Abstract

Before prion uptake and infection can occur in the lower gastrointestinal system, ingested prions are subjected to anaerobic digestion in the rumen of cervids and bovids. The susceptibility of soil-bound prions to rumen digestion has not been evaluated previously. In this study, prions from infectious brain homogenates as well as prions bound to a range of soils and soil minerals were subjected to in vitro rumen digestion, and changes in PrP levels were measured via western blot. Binding to clay appeared to protect noninfectious hamster PrPc from complete digestion, while both unbound and soil-bound infectious PrPSc proved highly resistant to rumen digestion. In addition, no change in intracerebral incubation period was observed following active rumen digestion of unbound hamster HY TME prions and HY TME prions bound to a silty clay loam soil. These results demonstrate that both unbound and soil-bound prions readily survive rumen digestion without a reduction in infectivity, further supporting the potential for soil-mediated transmission of chronic wasting disease (CWD) and scrapie in the environment.

Highlights

  • Prion diseases, or transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative diseases that afflict ruminants, including cattle, sheep and goats, and deer, elk, and moose, as well as humans (CreutzfeldJakob disease or CJD) [1,2]

  • Prion Source and protein misfolding cyclic amplification (PMCA) Substrate Prion-infected brain tissue was collected without prior buffer profusion from golden Syrian hamsters infected with the hyper (HY) strain of transmissible mink encephalopathy (TME) as previously described [29]

  • Standard methods, including standard rumen fluid sampling procedures and substrate and buffer compositions, were used [30,31,35]. pH values for the in vitro digestion were within normal in vivo ranges (Table 1), resazurin dye indicated a reduced environment in active samples but not inactive and buffer controls, and gas was produced throughout the 20 hr incubation, indicating anaerobic digestion occurred

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Summary

Introduction

Transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative diseases that afflict ruminants, including cattle (bovine spongiform encephalopathy, BSE, or ‘mad cow’ disease), sheep and goats (scrapie), and deer, elk, and moose (chronic wasting disease or CWD), as well as humans (CreutzfeldJakob disease or CJD) [1,2]. Natural transmission of CWD and scrapie occurs primarily or exclusively through ingestion or inhalation of prion-contaminated material shed from infected hosts or present in mortalities [2,4]. Once ingested by a ruminant (whether sheep, goat, cow, deer, elk, or moose), prions will be subjected to rumen digestion before entering the lower gastrointestinal tract, where agent uptake across the epithelium can initiate infection [8,9,10]

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