Murray Valley encephalitis (MVE), also known as Australian encephalitis, is one of many viral encephalitides and Flavivirus encephalitides, resulting from infection with the Murray Valley encephalitis virus.
Most patients have non-specific viral prodromal symptoms for approximately one week, including fevers, headache, nausea and vomiting, diarrhea, and generalized macular rash 1-3. This is followed by the emergence of neurological features, such as confusion and generalized or focal seizures 1-3.
These neurological features then progress in one of four distinct clinical courses:
- relentless progression (with parkinsonism, progressive motor decline, and stupor) to death 1-3
- prominent spinal cord involvement (a poliomyelitis-like syndrome) 1-3
- cranial nerve and brainstem involvement with tremor 1-3
- encephalitis followed by complete recovery 1-3
The causative agent is Murray valley encephalitis virus (MVEV), a single-stranded RNA flavivirus. Mosquitos and wild waterbirds, especially in the northern regions of Australia and in Papua New Guinea, are reservoirs for the virus, which is then spread by mosquitoes 1-3. Importantly, only 0.01-0.06% of patients with MVEV infection develop MVE 1.
The virus endemically spreads to more south-eastern regions of Australia, such as the Murray Valley regions, after extreme climate events that cause subsequent flooding of the Murray River and creation of ideal habitats for mosquitos that carry MVEV 1-3.
Symmetric early bilateral thalami involvement with later extension into the brain stem is classical regardless of CT or MRI imaging 1,3,4. Less commonly, the temporal lobes and cervical spinal cord may also be involved, depending on the clinical course 1.
Lesions may be subtle on CT but are most often hypodense involving the thalami and extending down into the brainstem as the disease progresses 1,3. These lesions often exert local mass-effect and may result in obstructive hydrocephalus 1,3.
MRI is the imaging modality of choice, however, is often unavailable due to the rurality of the regions affected by MVE, and thus MRI features are scarcely described in the literature 1,4.
However, the most striking features reported are symmetric high T2-weighted signal intensities classically affecting the thalami bilaterally and extending down into the brainstem 1,3,4. These lesions also demonstrate low signal on T1 with variable contrast enhancement and usually demonstrate high diffusion signal on DWI although this is likely due to T2 shine through as ADC maps are often isointense 4. As with CT, obstructive hydrocephalus secondary to mass-effect may also be noted 1.
Treatment and prognosis
There is no specific antiviral treatment available for MVE, and thus supportive management (e.g. antiepileptics, corticosteroids) is encouraged 1. Mortality is thought to be between 15-30%, with an additional 30-50% of patients having long-term neurological complications 1.
History and etymology
MVE was first formally recognized in Australia after an epidemic in 1951 in the Murray Valley region of Victoria 1.
- 1. Knox J, Cowan RU, Doyle JS, Ligtermoet MK, Archer JS, Burrow JN, Tong SY, Currie BJ, Mackenzie JS, Smith DW, Catton M, Moran RJ, Aboltins CA, Richards JS. Murray Valley encephalitis: a review of clinical features, diagnosis and treatment. The Medical journal of Australia. 196 (5): 322-6. Pubmed
- 2. Burrow JN, Whelan PI, Kilburn CJ, Fisher DA, Currie BJ, Smith DW. Australian encephalitis in the Northern Territory: clinical and epidemiological features, 1987-1996. Australian and New Zealand journal of medicine. 28 (5): 590-6. Pubmed
- 3. Niven DJ, Afra K, Iftinca M, Tellier R, Fonseca K, Kramer A, Safronetz D, Holloway K, Drebot M, Johnson AS. Fatal Infection with Murray Valley Encephalitis Virus Imported from Australia to Canada, 2011. Emerging infectious diseases. 23 (2): 280-283. doi:10.3201/eid2302.161161 - Pubmed
- 4. Einsiedel L, Kat E, Ravindran J, Slavotinek J, Gordon DL. MR Findings in Murray Valley Encephalitis. American Journal of Neuroradiology. 24 (7): 1379. Pubmed
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