Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos)
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
Gregory E. Phillips, Justin W. Fischer
United States Department of Agriculture, Animal and Plant Health Inspection
Service, Wildlife Services, National Wildlife Research Center, Fort Collins,
Colorado, United States of America
Abstract Top
Avian scavengers, such as American crows (Corvus brachyrhynchos), have
potential to translocate infectious agents (prions) of transmissible spongiform
encephalopathy (TSE) diseases including chronic wasting disease, scrapie, and
bovine spongiform encephalopathy. We inoculated mice with fecal extracts
obtained from 20 American crows that were force-fed material infected with
RML-strain scrapie prions. These mice all evinced severe neurological
dysfunction 196–231 d postinoculation ( = 198; 95% CI: 210–216) and tested
positive for prion disease. Our results suggest a large proportion of crows that
consume prion-positive tissue are capable of passing infectious prions in their
feces ( = 1.0; 95% CI: 0.8–1.0). Therefore, this common, migratory North
American scavenger could play a role in the geographic spread of TSE
diseases.
Citation: VerCauteren KC, Pilon JL, Nash PB, Phillips GE, Fischer JW (2012)
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos). PLoS ONE 7(10): e45774.
doi:10.1371/journal.pone.0045774
Editor: Jiyan Ma, Ohio State University, United States of America
Received: January 31, 2011; Accepted: August 24, 2012; Published: October
17, 2012
This is an open-access article, free of all copyright, and may be freely
reproduced, distributed, transmitted, modified, built upon, or otherwise used by
anyone for any lawful purpose. The work is made available under the Creative
Commons CC0 public domain dedication.
Funding: Funding was provided by U.S. Department of Agriculture, Animal and
Plant Health Inspection Service, Veterinary Services (VS). A representative of
VS served on a panel that provided input to the 5-year plan for the Chronic
Wasting Disease Project of the National Wildlife Research Center, within which
this project was conducted. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
Competing interests: The authors have declared that no competing interests
exist.
* E-mail: kurt.c.vercauteren@aphis.usda.gov
¤aCurrent address: Tolmar Inc., Fort Collins, Colorado, United States of
America
¤bCurrent address: Department of Biology, University of West Florida,
Pensacola, Florida, United States of America
snip...
Discussion
We tested the hypothesis that PrPRes would remain infectious after passage
through the digestive tract of crows. After inoculation with fecal supernatant
from crows gavaged with PrPRes-infected material, we observed clinical disease
and obtained positive results from ELISA in all 84 CF+ mice that survived >3
dpi. Thus, we confirmed passage of infectious PrPRes through all 20 crows
gavaged with infected material. We conclude that 83–100% of crows from the
population we sampled can excrete infectious RML PrPRes in feces under
conditions similar to those in our study.
The MB+ mice developed clinical scrapie 15 d earlier than CF+ mice
indicating inoculated dose of PrPRes infectivity was likely lower for CF+ mice.
We inoculated MB+ and MB− mice to demonstrate that brain source materials were
infectious or not infectious, respectively, not to serve as standards for titer
assessment. However, comparison with unpublished titration results from
intraperitoneal inoculation of RML mouse scrapie into C57BL10 mice (Ann Ward and
Sue Priola, Rocky Mountain Laboratories, personal communication) suggest MB+
mice received approximately 10-times more infectivity than CF+ mice. Dilutions
of brain and fecal material with SPBS (see Methods) indicate that the amount of
infectivity inoculated into MB+ mice would have been about double that of CF+
mice, assuming no influence on concentration of infectivity due to passage or
centrifuge processing. It is reasonable to expect some loss of infectivity after
removing solids from diluted crow feces by centrifugation. It is also possible
that some degradation or absorption of infectivity occurred during passage
through crow alimentary tracts.
Our study clearly shows that RML PrPRes can persist after passage through
the crow alimentary tract. As there is variability in resistance of different
strains of PrPRes to degradation [32]–[36], we cannot definitively state that
passage of strains of concern would occur. However, RML PrPRes has been shown
more sensitive to degradation than TSE field isolates after 4 h exposure to
enzymatic digestion [36]. Therefore, results of our study likely understate
potential for prion passage through the alimentary canal of crows. Further
experimental trials involving TSE prions obtained from ovine, bovine, and
cervine carcasses would be required to definitively evaluate passage of natural
TSEs through digestive systems of scavengers and predators. Other additional
research topics could include in-vitro evaluation of PrPRes degradation in crow
digestive fluids; effects of solid, semisolid, and liquid delivery of infective
materials on passage rate and residual infectivity in feces; postexcretion
continued enzymatic and bacterial degradation of infectivity in feces;
infectivity of feces excreted >4 h postgavage; susceptibility of crows to TSE
disease and potential for postinfection shedding of PrPRes in feces.
Sunday, November 01, 2009
AS THE CROW FLIES, SO DOES CWD
Sunday, November 01, 2009
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
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
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
;
Thursday, January 26, 2012
The Risk of Prion Zoonoses
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI:
10.1126/science.1218167
Thursday, January 26, 2012
Facilitated Cross-Species Transmission of Prions in Extraneural Tissue
Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI:
10.1126/science.1215659
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN,
AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY
PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF
FILE...TSS)
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
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 ;
Volume 18, Number 3—March 2012
Samuel E. Saunders1, Shannon L. Bartelt-Hunt, and Jason C. Bartz
Author affiliations: University of Nebraska-Lincoln, Omaha, Nebraska, USA
(S.E. Saunders, S.L. Bartelt-Hunt); Creighton University, Omaha (J.C. Bartz)
Synopsis
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
snip...
Most epidemiologic studies and experimental work have suggested that the
potential for CWD transmission to humans is low, and such transmission has not
been documented through ongoing surveillance (2,3). In vitro prion replication
assays report a relatively low efficiency of CWD PrPSc-directed conversion of
human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are
resistant to CWD infection (31); these findings indicate low zoonotic potential.
However, squirrel monkeys are susceptible to CWD by intracerebral and oral
inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans
than squirrel monkeys, are resistant to CWD infection (32). Regardless, the
finding that a primate is orally susceptible to CWD is of concern...
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...
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
Saturday, September 01, 2012
Resistance of Soil-Bound Prions to Rumen Digestion
Re: vCJD in the USA * BSE in U.S.
15 November 1999
Terry S Singeltary, NA
snip...
Our feeding and rendering practices have mirrored that of the U.K. for
years, some say it was worse. Everything from the downer cattle, to those
scrapie infected sheep, to any roadkill, including the city police horse and the
circus elephant went to the renders for feed and other products for consumption.
Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs,
chickens, dogs, and cats, and humans were exempt from that ban. So they can
still feed pigs and chickens those potentially TSE tainted by-products, and then
they can still feed those by-products back to the cows. I believe it was Dr. Joe
Gibbs, that said, the prion protein, can survive the digestinal track. So you
have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle
feeders, sent neurologically ill cattle, some with encephalopathy stamped on the
dead slips, were picked up and sent to the renders, along with sheep carcasses.
Speaking of autopsies, I have a stack of them, from CJD victims. You would be
surprised of the number of them, who ate cow brains, elk brains, deer brains, or
hog brains. ...
Saturday, October 6, 2012
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES 2011 Annual Report
Friday, October 12, 2012
Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule
Proposals for “Chronic Wasting Disease (CWD)”
Texas Animal Health Commission (TAHC)
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'
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, October 6, 2012 ***
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES 2011 Annual Report
TSS
posted by Terry S. Singeltary Sr. at
9:08 PM
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