Chronic Wasting Disease: Modeled Impacts of Chronic Wasting Disease on White-Tailed Deer in a Semi-Arid Environment

Modeled Impacts of Chronic Wasting Disease on White-Tailed Deer in a Semi-Arid Environment

Aaron M. Foley ,David G. Hewitt,Charles A. DeYoung,Randy W. DeYoung,Matthew J. Schnupp Published: October 6, 2016http://dx.doi.org/10.1371/journal.pone.0163592

Abstract White-tailed deer are a culturally and economically important game species in North America, especially in South Texas. The recent discovery of chronic wasting disease (CWD) in captive deer facilities in Texas has increased concern about the potential emergence of CWD in free-ranging deer. The concern is exacerbated because much of the South Texas region is a semi-arid environment with variable rainfall, where precipitation is strongly correlated with fawn recruitment. Further, the marginally productive rangelands, in combination with erratic fawn recruitment, results in populations that are frequently density-independent, and thus sensitive to additive mortality. It is unknown how a deer population in semi-arid regions would respond to the presence of CWD. We used long-term empirical datasets from a lightly harvested (2% annual harvest) population in conjunction with 3 prevalence growth rates from CWD afflicted areas (0.26%, 0.83%, and 2.3% increases per year) via a multi-stage partially deterministic model to simulate a deer population for 25 years under four scenarios: 1) without CWD and without harvest, 2) with CWD and without harvest, 3) with CWD and male harvest only, and 4) with CWD and harvest of both sexes. The modeled populations without CWD and without harvest averaged a 1.43% annual increase over 25 years; incorporation of 2% annual harvest of both sexes resulted in a stable population. The model with slowest CWD prevalence rate growth (0.26% annually) without harvest resulted in stable populations but the addition of 1% harvest resulted in population declines. Further, the male age structure in CWD models became skewed to younger age classes. We incorporated fawn:doe ratios from three CWD afflicted areas in Wisconsin and Wyoming into the model with 0.26% annual increase in prevalence and populations did not begin to decline until ~10%, ~16%, and ~26% of deer were harvested annually. Deer populations in variable environments rely on high adult survivorship to buffer the low and erratic fawn recruitment rates. The increase in additive mortality rates for adults via CWD negatively impacted simulated population trends to the extent that hunter opportunity would be greatly reduced. Our results improve understanding of the potential influences of CWD on deer populations in semi-arid environments with implications for deer managers, disease ecologists, and policy makers.

Discussion Our simulations suggest that additional adult mortality due to CWD will result in reduced or negative rates of population growth for populations of white-tailed deer in semi-arid environments. In regions with variable rainfall, adult survival must be high to overcome variable fawn recruitment [24]. The additive mortality of CWD in conjunction with higher prevalence rates in adult deer resulted in a reduced population size, even in the absence of hunter harvest of deer. Whereas CWD-afflicted deer populations elsewhere have been able to persist for over 30 years [42,74], the higher mean recruitment in conjunction with low prevalence rates in younger deer [12,28] likely enables population sustainability. Model projections based on fawn:doe ratios from temperate environments instead of semi-arid environments support the idea that high deer productivity increases likelihood of population sustainability. In our South Texas scenario with no harvest and slow CWD increase, a negative rate of population growth did not occur; therefore, deer populations in semi-arid regions may be able to persist after CWD introduction in the absence of harvest. For simplicity, we did not consider age-specific fecundity in our models. However, deer productivity in semi-arid environments is strongly influenced by age of the dam [58]. Therefore a decline in the age structure of females due to increased CWD prevalence [27,28] would likely result in a more rapid decline in our population simulations. The increased rate of population decline would be attributed to the reduced number of older, more productive, females available to produce offspring. Thus, young females (≤2.5 years old) would be the critical factor driving population sustainability in CWD-afflicted areas. However, there may not be sufficient healthy, and less productive, young females available to produce offspring in semi-arid environments because the lower and more variable fawn:doe ratio (0.35, SE = 0.03) results in a variable young female age structure [26].

CWD mortality was modeled to be additive because of the density-independent nature of deer dynamics in South Texas (22,24). It is possible that CWD mortality would be compensatory because of predation [75], deer-vehicle collisions [76], and harvest [77]. Mountain lions (Puma concolor) and coyotes (Canis latrans) exist in South Texas and may selectively prey on infected deer [74,75]; however, mountain lion density in South Texas is low (0.59–0.75 per 100 km2 [78]). Coyotes and bobcats occasionally kill adult deer [79] but primarily prey on fawns [80,81], which are not considered important to CWD dynamics [82]. Deer-vehicle collisions are not as frequent in South Texas compared to other states because of the relatively low road density; thus, it is unlikely deer-vehicle collisions would have an influence on CWD mortality. Deer mortality events due to harvest could be compensatory because both CWD prevalence and probability of being harvested increases with age [27]. However, CWD presumably does not discriminate by antler characteristics whereas hunters generally select for large-antlered mature males. Overall, it would be expected for CWD mortality to transition from compensatory to additive as prevalence rate increases because survival rates would be reduced [83,84]. The point in time when CWD mortality becomes additive is unknown but in deer populations that rely on high survivorship of adult deer, the transition from compensatory to additive is likely earlier relative to areas with higher recruitment typical of temperate environments.

If our hypothetical CWD-afflicted population was able to sustain itself, perhaps during a period of favorable rainfall and increased fawn:doe ratios [18,85,86], the higher prevalence rates in mature males is of concern. Our CWD simulations forecasted a male age structure with fewer mature (≥5.5 year old) males (Fig 7). Male harvest in south Texas is generally skewed towards mature males [60] and the change in CWD-modeled male age structures will likely be more pronounced because we modeled harvest to be equal among male age classes. Further, prevalence rates of ≥6.5 year old males at the end of simulated years were lower than expected (Fig 8) which suggest that CWD mortality rates would have a disproportionate effect on old (≥6.5 year old) males [27]. Culturally and economically, harvest of mature males is a critical component of hunting in South Texas [38]. With fewer mature males in CWD-afflicted populations, deer hunting may not be economically viable for privately owned ranches. Ranches may transition to alternative sources of income, such as agriculture or development which may not have the same ecosystem benefits as wildlife-cattle management programs on native rangelands [87–89].

Declines in our simulated CWD populations with only 1% female harvest suggest that a slight increase in additive mortality rates would be unsustainable for deer populations in semi-arid regions. This finding is not unexpected because deer managers have long known that harvest rates in native rangelands, where deer population density-independence occurs frequently, need to be conservative to prevent population declines due to the additive nature of harvest [24,90]. The additive mortality via harvest suggests that increased harvest in an attempt to suppress CWD [3,45,91,92], depending on the prevalence rate [44], may be a viable management strategy. However, the social nature of white-tailed deer (i.e., bachelor male groups and female family groups [93,94]) does not result in prevalence rates that are positively correlated with deer density [67,68]. Additionally, the persistence of prions in the environment complicates disease management strategies. This may be more so in semi-arid environments, where the availability of drinking water plays a critical part in habitat use during dry years [95]. One symptom of CWD is increased thirst [96]; thus, frequent visits to water catchments, troughs, stock tanks, and ephemeral pools [97] may increase disease transmission rates and congregate prion deposition [98]. Some natural water sources may be associated with impermeable clay soil, which may increase viability of CWD prions [12,13,99].

We acknowledge that our relatively simplistic population model contains both process variation (temporal, individual, and demographic variation) and sampling variation (variation in measured parameters) which could lead to bias in population projections [100,101]. However, we believe the impact of both types of variation on our models is relatively low. For instance, density dependence influences many life processes [25,63]. Because density dependence is rarely observed in south Texas [22,24], our model is unlikely to need density-dependent changes in vital rates as a result of a decrease in deer density. Another important component of population models is environmental stochasticity. In South Texas, environmental stochasticity is represented by variable rainfall which influences fawn production (i.e., fawn:doe ratios) [21], which was an integral part of our model. Further, it is well documented that fawn recruitment rates are the demographic parameter influencing deer population growth because adult deer have high natural survival rates [102]. Therefore, by controlling our models with known and critical region-specific parameters [103] and increasing prevalence rates at a rate observed in three CWD-afflicted areas [12,65,66], we feel our model is a fair demonstration of what could happen if CWD emerged in South Texas. The first CWD positive white-tailed deer identified in Texas was found in a captive deer breeder facility. The second CWD case occurred at a different captive facility was a result of an epidemiological investigation of deer purchased from the index facility. As of July 2016, 25 white-tailed deer in or originating from captive facilities have been confirmed positive for CWD in Texas [104]. Within Texas, there are >1,300 breeder facilities that house >110,000 white-tailed deer [105]. There is a risk of fence-line transmission between captive and free-ranging deer [106,107] but perhaps the bigger risk lies in the practice of deer translocation. In 2014, 27,684 deer were translocated from captive deer facilities to other captive deer facilities, high-fenced (surrounded by 2.5-m high woven-wire fence) properties, and low-fenced (1.25-m) properties [105]. Releasing a deer unknowingly infected with CWD may result in disease transmission to a native deer population via horizontal transmission or deposition of prions into a new environment.

Chronic wasting disease is a slow-spreading disease that may take years or decades to result in detectable prevalence rates [1]. Modeling is frequently used to project CWD consequences to cervid populations because field experiments are impractical [12,43,67]. Our simulations suggest that introduction of CWD into deer populations with low fawn production and that frequently exhibit density independence would have a significant impact on population size and age structure. Management efforts to enhance deer populations in this region in the event of CWD introduction would likely be difficult or infeasible. For instance, using supplemental nutrition may increase deer productivity to combat deleterious effects of drought years and CWD mortality; however, presence of feed stations would likely increase disease transmission rates [35,48,49]. Transplanting deer from CWD-free populations may be a feasible option; however, the prolonged existence of CWD prions in the environment will likely result in disease persistence. Therefore, prevention of CWD introduction into variable environments such as South Texas is a critical strategy to ensure deer continue to exist as a renewable natural resource.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0163592

SUNDAY, OCTOBER 02, 2016

What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016

http://chronic-wasting-disease.blogspot.com/2016/10/what-is-risk-of-cervid-tse-being.html

Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission

Author

item Moore, Sarah item Kunkle, Robert item West greenlee, Mary item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin

Submitted to: Emerging Infectious Diseases Publication Type: Peer reviewed journal Publication Acceptance Date: 8/29/2016 Publication Date: N/A Citation:

Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.

Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, and CWD was recently reported in a free-ranging reindeer of Norway. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrPcwd). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel reindeer although only 2 out of 6 developed clinical disease during the study period (< 57 months PI). We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.

Monday, September 05, 2016

*** Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway ***

https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261

Monday, September 05, 2016

Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway

http://chronic-wasting-disease.blogspot.com/2016/09/pathological-features-of-chronic.html

SUNDAY, OCTOBER 02, 2016

*** What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016

http://chronic-wasting-disease.blogspot.com/2016/10/what-is-risk-of-cervid-tse-being.html

Wednesday, September 7, 2016

*** An assessment of the long-term persistence of prion infectivity in aquatic environments

http://transmissiblespongiformencephalopathy.blogspot.com/2016/09/an-assessment-of-long-term-persistence.html

Friday, September 02, 2016

*** Chronic Wasting Disease Drives Population Decline of White-Tailed Deer

http://chronic-wasting-disease.blogspot.com/2016/09/chronic-wasting-disease-drives.html

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

http://jgv.sgmjournals.org/content/87/12/3737.full

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.

=========================

***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.

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

see ;

with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion. see ;

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

see ;

http://www.tandfonline.com/doi/pdf/10.4161/pri.28467

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.

https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson%20et%20al%20prions%20in%20soil.pdf

tse prion soil

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf

http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217

http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4

Wednesday, December 16, 2015

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full

The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf

>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<

Fate of Prions in Soil: A Review

Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*

Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160281/

P.161: Prion soil binding may explain efficient horizontal CWD transmission

Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<

Wednesday, December 16, 2015

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1

1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK

Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.

snip...

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

http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full

Wednesday, December 16, 2015

*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***

http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

http://jgv.sgmjournals.org/content/87/12/3737.full

Circulation of prions within dust on a scrapie affected farm

Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben C Maddison2*

Abstract

Prion diseases are fatal neurological disorders that affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk are contagious prion diseases where environmental reservoirs have a direct link to the transmission of disease. Using protein misfolding cyclic amplification we demonstrate that scrapie PrPSc can be detected within circulating dusts that are present on a farm that is naturally contaminated with sheep scrapie. The presence of infectious scrapie within airborne dusts may represent a possible route of infection and illustrates the difficulties that may be associated with the effective decontamination of such scrapie affected premises.

snip...

Discussion

We present biochemical data illustrating the airborne movement of scrapie containing material within a contaminated farm environment. We were able to detect scrapie PrPSc within extracts from dusts collected over a 70 day period, in the absence of any sheep activity. We were also able to detect scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m distance away from the scrapie contaminated buildings, suggesting that the chance of contamination of pasture by scrapie contaminated dusts decreases with distance from contaminated farm buildings. PrPSc amplification by sPMCA has been shown to correlate with infectivity and amplified products have been shown to be infectious [14,15]. These experiments illustrate the potential for low dose scrapie infectivity to be present within such samples. We estimate low ng levels of scrapie positive brain equivalent were deposited per m2 over 70 days, in a barn previously occupied by sheep affected with scrapie. This movement of dusts and the accumulation of low levels of scrapie infectivity within this environment may in part explain previous observations where despite stringent pen decontamination regimens healthy lambs still became scrapie infected after apparent exposure from their environment alone [16]. The presence of sPMCA seeding activity and by inference, infectious prions within dusts, and their potential for airborne dissemination is highly novel and may have implications for the spread of scrapie within infected premises. The low level circulation and accumulation of scrapie prion containing dust material within the farm environment will likely impede the efficient decontamination of such scrapie contaminated buildings unless all possible reservoirs of dust are removed. Scrapie containing dusts could possibly infect animals during feeding and drinking, and respiratory and conjunctival routes may also be involved. It has been demonstrated that scrapie can be efficiently transmitted via the nasal route in sheep [17], as is also the case for CWD in both murine models and in white tailed deer [18-20].

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

http://www.nature.com/articles/srep11573

***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.

P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion

Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2

1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWO

In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible.

***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.

PRION 2016 CONFERENCE TOKYO

http://prion2016.org/dl/newsletter_03.pdf

http://chronic-wasting-disease.blogspot.com/2016/09/wisconsin-governor-scott-walkers-dnr-et.html

Wednesday, September 21, 2016

*** TAHC Passes Authorized Personnel Rule at 396th Commission Meeting “Certified CWD Sample Collector” to “Certified CWD Postmortem Sample Collector” ***

http://chronic-wasting-disease.blogspot.com/2016/09/tahc-passes-authorized-personnel-rule.html

Wednesday, September 21, 2016

ILLINOIS -- Deer disease CWD meetings set Oct. 18 at the Nash Recreation Center in Oregon, Illinois, and Oct. 19 at the Big Rock Park District Community Building in Big Rock

http://chronic-wasting-disease.blogspot.com/2016/09/illinois-deer-disease-cwd-meetings-set.html

Wednesday, September 21, 2016

Pennsylvania Game commission to present forum on deer chronic wasting disease cwd tse prion

http://chronic-wasting-disease.blogspot.com/2016/09/pennsylvania-game-commission-to-present.html

Monday, August 29, 2016

*** NWHC USGS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE

http://chronic-wasting-disease.blogspot.com/2016/08/nwhc-usgs-chronic-wasting-disease-cwd.html

Thursday, August 18, 2016

*** PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL MEETING of the USAHA BSE, CWD, SCRAPIE, PORCINE TSE PRION October 22 28, 2015 ***

http://chronic-wasting-disease.blogspot.com/2016/08/proceedings-one-hundred-and-nineteenth.html

Sunday, August 28, 2016

*** TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS AND BEARS, OH MY! ***

http://transmissiblespongiformencephalopathy.blogspot.com/2016/08/transmissible-spongiform-encephalopathy.html

http://transmissiblespongiformencephalopathy.blogspot.com/

Saturday, December 12, 2015

NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE Prion REPORT December 14, 2015

http://transmissiblespongiformencephalopathy.blogspot.com/2015/12/notice-environmental-impact-statement.html

Friday, August 14, 2015

Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015

http://transmissiblespongiformencephalopathy.blogspot.com/2015/08/carcass-management-during-mass-animal.html

Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964

How Did CWD Get Way Down In Medina County, Texas?

Confucius ponders...

Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?

Epidemiology of Scrapie in the United States 1977

snip...

Scrapie Field Trial Experiments Mission, Texas

A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.

The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ...

snip...see full text ;

http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf

Thursday, June 09, 2016

Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964

How Did CWD Get Way Down In Medina County, Texas?

http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html

http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html

Friday, April 22, 2016

*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer

http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html

Friday, February 26, 2016

TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease CWD TSE Prion

http://chronic-wasting-disease.blogspot.com/2016/02/texas-hartley-county-mule-deer-tests.html

I understand that the 84th Legislation might have made some terrible mistakes with regards to Chronic Wasting Disease CWD TSE Prion aka mad cow type disease, by weakening CWD rules for breeders.

Sunday, December 14, 2014

TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry

http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-commencing-this.html

Tuesday, December 16, 2014

Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION

http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-2015-hr-no-2597.html

Monday, February 11, 2013

TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos

http://chronic-wasting-disease.blogspot.com/2013/02/texas-chronic-wasting-disease-cwd-four.html

Tuesday, July 10, 2012

Chronic Wasting Disease Detected in Far West Texas

http://chronic-wasting-disease.blogspot.com/2012/07/chronic-wasting-disease-detected-in-far.html