hunting over gut piles and CWD TSE prion disease
hunting over gut piles and CWD TSE prion disease, a reminder...just saying
Interspecies Transmission of Chronic Wasting Disease Wisconsin Species
Likely to be Exposed
Background Recent studies indicate that chronic wasting disease (CWD) may
be transmitted to deer by direct contact, from fecal or urine contamination, or
through environmental contamination associated with carcasses of infected deer.
The potential for environmental contamination with CWD provides a potential
source for transmission to wildlife that share habitat with white-tailed deer.
Carcasses of deer will also be consumed by wildlife, but little is known about
the frequency and range of species that eat deer carrion and could be exposed to
CWD from an infected carcass. In Wisconsin, the primary carrion consumers will
likely include Eastern coyote (Canis latrans), red fox (Vulpes vulpes), common
raccoon (Procyon lotor), striped skunk (Mephitis mephitis) and Virginia opossum
(Didelphis virginiana). Although these species may consume infected deer tissue,
it is unknown whether CWD can successfully cross the species barrier to infect
these animals.
snip..
see full text with slides, and thanks for your hard work !...tss
Monday, July 13, 2009
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic
Wasting Disease Journal of Wildlife Management 73(5):655-662. 2009 doi:
10.2193/2008-282
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic
Wasting Disease Christopher S. Jennelle1a, Michael D. Samuelb, Cherrie A.
Noldenc, and Elizabeth A. Berkleyd
aDepartment of Forest and Wildlife Ecology, University of Wisconsin, 1630
Linden Drive, Madison, WI 53706, USA
bUnited States Geological Survey, Wisconsin Cooperative Wildlife Research
Unit, University of Wisconsin, 1630 Linden Drive, Madison, WI 53706, USA
cDepartment of Forest and Wildlife Ecology, University of Wisconsin, 1630
Linden Drive, Madison, WI 53706, USA
dDepartment of Forest and Wildlife Ecology, University of Wisconsin, 1630
Linden Drive, Madison, WI 53706, USA
1E-mail:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000092/!x-usc:mailto:jennelle@wisc.edu
Abstract
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy
afflicting the Cervidae family in North America, causing neurodegeneration and
ultimately death. Although there are no reports of natural cross-species
transmission of CWD to noncervids, infected deer carcasses pose a potential risk
of CWD exposure for other animals. We placed 40 disease-free white-tailed deer
(Odocoileus virginianus) carcasses and 10 gut piles in the CWD-affected area of
Wisconsin (USA) from September to April in 2003 through 2005. We used photos
from remotely operated cameras to characterize scavenger visitation and relative
activity. To evaluate factors driving the rate of carcass removal
(decomposition), we used Kaplan–Meier survival analysis and a generalized linear
mixed model. We recorded 14 species of scavenging mammals (6 visiting species)
and 14 species of scavenging birds (8 visiting species). Prominent scavengers
included American crows (Corvus brachyrhynchos), raccoons (Procyon lotor), and
Virginia opossums (Didelphis virginiana). We found no evidence that deer
consumed conspecific remains, although they visited gut piles more often than
carcasses relative to temporal availability in the environment. Domestic dogs,
cats, and cows either scavenged or visited carcass sites, which could lead to
human exposure to CWD. Deer carcasses persisted for 18 days to 101 days
depending on the season and year, whereas gut piles lasted for 3 days. Habitat
did not influence carcass decomposition, but mammalian and avian scavenger
activity and higher temperatures were positively associated with faster removal.
Infected deer carcasses or gut piles can serve as potential sources of CWD
prions to a variety of scavengers. In areas where surveillance for CWD exposure
is practical, management agencies should consider strategies for testing primary
scavengers of deer carcass material.
Friday, August 8, 2008
PS 76-59: White-tailed deer carcass decomposition and risk of chronic
wasting disease exposure to scavenger communities in Wisconsin
Chris S. Jennelle, Michael D. Samuel, Cherrie A. Nolden, and Elizabeth A.
Berkley. University of Wisconsin
snip...
Chronic wasting disease (CWD) is an infectious transmissible spongiform
encephalopathy (TSE) afflicting members of the family Cervidae, and causes
neurodegeneration and ultimately death. While there have been no reports of
natural cross-species transmission of CWD outside this group, we addressed the
role of white-tailed deer (Odocoileus virginianus) carcasses as environmental
sources of CWD in Wisconsin. Our objectives were to estimate rates of deer
carcass and gut pile decomposition in the environment, characterize vertebrate
scavenger communities, and quantify the relative activity of scavengers to
determine CWD exposure risk. We placed 40 disease-free deer carcasses and nine
gut piles in the CWD-affected area of Wisconsin from September to April in 2003
through 2005. We used photos from remotely operated cameras to characterize
scavenger communities and relative activity. We used Kaplan-Meier survival
analysis and a generalized linear mixed model to quantify the driving factors
and rate of carcass removal (decomposition) from the environment.
Results/Conclusions
We recorded 14 species of scavenging mammals (six visiting species), and
eight species of scavenging birds (14 visiting species). Prominent scavengers
included American crows (Corvus brachyrhynchos), raccoons (Procyon lotor), and
Virginia opossums (Didelphis virginiana). We found no evidence that deer
directly consumed conspecific remains, although they visited them frequently.
Domestic dogs (Canis familiaris), cats (Felis catus), and cows (Bos spp.) either
scavenged or visited carcass sites, which could increase exposure risk of CWD to
humans and human food supplies. Deer carcasses persisted for a median of 18 to
101 days, while gut piles lasted for a median of three days. Habitat did not
influence carcass decomposition, but mammalian and avian scavenger activity and
higher temperatures (proxy for microbial and arthropod activity) were associated
with greater rates of carcass removal. Infected deer carcasses serve as
environmental sources of CWD prions to a wide variety of mammalian and avian
scavengers. Such sources of infectious material likely influence the maintenance
and spread of CWD (in particular), and should be considered in the dynamics of
other disease systems as well. Prudence would dictate the use of preemptive
management strategies, and we highlight strategies for carcass disposal to
mitigate the influence of carcasses as environmental sources of infectious
diseases.
See more of PS 76 - Latebreaking: Disease and Epidemiology See more of
Latebreakers
See more of The 93rd ESA Annual Meeting (August 3 -- August 8, 2008)
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
Title: Chronic wasting disease in bank voles: characterisation of the
shortest incubation time model for prion diseases
Authors
item Di Bari, Michele - item Nonno, Romolo - item Castilla, Joaquín - item
D'Agostino, Claudia - item Pirisinu, Laura - item Riccardi, Geraldina - item
Conte, Michela - item Richt, Juergen item Kunkle, Robert item Langeveld, Jan -
item Vaccari, Gabriele - item Agrimi, Umberto -
Submitted to: PLoS Pathogens Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 14, 2013 Publication Date: March 7, 2013
Repository URL: http://handle.nal.usda.gov/10113/55901
Citation: Di Bari, M.A., Nonno, R., Castilla, J., D'Agostino, C., Pirisinu, L.,
Riccardi, G., Conte, M., Richt, J., Kunkle, R., Langeveld, J., Vaccari, G.,
Agrimi, U. 2013. Chronic wasting disease in bank voles: characterisation of the
shortest incubation time model for prion diseases. PLoS Pathogens.
9(3):e1003219.
Interpretive Summary: Chronic wasting disease (CWD) is a prion disease that
affects free-ranging and captive cervids and is slowly spreading in certain
regions of the United States and Canada. Animal models are of key importance in
the study of prion diseases but their development for CWD has long been hampered
by its very inefficient transmission to wild-type mice traditionally used in
research. Significant progress was made following genetic manipulation of
laboratory mice making them transgenic (mice that over-express the cervid prion
genes instead of mouse prion genes). Studies reported here show that the bank
vole (Myodes glareolus), a wild rodent species that has been demonstrated to be
susceptible to many animal and human prion diseases, is also unique in its
susceptibility to CWD from elk, mule deer and white-tailed deer. Moreover,
experimental studies reported here found passage of CWD to bank voles led to the
isolation of a prion strain with peculiar characteristics; most notable are the
unprecedented short incubation and survival times, respectively of 25-28 and ~35
days. Development of a rapid animal model for prion diseases that leads to
disease in less than one month represents a significant tool for investigating,
neurodegenerative diseases (like prion diseases) where no known treatments or
cures exist.
Technical Abstract: In order to assess the susceptibility of bank voles to
chronic wasting disease (CWD), we inoculated voles carrying isoleucine or
methionine at codon 109 (Bv109I and Bv109M, respectively) with CWD isolates from
elk, mule deer and white-tailed deer. Efficient transmission rate (100%) was
observed with mean survival times ranging from 156 to 281 days post inoculation.
Subsequent passages in Bv109I allowed us to isolate from all CWD sources the
same vole-adapted CWD strain (Bv**I/ICWD), typified by unprecedented short
incubation times of 25-28 days and survival times of ~35 days. Neuropathological
and molecular characterisation of Bv**I/ICWD showed that the classical features
of mammalian prion diseases were all recapitulated in less than one month after
intracerebral inoculation. Bv**I/ICWD was characterised by a mild and discrete
distribution of spongiosis and relatively low levels of protease-resistant
PrP**Sc (PrP**res) in the same brain regions. Despite the low PrP**res levels
and the short time lapse available for its accumulation, end-point titration
revealed that brains from terminally-ill voles contained up to 108,4 i.c. ID50
infectious units per gram. Bv**I/ICWD was efficiently replicated by protein
misfolding cyclic amplification (PMCA) and the infectivity faithfully generated
in vitro, as demonstrated by the preservation of the peculiar Bv**I/ICWD strain
features on re-isolation in Bv109I. Overall, we provide evidence that the same
CWD strain was isolated in Bv109I from the three-cervid species. Bv**I/ICWD
showed unique characteristics of "'virulence"', low PrP**res accumulation and
high infectivity, thus providing exceptional opportunities to improve basic
knowledge of the relationship between PrP**Sc, neurodegeneration and
infectivity.
Project Team Nicholson, Eric Kunkle, Robert Greenlee, Justin Publications
Publications Related National Programs Animal Health (103) Last Modified:
09/01/2013
Sunday, July 07, 2013
Could avian scavengers translocate infectious prions to disease-free areas
initiating new foci of chronic wasting disease?
Prion. 2013 Jul 3;7(4). [Epub ahead of print]
The results of this study indicate raccoons are susceptible to infection
with bovine-passaged TME, but not hamster-adapted DY and HY strains. RacTME and
bovTME exhibited similar clinicopathologic and immunohistochemical
characteristics, suggesting a commonality in the TME isolates or host response
to the agent.
Prion diseases
Although naturally occurring transmissible spongiform encephalopathies
(TSEs) have not been reported in the raccoon, reports of successful experimental
transmission of similar spongiform diseases, transmissible encephalopathy of
mink (TME) and sheep scrapie, have been documented in this species21,49,52,53 by
intracerebral (IC) and oral inoculations.21 In the IC-infected route, the
raccoons were administered TME and developed a rapidly progressive disease
within 190 days, whereas the orally infected raccoon developed neurologic signs
after 306 days, which included weakness, behavior change, and incoordination.
Scrapie-infected raccoons required a 2-year period to develop the disease when
inoculated by the IC route.49,52,53 Microscopically, the lesions were identical
in both groups (TME and scrapie) and consisted of widespread vacuolar changes,
neuronal degeneration, and astrocytosis in the brain (except in cerebellum).
Neuronal vacuolar changes, although described in scrapie and related diseases
including naturally occurring TME, were rare.49,52,53
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
"although the infection rate was low (4 of 13 animals [Hamir et al.
2001])."
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
----- Original Message -----
From: David Colby
To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter.
Warm Regards, David Colby
--
David Colby, PhDAssistant ProfessorDepartment of Chemical
EngineeringUniversity of Delaware
====================END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904
6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long
delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform
Encephalopathy Advisory Committee (SEAC), the UK Government's independent
Advisory Committee on all aspects related to BSE-like disease, gave the hound
study detailed consideration at their meeting in January 1994. As a summary of
this meeting published in the BSE inquiry noted, the Committee were clearly
concerned about the work that had been carried out, concluding that there had
clearly been problems with it, particularly the control on the histology, and
that it was more or less inconclusive. However was agreed that there should be a
re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound
study to see if any useful results could be gained from it. The Chairman
concluded that there were varying opinions within the Committee on further work.
It did not suggest any further transmission studies and thought that the lack of
clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as
conducted. As a result it is likely that the authors felt that it would not
stand up to r~eer review and hence it was never published. As noted above, and
in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether
additional work should be performed to examine dogs for evidence of TSE
infection. Although the Committee had mixed views about the merits of conducting
further work, the Chairman noted that when the Southwood Committee made their
recommendation to complete an assessment of possible spongiform disease in dogs,
no TSEs had been identified in other species and hence dogs were perceived as a
high risk population and worthy of study. However subsequent to the original
recommendation, made in 1990, a number of other species had been identified with
TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
As this study remains unpublished, my understanding is that the ownership
of the data essentially remains with the original researchers. Thus
unfortunately, I am unable to help with your request to supply information on
the hound survey directly. My only suggestion is that you contact one of the
researchers originally involved in the project, such as Gerald Wells. He can be
contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases
of spongiform encephalopathy in animals and poultry were made notifiable. Hence
since that date there has been a requirement for vets to report any suspect SE
in dogs for further investigation. To date there has never been positive
identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's minute.
I do NOT think that we can justify devoting any resources to this study,
especially as larger and more important projects such as the pathogenesis study
will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound
brains then it should be passed entirely to the VI Service.
J W WILESMITH Epidemiology Unit 18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would
by the end of the year, indentify the three brains that were from the
''POSITIVE'' end of the lesion spectrum.
TSE in dogs have not been documented simply because OF THE ONLY STUDY,
those brain tissue samples were screwed up too. see my investigation of this
here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS
BRAIN TISSUE SAF's. ...TSS
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to
other species will invariably present pathology typical of a scrapie-like
disease.
snip...
76 pages on hound study;
snip...
***2012***
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an
unrecognized sporadic or genetic case of bovine prion disease incorporated into
cattle feed or even cattle feed contaminated with prion-infected human remains.1
However, strong support for a genetic origin of BSE has recently been
demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2
Furthermore, a specific prion protein strain causing BSE in cattle is believed
to be the etiological agent responsible for the novel human prion disease,
variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in
a number countries, including France, Italy, Ireland, the Netherlands, Canada,
Japan, US and the UK with the largest number of cases. Naturally occurring
feline spongiform encephalopathy of domestic cats4 and spongiform
encephalopathies of a number of zoo animals so-called exotic ungulate
encephalopathies5,6 are also recognized as animal prion diseases, and are
thought to have resulted from the same BSE-contaminated food given to cattle and
humans, although and at least in some of these cases, a sporadic and/or genetic
etiology cannot be ruled out. The canine species seems to display resistance to
prion disease and no single case has so far been reported.7,8 Here, we describe
a case of a 9 week old male Rottweiler puppy presenting neurological deficits;
and histological examination revealed spongiform vacuolation characteristic of
those associated with prion diseases.9 Initial biochemical studies using
anti-PrP antibodies revealed the presence of partially proteinase K-resistant
fragment by western blotting. Furthermore, immunohistochemistry revealed
spongiform degeneration consistent with those found in prion disease and
displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross
the species barrier transmitted to hamster in vitro with PMCA and in vivo (one
hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100%
attack rate (n = 4) and animals displayed untypical lesional profile and shorter
incubation period.
In this study, we show that the canine species might be sensitive to prion
disease and that PrPSc isolated from a dog can be transmitted to dogs and
hamsters in vitro using PMCA and in vivo to hamsters.
If our preliminary results are confirmed, the proposal will have a major
impact on animal and public health and would certainly lead to implementing new
control measures for ‘canine spongiform encephalopathy’ (CSE).
References 1. Colchester AC, Colchester NT. The origin of bovine spongiform
encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61;
PMID:16139661; http://
dx.doi.org/10.1016/S0140-6736(05)67218-2.
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation.
PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal.
ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy
(BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/
hmg/6.10.1699.
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith
JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic
cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus
angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI.
Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu
(Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink
encephalopathy species barrier effect between ferret and mink: PrP gene and
protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317-
75-11-2947.
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et
al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad
Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30;
PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.
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
AD.63: Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1
1Colorado State University; Fort Collins, CO USA; 2University of Minnesota;
Saint Paul, MN USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by 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 the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD. These results demonstrate that
CWD can be transmitted and adapted to the domestic cat, thus raising the issue
of potential cervid-to- feline transmission in nature.
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Monday, August 8, 2011
Susceptibility of Domestic Cats to CWD Infection
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Sunday, August 25, 2013
Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats,
blood, and mother to offspring transmission
Sunday, September 1, 2013
Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy
We previously described the biochemical similarities between PrPres derived
from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations
suggest a link between these two uncommon prion phenotypes in a primate model
(it is to note that such a link has not been observed in other models less
relevant from the human situation as hamsters or transgenic mice overexpressing
ovine PrP [28]). We speculate that a group of related animal prion strains
(L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion
diseases in humans with a type 2 PrPres molecular signature (and more
specifically type 2B for vCJD)
snip...
Together with previous experiments performed in ovinized and bovinized
transgenic mice and hamsters [8,9] indicating similarities between TME and
L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME
outbreaks in North America and Europe during the mid-1900s.
kind regards, terry
posted by Terry S. Singeltary Sr. at
12:13 PM
0 Comments:
Post a Comment
Subscribe to Post Comments [Atom]
<< Home