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]
Could avian scavengers translocate infectious prions to disease-free areas
initiating new foci of chronic wasting disease?
Fischer JW, Phillips GE, Nichols TA, Vercauteren KC. Source United States
Department of Agriculture; Animal and Plant Health Inspection Service; Wildlife
Services; National Wildlife Research Center; Fort Collins, CO USA.
Abstract Mechanisms for the spread of transmissible spongiform
encephalopathy diseases, including chronic wasting disease (CWD) in North
American cervids, are incompletely understood, but primary routes include
horizontal and environmental transmission. Birds have been identified as
potential vectors for a number of diseases, where they ingest or are exposed to
infected material and later shed the disease agent in new areas after flying
substantial distances. We recently identified American crows (Corvus
brachyrhynchos) as having the potential to translocate infectious prions in
their feces. Our results suggest that this common, migratory North American
scavenger is capable of translocating infectious prions to disease-free areas,
potentially seeding CWD infection where no other initial source of pathogen
establishment is forthcoming. Here we speculate on the role avian scavengers,
like American crows, might play in the spatial dissemination of CWD. We also
consider the role mammalian scavengers may play in dispersing prions.
KEYWORDS: American crows, CWD, Corvus brachyrhynchos, TSE, disease
transmission, transmissible spongiform encephalopathy
PMID: 23822910 [PubMed - as supplied by publisher]
Greetings,
this is another example of why it is so important to properly dispose of
carcasses, due to CWD risk factor, and if you bury it (incineration is much
better), if you bury it, you better bury it deep, deep, deep, so scavengers
cannot smell it and dig it up later, however, you risk tainting your water table
with the CWD TSE prion in doing so.
I have also witnessed birds eating pet food. I have witnessed in a domestic
aspect, and in the wild while hunting at livestock feeding stations.
so really, since in the USA, it is still legal to feed cervids back to
cervids (as in ruminant/cervid protein), even if it is from a HIGH RISK CWD
AREA, it would be futile to try and stop scavengers from eating CWD infected
cervids, when humans are doing this through legal feed for cervids, that contain
cervids from high risk CWD areas. ...
just my take...
kind regards,
terry
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
Sunday, November 01, 2009
AS THE CROW FLIES, SO DOES CWD
American crows (Corvus brachyrhynchos) and potential spreading of CWD
through feces of digested infectious carcases
Monday, July 13, 2009
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic
Wasting Disease
[226] CHRONIC WASTING DISEASE AND CARNIVORES: A ONE-HEALTH APPROACH TO
CONSERVATION
Christine Avena1,3, Allen Rutberg2, Gretchen Kaufman1 1Center for
Conservation Medicine, Tufts Cummings School of Veterinary Medicine, MA., USA;
2Center for Animals and Public Policy, Tufts Cummings School of Veterinary
Medicine, MA, USA; 3EMail: Christine.Avena@tufts.edu
Chronic wasting disease (CWD) is a progressive, fatal, transmissible prion
disease first identified in captive mule deer in 1967 in Colorado, USA.
Currently, the disease is known to infect mule deer, white-tailed deer, elk, and
moose located in fourteen states and Canada. The method of disease transmission
to naïve animals is still uncertain, although contact with contaminated
environment is identified as a risk factor. There is no known way to contain or
treat CWD. Although other transmissible spongiform encephalopathies (TSEs)
infect humans and animals, CWD is currently only found in cervids. As a
precaution, the Centers for Disease Control and Prevention (CDC) warns against
exposure to CWD infected animals and meat products. The reintroduction of the
wolf to the western U.S. in 1995 offered a unique opportunity to monitor changes
to ecosystem health. The
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND
NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease
Association 2011
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
=======================================
2013
Strain characteristics of the in vitro-adapted rabbit and dog BSE agent
remained invariable with respect to the original cattle BSE prion, suggesting
that the naturally low susceptibility of rabbits and dogs to prion infections
should not alter their zoonotic potential if these animals became infected with
BSE.
=======================================
Neurobiology of Disease
Bovine Spongiform Encephalopathy Induces Misfolding of Alleged
Prion-Resistant Species Cellular Prion Protein without Altering Its
Pathobiological Features
Enric Vidal3, Natalia Fernández-Borges1, Belén Pintado4, Montserrat
Ordóñez3, Mercedes Márquez6, Dolors Fondevila5,6, Juan María Torres7, Martí
Pumarola5,6, and Joaquín Castilla1,2 + Author Affiliations
1CIC bioGUNE, 48160 Derio, Bizkaia, Spain,
2IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Bizkaia, Spain,
3Centre de Recerca en Sanitat Animal, Campus de la Universitat Autònoma de
Barcelona (UAB)-IRTA, 08193 Bellaterra, Barcelona, Spain,
4Centro Nacional de Biotecnología, Campus de Cantoblanco, 28049
Cantoblanco, Madrid, Spain,
5Department of Animal Medicine and Surgery, Veterinary Faculty, UAB, 08193
Bellaterra (Cerdanyola del Vallès), Barcelona, Spain,
6Murine Pathology Unit, Centre de Biotecnologia Animal i Teràpia Gènica,
UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, and
7Centro de Investigación en Sanidad Animal-Instituto Nacional de
Investigación y Tecnología Agraria y Alimentaria, 28130 Valdeolmos, Madrid,
Spain
Author contributions: E.V., N.F.-B., and J.C. designed research; E.V.,
N.F.-B., B.P., M.O., M.M., D.F., and J.C. performed research; E.V., N.F.-B.,
B.P., and J.C. contributed unpublished reagents/analytic tools; E.V., N.F.-B.,
B.P., M.O., M.M., D.F., J.M.T., M.P., and J.C. analyzed data; E.V. and J.C.
wrote the paper.
Abstract
Bovine spongiform encephalopathy (BSE) prions were responsible for an
unforeseen epizootic in cattle which had a vast social, economic, and public
health impact. This was primarily because BSE prions were found to be
transmissible to humans. Other species were also susceptible to BSE either by
natural infection (e.g., felids, caprids) or in experimental settings (e.g.,
sheep, mice). However, certain species closely related to humans, such as canids
and leporids, were apparently resistant to BSE. In vitro prion amplification
techniques (saPMCA) were used to successfully misfold the cellular prion protein
(PrPc) of these allegedly resistant species into a BSE-type prion protein. The
biochemical and biological properties of the new prions generated in vitro after
seeding rabbit and dog brain homogenates with classical BSE were studied.
Pathobiological features of the resultant prion strains were determined after
their inoculation into transgenic mice expressing bovine and human PrPC. Strain
characteristics of the in vitro-adapted rabbit and dog BSE agent remained
invariable with respect to the original cattle BSE prion, suggesting that the
naturally low susceptibility of rabbits and dogs to prion infections should not
alter their zoonotic potential if these animals became infected with BSE. This
study provides a sound basis for risk assessment regarding prion diseases in
purportedly resistant species.
Received January 18, 2013. Revision received March 7, 2013. Accepted March
23, 2013. Copyright © 2013 the authors 0270-6474/13/337778-09$15.00/0
Friday, March 8, 2013
Dogs may have been used to make Petfood and animal feed
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A.
Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel
J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary
Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI
53706, USA 2US Geological Survey, National Wildlife Health Center, 6006
Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural
Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary
Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author
email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents
that inhabit locations undergoing cervid chronic wasting disease (CWD)
epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed
mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles
(Myodes gapperi). The inocula were prepared from the brains of hunter-harvested
white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles
proved to be most susceptible, with a median incubation period of 272 days.
Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the
brains of all challenged meadow voles. Subsequent passages in meadow voles lead
to a significant reduction in incubation period. The disease progression in
red-backed voles, which are very closely related to the European bank vole (M.
glareolus) which have been demonstrated to be sensitive to a number of TSEs, was
slower than in meadow voles with a median incubation period of 351 days. We
sequenced the meadow vole and red-backed vole Prnp genes and found three amino
acid (AA) differences outside of the signal and GPI anchor sequences. Of these
differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is
particularly intriguing due its postulated involvement in "rigid loop" structure
and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5
years post-inoculation, but appear to be exhibiting a high degree of disease
penetrance. White-footed mice have an even longer incubation period but are also
showing high penetrance. Second passage experiments show significant shortening
of incubation periods. Meadow voles in particular appear to be interesting lab
models for CWD. These rodents scavenge carrion, and are an important food source
for many predator species. Furthermore, these rodents enter human and domestic
livestock food chains by accidental inclusion in grain and forage. Further
investigation of these species as potential hosts, bridge species, and
reservoirs of CWD is required.
please see ;
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO
CAMELUS) - SPONGIFORM ENCEPHALOPATHY
4.21 Three cases of SE’s with an unknown infectious agent have been
reported in ostriches (Struthio Camellus) in two zoos in north west Germany
(Schoon @ Brunckhorst, 1999, Verh ber Erkeg Zootiere 33:309-314). These birds
showed protracted central nervous symptoms with ataxia, disturbances of balance
and uncoordinated feeding behaviour. The diet of these birds had included
poultry meat meal, some of which came from cattle emergency slaughter
cases.
SE1806
TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN
HOMOGENATE
1 challenged cock bird was necropsied (41 months p.i.) following a period
of ataxia, tremor, limb abduction and other neurological signs.
Histopathological examination failed to reveal any significant lesions of the
central or peripheral nervous systems...
1 other challenged cock bird is also showing ataxia (43 months p.i.).
snip...
94/01.19/7.1
A notification of Spongiform Encephalopathy was introduced in October 1996
in respect of ungulates, poultry and any other animal.
4.23 MAFF have carried out their own transmission experiments with hens. In
these experiments, some of the chickens exposed to the BSE agent showed
neurological symptoms. However MAFF have not so far published details of the
symptoms seen in chickens. Examination of brains from these chickens did not
show the typical pathology seen in other SE’s. 4.24 A farmer in Kent in November
1996 noticed that one of his 20 free range hens, the oldest, aged about 30
months was having difficulty entering its den and appeared frightened and tended
to lose its balance when excited. Having previously experienced BSE cattle on
his farm, he took particular notice of the bird and continued to observe it over
the following weeks. It lost weight, its balance deteriorated and characteristic
tremors developed which were closely associated with the muscles required for
standing. In its attempts to maintain its balance it would claw the ground more
than usual and the ataxia progressively developed in the wings and legs, later
taking a typical form of paralysis with a clumsy involuntary jerky motion.
Violent tremors of the entire body, particularly the legs, became common,
sparked off by the slightest provocation. This is similar to that seen in many
BSE cases where any excitement may result in posterior ataxia, often with
dropping of the pelvis, kicking and a general nervousness. Three other farmers
and a bird breeder from the UK are known to have reported having hens with
similar symptoms. The bird breeder who has been exhibiting his birds for show
purposes for 20 years noticed birds having difficulty getting on to their perch
and holding there for any length of time without falling. Even though the bird
was eating normally, he noticed a weight loss of more than a pound in a bird the
original weight of which was 5 pounds. 4.25 Histological examination of the
brain revealed degenerative pathological changes in hens with a minimal
vacuolation. The presence of PrP immunostaining of the brain sections revealed
PrP-sc positive plaques and this must be regarded as very strong evidence to
demonstrate that the hens had been incubating Spongiform Encephalopathy.
OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED
BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002
OPINION
1. Necrophagous birds as possible transmitters of BSE. The SSC considers
that the evaluation of necrophagous birds as possible transmitters of BSE,
should theoretically be approached from a broader perspective of mammals and
birds which prey on, or are carrion eaters (scavengers) of mammalian species.
Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons,
eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could
be considered possible vectors of transmission and/or spread of TSE infectivity
in the environment. In view also of the occurrence of Chronic Wasting Disease
(CWD) in various deer species it should not be accepted that domestic cattle and
sheep are necessarily the only source of TSE agent exposure for carnivorous
species. While some information is available on the susceptibility of
wild/exotic/zoo animals to natural or experimental infection with certain TSE
agents, nothing is known of the possibility of occurrence of TSE in wild animal
populations, other than among the species of deer affected by CWD in the
USA.
1 The carrion birds are animals whose diet regularly or occasionally
includes the consumption of carcasses, including possibly TSE infected ruminant
carcasses.
C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc
snip...
skroll down to the bottom ;
Date: Mon, 11 Jun 2001 16:24:51 –0700
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs
'THE AUTOPSY'
Wednesday, October 14, 2009
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD
;
Friday, February 08, 2013
Behavior of Prions in the Environment: Implications for Prion Biology
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-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.
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.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients.
*** For elk and deer considered at high risk for CWD, the FDA recommends
that these animals do not enter the animal feed system. However, this
recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and
behavioural changes that can span weeks or months (Williams, 2005). In addition,
signs might include excessive salivation, behavioural alterations including a
fixed stare and changes in interaction with other animals in the herd, and an
altered stance (Williams, 2005). These signs are indistinguishable from cervids
experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB,
for example, infected deer populations would need to be tested to differentiate
if they were infected with CWD or BSE to minimise the risk of BSE entering the
human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
see full text report here ;
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
LANCET INFECTIOUS DISEASE JOURNAL
Volume 3, Number 8 01 August 2003
Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people who have remained
largely unsatisfied after being told that a close relative died from a rapidly
progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease
(CJD). So he decided to gather hundreds of documents on transmissible spongiform
encephalopathies (TSE) and realised that if Britons could get variant CJD from
bovine spongiform encephalopathy (BSE), Americans might get a similar disorder
from chronic wasting disease (CWD)the relative of mad cow disease seen among
deer and elk in the USA. Although his feverish search did not lead him to the
smoking gun linking CWD to a similar disease in North American people, it did
uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the
occurrence of CJD and CWD in the USA. Only a few states have made CJD
reportable. Human and animal TSEs should be reportable nationwide and
internationally, he complained in a letter to the Journal of the American
Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue
to expect us to still believe that the 85% plus of all CJD cases which are
sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small
region in Colorado. But since early 2002, it has been reported in other areas,
including Wisconsin, South Dakota, and the Canadian province of Saskatchewan.
Indeed, the occurrence of CWD in states that were not endemic previously
increased concern about a widespread outbreak and possible transmission to
people and cattle.
To date, experimental studies have proven that the CWD agent can be
transmitted to cattle by intracerebral inoculation and that it can cross the
mucous membranes of the digestive tract to initiate infection in lymphoid tissue
before invasion of the central nervous system. Yet the plausibility of CWD
spreading to people has remained elusive.
Getting data on TSEs in the USA from the government is like pulling teeth,
Singeltary argues. You get it when they want you to have it, and only what they
want you to have.
SNIP...FULL TEXT ;
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
Saturday, March 09, 2013
Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest
Incubation Time Model for Prion Diseases
Tuesday, April 24, 2012
MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA
Wednesday, April 25, 2012
4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012
Wednesday, May 2, 2012
ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND
ANIMAL HEALTH
==============================================
Saturday, August 4, 2012
***Final Feed Investigation Summary - California BSE Case - July 2012
=============================================
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
Saturday, July 6, 2013
Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy
Research Article
TSS
posted by Terry S. Singeltary Sr. at
12:41 PM
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