In the past 12 years (1967-79) a syndrome we identify as chronic wasting disease has been observed in 53 mule deer (Odocoileus hemionus hemionus) and one black-tailed deer (Odocoileus hemionus columbianus) held in captivity in several wildlife facilities in Colorado and more recently in Wyoming. Clinical signs were seen in adult deer and included behavioral alterations, progressive weight loss and death in 2 weeks to 8 months. Gross necropsy findings included emaciation and excess rumen fluid admixed with sand and gravel. Consistent histopathologic change was limited to the central nervous system and characterized by widespread spongiform transformation of the neuropil, single or multiple intracytoplasmic vacuoles in neuronalperikaryons and intense astrocytic hypertrophy and hyperplasia. Presented is a clinical characterization of chronic wasting disease and pathologic evidence supporting the conclusion that the disease is a specific spontaneously occurring form of spongiform encephalopathy. mouflon (Ovis musimon).
Abstract. Chronic wasting disease (CWD) is a unique transmissible spongiform encephalopathy (TSE) of mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), and Rocky Mountain elk (Cervus elaphus nelsoni). The natural history of CWD is incompletely understood, but it differs from scrapie and bovine spongiform encephalopathy (BSE) by virtue of its occurrence in nondomestic and free-ranging species. CWD has many features in common with scrapie, including early widespread distribution of disease-associated prion protein (PrP d ) in lymphoid tissues, with later involvement of central nervous system (CNS) and peripheral tissues. This distribution likely contributes to apparent efficiency of horizontal transmission and, in this, is similar to scrapie and differs from BSE. Clinical features and lesions of CWD are qualitatively similar to the other animal TSEs. Microscopically, marked spongiform lesions occur in the central nervous system (CNS) after a prolonged incubation period and variable course of clinical disease. During incubation, PrP d can be identified in tissues by antibody-based detection systems. Although CWD can be transmitted by intracerebral inoculation to cattle, sheep, and goats, ongoing studies have not demonstrated that domestic livestock are susceptible via oral exposure, the presumed natural route of exposure to TSEs. Surveillance efforts for CWD in captive and free-ranging cervids will continue in concert with similar activities for scrapie and BSE. Eradication of CWD in farmed cervids is the goal of state, federal, and industry programs, but eradication of CWD from free-ranging populations of cervids is unlikely with currently available management techniques.Key words: Chronic wasting disease; elk; mule deer; prion disease; transmissible spongiform encephalopathy; white-tailed deer.The transmissible spongiform encephalopathies (TSEs) are unusual infectious diseases of animals and humans. The TSEs, including chronic wasting disease (CWD), are designated prion diseases because of their association with aberrantly refolded isoforms of the prion protein, a normal cellular glycoprotein (PrP C ). 120 CWD-associated prion protein (PrP CWD or PrP d ) 82 is widespread in the lymphoid tissues and the CNS from early in the incubation phase until death. 98,132,137 Scrapie, the first TSE identified, was the focus of considerable research and even controversy concerning its origin and nature (genetic versus infectious) for many years. 2,114,115 However, it was the recognition that prion diseases were transmissible and affected humans as well as animals that stimulated much of the current scientific interest in the nature of these diseases.Scrapie has been recognized for hundreds of years, transmissible mink encephalopathy (TME) for more than 50 years, CWD for more than 30 years, and bovine spongiform encephalopathy (BSE) for fewer than 20 years. Although CWD is now well known, it was just a few years ago considered an obscure disease of mule deer (Odocoileus hemionus) and elk (Cervus elaphus nelso...
Whether transmission of the chronic wasting disease (CWD) prion among cervids requires direct interaction with infected animals has been unclear. We report that CWD can be transmitted to susceptible animals indirectly, from environments contaminated by excreta or decomposed carcasses. Under experimental conditions, mule deer (Odocoileus hemionus) became infected in two of three paddocks containing naturally infected deer, in two of three paddocks where infected deer carcasses had decomposed in situ ≈1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier. Indirect transmission and environmental persistence of infectious prions will complicate efforts to control CWD and perhaps other animal prion diseases.
Surveillance and epidemic modeling were used to study chronic wasting disease (CWD), a transmissible spongiform encephalopathy that occurs naturally among sympatric, free-ranging deer (Odocoileus spp.) and Rocky Mountain elk (Cervus elaphus nelsoni) populations in contiguous portions of northeastern Colorado and southeastern Wyoming (USA). We used clinical case submissions to identify endemic areas, then used immunohistochemistry to detect CWD-infected individuals among 5,513 deer and elk sampled via geographically-focused random surveys. Estimated overall prevalence (prevalence, 95% confidence interval) in mule deer (4.9%, 4.1 to 5.7%) was higher than in white-tailed deer (2.1%, 0.5 to 3.4%) or elk (0.5%, 0.001 to 1%) in endemic areas; CWD was not detected in outlying portions of either state. Within species, CWD prevalence varied widely among biologically- or geographically-segregated subpopulations within the 38,137 km2 endemic area but appeared stable over a 3-yr period. The number of clinical CWD cases submitted from an area was a poor predictor of local CWD prevalence, and prevalence was typically > or =1% before clinical cases were first detected in most areas. Under plausible transmission assumptions that mimicked field data, prevalence in epidemic models reached about 1% in 15 to 20 yr and about 15% in 37 to 50 yr. Models forecast population declines once prevalence exceeded about 5%. Both field and model data supported the importance of lateral transmission in CWD dynamics. Based on prevalence, spatial distribution, and modeling, we suggest CWD has been occurring in northeastern Colorado and southeastern Wyoming for >30 yr, and may be best represented as an epizootic with a protracted time-scale.
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