Potential Role of Soil in the Transmission of Prion Disease

Schramm, Peter T; Johnson, Christopher; Mathews, Nancy E.; McKenzie, Debbie; Aiken, Judd M.; Pedersen, Joel A.

doi:10.2138/rmg.2006.64.5

Cited by 51 publications

(41 citation statements)

References 143 publications

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“…An environmental reservoir of prion infectivity appears to contribute to the transmission of CWD and scrapie (5). Several lines of evidence support the concept that soil comprises a component of this reservoir (5).…”

Section: Introductionmentioning

confidence: 95%

“…PrP Sc adsorption to quartz sand particles was examined as a function of pH, I, and prion protein concentration in batch sorption experiments. Solution pH was maintained using 0.01 M acetate (pH [3][4][5], MOPS (pH 6-7), or Tris (pH 8-9); the desired I was achieved by NaCl addition.…”

Section: Prpmentioning

confidence: 99%

“…Oral transmission of CWD via saliva from infected deer has been demonstrated (7), and shedding of prions in urine from animals with chronic kidney inflammation has been reported (9). Since herbivores consume soil both deliberately and incidentally (10,11), ingestion of prion-contaminated soil may contribute to the natural CWD and scrapie transmission (5,12). Montmorillonite-associated prions were recently demonstrated to retain infectivity despite extremely avid adsorption of PrP Sc to the clay particles (12).…”

Section: Introductionmentioning

confidence: 99%

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Adsorption of Pathogenic Prion Protein to Quartz Sand

Benson

McKenzie

et al. 2007

Environ. Sci. Technol.

123

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Management responses to prion diseases of cattle, deer, and elk create a significant need for safe and effective disposal of infected carcasses and other materials. Furthermore, soil may contribute to the horizontal transmission of sheep scrapie and cervid chronic wasting disease by serving as an environmental reservoir for the infectious agent. As an initial step toward understanding prion mobility in porous materials such as soil and landfilled waste, the influence of pH and ionic strength (I) on pathogenic prion protein (PrP Sc ) properties (viz. aggregation state and ζ-potential) and adsorption to quartz sand was investigated. The apparent average isoelectric point of PrP Sc aggregates was 4.6. PrP Sc aggregate size was largest between pH 4 and 6, and increased with increasing I at pH 7. Adsorption to quartz sand was maximal near the apparent isoelectric point of PrP Sc aggregates and decreased as pH either declined or increased. PrP Sc adsorption increased as suspension I increased, and reached an apparent plateau at I ∼ 0.1 M. While trends with pH and I in PrP Sc attachment to quartz surfaces were consistent with predictions based on Born-DLVO theory, non-DLVO forces appeared to contribute to adsorption at pH 7 and 9 (I ) 10 mM). Our findings suggest that disposal strategies that elevate pH (e.g., burial in lime or fly ash), may increase PrP Sc mobility. Similarly, PrP Sc mobility may increase as a landfill ages, due to increases in pH and decreases in I of the leachate.

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Section: Introductionmentioning

confidence: 95%

Section: Prpmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adsorption of Pathogenic Prion Protein to Quartz Sand

Benson

McKenzie

et al. 2007

Environ. Sci. Technol.

123

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“…Prion protein and other soil exogenous proteins can also easily interact with organomineral complexes that likely are in soil more abundant than the mineral or organic components alone. Soil has been suggested to act as a reservoir of TSE infectivity [17,18] and even to enhance the transmissibility of prion disease by oral uptake of soil complexed PrP Sc [16]. While biotic PrP Sc degradation by some proteases can be reduced because of persistent PrP Sc aggregates, its inactivation may arise by abiotic oxidative reactions.…”

Section: Introductionmentioning

confidence: 99%

Interaction of a Recombinant Prion Protein with Organo-Mineral Complexes as Assessed by FT-IR and CPMAS 13C NMR Analysis

Russo¹,

Gianfreda²,

Conte³

et al. 2010

TOMRJ

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Prion proteins are considered as the main agents for the Transmissible Spongiform Encephalopathies (TSE). The misfolded form, PrP Sc , which is also indicated as the etiological agent for TSE, exhibits high resistance to degradation in environmental processes. Soil contamination by prion proteins is a real environmental issue since contaminated soils can become potential reservoir and diffuser for TSE infectivity. In this work, the interaction of prion protein with organomineral complexes was studied by using a recombinant non pathogenic prion protein and a model soil system. This latter was represented by a soil manganese mineral coated with polymerized catechol. FT-IR spectra showed amide I and II signals which revealed protein involvement in catechol polymers coating manganese oxide surface. CPMAS 13 C-NMR was applied to follow the complexation of the protein to the soil-like system. All the signals were attributed to C-N in peptidic bonds, alkyl chains and methyl groups. The NMR spectrum of the prion protein interacting directly with birnessite revealed disappearance of signals due to the paramagnetic nature of manganese oxide or protein abiotic degradation, while the presence of organic matter strongly reduced the disappearance of prion protein signals.

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“…11 Although various aspects of prions in the environment have been reviewed previously, a complete review of literature related to prion occurrence, fate and mitigation in the environment is lacking. The potential role of soil in prion transmission was reviewed in 2006, 12 but over 30 pertinent studies have been published during the ensuing two years. Snow and colleagues separately reported the prion environmental literature published in 2006 13 and 2007.…”

Section: Introductionmentioning

confidence: 99%

Prions in the environment

Saunders

Bartelt–Hunt

Bartz

2008

Prion

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Scrapie and CWD are horizontally transmissible, and the environment likely serves as a stable reservoir of infectious prions, facilitating a sustained incidence of CWD in free-ranging cervid populations and complicating efforts to eliminate disease in captive herds. Prions will enter the environment through mortalities and/ or shedding from live hosts. Unfortunately, a sensitive detection method to identify prion contamination in environmental samples has not yet been developed. An environmentally-relevant prion model must be used in experimental studies. Changes in PrP Sc structure upon environmental exposure may be as significant as changes in PrP Sc quantity, since the structure can directly affect infectivity and disease pathology. Prions strongly bind to soil and remain infectious. Conformational changes upon adsorption, competitive sorption and potential for desorption and transport all warrant further investigation. Mitigation of contaminated carcasses or soil might be accomplished with enzyme treatments or composting in lieu of incineration.

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Potential Role of Soil in the Transmission of Prion Disease

Cited by 51 publications

References 143 publications

Adsorption of Pathogenic Prion Protein to Quartz Sand

Adsorption of Pathogenic Prion Protein to Quartz Sand

Interaction of a Recombinant Prion Protein with Organo-Mineral Complexes as Assessed by FT-IR and CPMAS 13C NMR Analysis

Prions in the environment

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