Thursday, July 10, 2025

Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) Published: July 9, 2025

Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) Published: July 9, 2025
Abstract
Cervids susceptible to chronic wasting disease (CWD) are sympatric with multiple other animal species that can interact with infectious prions. Several reports have described the susceptibility of other species to CWD prions, or their potential to transport them. One of these species is the coyote (Canis latrans), which has been previously shown to pass transmission-relevant prion titers in their feces for at least three days after ingesting prion-positive brain material. The current study followed up on these findings and evaluated the distribution of prions in multiple tissues from the same coyotes. Our results show that prions persist in the digestive tract of prion-exposed coyotes five days after exposure. Moreover, prion seeding activity was identified in other tissues, including lymph nodes and lungs. These results provide additional information about the dynamics of CWD prions in the environment and show the initial fate of prions after ingestion by a canid species that is a carnivorous predator and scavenger.
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Despite the strong species barriers, predators and scavengers may still be relevant as spreaders of infectious prion particles. In fact, both experimental research and natural observations indicate that insects, parasites, and various wild and domestic animals that co-exist with cervids can act as passive carriers of CWD prions [16–23]. For example, coyotes (Canis latrans) are relevant deer predators and scavengers. Previous studies showed that coyotes fed with an elk brain infected with CWD passed prions through their feces for at least three days after ingestion [23]. Similar observations were reported for cougars (Puma concolor) [21]. In contrast, crows (Corvus brachyrhynchos) passed prions for only few hours after ingesting infected materials [22]. Importantly, previous research in coyotes and cougars suggest that excreted prions contain decreased infectivity titers compared with the ingested material, suggesting that infectious particles are being retained in tissues within these animals, or degraded. In natural settings, prions have been identified in scat from multiple species of sympatric animals [20]. Overall, data indicates that predators and scavengers can excrete infectious prions after ingesting contaminated tissues. This, in turn, may contribute to the environmental spread of prions.
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Our results confirmed the previous results communicated by Nichols et al. [23] which found no CWD prions in feces collected before exposure, or in feces collected from coyotes treated with the CWD-free brain (Coyote #132 and Coyote #134, Fig 2). In contrast, prion seeding activity was readily detected in feces from the coyotes fed with prion-infected brains (Coyote #133, Coyote #135 and Coyote #137, Fig 2). It is important to mention that CWD prions were only detected in feces after two or three PMCA rounds (Fig 3), irrespective of when the samples were collected. A single coyote (#133, Fig 3) provided signals at Day 1 in a second PMCA round, suggesting a higher load of prions at that specific time point. It is important to note that the previous study detected prions in coyotes’ feces only on days one and two after CWD exposure, demonstrating the increased sensitivity of the PMCA format used here. These changes in sensitivity may be due to different factors, including the addition of digitonin and Teflon beads that increase the sensitivity and reproducibility of this prion amplification method [28].
Previous reports by us [25] and others [24] used prion amplification assays to study the distribution of prions in animal tissues shortly after administration. Here, we tested nine separate tissue types (intestine, cecum, liver, tonsil, mesenteric lymph nodes, spleen, brain, lung and heart) from prion-exposed coyotes to explore similar paradigms. PMCA positive results were obtained from the cecum of the CWD-exposed animals, suggesting that prions are retained in this tissue several days after ingestion. The presence of CWD prions in the intestine of a single prion-exposed coyote (#135) further support the intestinal retention of ingested prions. Although gastrointestinal tissues were thoroughly washed to remove traces of ingested homogenate and feces from them, it is possible that some of the positive results observed were due to these materials. Nevertheless, positive signals were observed in tissues other than those of the gastrointestinal tract. Specifically, CWD-prions were also identified in the tonsils and mesenteric lymph nodes of single CWD-exposed coyotes (#137 and #135, respectively). These results suggest that CWD-prions were internalized after ingestion and reached some lymphoid tissues. This is consistent with a previous report showing that CWD prions readily migrate to lymph nodes in white-tailed deer [24]. Nevertheless, we acknowledge that the direct contact of prions with tonsils, due to ingestion, can explain the detection of CWD prions for this particular tissue. Another tissue showing positive prion detection was the lung (Fig 2). The detection in this tissue was obtained in only one of the three replicates tested for two different animals (#135 and #137). Importantly, all tissues from the coyotes fed with the CWD-free brains did not provide positive signals in our prion amplification assay (Fig 2).
Discussion
Here, we confirmed previous findings [23] demonstrating that predators and scavengers can spread CWD prions via feces while retaining some infectious prions in their bodies. As previously suggested, these animals may act in a dual manner, by sequestering a low proportion of the infectious particles in their bodies while also disseminating transmission-relevant titers into the environment. We explored the fate of CWD prions after entering the coyotes’ bodies by testing multiple tissues five days after ingestion. We effectively found that a number of the tissues contained in vitro (PMCA) prion seeding activities, demonstrating that some of the ingested infectious particles are retained in these animals [21]. Although some studies show that prions can be degraded by elements of the digestive tract [31], others demonstrate that their binding to other particles such as soils protects them from this degradation [32]. Further studies should explore the potential role of gastrointestinal retention and degradation in the prion infectivity titers present in excreta and whether this varies in different animal species (specifically focused in ruminants and carnivore predators).
The role of wildlife species that share environments with cervids in the translocation of CWD via feces has been experimentally explored, as well as their ability to become infected by CWD prions. The latter creates a worrisome scenario as prions adapted in a new species may generate new prion strains of unknown infectivity and host ranges [7–9]. This possibility was not explored here, due to the short post-exposure periods of this study. Previous reports suggesting that canids are resistant to prion infection [33,34] makes this possibility unlikely. Regardless, our data demonstrate that a fraction of CWD prions ingested by coyotes are incorporated in their tissues, while larger levels are released in feces. The presumable reduction of prion titers after crossing the gastrointestinal tract of predators [23] suggest that the presence of coyotes in specific environments may be beneficial in reducing CWD prions. Along this line, the expanding geographic range of coyotes in North America [35] may result in additional benefits. However, the fact that infectious relevant levels of prions are released in coyotes’ feces several days post ingestion suggest that they might promote the environmental spreading of CWD. Considering this, evaluating the dual implications of the CWD-coyote interactions in the spread and prevalence of CWD will need substantial epidemiological and molecular research efforts.
It is important to clarify certain discrepancies between the findings found in the present study compared to those communicated in the original report [23]. First, the previous article by Nichols et al. used different PMCA settings compared to those used in the current study. Specifically, the current PMCA protocol results in a considerable higher sensitivity. This explains the fact that here we detected CWD-prions in feces for additional days after prion exposure compared to the first publication.
The results presented here provide additional information on the fate of CWD prions consumed by a canid mesopredator and sheds additional light on the potential role of cervid sympatric species, specifically predators, in the ecology of CWD.
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These results provide strong evidence for the emergence of a novel strain of CWD after passage in meadow voles and raccoons. Therefore, interspecies transmission of CWD prions between cervids and noncervid species that share the same habitat might represent a confounding factor in CWD-management programs. In addition, passage of CWD prions through off-target species might represent a source of novel CWD strains with unknown biologic characteristics, including zoonotic potential. Characterization of the biologic behavior of CWD isolates after cross-species transmission will help us develop more effective management strategies for CWD-affected populations.
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Project Type: In-House Appropriated
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***> The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons <***
8 The chronic wasting disease agent from white-tailed deer is infectious to humanized mice after passage through raccoons 
Eric Cassmann', Xu Qi?, Qingzhong Kong?, Justin Greenlee' 'USDA ARS, Ames, USA. 2Case Western Reserve University, Cleveland, USA 
Abstract The aim of this study was to evaluate the zoonotic potential of the raccoon passaged chronic wasting disease (CWD) agent in humanized transgenic mice in comparison with the North American CWD agent from the original white-tailed deer (WTD) host. Pooled brain (GG96) from CWD positive white-tailed deer was used to intracranially inoculate two WTD and one raccoon. Brain homogenates (10% w/v) from the raccoon and the WTD were used to intracranially inoculate transgenic mice (Tg40h) expressing the methionine 129 human prion protein. Brains and spleens were collected from mice at experimental endpoints of clinical disease or approximately 700 days post-inoculation. Tissues were divided and homogenized or fixed in 10% buffered neutral formalin. Immunohistochemistry, enzyme immunoassay, and western blot were used to detect misfolded prion protein (PrpSc) in tissue. Tg40h mice inoculated with the raccoon passaged CWD agent from WTD exhibited a 100% (12/12) attack rate with an average incubation period of 605 days. Prpsc was detected in brain tissue by enzyme immunoassay with an average optical density of 3.6/4.0 for positive brains. Prpsc also was detected in brain tissue by western blot and immunohistochemistry. No Prpsc was detected in the spleens of mice inoculated with the raccoon passaged CWD agent. Humanized mice inoculated with the CWD agent from WTD did not have detectable Prps using conventional immunoassay techniques. These results demonstrated that the host range of the CWD agent from WTD was expanded in our experimental model after one passage through raccoons.
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogenesis. We orally inoculated white-tailed deer with either single or multiple divided doses of prions of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.
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In conclusion, we have attempted to model and better understand CWD infection relative to natural exposure. The results demonstrate: (a) that the minimum CWD oral infectious dose is vastly lower than historical studies used to establish infection; (b) that a direct relationship exists between dose and incubation time to first prion replication detection in tonsils, irrespective of genotype; (c) that a difference was not discernible between brain vs. saliva source prions in ability to establish infection or in resultant disease course; and (d) that the CWD infection process appears to conform more to a threshold dose than an accumulative dose dynamic.
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kindest regards, terry

posted by Terry S. Singeltary Sr. at 1:31 PM

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