Wednesday, October 17, 2012
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
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: email@example.com
¤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
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 –, 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 . 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
SCRAPIE TRANSMISSION TO CHIMPANZEES
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: firstname.lastname@example.org
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)
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
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...
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,...
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
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.
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.).
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
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.
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
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