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The article presents an analysis of various factors influencing the attachment of prion protein to soil constituents. It discusses the potential implications of prions as agents of transmissible spongiform encephalopathies (TSEs), that is a form of neurodegenerative disease and explains the structure of pathogenic prion protein. It informs that environmental routes of TSE transmission are shown in TSE if deer, mouse and elk and stresses on the need of assessing the persistence, mobility and bioavailability of prions in soil for the management of TSE-contaminated soils.

Chronic wasting disease (CWD) was found in wild deer populations in the province of Alberta, Canada, in 2005, and there is concern that this finding could create significant costs related to the farmed elk and deer industry. These potential costs or “values at risk” can be used to assess the economic returns from CWD containment and eradication programs. Cost estimates of CWD to cervid farms range from $12 million for additional farm fencing to hundreds of millions of dollars in payments by governments to discontinue cervid farming. [ABSTRACT FROM AUTHOR]

Chronic wasting disease (CWD) is increasingly prevalent in multiple wild mule (Odocoileus hemionus) and white-tailed deer (O. virginianus) herds in North America. CWD was first found in Canadian wild mule deer in Saskatchewan in 2000 and has since spread into the neighboring province of Alberta. The infectious agent for CWD is a misfolded prion protein encoded by the PRNP gene. Previous studies revealed association between PRNP genotype and susceptibility to CWD in both mule and white-tailed deer in other regions. To investigate this link in Canadian populations, PRNP gene sequence was examined in 166 CWD- and 83 CWD+ mule deer, and 197 CWD- and 30 CWD+ white-tailed deer from Saskatchewan and Alberta. Two variable sites were found in mule deer, and 15 in white-tailed deer. In both species PRNP genotype was associated with CWD status. Mule deer possessing at least one copy of the common allele at codon 20 were less likely to test positive for CWD than expected, given the frequency of this allele in the population. A variant at codon 96 in white-tailed deer was also linked with reduced incidence of CWD. A greater knowledge of the genetic sources of heterogeneity in CWD susceptibility may improve our understanding of the mechanisms underlying the CWD epidemic in western Canada. [ABSTRACT FROM AUTHOR]

Summary: Chronic wasting disease (CWD), a prion disease of North American deer, elk and moose, affects both free-ranging and captive cervids. The potential host range for CWD remains uncertain. The susceptibility of the ferret to CWD was examined experimentally by administering infectious brain material by the intracerebral (IC) or oral (PO) route. Between 15 and 20 months after IC inoculation, ferrets developed neurological signs consistent with prion disease, including polyphagia, somnolence, piloerection, lordosis and ataxia. Upon first sub-passage of ferret-adapted CWD, the incubation period decreased to 5 months. Spongiform change in the neuropil was most marked in the basal ganglia, thalamus, midbrain and pons. The deposition of PrPCWD was granular and was occasionally closely associated with, or localized within, neurons. There were no plaque-like or perivascular PrP aggregates as seen in CWD-infected cervids. In western blots, the PrPCWD glycoform profile resembled that of CWD in deer, typified by a dominant diglycosylated glycoform. CWD disease in ferrets followed IC but not PO inoculation, even after 31 months of observation. These findings indicate that CWD-infected ferrets share microscopical and biochemical features of CWD in cervids, but appear to be relatively resistant to oral infection by primary CWD inoculum of deer origin. [Copyright &y& Elsevier]

Reports on a study which provides the evidence that chronic wasting disease can be transmitted through environments contaminated by carcasses or excrement of infected animals, in addition to spreading through direct interactions between animals. Need to consider potential exposure routes when attempting to control this disease; History of the identification of the disease; Significance of the findings for veterinary medicine.