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Wasting Disease (wasting + disease)
Selected AbstractsA Griscelli syndrome type 2 murine model of hemophagocytic lymphohistiocytosis (HLH)EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 11 2008Jana Pachlopnik Schmid Abstract Griscelli syndrome type 2 is caused by mutations in the RAB27A gene and is a rare and potentially fatal immune disorder associated with hemophagocytic lymphohistiocytosis (HLH). Animal models could provide assistance for better understanding the mechanisms and finding new treatments. Rab27a-deficient (ashen) mice do not spontaneously develop HLH. When injected with lymphocytic choriomeningitis virus (LCMV) strain WE, Rab27a-deficient C57BL/6 mice developed wasting disease, hypothermia, splenomegaly, cytopenia (anemia, neutropenia and thrombocytopenia), hypertriglyceridemia and increased levels of IFN-,, TNF-,, GM-CSF, IL-12, CCL5 and IL-10. Activated macrophages with hemophagocytosis were found in liver sections of these mice. Compared with perforin-deficient mice, LCMV-infected Rab27a-deficient mice showed a substantially better survival rate and slightly higher viral doses were needed to trigger HLH in Rab27a-deficient mice. This study demonstrates that LCMV-infected Rab27a-deficient C57BL/6 mice develop features consistent with HLH and, therefore, represent a murine model of HLH in human Griscelli syndrome type 2. [source] Host culling as an adaptive management tool for chronic wasting disease in white-tailed deer: a modelling studyJOURNAL OF APPLIED ECOLOGY, Issue 2 2009Gideon Wasserberg Summary 1Emerging wildlife diseases pose a significant threat to natural and human systems. Because of real or perceived risks of delayed actions, disease management strategies such as culling are often implemented before thorough scientific knowledge of disease dynamics is available. Adaptive management is a valuable approach in addressing the uncertainty and complexity associated with wildlife disease problems and can be facilitated by using a formal model. 2We developed a multi-state computer simulation model using age, sex, infection-stage, and seasonality as a tool for scientific learning and managing chronic wasting disease (CWD) in white-tailed deer Odocoileus virginianus. Our matrix model used disease transmission parameters based on data collected through disease management activities. We used this model to evaluate management issues on density- (DD) and frequency-dependent (FD) transmission, time since disease introduction, and deer culling on the demographics, epizootiology, and management of CWD. 3Both DD and FD models fit the Wisconsin data for a harvested white-tailed deer population, but FD was slightly better. Time since disease introduction was estimated as 36 (95% CI, 24,50) and 188 (41,>200) years for DD and FD transmission, respectively. Deer harvest using intermediate to high non-selective rates can be used to reduce uncertainty between DD and FD transmission and improve our prediction of long-term epidemic patterns and host population impacts. A higher harvest rate allows earlier detection of these differences, but substantially reduces deer abundance. 4Results showed that CWD has spread slowly within Wisconsin deer populations, and therefore, epidemics and disease management are expected to last for decades. Non-hunted deer populations can develop and sustain a high level of infection, generating a substantial risk of disease spread. In contrast, CWD prevalence remains lower in hunted deer populations, but at a higher prevalence the disease competes with recreational hunting to reduce deer abundance. 5Synthesis and applications. Uncertainty about density- or frequency-dependent transmission hinders predictions about the long-term impacts of chronic wasting disease on cervid populations and the development of appropriate management strategies. An adaptive management strategy using computer modelling coupled with experimental management and monitoring can be used to test model predictions, identify the likely mode of disease transmission, and evaluate the risks of alternative management responses. [source] Myiasis as a risk factor for prion diseases in humansJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 9 2006O Lupi Abstract Prion diseases are transmissible spongiform encephalopathies of humans and animals. The oral route is clearly associated with some prion diseases, according to the dissemination of bovine spongiform encephalopathy (BSE or mad cow disease) in cattle and kuru in humans. However, other prion diseases such as scrapie (in sheep) and chronic wasting disease (CWD) (in cervids) cannot be explained in this way and are probably more associated with a pattern of horizontal transmission in both domestic and wild animals. The skin and mucous membranes are a potential target for prion infections because keratinocytes and lymphocytes are susceptible to the abnormal infective isoform of the prion protein. Iatrogenic transmission of Creutzfeldt,Jakob disease (CJD) was also recognized after corneal transplants in humans and scrapie was successfully transmitted to mice after ocular instillation of infected brain tissue, confirming that these new routes could also be important in prion infections. Some ectoparasites have been proven to harbour prion rods in laboratory experiments. Prion rods were identified in both fly larvae and pupae; adult flies are also able to express prion proteins. The most common causes of myiasis in cattle and sheep, closely related animals with previous prion infections, are Hypoderma bovis and Oestrus ovis, respectively. Both species of flies present a life cycle very different from human myiasis, as they have a long contact with neurological structures, such as spinal canal and epidural fat, which are potentially rich in prion rods. Ophthalmomyiases in humans is commonly caused by both species of fly larvae worldwide, providing almost direct contact with the central nervous system (CNS). The high expression of the prion protein on the skin and mucosa and the severity of the inflammatory response to the larvae could readily increase the efficiency of transmission of prions in both animals and humans. [source] | ||||||||||