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Clinical and Radiological Predictors of Outcome for Murray Valley Encephalitis

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  • Department of Microbiology, PathWest Laboratory Medicine WA, Nedlands, Western Australia, Australia; School of Medicine and Pharmacology, University of Western Australia, Crawley, Western Australia, Australia; Department of Microbiology, PathWest Laboratory Medicine WA, Royal Perth Hospital, Perth, Western Australia, Australia; Princess Margaret Hospital for Children, Subiaco, Western Australia, Australia; School of Paediatrics and Child Health, University of Western Australia, Crawley, Western Australia, Australia; Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia; Department of Microbiology, PathWest Laboratory Medicine WA, Fremantle Hospital, Fremantle, Western Australia, Australia; Fremantle Hospital, Fremantle, Western Australia, Australia; School of Pathology and Laboratory Medicine, University of Western Australia, Crawley, Western Australia, Australia
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A review of the laboratory-confirmed cases of Murray Valley encephalitis (MVE) from Western Australia between 2009 and 2011 was conducted to describe the clinical, laboratory, and radiological features of the disease. The nine encephalitis patients presented with altered mental state and seizures, tremor, weakness, or paralysis. All patients developed a raised C-reactive protein, whereas most developed acute liver injury, neutrophilia, and thrombocytosis. All patients with encephalitis developed cerebral peduncle involvement on early magnetic resonance imaging (MRI). The absence of thalamic MRI hyperintensity during the acute illness, with or without leptomeningeal enhancement, predicted a better neurological outcome, whereas those patients with widespread abnormalities involving the thalamus, midbrain, and cerebral cortex or the cerebellum had devastating neurological outcomes. MRI scans repeated months after acute illness showed destruction of the thalamus and basal ganglia, cortex, or cerebellum. These findings may help clinicians predict the neurological outcome when evaluating patients with MVE.

Author Notes

* Address correspondence to David J. Speers, Department of Microbiology, PathWest Laboratory Medicine WA, Queen Elizabeth II Medical Centre, Hospital Avenue, Nedlands 6009, Western Australia, Australia. E-mail: david.speers@health.wa.gov.au

Authors' addresses: David J. Speers, Department of Microbiology, PathWest Laboratory Medicine WA, Nedlands, Western Australia, Australia, and School of Medicine and Pharmacology, University of Western Australia, Crawley, Western Australia, Australia, E-mail: david.speers@health.wa.gov.au. James Flexman, Department of Microbiology, PathWest Laboratory Medicine WA, Royal Perth Hospital, Perth, Western Australia, Australia, E-mail: james.flexman@health.wa.gov.au. Christopher C. Blyth, Princess Margaret Hospital for Children, Subiaco, Western Australia, Australia, and School of Paediatrics and Child Health, University of Western Australia, Crawley, Western Australia, Australia, E-mail: christopher.blyth@uwa.edu.au. Nirooshan Rooban, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia, E-mail: nirooshan@doctors.org.uk. Edward Raby, Department of Microbiology, PathWest Laboratory Medicine WA, Fremantle Hospital, Fremantle, Western Australia, Australia, E-mail: edward.raby@health.wa.gov.au. Ganesh Ramaseshan, Fremantle Hospital, Fremantle, Western Australia, Australia, E-mail: katcheri@yahoo.com.au. Susan Benson, School of Pathology and Laboratory Medicine, University of Western Australia, Crawley, Western Australia, Australia, E-mail: susan.benson@iinet.net.au. David W. Smith, Department of Microbiology, PathWest Laboratory Medicine WA, Nedlands, Western Australia, Australia, and School of Pathology and Laboratory Medicine, University of Western Australia, Crawley, Western Australia, Australia, E-mail: david.smith@health.wa.gov.au.

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