Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Passage of the CWD agent through meadow voles results in increased attack rates and decreased incubation periods in raccoons
Author item MOORE, SARA JO - Orise Fellow item CARLSON, CHRISTINA - Us Geological Survey (USGS) item SCHNEIDER, JAY - Us Geological Survey (USGS) item JOHNSON, CHRISTOPHER - Us Geological Survey (USGS) item Greenlee, Justin Submitted to: Emerging Infectious Diseases Publication Type: Peer Reviewed Journal Publication Acceptance Date: 12/13/2021 Publication Date: N/A Citation: N/A Interpretive
Summary: Transmissible spongiform encephalopathies (TSEs) are a group of fatal diseases caused by the accumulation of misfolded prion protein in the brain. Several livestock species including cattle, sheep, deer, and elk are afflicted by prion diseases. In sheep the disease is called scrapie. In deer and elk, the disease is called chronic wasting disease (CWD). Due to the human consumption of cervid meat products and intermingling of various livestock species with wild cervid populations, there is significant interest in characterizing the possible host range of CWD. This study reports the successful transmission of the CWD agent to raccoons, a ubiquitous omnivore present throughout North America. In addition, passage of the CWD agent from deer through meadow voles, a scavenger present in much of the range where CWD occurs, results in changes in the biological behavior of the CWD agent when that material is used to inoculate raccoons. This research is of interest to regulatory officials or anyone interested in controlling CWD in wildlife or captive cervid herds.
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring neurodegenerative disease of cervids. Raccoons (Procyon lotor) and meadow voles (Microtus pennsylvanicus) have previously been shown to be susceptible to CWD and their scavenging habits could expose them to environmental CWD infectivity. To investigate the potential for transmission of the agent of CWD from white-tailed deer to voles and subsequently to raccoons, we intracranially inoculated raccoons with brain homogenate from a CWD-affected white-tailed deer (CWDWtd), or derivatives of this isolate after it had been passaged through voles one or five times. We found that passage of the CWDWtd isolate through voles led to a change in the biological behavior of the CWD agent, including increased attack rates and decreased incubation periods in raccoons. A better understanding of the dynamics of cross-species transmission of CWD prions will help us to better manage and control the spread of CWD in free-ranging and farmed cervid populations.
''We found that passage of the CWDWtd isolate through voles led to a change in the biological behavior of the CWD agent, including increased attack rates and decreased incubation periods in raccoons.''
Disturbing...terry
ORIGINAL RESEARCH ARTICLE
Front. Vet. Sci., 02 March 2018 | https://doi.org/10.3389/fvets.2018.00004
Consumption of Big Game Remains by Scavengers: A Potential Risk as Regards Disease Transmission in Central Spain
imageRicardo Carrasco-Garcia, imagePatricia Barroso, imageJavier Perez-Olivares, imageVidal Montoro and imageJoaquÃn Vicente* SaBio group, Instituto de Investigación en Recursos Cinegéticos (CSIC-UCLM-JCCM), Ciudad Real, Spain
Understanding the role that facultative scavenger species may play in spreading infectious pathogens, and even becoming reservoirs for humans, domestic and wild ungulates or, on the contrary, preventing the spread of disease, requires a prior understanding of the pattern of carrion scavenging in specific scenarios. The objectives of this paper are (i) to describe the guild of vertebrate scavengers and (ii) to study the species-specific, habitat, and management-related factors involved in the usage of gut piles in South Central Spain (SCS), a tuberculosis (TB) endemic area. We used camera trapping at 18 hunting piles on seven hunting estates. A total of eight bird and five mammal taxa were detected at the remains of hunting piles. The most frequently detected species in terms of number of gut piles visited (78%) and scavenged (61%) was the red fox Vulpes vulpes, followed by the griffon vulture Gyps fulvus (56% as regards both presence and scavenging) and the raven Corvus corax (61 and 39% as regards presence and scavenging, respectively). We evidenced that griffon vultures accounted for most of the scavenging activity in open habitats, while facultative mammal scavengers, red fox, and wild boar Sus scrofa made the highest contribution to scavenging in vegetation-covered habitats. In the case of wild boar, the gut piles deposited during the evening and night favored higher rates of scavenging, while the opposite pattern was observed for griffons. Overall, our findings suggest that when disposing of hunting remains in areas of risk as regards disease transmission it is particularly important to consider the access that facultative mammals, and especially wild boar, have to material, while the presence of the resource needs to be safeguarded to protect specialist scavengers of conservation value. These results are of particular relevance in the case of wild boar in the current context of re-emerging TB and emerging African swine fever (ASF) in Europe.
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Results
The general descriptors concerning the monitoring and the usage of hunting piles are shown in Table 1. Overall, the mean (±SD) period of monitoring per pile (time between the beginning and the end of the monitoring) was 14.75 ± 9.08 days. The mean period before the first activity (time between the start of the carrion monitoring and the first activity detected) was 2.58 ± 3.39 days. The mean period of activity per gut pile (time between the first and last activities detected) was 11.47 ± 8.22 days. Scavenging activity was detected at all the study hunting piles except one. The mean number of pictures per camera was 516 ± 541.
A total of eight bird and five mammal taxa were detected by the camera traps around the hunting remains (Table 2). In terms of the total number of pictures, the griffon vulture was the most frequently detected species, followed by ravens, monk vultures, azure-winged magpies Cyanopica cyanus, magpies Pica pica, wild boar, red fox, and red deer. Domestic dogs, usually hunting dogs that could not be retrieved by the hunters immediately after the hunting day, were found in 44 pictures (four gut piles). The Imperial eagle was recorded in only 19 pictures (two piles), while the Egyptian vulture Neophron percnocterus, Golden eagle, and common genet Genetta genetta were detected in 4, 4, and 1 pictures, respectively (in one pile). With regard to wild boar, we recorded activity in 17% of all 207 camera-nights (during the period of activity), and two or more visits were made by this species in 5% of these cases.
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It has been reported (8) the ability of chronic wasting disease (CWD) -infected brain material to pass through the gastrointestinal tract of coyotes (Canis latrans) following oral ingestion, and be infectious, demonstrating that mammalian scavengers could contribute to the translocation and contamination of CWD in the environment.
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Discussion This research provides the first results on the factors that determine the usage of big game remains by scavengers in South Western Europe, a TB endemic region. The guild of vertebrates using big game remains in Mediterranean habitats in SCS appeared rich as regards the number of species, which supports the prevalence of facultative scavenging (14). Vultures and corvids were the most common diurnal scavenger at gut piles in the study area, especially in open habitats, and benefited from most of the piles available. While vultures, which are generally very resistant to ungulate infectious diseases, may contribute to the removal of most pathogenic microorganisms from dead animals (12, 23), the role of mammal scavengers such as wild boar and red fox requires further research. We evidenced that these mammal species prevailed at hunting piles located in covered areas (woodlands and scrublands), and that the moment of gut pile deposition influenced their subsequent usage. In the case of wild boar, those plies deposited during the evening and night favored scavenging by this species. Overall, our findings suggest that the disposal of hunting remains in areas of risk for disease transmission, and particularly TB in our study area, must particularly consider the access of facultative mammals, especially wild boar, to material, while the presence of the resource needs to be safeguarded in order to protect specialist scavengers of conservation value. We also raise concerns about the potential role of cannibalism by wild boar in relation to other pathogens not present in our study area, such as ASF (16).
The contribution made by azure-winged magpies and magpies to the consumption of hunting remains is limited, since these birds’ activity around the gut piles probably consisted of searching for decomposer insects, and their ingestion rate is very low when compared with that of larger birds. Vultures and ravens accounted for a relevant proportion of scavenging in open habitats, and particularly those which took place during the daytime. For instance, corvids were frequently involved in the early discovery of gut piles: they were detected 2.5 times faster in open habitats than in covered ones (1.6 and 4.3 days, respectively). The early consumption by birds determined the subsequent use of the hunting remains, and prevented the subsequent access of facultative mammal scavengers (usually nocturnal) once remains were left.
In woodlands, wild boar and red fox made the highest average contribution to scavenging (wild boar made 37% of the average contribution per species and gut pile, and red fox, 31%), whereas vultures were much less relevant (Table 3). From the ecological perspective, factors limiting vultures’ access to big game remains may have an effect on the ecology of facultative scavengers. For instance, the presence of vultures may reduce the scavenging opportunities of mesocarnivores (facultative scavengers, particularly red fox) through their indirect effect on abundance, as evidenced in two neighboring areas in South-eastern Spain (24).
Interestingly, in this study wild boar scavenged both cervid and wild boar guts, contrary to that which usually occurs with entire carcasses [the authors, unpublished (16)], when it (at least partially) avoids feeding on conspecifics. The red fox has been described as behaving in a similar manner (25). This highlights that feeding on conspecific gut piles, as compared with entire carcasses, probably involves an increased risk of pathogen transmission. In Mediterranean ecosystems the gut piles of big game may, therefore, be a source of inter and intraspecific transmission of pathogens, particularly in the case of wild boar.
The scavenging activity of wild boar should be considered as a risk factor to consider when applying control strategies for diseases such as TB and, eventually, ASF. This must be contextualized in integral disease–control approaches [e.g., the reduction of population abundance and aggregation, the management of risk factors, etc. (26)]. In central and East Europe, ASF virus infecting wild boar and pigs has a great ability to persist in the tissues of dead animals (27). As this viral disease becomes more chronic or carrier host status is possible, the importance of managing wild boar hunting remains and carcasses increases. It had been considered that carnivores, such as the endangered Iberian lynx, the badger and the red fox, may possibly have been infected by TB as a result of their consuming infected prey or carrion [e.g., Ref. (28, 29)] in South Central Spain, and this may similarly occur with carnivores in other latitudes [e.g., Ref. (30)]. Some relevant pathogens that may be transmitted via scavenging are the nematodes of the genus Trichinella, Aujeszky’s disease virus (from wild boar) or Hepatitis E virus. On the contrary, facultative scavengers, such as carnivores, are likely to reduce the intraspecific transmission risk of some pathogens, as in the case of brucellosis (31). We consider the presence of a male red deer at two gut piles as anecdotal. Dietary deficits and unhealthy conditions have been proposed as the origin of abnormal and stereotypic oral and diet behaviors in ungulates (32).
Management Applications
The findings of this study recommend improving the previous detailed veterinary inspection of hunting remains in areas of risk as regards diseases (e.g., TB), followed by their appropriate disposal, preferably on mammal-proof sites (bird feeding stations) in order to deal with conservation issues, or the elimination by other authorized means when risk of disease spread is present. We evidenced that, in open localizations, avian scavengers are a suitable and ecological option for the removal of hunting remains. An interesting approach might be a combination of strategies: the use of open habitats, depositing hunting remains during the daytime, and implementing temporary fences that effectively limit access by mammals. Moreno-Opo et al. (33) have proposed cheap, mobile, and easily manageable enclosure models, such as electrified mesh, that prevent facultative mammalian scavengers from entering feeding stations, at least temporarily while remains are totally scavenged by specialists.
Research Papers
CWD prions remain infectious after passage through the digestive system of coyotes (Canis latrans)
Tracy A Nichols, Justin W Fischer, Terry R Spraker, Qingzhong Kong & Kurt C VerCauteren Pages 367-375 | Received 07 Jul 2015, Accepted 18 Aug 2015, Accepted author version posted online: 04 Dec 2015, Published online: 04 Dec 2015 Download citation https://doi.org/10.1080/19336896.2015.1086061
ABSTRACT
Chronic wasting disease (CWD) is a geographically expanding prion disease of wild and captive cervids in North America. Disease can be transmitted directly, animal to animal, or indirectly via the environment. CWD contamination can occur residually in the environment via soil, water, and forage following deposition of bodily fluids such as urine, saliva, and feces, or by the decomposition of carcasses. Recent work has indicated that plants may even take up prions into the stems and leaves. When a carcass or gut pile is present in the environment, a large number of avian and mammalian species visit and consume the carrion. Additionally, predators like coyotes, likely select for disease-compromised cervids. Natural cross-species CWD transmission has not been documented, however, passage of infectious prion material has been observed in the feces of crows. In this study we evaluated the ability of CWD-infected brain material to pass through the gastrointestinal tract of coyotes (Canis latrans) following oral ingestion, and be infectious in a cervidized transgenic mouse model. Results from this study indicate that coyotes can pass infectious prions via their feces for at least 3 days post ingestion, demonstrating that mammalian scavengers could contribute to the translocation and contamination of CWD in the environment.
Keywords: chronic wasting disease, coyotes, environmental contamination, feces, prions, scavengers, transmission
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Discussion The continued spread of CWD is of concern to the health of both wild and captive cervid populations. Indirect transmission through the environment has been demonstrated in captive animals living in paddocks where CWD-positive animals had lived,3 Miller MW, Williams ES, Hobbs NT, Wolfe LL. Environmental sources of prion transmission in mule deer. Emerg Infect Dis 2004; 10:1003-6; PMID:15207049; http://dx.doi.org/10.3201/eid1006.040010 [Crossref], [PubMed], [Web of Science ®], [Google Scholar] and is a particular challenge due to the long persistence of CWD within the environment.7,28 Johnson CJ, Phillips KE, Schramm PT, McKenzie D, Aiken JM, Pedersen JA. Prions adhere to soil minerals and remain infectious. PLoS Pathog 2006; 2:e32; PMID:16617377; http://dx.doi.org/10.1371/journal.ppat.0020032 Wiggins RC. Prion stability and infectivity in the environment. Neurochem Res 2009; 34:158-68; PMID:18483857; http://dx.doi.org/10.1007/s11064-008-9741-6 Infectious material can be deposited in the environment by the decay of infected carcasses, from urine, feces, and saliva,5,6,29 Pulford B, Spraker TR, Wyckoff AC, Meyerett C, Bender H, Ferguson A, Wyatt B, Lockwood K, Powers J, Telling GC, et al. Detection of PrPCWD in feces from naturally exposed Rocky Mountain elk (Cervus elaphus nelsoni) using protein misfolding cyclic amplification. J Wildl Dis 2012; 48:425-34; PMID:22493117; http://dx.doi.org/10.7589/0090-3558-48.2.425 Mathiason CK, Powers JG, Dahmes SJ, Osborn DA, Miller KV, Warren RJ, Mason GL, Hays SA, Hayes-Klug J, Seelig DM, et al. Infectious prions in the saliva and blood of deer with chronic wasting disease. Science 2006; 314:133-6; PMID:17023660; http://dx.doi.org/10.1126/science.1132661 Haley NJ, Mathiason CK, Zabel MD, Telling GC, Hoover EA. Detection of sub-clinical CWD infection in conventional test-negative deer long after oral exposure to urine and feces from CWD+ deer. PLoS One 2009; 4:e7990; PMID:19956732; http://dx.doi.org/10.1371/journal.pone.0007990 and the spread of infected material may be aided by scavengers and predators. In this study we illustrated the ability of coyotes to pass infectivity in their feces after the ingestion of CWD-infected brain homogenate.
Coyotes have the ability to travel significant distances. This distance, however, is based upon social structure, which is generally placed in 2 categories; resident or transient.30 Gese EM, Rongstad OJ, Mytton WR. Home range and habitat use of coyotes in southeastern Colorado. Journal of Wildlife Management 1988; 52:640-6; http://dx.doi.org/10.2307/3800923 [Crossref], [Web of Science ®], [Google Scholar] Resident animals are those that utilize a specific territory and are comprised of a mated pair and sometimes pups from a previous year, while transient animals are individuals that are nomadic, more commonly male, and have no affinity for a specific territory.30 Gese EM, Rongstad OJ, Mytton WR. Home range and habitat use of coyotes in southeastern Colorado. Journal of Wildlife Management 1988; 52:640-6; http://dx.doi.org/10.2307/3800923 [Crossref], [Web of Science ®], [Google Scholar] In a study evaluating the range of coyotes in southern Colorado, transient animals, which represented 22% of the population, ranged over 106.5 ± 27 km2, versus resident groups which ranged over 11.3 ± 5.8 km.2,30 Miller MW, Williams ES. Prion disease: horizontal prion transmission in mule deer. Nature 2003; 425:35-6; PMID:12955129; http://dx.doi.org/10.1038/425035a Gese EM, Rongstad OJ, Mytton WR. Home range and habitat use of coyotes in southeastern Colorado. Journal of Wildlife Management 1988; 52:640-6; http://dx.doi.org/10.2307/3800923 Transient coyotes are therefore provided an opportunity to translocate disease to previously CWD-negative localities.
Control coyotes readily consumed the homogenized elk brain. Of the treatment coyotes, which were moved indoors 2 days prior to the initiation of the study, only one (#135) immediately ate the brain homogenate. The other coyotes required supplementation with diced, raw chicken, or fish-flavored soft cat food. Although the numbers are too small to come to any definitive conclusions, it is interesting to note that the coyote that ingested the brain homogenate without chicken or cat food supplementation did not appear to transfer infectivity to any of the mice in the bioassay. Neither age nor sex appeared to have any effect on fecal shedding. However, it is possible that individual variation within the stomach environment, such as pH and flora could have influenced the passage of the infectious prions through the gastrointestinal tract.
Our experimental design was based on detection of CWD in coyote feces by PMCA prior to initiation of the bioassay. PMCA was able to repeatedly detect the presence of proteinase K-resistant prions signal in feces from DPI 1, so the bioassay was designed to evaluate feces for 2 days following, to account for any uncertainty in prion detection in feces. Results from the bioassay showed transmission of disease to 2/4 mouse groups in DPI 3, suggesting that infectivity may continue to be present in the feces more than 3 days after ingestion. We were unable to go back and increase the bioassay to include DPI 4 and 5, due to logistical reasons.
The 50 mL oral dose ingested by coyotes in this study was comprised solely of infected brain tissue and represented a high dose. In the wild, coyotes would opportunistically consume a wide variety of tissues from a kill or scavenged deer or elk carcass, likely making their actual ingested infective dose much smaller. This study was not designed to mimic a naturally consumed dose of CWD, but rather as a proof of concept to determine if infectivity could pass into coyote feces. The passage of disease in feces is a common route of translocation for many viral, bacterial and parasitic diseases.
The results of this bioassay indicate that infectious CWD prions are able to be passed in the feces of coyotes fed infected elk brain homogenate for at least 3 DPI, making them a potential vector for CWD prion transport and contamination within the environment.
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
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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)
SUNDAY, SEPTEMBER 01, 2013
hunting over gut piles and CWD TSE prion disease
hunting over gut piles and CWD TSE prion disease, a reminder...just saying
SUNDAY, JULY 07, 2013
Could avian scavengers translocate infectious prions to disease-free areas initiating new foci of chronic wasting disease?
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
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.
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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 MarÃa Torres7, Martà Pumarola5,6, and JoaquÃn 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 BiotecnologÃa, 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 Terà pia Gènica, UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, and
7Centro de Investigación en Sanidad Animal-Instituto Nacional de Investigación y TecnologÃa 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.).
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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.
Necrophagous_OPINION_0209_FINAL.doc
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skroll down to the bottom ;
AUTOPSY OF THE RED-NECKED OSTRICH SPONGIFORM ENCEPHALOPATHY
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.
MONDAY, AUGUST 8, 2011
Susceptibility of Domestic Cats to CWD Infection Oral.29: Susceptibility of Domestic Cats to CWD Infection
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.
WILD HOGS AND CHRONIC WASTING DISEASE CWD TSE PRION
i have been worried about this for some time, but i don't see why others are not worried as well. these feral hogs that run rampant across states, can dig up a great deal of territory. what else can they dig up? i.e. CWD TSE PRION, and can they spread cwd tse prion to hell and back?
CWD TO PIGS
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
WEDNESDAY, APRIL 05, 2017
*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***
cattle are highly susceptible to white-tailed deer CWD and mule deer CWD
***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.
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price of prion poker goes up for cwd to cattle;
Monday, April 04, 2016
*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***
MONDAY, JUNE 12, 2017
Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?
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
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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.
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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.
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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).
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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.
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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.
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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.
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i am thinking of that 10,000,000 POUNDS OF BLOOD LACED MEAT AND BONE MEAL IN COMMERCE WARNING LETTER back in 2007, see;
SATURDAY, NOVEMBER 4, 2017
FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006
FRIDAY, NOVEMBER 3, 2017
BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW
''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''
IN CONFIDENCE
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
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It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
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The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS AND BEARS, OH MY!
Please be assured, the USA does NOT have any clue as to what the real perspective on the TSE prion disease in domestic feline and canine, much less our big wild cats, OR any other species including humans for that matter, but one thing for sure, the studies and history of the mad cow debacle below are deeply concerning with regards, to humans and wild big cats like mountain lions, cougars, lynx, Jaguar, and such, that feed on cervids that are infected with CWD. one thing for sure, don’t kid yourselves, all are very much susceptible to the TSE Prion disease, and if you don’t look, you don’t find, problems solved$$$
are we as humans, not only witnessing the 6th extinction, but more importantly, are we as humans the cause?
I would say yes to both...imo.
and please, before going any further, please remember this ;
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** 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.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION
*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
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***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
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Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
the tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
***URINE***
SUNDAY, JULY 16, 2017
*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***
Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20).
Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22).
Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing.
Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building.
Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9).
The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep.
Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease.
It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases.
Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA.
Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice.
In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals.
In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions).
As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28).
This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm.
This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc.
In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc.
Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing.
The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material.
In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12).
A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30).
This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model.
Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
TSE Scrapie, CWD, BSE, Prion, Soil
Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois
Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla
Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x
Download Citation
Ecological epidemiology Ecological modelling Infectious diseases Prions
Received: 21 August 2017
Accepted: 08 December 2017
Published online: 22 December 2017
Abstract
Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.
tse prion soil
cwd tse prion and soil, see more ;
BSE TSE Prion in zoo animals, exotic ruminants, domestic cats, and CPD Camel Prion Disease, a review 2020
The BSE Inquiry / Statement No 324
Dr James Kirkwood
(not scheduled to give oral evidence)
Statement to the BSE Inquiry
James K Kirkwood BVSc PhD FIBiol MRCVS
[This witness has not been asked to give oral evidence in Phase 1 of the Inquiry] 1. I became involved in the field of TSEs through my work as Head of the Veterinary Science Group at the Zoological Society of London’s Institute of Zoology. I held this post from November 1984 until June 1996, when I took up my present post at UFAW. During this time, concurrent with the BSE epidemic, cases of scrapie-like spongiform encephalopathies occurred in animals at the Zoological Society of London’s collections at Regent’s Park and Whipsnade and in other zoos. It was appropriate to investigate the epidemiology of these cases in order to try to determine the possible impact on zoo animals and breeding programmes, and to consider how the disease in zoo animals might be controlled.
2. Throughout the period from 1985 to March 1996, I worked at the Institute of Zoology (IoZ). I was Head of the Veterinary Science Group of the IoZ and Senior Veterinary Officer of the Zoological Society of London (ZSL). I was responsible for the provision of the veterinary service for the ZSL collections.
3. During the period from 1985 to March 1996, scrapie-like spongiform encephalopathies were diagnosed in the following animals which died, or were euthanased, at London Zoo and Whipsnade:
Animal Sex Date of Death Age (mos)
Arabian Oryx Oryx leucoryx F 24.3.89 38
Greater kudu Tragelaphus strepsiceros (Linda) F 18.8.89 30
Greater kudu (Karla) F 13.11.90 19
Greater kudu (Kaz) M 6.6.91 37
Greater kudu (Bambi) M 24.10.91 36
Greater kudu (346/90) M 26.2.92 18
Greater kudu (324/90) F 22.11.92 38
Cheetah Acinonyx jubatus (Michelle) F 22.12.93 91
All these cases were described in papers published in the scientific literature (as cited below).
4. All the animals listed above were bred in captivity. The greater kudu were from a highlyinbred group whose founders were Koo (imported from West Africa in 1967), Doo (imported from a Danish Zoo in 1969) and Chester (transferred to London from Chester Zoo in 1982). The family tree of the group is shown in: Kirkwood, J.K., Cunningham, A.A., Wells, G.A.H., Wilesmith, J.W. & Barnett, J.E.F. (1993) Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros: epidemiological observations. Veterinary Record 133, 360-364: (J/VR/133/360)
5. The first case diagnosed among the ZSL’s animals was in the greater kudu ‘Linda’, which died in August 1989. Retrospective examination of the brain of the Arabian oryx that had died 5 months earlier, revealed that this animal also had brain lesions characteristic of a scrapielike spongiform encephalopathy. Diagnostic histopathology of these (and of all the other cases that occurred at London and Whipsnade) was undertaken by the Central Veterinary Laboratory. The clinical features, diagnosis and possible aetiology of these first two ZSL cases was discussed in a paper published in 1990 (Kirkwood, J.K., Wells, G.A.H., Wilesmith, J.W., Cunningham, A.A. & Jackson, S.I. (1990) Spongiform encephalopathy in an Arabian oryx Oryx leucoryx and a greater kudu Tragelaphus strepsiceros. Veterinary Record 127, 418-420).(J/VR/127/418). We noted, in this paper, that it seemed probable that these cases had a common aetiology with BSE.
6. A greater kudu ‘Frances’ which had died some 18 months earlier (17.11.87) had shown clinical signs which, in retrospect, could have been due to SE but CNS tissue had not been saved for examination so this could not be checked (Kirkwood, J.K., Cunningham, A.A., Wells, G.A.H., Wilesmith, J.W. & Barnett, J.E.F. (1993) Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros: epidemiological observations. Veterinary Record 133, 360-364)(J/VR/133/360).
7. During the following 3 years, SE was diagnosed in 5 further greater kudu in the ZSL collections (see list in point 3 above). The second confirmed case in a greater kudu occurred in the 19-month old calf (Karla) born to the first confirmed case (Linda). This case gave us concern since the calf was born after the July 1988 ban on inclusion of ruminant derived protein in ruminant feeds and it was considered to be extremely unlikely that this animal could have been exposed to contaminated feeds (the kudu diet prior to February 1987 had included a cattle pellet but pelleted diets fed from then on were thought not to contain RDP). We speculated that maternal transmission may have occurred (Kirkwood, J.K., Wells, G.A.H., Cunningham, A.A., Jackson, S.I., Scott, A.C., Dawson, M. & Wilesmith, J.W. (1992). Scrapie-like encephalopathy in greater kudu (Tragelaphus strepsiceros) which had not been fed on ruminant-derived protein. Veterinary Record 130, 365-367:J/VR/130/365).
8. Since the next three animals in which the disease was confirmed (Kaz, Bambi and 346/90) were not thought to have been exposed to contaminated feeds, and were not born to dams who had been clinical cases (Cunningham, A.A., Wells, G.A.H., Scott, A.C., Kirkwood, J.K. & Barnett, J.E.F. (1993) Transmissible spongiform encephalopathy in greater kudu (Tragelaphus strepsiceros). Veterinary Record 132, 68), we considered the possibility that horizontal transmission may have occurred (Kirkwood, J.K., Cunningham, A.A., Wells, G.A.H., Wilesmith, J.W. & Barnett, J.E.F. (1993) Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros: epidemiological observations. Veterinary Record 133, 360-364: J/VR/132/68). The occurrence of SE in a greater kudu (324/90), that had been born in another zoo and was not thought to have been exposed to feeds contaminated with RDP, 27 months after being introduced to the group at Regent’s Park, was further cause for concern that transmission may have occurred between animals (Kirkwood, J.K., Cunningham, A.A., Austin, A.R.,Wells, G.A.H & Sainsbury, A.W. (1994) Spongiform encephalopathy in a Greater kudu Tragelaphus strepsiceros introduced into an affected group. Veterinary Record 134, 167-168: J/VR/134/167).
9. At that time, around 1993, the most likely explanation of the pattern of events seemed to be that the disease in kudu was the same as that in cattle: that it had originally entered the group in contaminated feed but that thereafter transmission may have occurred between individuals (Cunningham, A.A., Wells, G.A.H., Scott, A.C., Kirkwood, J.K. & Barnett, J.E.F. (1993) Transmissible spongiform encephalopathy in greater kudu (Tragelaphus strepsiceros).Veterinary Record 132, 68). In view of this and the likelihood that individuals of a wide range of species of zoo animals had been exposed we recommended (Kirkwood, J.K., Cunningham, A.A., Wells, G.A.H., Wilesmith, J.W. & Barnett, J.E.F. (1993) Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros: epidemiological observations. Veterinary Record 133, 360-364 ) that all zoo animals that may have been exposed to contaminated feeds should be observed closely and that because of the potentially serious implications for captive breeding programmes, well-described by my colleague Mr Andrew Cunningham (Cunningham, A.A. (1991) Bovine spongiform encephalopathy and British Zoos. Journal of Zoo and Wildlife Medicine 11, 605-634: J/ZWM/11/605), there was a need for caution about exporting such animals. In addition the kudu were kept isolated from other zoo animals. A very cautious approach was taken and the keeper staff used separate tools for cleaning out the kudu dens and paddocks, changed overalls and boots, used latex gloves, and, for a period until it seemed (for reasons mentioned below) less likely that the situation in kudu differed from that in cattle, collected wastes for incineration. Management practices were reviewed again in March 1996 when it was announced that cases of new variant CJD had occurred which might be related to the BSE agent. In order to pre-empt any public concern that might follow this announcement, the walkways past the kudu paddock were closed to the public. No cases have occurred in the kudu group since 1992.
10. The case of SE in a cheetah that occurred during the period, involved a 7 year-old female which had been born and lived all her life at Whipsnade (except for the final stages when she was moved to the Animal Hospital at Regent’s Park for diagnosis and treatment). This animal, which died in December 1993, had been fed on cuts of meat and bone from carcases of cattle unfit for human consumption and it was thought likely that she had been exposed to spinal cord (Kirkwood, J.K., Cunningham, A.A., Flach, E.J., Thornton, S.M. & Wells, G.A.H. (1995) Spongiform encephalopathy in another captive cheetah (Acinonyx jubatus): evidence for variation in susceptibility or incubation periods between species. Journal of Zoo and Wildlife Medicine 26, 577-582: J/ZWM/26/577).
11. During the period we also collated information on cases of SE that occurred in wild animals at or from other zoos in the British Isles. The total number of cases of which I was aware in June 1996, when I presented a review on occurrence of spongiform encephalopathies in zoo animals (at the Royal College of Pathologists’ Symposium on Transmitting prions: BSE, CJD, and other TSEs, The Royal Society, London, 4th July 1996), was 25, involving 10 species. The animals involved were all from the families Bovidae and Felidae, and comprised: 1 Nyala Tragelaphus angasi, 5 Eland Taurotragus oryx, 6 greater kudu Tragelaphus strepsiceros, 1 Gemsbok Oryx gazella, 1 Arabian oryx Oryx leucoryx, 1 Scimitar-horned oryx Oryx dammah, 4 Cheetah Acinonyx jubatus, 3 Puma Felis concolor 2 Ocelot Felis pardalis, and 1 Tiger Panthera tigris. (A spongiform encephalopathy, which was thought probably to have a different aetiology, had also been reported in 3 ostriches Struthio camelus in Germany). This list did not include cases of BSE in domesticated species in zoos (ie BSE in Ankole or other cattle, or SEs, assumed to be scrapie, in mouflon sheep Ovis musimon).
12. Since the time the above statistics were published, a few further cases have occurred in animals at or from zoos in the British Isles. The total number of cases in cheetah that have now been documented has, as far as I am aware, risen to seven (Vitaud, C., Flach, E.J., Thornton, S.M. & Capello, R. (1998) Clinical observations on four cases of feline spongiform encephalopathy in cheetahs (Acinonyx jubatus). Proceedings of the European Association of Zoo and Wildlife Veterinarians, Chester, UK, 21st-24th May 1998. Pp 133-138). There has also been a case in a bison.
13. Epidemiological aspects of the majority of these cases (those diagnosed up to the end of 1993) were considered in paper published in 1994 (Kirkwood, J.K. & Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record 135, 296-303:J/VR/135/296.) This paper was based on a paper presented at the Consultation on BSE with the Scientific Veterinary Committee of the Commission of the European Communities held in Brussels, 14-15th September 1993 (Kirkwood, J.K. & Cunningham, A.A. (1993) Spongiform encephalopathy in captive wild animals in Britain: epidemiological observations. In R. Bradley & B Marchant (Eds) Transmissible spongiform encephalopathies. Proceedings of a Consultation on BSE with the Scientific Veterinary Committee of the Commission of the European Communities, 14-15 September 1993, Brussels. European Commission. Pp 29-47:M9 tab 46). It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
14. Among the affected bovids were others (including scimitar horned oryx and eland) which, like some of the kudu, were born some considerable time after the July 1988 ban on inclusion of RDP in ruminant feeds (Kirkwood, J.K. & Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record 135, 296-303:J/VR/135/296). The source of infection to these animals was puzzling. However, as it emerged that many cases of BSE were continuing to occur in domestic cattle born after the July 1988 ban on inclusion of RDP in ruminant feeds, it was clear that the ban had not been immediately effective, and it was therefore possible (or, at least, impossible to rule out) that the late cases in zoo ungulates were also due to exposure to contaminated feeds.
15. We drew attention to the fact that, from a taxonomic perspective, the incidence of cases was strikingly patchy (Kirkwood, J.K. & Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record 135, 296-303. Also Kirkwood, J.K., Cunningham, A.A., Flach, E.J., Thornton, S.M. & Wells, G.A.H. (1995) Spongiform encephalopathy in another captive cheetah (Acinonyx jubatus): evidence for variation in susceptibility or incubation periods between species? Journal of Zoo and Wildlife Medicine 26, 577-582) Compared with many other species of exotic ruminants, few kudu were present in the UK but there had been 6 cases of SE among them. The picture seemed similar in the felids. Compared with other species of exotic felids (eg lions in which no cases had occurred), there were relatively small numbers of puma and cheetah in the UK but (at that time) there had been 3 and 4 cases among these respectively. Almost certainly a wider range of species were exposed to contaminated feeds than those in which cases have occurred or been detected. However, we were cautious about drawing firm conclusions about variation in susceptibility between species because (i) incubation periods vary between species and we thought other cases may emerge and (ii) because the variation might be related to differences in intensity of exposure.
TSEs in Exotic Ruminants
TSEs have been detected in exotic ruminants in UK zoos since 1986. These include antelopes (Eland, Gemsbok, Arabian and Scimitar oryx, Nyala and Kudu), Ankole cattle and Bison. With hindsight the 1986 case in a Nyala was diagnosed before the first case of BSE was identified. The TSE cases in exotic ruminants had a younger onset age and a shorter clinical duration compared to that in cattle with BSE. All the cases appear to be linked to the BSE epidemic via the consumption of feed contaminated with the BSE agent. The epidemic has declined as a result of tight controls on feeding mammalian meat and bone meal to susceptible animals, particularly from August 1996.
SPONGIFORM ENCEPHALOPATHY IN A CAPTIVE PUMA
an article in yesterday's Times (attached) which suggested that the puma concerned had never ''eaten any part of a cow or sheep which, in the opinion of Government Scientists, could transmit the species to a different species''.
3. You explained to me that this was INCORRECT. The position was as set out in the briefing for Prime Minister's questions attached to Mr Taylor's note. The puma had probably been fed low quality beef meat in the form of split carcasses. ...
http://web.archive.org/web/20090506032628/http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf
Spongiform Encephalopathy in Captive Wild Animals in Britain
Sun, Dec 20, 2020 4:54 pm
Subject: TSE in exotic ruminants
TSE in exotic ruminants
NUMBER OF CONFIRMED CASES OF FSE IN DOMESTIC CATS BY YEAR Year Reported No. of cases Year of Onset No. of cases
1988 0 1988 0
1989 0 1989 1
1990 12 1990 16
1991 12 1991 11
1992 10 1992 14
1993 11 1993 10
1994 16 1994 14
1995 8 1995 4
1996 6 1996 7
1997 6 1997 8
1998 4 1998 1
1999 2 1999 1
2000 1 2000 1
2001 1 2001 1
2002 0 2002 0
2003 0 2003 0
2004 0 2004 0
2005 0 2005 0
2006 0 2006 0
2007 0 2007 0
2008 0 2008 0
2009 0 2009 0
2010 0 2010 0
2011 0 2011 0
2012 0 2012 0
2013 0 2013 0
2014 0 2014 0
2015 0 2015 0
2016 0 2016 0
2017 0 2017 0
2018 0 2018 0
2019 0 2019 0
2020 0 2020 0
Total 89 Total 89 Data valid to 30 November 2020 Includes one case from Guernsey
Published 11 February 2015 Last updated 21 December 2020 - hide all updates
SE DIAGNOSES IN EXOTIC SPECIES
KUDU 6
GEMSBOK 1
NYALA 1
ORYX 2
ELAND 6
CHEETAH 4*
PUMA 3
TIGER 1
OCELOT 2
BISON (bison bison) 1
ANKOLE COW 2
* Excludes one cheetah in Australia and one in ROI - litter mates born in GB, and another in France also born in G.B. [figures to 1 January 1998]
FELINE SPONGIFORM ENCEPHALOPATHY
TOTAL TO DATE 81 (Plus 1 in N Ireland, 1 in Norway, 1 in Lichtenstein )
YEAR Cases
1990 12
1991 12
1992 10
1993 11
1994 16
1995 8
1996 6
1997 6
Exotic species
Species Number of cases Dates affected
Ankole Cow 2 1991, 95
Bison 1 1996
Asian Leopard Cat (1) 1 2005
Cheetah 5 1992, 98
Eland 6 1989, 95
Gemsbok 1 1987
Kudu 6 1989, 92
Lion 4 1998, 2001
Nyala 1 1986
Ocelot 3 1994, 99
Oryx 2 1989, 92
Puma 3 1992, 95
Tiger 3 1995, 99
As at 12 January 2006.
A total of 38 cases of spongiform encephalopathy have been confirmed in exotic species, the last one in 2005.
(1) Felis (Prionailurus) bengalensis.
BSE TSE PRION STATISTICS
ZOO ANIMALS AND TSE PRION DISEASE
The 82 zoo animals with BSE:
Id TSE Genus Species Subsp Birth Origin Death Place of Death
654 x Microcebus murinus - 1997 U.Montpellier 1998 U.Montpellier
656 x Microcebus murinus - 1997 U.Montpellier 1998 U.Montpellier
481 + Eulemur fulvus mayottensis 1974 Madagascar 1992 Montpellier zoo
474 + Eulemur fulvus mayottensis 1974 Madagascar 1990 Montpellier zoo
584 - Eulemur fulvus mayottensis 1984 Montpellier 1991 Montpellier zoo
455 + Eulemur fulvus mayottensis 1983 Montpellier 1989 Montpellier zoo
- + Eulemur fulvus mayottensis 1988 Montpellier 1992 Montpellier zoo
- + Eulemur fulvus mayottensis 1995 Montpellier 1996 Montpellier zoo
- + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo
- + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo
- + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo
456 + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo
586 + Eulemur mongoz - 1979 Madagascar 1998 Montpellier zoo
- p Eulemur mongoz - 1989 Mulhouse 1991 Montpellier zoo
- p Eulemur mongoz - 1989 Mulhouse 1990 Montpellier zoo
- p Eulemur macaco - 1986 Montpellier 1996 Montpellier zoo
- p Lemur catta - 1976 Montpellier 1994 Montpellier zoo
- p Varecia variegata variegata 1985 Mulhouse 1990 Montpellier zoo
- p Varecia variegata variegata 1993 xxx 1994 Montpellier zoo
455 + Macaca mulatta - 1986 Ravensden UK 1992 Montpellier zoo
- p Macaca mulatta - 1986 Ravensden UK 1993 Montpellier zoo
- p Macaca mulatta - 1988 Ravensden UK 1991 Montpellier zoo
- p Saimiri sciureus - 1987 Frejus France 1990 Frejus zoo
700 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
701 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
702 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
703 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
704 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
705 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
706 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
707 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
708 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
709 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
710 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
711 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
712 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
713 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
714 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
715 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
716 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
717 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
x p genus species - - Lille zoo 1996 Lille zoo
y p genus species - - Lille zoo 1996 Lille zoo
z p genus species - - Lille zoo 1996 Lille zoo
1 + Actinonyx jubatus cheetah 1986 Marwell zoo 1991 Pearle Coast AU
Duke + Actinonyx jubatus cheetah 1984 Marwell zoo 1992 Colchester zoo? UK
Saki + Actinonyx jubatus cheetah 1986 Marwell zoo 1993 unknown UK
Mich + Actinonyx jubatus cheetah 1986 Whipsnade 1993 Whipsnade UK
Fr1 + Actinonyx jubatus cheetah 1987 Whipsnade 1997 Safari de Peaugres FR
Fr2 + Actinonyx jubatus cheetah 1991 Marwell zoo 1997 Safari de Peaugres Fr
xx + Actinonyx jubatus cheetah 19xx xxx zoo 199x Fota zoo IR
yy + Actinonyx jubatus cheetah 19xx yyy zoo 1996+ yyyy zoo UK
zz + Actinonyx jubatus cheetah 19xx zzz zoo 1996+ yyyy zoo UK
aaa + Felis concolor puma 1986 Chester zoo 1991 Chester zoo UK
yy + Felis concolor puma 1980 yyy zoo 1995 yyyy zoo UK
zz + Felis concolor puma 1978 zzz zoo 1995 zzzz zoo UK
xxx + Felis pardalis ocelot 1987 xxx 1994 Chester zoo UK
zzz + Felis pardalis ocelot 1980 zzz 1995 zzzz zoo UK
85 + Felis catus cat 1990+ various 1999+ various UK LI NO
19 + Canis familia. dog 1992+ various 1999+ various UK
Fota + Panthera tigris tiger 1981 xxx zoo 1995 xxxx zoo UK
yy + Panthera tigris tiger 1983 yyy zoo 1998 yyyy zoo UK
Lump + Panthera leo lion 1986 Woburn SP 1998 Edinburgh zoo UK [since 1994]
1 + Taurotragus oryx eland 1987 Port Lympne 1989 Port Lympne zoo UK
Moll + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK
Nedd + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK
Elec + Taurotragus oryx eland 1990 xx UK 1992 not Port Lympne Uk
Daph p Taurotragus oryx eland 1988 xx UK 1990 not Port Lympne UK
zzz + Taurotragus oryx eland 1991 zz UK 1994 zzz UK
yyy + Taurotragus oryx eland 1993 yy UK 1995 yyy UK
Fran p Tragelaphus strepsi. kudu 1985 London zoo 1987 London zoo UK
Lind + Tragelaphus strepsi. kudu 1987 London zoo 1989 London zoo UK
Karl + Tragelaphus strepsi. kudu 1988 London zoo 1990 London zoo UK
Kaz + Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK
Bamb pc Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK
Step - Tragelaphus strepsi. kudu 1984 London zoo 1991 London zoo UK
346 pc Tragelaphus strepsi. kudu 1990 London zoo 1992 London zoo UK
324 + Tragelaphus strepsi. kudu 1989 Marwell zoo 1992 London zoo UK
xxx + Tragelaphus angasi nyala 1983 Marwell zoo 1986 Marwell zoo UK
yy + Oryx gazella gemsbok 1983 Marwell zoo 1986 Marwell zoo UK
zz + Oryx gazella gemsbok 1994+ zzz zoo 1996+ zzzz zoo UK
xx + Oryx dammah scim oryx 1990 xxxx zoo 1993 Chester zoo UK
yy + Oryx leucoryx arab oryx 1986 Zurich zoo 1991 London zoo UK
yy + Bos taurus ankole cow 1987 yyy zoo 1995 yyyy zoo UK
zz + Bos taurus ankole cow 1986 zzz zoo 1991 zzzz zoo UK
xx + Bison bison Eu bison 1989 xxx zoo 1996 xxxx zoo UK
Vet Rec 1997 Sep 13;141(11):270-1 Baron-T, Belli-P Madec-J-Y Moutou-F Vitaud-C Savey-M Spongiform encephalopathy in an imported cheetah in France. CNEVA-Lyon, Laboratoire de Pathologie Bovine, France.
Proc Soc Exp Biol Med 1996 Apr;211(4):306-22 Narang H Origin and implications of bovine spongiform encephalopathy. [tiger]
Vet Rec. 1994 Nov 12;135(20):488. Benbow G. Spongiform encephalopathies in zoo animals. comment
Vet Rec 1994 Oct 29;135(18):440 Swainston J. comment
Vet Rec 1994 Sep 24;135(13):296-303 Kirkwood JK, Cunningham AA Epidemiological observations on spongiform encephalopathies
Vet Rec 1994 Feb 12;134(7):167-8 Kirkwood JK, Cunningham AA, Austin AR, Wells GA, Sainsbury AW Spongiform encephalopathy in a greater kudu
Vet Rec. 1993 Oct 9;133(15):360-4. Kirkwood JK, et al. Spongiform encephalopathy in a herd of greater kudu
Vet Rec. 1993 Jan 16;132(3):68. Cunningham AA, et al. Transmissible spongiform encephalopathy in greater kudu
Vet Rec. 1992 Nov 7;131(19):431-4. Willoughby K, et al. Spongiform encephalopathy in a captive puma
Aust Vet J 1992 Jul;69(7):171 Peet RL, Curran JM Spongiform encephalopathy in an imported cheetah
Vet Rec 1992 Apr 25;130(17):365-7 Kirkwood JK, Wells GA, Cunningham AA, Jackson SI, Scott AC, Dawson M, Wilesmith JW Scrapie-like encephalopathy in a greater kudu
Acta Neuropathol (Berl) 1992;84(5):559-69 Jeffrey M, Scott JR, Williams A, Fraser H Ultrastructural features of spongiform encephalopathy
Vet Rec. 1991 Oct 5;129(14):320 Synge BA, et al. Spongiform encephalopathy in a Scottish cat.
Vet Rec 1991 Sep 14;129(11):233-6 Wyatt JM, Pearson GR, Naturally occurring scrapie-like s
Vet Rec. 1991 Jun 1;128(22):532. Pearson GR, et al. Feline spongiform encephalopathy.
Vet Rec. 1991 Mar 30;128(13):311. Kock R. Spongiform encephalopathies in ungulates.
Vet Rec. 1991 Feb 2;128(5):115. Gibson PH. Spongiform encephalopathies in ungulates. comment
Vet Rec 1990 Dec 15;127(24):586-8 Leggett MM, Dukes J, Pirie HM A spongiform encephalopathy in a cat.
Done JT. Vet Rec. 1990 Nov 10;127(19):484. Spongiform encephalopathy in pigs.
Vet Rec. 1990 Oct 27;127(17):418-20. Kirkwood JK, et al. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu.
Vet Rec. 1990 Sep 29;127(13):338. Dawson M, et al. Primary parenteral transmission of bovine spongiform encephalopathy to the pig.
Vet Rec. 1990 May 19;126(20):513 no authors listed Spongiform encephalopathy in a cat.
Vet Rec 1990 May 12;126(19):489-90 Gibson PH Spongiform encephalopathy in an eland.
Nature. 1990 Mar 15;344(6263):183 Aldhous P. Antelopes die of "mad cow" disease.
Vet Rec 1990 Apr 21;126(16):408-9 Fleetwood AJ, Furley CW Spongiform encephalopathy in an eland.
Vet Pathol. 1988 Sep;25(5):398-9 Jeffrey M, Wells GA Spongiform encephalopathy in a nyala (Tragelaphus angasi) Lasswade Veterinary Laboratory, Midlothian
2020
Monday, November 30, 2020
Tunisia has become the second country after Algeria to detect a case of CPD Camel Prion Disease within a year
REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019
Scientific Commission/September 2019
Tunisia has become the second country after Algeria to detect a case of CPD within a year
10.2. Prion disease in dromedary camels
snip...see full text;
MONDAY, DECEMBER 21, 2020
BSE TSE Prion in zoo animals, exotic ruminants, domestic cats, and CPD Camel Prion Disease, a review 2020
TUESDAY, FEBRUARY 11, 2020
Predators, Scavengers, and trans locating the CWD TSE Prion
MONDAY, FEBRUARY 25, 2019
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
Terry S. Singeltary Sr.
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