Clay Components in Soil Dictate Environmental Stability and Bioavailability of Cervid Prions in Mice

Wyckoff, A. Christy; Kane, Sarah J.; Lockwood, Krista; Seligman, Jeff; Michel, Brady; Hill, D. Ashley; Ortega, Aimee; Mangalea, Mihnea R.; Telling, Glenn C.; Miller, Michael W.; VerCauteren, Kurt C.; Zabel, Mark D.

doi:10.3389/fmicb.2016.01885

Cited by 19 publications

(24 citation statements)

References 36 publications

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“…As such, factors that increase M-cell density in the gut epithelium (coinfections or miscellaneous inflammatory conditions) may also increase susceptibility to orally acquired prion infections. A study by Wyckoff et al [142] mentions the binding of prions to certain types of soil particles that may result in an increased uptake of prions from the gut lumen, but it is not yet clear if this uptake is mediated by M cells. Host infection by M-cell-independent mechanisms cannot be disregarded, namely, those involving directly enterocytes from the follicle-associated epithelium [143] or other M-cellindependent pathways [144].…”

Section: Cellsmentioning

confidence: 99%

TSE Monitoring in Wildlife Epidemiology, Transmission, Diagnosis, Genetics and Control

Machado¹,

Orge²,

Pires³

et al. 2019

Wildlife Population Monitoring

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Among the transmissible spongiform encephalopathies (TSEs), chronic wasting disease (CWD) in cervids is now the rising concern within Europe. CWD will be outlined in this chapter gathering its epidemiology, transmission, diagnosis, genetics, and control. Prion diseases are fatal neurodegenerative diseases characterized by the accumulation of an abnormal isoform of the prion protein (PrP c), usually designated by PrP sc or prion. CWD is a prion disease of natural transmission affecting cervids detected mainly in North America. The first European case was detected in Norway, in 2016, in a wild reindeer; until April 2018, a total of 23 cases were described. The definite diagnosis is postmortem, performed in target areas of the brain and lymph nodes. Samples are first screened using a rapid test and, if positive, confirmed by immunohistochemistry and Western immunoblotting. It is not possible to establish a culling plan based on the genotype, once affected animals appear with all genotypes. However, some polymorphisms seem to result in longer incubation periods or confer a reduced risk. The control is not easy in captive cervids and even more in the wildlife; some recommendations have been proposed in order to understand the danger and impact of CWD on animal and public health.

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Section: Cellsmentioning

confidence: 99%

TSE Monitoring in Wildlife Epidemiology, Transmission, Diagnosis, Genetics and Control

Machado¹,

Orge²,

Pires³

et al. 2019

Wildlife Population Monitoring

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“…Studies show that on farms with an incidence of prion disease, the prions may persist within the environment for long periods [ 28 ]. Prions may persist in soil for at least 18 months [ 29 , 30 ] and can retain their infectious properties, even when bound to plants [ 31 ]. Although the mechanism of action is not known, the binding of prions to soil may also enhance their ability to infect the host after oral exposure [ 32 ].…”

Section: Transmission Of Prp Sc Prions Between mentioning

confidence: 99%

How do PrPSc Prions Spread between Host Species, and within Hosts?

Mabbott

2017

Pathogens

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Prion diseases are sub-acute neurodegenerative diseases that affect humans and some domestic and free-ranging animals. Infectious prion agents are considered to comprise solely of abnormally folded isoforms of the cellular prion protein known as PrPSc. Pathology during prion disease is restricted to the central nervous system where it causes extensive neurodegeneration and ultimately leads to the death of the host. The first half of this review provides a thorough account of our understanding of the various ways in which PrPSc prions may spread between individuals within a population, both horizontally and vertically. Many natural prion diseases are acquired peripherally, such as by oral exposure, lesions to skin or mucous membranes, and possibly also via the nasal cavity. Following peripheral exposure, some prions accumulate to high levels within the secondary lymphoid organs as they make their journey from the site of infection to the brain, a process termed neuroinvasion. The replication of PrPSc prions within secondary lymphoid organs is important for their efficient spread to the brain. The second half of this review describes the key tissues, cells and molecules which are involved in the propagation of PrPSc prions from peripheral sites of exposure (such as the lumen of the intestine) to the brain. This section also considers how additional factors such as inflammation and aging might influence prion disease susceptibility.

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“…Soil properties are a key factor for CWD persistence and transmission in the environment [8,15,16]. Whereas the soil mineral montmorillonite (Mte) avidly binds abnormal prion protein, enhancing infectivity [17,18], an organic soil constituent, humic acids can decrease CWD infectivity [19]. Prion persistence under harsh environmental conditions has been described [20,21], demonstrating prions shed in native soil maintain infectivity for years [6,22].…”

Section: Introductionmentioning

confidence: 99%

Long-Term Incubation PrPCWD with Soils Affects Prion Recovery but Not Infectivity

et al. 2020

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Chronic wasting disease (CWD) is a contagious prion disease of cervids. The infectious agent is shed from animals at the preclinical and clinical stages of disease where it persists in the environment as a reservoir of CWD infectivity. In this study, we demonstrate that long-term incubation of CWD prions (generated from tg-mice infected with deer or elk prions) with illite, montmorillonite (Mte) and whole soils results in decreased recovery of PrP CWD , suggesting that binding becomes more avid and irreversible with time. This continual decline of immunoblot PrP CWD detection did not correlate with prion infectivity levels. Bioassay showed no significant differences in incubation periods between mice inoculated with 1% CWD brain homogenate (BH) and with the CWD-BH pre-incubated with quartz or Luvisolic Ae horizon for 1 or 30 weeks. After 55 weeks incubation with Chernozem and Luvisol, bound PrP CWD was not detectable by immunoblotting but remained infectious. This study shows that although recovery of PrP CWD bound to soil minerals and whole soils with time become more difficult, prion infectivity is not significantly altered. Detection of prions in soil is, therefore, not only affected by soil type but also by length of time of the prion-soil interaction.Pathogens 2020, 9, 311 2 of 9 soils [12]. A number of laboratory studies have, however, suggested a time-dependent decline in the ability to detect rodent prions when bound to soils [22,25]. A decline in recoverable PrP Sc , after prolonged incubation, was found to be soil type specific with less PrP Sc recovery from clay compared to sandy soils [23].Sensitive detection of infectious CWD prions from environmental samples would have clear benefits for monitoring CWD spread. We demonstrate that, with time, PrP CWD becomes more difficult to recover from variety of soil types, yet CWD infectivity does not significantly decrease. Our findings suggest significant limitations to soil-bound PrP CWD detection especially for soils with montmorillonite minerology, impacting both surveillance and mitigation approaches.

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Clay Components in Soil Dictate Environmental Stability and Bioavailability of Cervid Prions in Mice

Cited by 19 publications

References 36 publications

TSE Monitoring in Wildlife Epidemiology, Transmission, Diagnosis, Genetics and Control

TSE Monitoring in Wildlife Epidemiology, Transmission, Diagnosis, Genetics and Control

How do PrPSc Prions Spread between Host Species, and within Hosts?

Long-Term Incubation PrPCWD with Soils Affects Prion Recovery but Not Infectivity

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