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Extended detection and isolation of Murray Valley encephalitis virus in whole blood and urine

Leon Caly, Natalie Davidson, Ram Ghimire, Brinthan Rajaratnam, Jonathan Marrow, Rob Baird, Ella M Meumann and Julian Druce
Med J Aust 2019; 211 (11): . || doi: 10.5694/mja2.50423
Published online: 9 December 2019

A 23‐year‐old Indigenous woman from Arnhem Land, Northern Territory, presented with a 2‐day history of fever, arthralgia and headache. She had a background of systemic lupus erythematosus treated with daily azathioprine 100 mg and prednisolone 20 mg, and rheumatic heart disease treated with monthly intramuscular benzathine penicillin. After admission, she developed generalised seizures and confusion requiring intensive care unit admission and intubation. Magnetic resonance imaging (MRI) of the brain on Day 6 after admission demonstrated increased T2 and fluid‐attenuated inversion recovery (FLAIR) signal in the medial temporal lobes bilaterally (Box 1). Electroencephalogram was suggestive of episodic bifrontal delta wave activity not corresponding to seizure activity and generalised slowing. Cerebrospinal fluid (CSF) white cell count was 287 × 106/L with 90% mononuclear cells, CSF protein elevated at 1.49 g/L (normal range [NR], 0.15–0.45 g/L), and CSF glucose 4.5 mmol/L (NR, 2.7–4.2 mmol/L). The most likely diagnosis was thought to be encephalitis associated with systemic lupus erythematosus, and she initially received intravenous immunoglobulin and intravenous methylprednisolone 1 g daily. However, infection, including Murray Valley encephalitis virus (MVEV) — peak risk February to July — was considered in the differential diagnosis.


  • 1 Victorian Infectious Diseases Reference Laboratory, Royal Melbourne Hospital, Peter Doherty Institute for Infection and Immunity, Melbourne, VIC
  • 2 Royal Darwin Hospital, Darwin, NT
  • 3 Menzies School of Health Research, Darwin, NT


Correspondence: leon.caly@mh.org.au

Competing interests:

No relevant disclosures.

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