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Murray Valley Encephalitis (murray + valley_encephalitis)
Selected AbstractsMorphological features of Murray Valley encephalitis virus infection in the central nervous system of swiss miceINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 1 2000Vance Matthews We have examined the histological and ultrastructural features of CNS infection with Murray Valley encephalitis (MVE) virus in mice inoculated with a virulent parental strain (BH3479). Light microscopic examination revealed neuronal necrosis in the olfactory bulb and hippocampus of MVE-infected brains by 5 days post-infection (pi). Electron microscopy of these regions showed endoplasmic reticulum membrane proliferation, and tubular and spherical structures in the cisternae of the endoplasmic reticulum, Golgi complex and nuclear envelope. At seven to eight days pi, infected neurones exhibited chromatin condensation and extrusion, nuclear fragmentation, loss of segments of the nuclear envelope, reduced surface contact with adjacent cells and loss of cytoplasmic organelles. This cell injury was particularly noticeable in the proximal CA3 and distal CA1 regions of the hippocampus. The inflammatory cell profile consisted of macrophages, lymphocytes and especially neutrophils, and many of these inflammatory cells were apoptotic. High mortality rates in the BH3479-infected population of mice correlated with the intense polymorphonuclear and mononuclear leucocyte inflammatory infiltrate in the CNS. [source] Murray Valley encephalitis: Case report and review of neuroradiological featuresJOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 1 2003N Kienzle SUMMARY We report on a child with diffuse symmetrical thalamic enlargement and signal increase on MRI, representing changes caused by Murray Valley encephalitis (MVE). Very little has previously been reported on the neuroradiological findings of MVE, also known as Australian encephalitis. It is endemic to tropical North Australia, particularly Western Australia and the Northern Territory, but can occur in other parts of Australia. The last epidemic was in south-eastern Australia in 1974. Australian encephalitis is the second most serious acute viral encephalitis to be encountered in Australia. Clinicians need to be aware of MVE in this era of ever-increasing travel. Our aim is to highlight these finding and further define the neuroradiological features. [source] Mosquito-borne disease and climate change in Australia: time for a reality checkAUSTRALIAN JOURNAL OF ENTOMOLOGY, Issue 1 2009Richard C Russell Abstract Will warming climate increase the risk or prevalence of mosquito-borne disease in Australia, as has been projected in a number of scientific publications and governmental reports? Unfortunately, most of these ,predictions' do not adequately consider the current and historical distribution of the vectors and diseases, their local ecology and epidemiology and the impact of societal features and the capacity for public health interventions in Australia. Overall, a strong case can be made that we are unlikely to see significant changes in the distribution of transmission of the exotic pathogens causing malaria and dengue, and while activity of endemic arboviruses such as Murray Valley encephalitis and Ross River viruses may possibly increase in some areas, it is likely to decrease in others. The ecologies of mosquito-borne diseases can be complex and difficult to predict, and any evaluation of potential effects of changes in climate will need a detailed examination of site-specific vector, host and other factors likely to influence the outcomes on human health. Of itself, climate change as currently projected, is not likely to provide great cause for public health concern with mosquito-borne disease in Australia. [source] | ||||||||||