was either done by direct
injection of 10 mg CWDWTD to two animals (> 880 dpi) or by surgical
implantation of CWD-WTD or CWD-elk contaminated steel wires in two animals (>
750 dpi) or three animals (> 400 dpi), respectively.
To address the risk of hunters while field dressing carcasses, we
inoculated two animals with CWD-WTD by dermal scarification (> 920 dpi). To
simulate human consumption of CWDinfected food products, we orally challenged
three animals with 10 g CWD-WTD brain (> 820 dpi) and three animals with 3 kg
CWD muscle tissue from different cervid species (> 950 dpi) by repeated
feeding. Mock-inoculated macaques are co-housed in the same cage allowing
exposure to saliva and faeces of CWDinoculated macaques.
To date, all inoculated animals remain asymptomatic. Cerebrospinal fluid
and blood from all animals were and are going to be collected bimonthly,
processed and stored in a repository. Analysis of these samples using
ultrasensitive prion detection methods has been initiated. Oral challenge of 50
mg BSE to cynomolgus macaques can lead to fatal disease only after more than 5 y
of incubation time (1952 dpi).
Thus, to estimate whether CWD could be transmitted to macaques or not, we
assume that observation of challenged animals would be necessary for at least
8–10 y.
PO-248: TSE infectivity survives burial for five years with little
reduction in titer
Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and
R(D)SVS; University of Edinburgh; Edinburgh, UK
BSE infected animals, BSE-contaminated materials and other sources of TSE
(prion) infection, such as carcasses from scrapie infected sheep, CWD infected
deer and cadavers of individuals infected with CJD may all end up in the
environment through burial or other methods of disposal. They may continue to
act as a reservoir of TSE infectivity if cattle or other susceptible animals
were to be exposed to these sources in the future. In order to address these
concerns, we performed two large scale demonstration experiments under field
conditions which were designed to mimic some of the ways by which TSE infected
materials may have been disposed of. The project examined the fate of TSE
infectivity over a period of five years in two scenarios; when the infectivity
was contained within bovine heads and when the infectivity was buried without
any containment. Two soil types were compared: a sandy loam and a clay loam. We
used the 301V TSE strain which was derived by serial passage of BSE in VM
mice.
TSE infectivity was recovered from all the heads exhumed annually for five
years from both types of soil, with little reduction in the amount of
infectivity throughout the period of the experiment. Small amounts of
infectivity were found in the soil immediately surrounding the heads, but not in
samples remote from them. Similarly there was no evidence of significant lateral
movement of infectivity from the buried bolus. However large amounts of TSE
infectivity were recovered at the site of burial of both boluses. There was
limited vertical upward movement of infectivity from the bolus buried in clay
soil and downward movement from the bolus buried in sandy soil.
Now that these experiments are completed we conclude that TSE infectivity
is likely to survive burial for long periods of time with minimal loss of
infectivity and restricted movement from the site of burial. These experiments
emphasize that the environment is a viable reservoir for retaining large
quantities of TSE infectivity, and reinforce the importance of risk assessment
when disposing of this type of infectious material.
see more here ;
Epidemiology Update March 23, 2006
As of today, 13 locations and 32 movements of cattle have been examined
with 27 of those being substantially completed. Additional investigations of
locations and herds will continue. In addition, state and federal officials have
confirmed that a black bull calf was born in 2005 to the index animal (the red
cow). The calf was taken by the owner to a local stockyard in July 2005 where
the calf died. The calf was appropriately disposed of in a local landfill and
did not enter the human or animal food chain. http://www.aphis.usda.gov/newsroom/hot_issues/bse/bse_al_epi-update.shtml
> The calf was appropriately disposed of in a local
> landfill and did not enter the human or animal food chain.
Wednesday, May 30, 2012
PO-248: TSE infectivity survives burial for five years with little
reduction in titer
TSS
Friday, May 25, 2012
Chronic Wasting Disease CWD found in a farmed red deer from Ramsey County Minnesota
News Release
For immediate release: Friday, May 25, 2012
Contact: Malissa Fritz, BAH Communications Director, 651-201-6830
Chronic Wasting Disease found in a farmed red deer from Ramsey County
Mandatory surveillance program leads to detection of the disease
St. Paul, Minn – The Minnesota Board of Animal Health today announced that
a farmed red deer from a Ramsey County herd tested positive for Chronic Wasting
Disease (CWD).
The brain stem from a two-year-old female red deer was submitted for
testing at the University of Minnesota Veterinary Diagnostic Laboratory, where
preliminary results were positive for CWD. The National Veterinary Services
Laboratory today confirmed the positive test. The Board of Animal Health has
placed the herd under quarantine and is working with the owners to determine the
herd’s future.
The red deer died on the farm on May 10. The animal was tested for the
disease as part of Minnesota’s mandatory CWD surveillance program, which has
been in place since 2003. Farmed cervidae producers in Minnesota must CWD test
all deer and elk over 16 months of age that die or are slaughtered.
This herd has been registered with the Board of Animal Health since 2000.
“This herd is an example of farmers who take great care in the management of
their animals,” said Dr. Paul Anderson, assistant director of the Board of
Animal Health. “In their 12 years of herd registration with the Board, this
producer has met all of the requirements.”
The Board of Animal Health is coordinating with the Minnesota Department of
Natural Resources (DNR). The DNR is currently evaluating the situation and will
likely test wild white-tailed deer in the area this fall.
CWD is a fatal brain and nervous system disease found in cervidae in
certain parts of North America. The disease is caused by an abnormally shaped
protein called a prion, which can damage brain and nerve tissue. Infected
animals may show signs of the disease including progressive loss of body weight,
behavioral changes, staggering, increased water consumption and drooling. In
later stages of the disease, animals become emaciated (thus “wasting” disease).
According to state health officials and the federal Centers for Disease
Control and Prevention, there is no evidence that CWD can be transmitted to
humans.
For more information on CWD and the Board of Animal Health, visit
www.bah.state.mn.us.
--30--
Chronic wasting disease found in a red deer from North Oaks farm herd
By Dennis Lien
Posted: 05/25/2012 12:01:00 AM CDT
May 26, 2012 1:45 AM GMTUpdated: 05/25/2012 08:45:21 PM CDT
A farmed red deer from a large northern Ramsey County herd has tested
positive for chronic wasting disease.
The Minnesota Board of Animal Health said the 2-year-old female deer died
on the farm May 10, and a required examination of its brain stem tested positive
for the fatal brain and nervous system disease affecting elk and deer.
The 500-head North Oaks herd remains under quarantine, and officials are
trying to figure out how the disease got there and what to do with the rest of
the red deer, a large species native to Europe and Asia.
It marks the fifth case of farmed cervids testing positive in Minnesota for
chronic wasting disease, according to Dr. Paul Anderson, a board veterinarian.
Three were elk; the fourth, a white-tailed deer.
In those instances, including the most recent one in Olmsted County in
2009, all other herd members were slaughtered and tested for the disease.
"It's way too early to tell (in this case),'' said Anderson, noting the
investigation will take weeks.
"The one thing I will say, this particular operation has had absolutely
perfect surveillance for CWD,'' he added. "They have never missed an animal they
needed to test, and all the animals have tested negative. This farm is one of
the best-run in the state, and it's going to take some work to see if we can
figure out where this came from.''
A man answering a telephone number listed at northoaksfarms.com declined to
comment.
"I would refer you to the Board of Animal Health. We're working closely
with them. Goodbye,'' he said and hung up.
That herd of red deer has been registered with the Board of Animal Health
since 2000.
Chronic wasting disease, which is found in elk and deer in parts of North
America, is caused by an abnormally shaped protein called a prion, which can
damage brain and nerve tissue. Infected animals show progressive loss of body
weight with accompanying behavioral changes, including staggering, drinking
large amounts of water, excessive urinating and drooling.
There is no evidence the disease can be transmitted to humans or other
animals such as cattle or sheep, according to federal and state health experts.
Authorities believe it most likely is transmitted by animal-to-animal contact or
exposure to contaminated habitat.
The disease can have a long incubation period, making it difficult to
figure out how animals became infected.
In the North Oaks case, the brain stem from the red deer was submitted to
the University of Minnesota Veterinary Diagnostic Laboratory, where preliminary
results were positive. The U.S. Department of Agriculture's National Veterinary
Services Laboratory in Ames, Iowa, confirmed the positive test Friday, May 25.
The deer was tested as part of the state's mandatory CWD surveillance
program.
Since 2003, Minnesota has required registration and chronic wasting disease
surveillance programs for farmed cervid herds. When animals 16 months or older
die or are slaughtered, herd owners must submit brain samples for testing.
The Minnesota Department of Natural Resources plans to meet with the board
soon and likely will test wild white-tailed deer in the area.
"We haven't had any reports of sick deer in the area,'' said Lou
Cornicelli, DNR wildlife research manager.
Although the other farmed herds have been destroyed, Anderson said
decisions are made on a case-by-case basis.
"Whenever something like this happens, we do what is best for the herd and
figure out a way to make sure this disease is eradicated,'' Anderson said.
Dennis Lien can be reached at 651-228-5588.
CHRONIC WASTING DISEASE UPDATE September 6, 2002
Minnesota has announced the finding of CWD in a captive elk in Aitkin
County. The animal was a five-year-old male. It had been purchased from a
captive facility in Stearns County in August of 2000. The herd where the elk was
found has been placed under quarantine as has two additional facilities where
the infected elk had resided prior to it coming to the farm in Aitkin County.
Minnesota DNR officials will test wild deer in the area to determine if there is
any sign of CWD in the free-ranging population. This is the first case of CWD in
either captive or freeranging cervids in Minnesota. Several more states have
passed bans on the importation of deer and elk carcasses from states where CWD
has been found in wild animals. Previously the states of Colorado, Illinois and
Iowa and the province of Manitoba had passed such bans. The states of Vermont,
Oregon and Missouri have enacted similar bans. Numerous states have issue
voluntary advisories to their out-of-state hunters encouraging them not to bring
the carcass or carcass parts of deer and elk into their state. The bans do
permit the importation of boned out meat, hides or cape with no meat attached,
clean skull cap with antler attached, finished taxidermy heads or the ivories of
elk. The state of Georgia has recently banned the importation of live cervids
into that state also. Some citizens of Colorado have formed a new political
action group called Colorado Wildlife Defense (just happens that the acronym is
CWD). The stated goal of this group are; Elimination of big game diseases,
especially CWD; promotion of healthy wildlife habitat; promotion of
scientifically sound wildlife research; promotion of a discussion of the ethics
of hunting and wildlife management; education of the hunting and non hunting
public. Their action plan calls for; requiring double fencing of all game farms
at owners expense; all game farmers provide annual proof of bonding; prohibit
new licenses for deer and elk farms; prohibit expansion in acreage of existing
game farms; prohibit the transfer of game farm licenses; prohibit charging for
hunting behind high wire; prohibit blocking of traditional migratory paths by
high fences; requiring game farms to maintain environmental controls and
prohibit the escape of contaminated water or soil; requiring immediate reporting
of missing deer or elk from game farms; and requiring all game farm deer and elk
to be tested for brucellosis and TB. Wisconsin has announced that 7 more
free-ranging deer have tested positive for CWD. They have expanded their
eradication zone by an additional 15 square miles to cover these findings. The
total number of free-ranging CWD positive in Wisconsin is now 31 white-tail
deer.
In 2000, a elk farmer in Wisconsin received elk from a CWD exposed herd in
Colorado. At that time, the farmer advised the Wisconsin Department of
Agriculture that both animals from the exposed herd in Colorado were dead. He
has now advised Wisconsin Ag. that he was mistaken and that one of the animals
is still alive in his herd. The second draft of the implementation documents for
the National CWD Plan was distributed to committee members and others on Friday,
August 30. The final documents are due to APHIS and USFWS on Friday, September
13. The herd of captive elk in Oklahoma that had been exposed to CWD will be
destroyed this week. This herd had an elk test positive for CWD in 1997 but the
depopulation of the herd was not agreed to by the owners and federal
representatives until this week. Since the discovery of CWD in the herd, the
remaining animals have been under quarantine, however, in the meantime the herd
has dropped from 150 animals to 74. Due to a lack of communication, not all of
the 76 animals that died in the interim were tested for CWD. All remaining
animals will be tested but the true degree of infection rate of the herd will
never be known.
The owners of the facility will not be permitted to restock the area with
cervids for a period of five years. A New York based organization, BioTech
Research Fund I LLC has committed a $1 million line of credit to fund
commercialization of tests for brain-wasting disorders and production of various
vaccines to Gene-Thera of Wheat Ridge, Colorado. Gene-Thera has spent three
years developing new ways not only to diagnose CWD, but create vaccines for mad
cow disease, E. coli contaminants and foot-and-mouth disease. Its tests for CWD
have been successful in more than 100 samples from Colorado and Wisconsin
according to company officials. Gene-Thera plans to license and market some o
fits disease test kits by the end of the year, then begin volume distribution by
mid-2003. The abstracts of the presentations from the CWD Conference in Denver
August 6 and 7 have been posted on the Colorado Division of Wildlife web site.
You will need adobe acrobat reader to read them.
The Division web site is: http://wildlife.state.co.us/CWD/Symposium_booklet.pdf
If you don’t have adobe acrobat, you can download it free at http://www.adobe.com/products/acrobat/readstep.html
Minnesota: Second case in a game farmed elk discovered in Stearns Co.
This is a trace forward from the previously affected game farm in Aitkins
Co. An additional game farm in Benton Co is under quarantine.
snip...
Supporting Documents: Colorado: CWD-Exposed Elk Used in 1990 Study-
Wildlife officials call W. Slope move a mistake Date: January 17, 2003 Source:
Denver Post Contacts: Theo Stein Environment Writer
The Colorado Division of Wildlife knowingly used a herd of captive elk
exposed to chronic wasting disease in a grazing study on the Western Slope in
January 1990, possibly introducing the disease to the elk-rich area. "It was a
bad call," said Jeff Ver Steeg, the division's top game manager. "I can't deny
it." About 150 wild elk were allowed to graze in the same pens near Maybell
after the research herd was removed and may have picked up the abnormal protein
that causes the disease from the feces and urine left by the captive elk. While
the Division of Wildlife has expressed concern before that its animals might
have helped spread CWD, this is the first time the agency has acknowledged it
knowingly moved elk exposed to CWD deep into an area where the disease was not
known to already exist. Studies that could help determine the source of CWD on
the Western Slope are incomplete, and officials say what data that do exist are
so new and so spotty they may not provide all the answers. So far, it appears
that less than 1 percent of deer and elk in the area are infected, compared with
as much as 15 to 20 percent in hotspots in northeastern Colorado. But as
wildlife officials grapple with CWD's appearance in northwestern Colorado,
officials now admit the decision to continue the grazing study over the
objections of some biologists was an error. At the time, biologists wanted to
see whether elk grazing on winter range depleted forage that ranchers wanted for
fattening cattle in spring. "I think in hindsight a lot of good people probably
did some dumb things, myself included," said Bruce Gill, a retired wildlife
manager who oversaw research efforts and remembers the debate over the project.
"Had we known CWD would explode into such a potentially volatile ecologic and
economic issue, we wouldn't have done it." Elk ranchers, who have been blamed
for exporting the disease from its stronghold on the Colorado and Wyoming plains
to seven states and two Canadian provinces, say the agency's belated disclosure
smacks of a coverup. "It's pure negligence," said Jerry Perkins, a Delta banker
and rancher who is now demanding a legislative inquiry. "If I'd have moved
animals I knew to be infected around like that, I'd be in jail." Grand Junction
veterinarian and sportsman Dick Steele said he faults the agency for not
disclosing information about CWD-exposed research animals before October, when
information was posted on the Division of Wildlife website. "This went way
beyond poor judgment," he said. "My main concern is that this has been hidden
for the last 12 years. It would have been real important to our decision-making
process on how to deal with CWD." While the Maybell information is new, Perkins
and other ranchers have long suspected Division of Wildlife research facilities
near Meeker and Kremmling, which temporarily housed mule deer kept in heavily
infected pens at the Fort Collins facility, have leaked CWD to the wild. Fear of
an outbreak led the agency to sample 450 deer around the Meeker and Kremmling
facilities. None tested positive, but the sample size was only large enough to
detect cases if the infection rate was greater than 1 percent. This fall, tests
on 23,000 deer and elk submitted by hunters statewide have revealed 48 CWD cases
north of Interstate 70 and west of the Continental Divide. Biologists believe
the infection rate in that area, which includes the Maybell, Meeker and
Kremmling sites, is still well below 1 percent. But CWD has never been contained
in a wild population, so experts fear the problem will grow worse.
The Division of Wildlife says it will be months before a statistical
analysis of the fall's sampling results can be completed, an exercise that may
shed light on the disease's origin on the Western Slope. "We're just not going
to speculate at this point," said Ver Steeg of the possible Maybell connection.
"This is one possibility, but certainly not the only possibility." Some
biologists think a defunct elk ranch near Pagoda, which had dozens of
unexplained deaths in the mid-'90s, is another, a suggestion Perkins rejects.
"It may be inconclusive to them," said Perkins. "It isn't inconclusive to
us."
To date, 19 CWD-positive
animals have been found on six Wisconsin farms. All have been white-tailed deer
except for one elk imported from a Minnesota herd later found to be infected.
More than 8,000 farm-raised deer and elk have been tested in Wisconsin, and
about 540 herds are enrolled in the CWD monitoring program.
Subject: CWD disease detected on Lac qui Parle County cervid farm
southwestern Minnesota (2006-03-15) Date: March 15, 2006 at 12:36 pm PST
Chronic wasting disease detected on Lac qui Parle County cervid farm
(2006-03-15) The Board of Animal Health announced today that chronic wasting
disease (CWD) has been detected in one domestic white-tailed deer on a cervid
farm in Lac qui Parle County, which is located in southwestern Minnesota.
Immediately, DNR officials will conduct a local deer survey to determine
the number of wild deer in the area. It is expected that not many deer will be
found because the area is highly agricultural, with little deer habitat
surrounding the farm. DNR will conduct opportunistic sampling of deer, like road
kills, in the immediate area now and will conduct intensive hunter-harvested
surveillance during the 2006 firearm deer season.
Although this positive animal is a captive deer, DNR has conducted
surveillance for CWD in wild deer in the area. The farm is located near the
northern boundary of deer permit area 447, where wild deer surveillance for CWD
last occurred in 2003.
Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we
conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447.
In total, we collected 392 samples from those permit areas during the regular
firearm deer season and CWD was not detected."
The sampling of wild deer was designed statistically to have a 95 percent
confidence of detecting a 1 percent infection rate, according to Mike DonCarlos,
DNR wildlife programs manager.
"This situation is very similar to the positive elk farm discovered in
Stearns County in 2003, which followed the first discovery of CWD in an Aitkin
County elk farm," DonCarlos said. “The DNR response will be similar to the
Stearns County action and will include an initial assessment of wild deer
populations in the area and development of a surveillance program for next
fall."
From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide
and no disease found in the wild herd.
"The intensive surveillance conducted in 2003 indicated CWD was not present
in wild deer," Cornicelli said. “In addition, all indications are that this
positive captive deer has not contacted any wild deer, but we will conduct
additional surveillance this fall to be sure."
Subject: CWD disease detected on Lac qui Parle County cervid farm
southwestern Minnesota (2006-03-15) Date: March 15, 2006 at 12:36 pm PST Chronic
wasting disease detected on Lac qui Parle County cervid farm (2006-03-15) The
Board of Animal Health announced today that chronic wasting disease (CWD) has
been detected in one domestic white-tailed deer on a cervid farm in Lac qui
Parle County, which is located in southwestern Minnesota.
Immediately, DNR officials will conduct a local deer survey to determine
the number of wild deer in the area. It is expected that not many deer will be
found because the area is highly agricultural, with little deer habitat
surrounding the farm. DNR will conduct opportunistic sampling of deer, like road
kills, in the immediate area now and will conduct intensive hunter-harvested
surveillance during the 2006 firearm deer season.
Although this positive animal is a captive deer, DNR has conducted
surveillance for CWD in wild deer in the area. The farm is located near the
northern boundary of deer permit area 447, where wild deer surveillance for CWD
last occurred in 2003.
Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we
conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447.
In total, we collected 392 samples from those permit areas during the regular
firearm deer season and CWD was not detected."
The sampling of wild deer was designed statistically to have a 95 percent
confidence of detecting a 1 percent infection rate, according to Mike DonCarlos,
DNR wildlife programs manager.
"This situation is very similar to the positive elk farm discovered in
Stearns County in 2003, which followed the first discovery of CWD in an Aitkin
County elk farm," DonCarlos said. “The DNR response will be similar to the
Stearns County action and will include an initial assessment of wild deer
populations in the area and development of a surveillance program for next
fall."
From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide
and no disease found in the wild herd.
"The intensive surveillance conducted in 2003 indicated CWD was not present
in wild deer," Cornicelli said. “In addition, all indications are that this
positive captive deer has not contacted any wild deer, but we will conduct
additional surveillance this fall to be sure."
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
SNIP...
Reasons for Caution There are several reasons for caution with respect to
zoonotic and interspecies CWD transmission. First, there is strong evidence that
distinct CWD strains exist (36). Prion strains are distinguished by varied
incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc
depositions (3,32). Strains have been identified in other natural prion
diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies
transmission of prions from CWD-positive deer and elk isolates resulted in
identification of >2 strains of CWD in rodent models (36), indicating that
CWD strains likely exist in cervids. However, nothing is currently known about
natural distribution and prevalence of CWD strains. Currently, host range and
pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of
CWD may also vary with CWD strain. In addition, diversity in host (cervid) and
target (e.g., human) genotypes further complicates definitive findings of
zoonotic and interspecies transmission potentials of CWD. Intraspecies and
interspecies passage of the CWD agent may also increase the risk for zoonotic
CWD transmission. The CWD prion agent is undergoing serial passage naturally as
the disease continues to emerge. In vitro and in vivo intraspecies transmission
of the CWD agent yields PrPSc with an increased capacity to convert human PrPc
to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and
yield multiple novel prion strains (3,28). The potential for interspecies CWD
transmission (by cohabitating mammals) will only increase as the disease spreads
and CWD prions continue to be shed into the environment. This environmental
passage itself may alter CWD prions or exert selective pressures on CWD strain
mixtures by interactions with soil, which are known to vary with prion strain
(25), or exposure to environmental or gut degradation. Given that prion disease
in humans can be difficult to diagnose and the asymptomatic incubation period
can last decades, continued research, epidemiologic surveillance, and caution in
handling risky material remain prudent as CWD continues to spread and the
opportunity for interspecies transmission increases. Otherwise, similar to what
occurred in the United Kingdom after detection of variant CJD and its subsequent
link to BSE, years of prevention could be lost if zoonotic transmission of CWD
is subsequently identified, SNIP...SEE FULL TEXT ;
SNIP...SEE FULL TEXT ;
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
WHICH CAME FIRST, THE CART OR THE HORSE $$$
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
please see full text ;
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
see much more here ;
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Tuesday, December 20, 2011
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.
snip...see full text and much more here ;
SNIP...SEE FULL TEXT ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
THIRD CJD REPORT UK 1994
snip...
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats, there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER
AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages
858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of
the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
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 ;
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE
RISE IN NORTH AMERICA
Sunday, February 12, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1
(August 19, 2011) including Texas
TSS