Nipah virus encephalitis (NiV encephalitis) is a zoonotic illness caused by the Nipah virus resulting in a severe and often fatal encephalitis.
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Epidemiology
As the virus is thought to be spread from pigs to humans, pig farmers and abattoir workers are at the highest risk of exposure 2. Several outbreaks of the disease has occurred in Malaysia, Singapore, Bangladesh and India 5.
Clinical presentation
On presentation the clinical features ranging from most common to least common include 2:
- fever
- headache
- dizziness
- vomiting
- altered level of consciousness
- focal neurological signs (e.g. cerebellar, segmental myoclonus)
- respiratory symptoms
However, the infection may also be asymptomatic in some patients.
Pathology
Etiology
Nipah virus is a single stranded RNA virus and a member of the paramyxovirus family and the Henipavirus genus. The Henipavirus genus includes two of the most lethal viruses known to man: Hendra and Nipah. The natural reservoir of the virus is the fruit bat 2. The incubation time from exposure to symptom onset is around 9 days 6. However, delayed onset of symptoms has also been reported more than 11 weeks after exposure 2. Most human cases are thought to be related to exposure to porcine hosts which can also be infected with the virus 2. However, direct bat-human transmission and human-human transmission have also been described 5.
Microscopic appearance
Autopsies performed on confirmed cases of Nipah showed widespread endothelial damage and vasculitis. Surrounding the vasculitic areas were regions of microinfarction 1,3. The brain is the main organ affected, but the kidneys, heart and lungs also show evidence of viral infection 3.
Markers
The virus is detectable in the CSF through viral culture and nucleic acid amplification. Hendra virus IgM and IgG ELISA tests can also detect Nipah 2.
Radiographic features
CT
In cases of Nipah virus encephalitis, CT is usually unremarkable 3.
MRI
In one study, lesions on MRI were seen in 100% of cases of Nipah virus encephalitis 1. Typical appearances include 1,4,7:
-
T1:
- hyperintense
- small discrete lesions, may range in number from 2 to >10
- appear round or as strips
- present in deep white matter cortex (44%), temporal lobe (30%), pons (22%), penducles (10%) 1
- may be present as large confluent areas
- absence of surrounding or generalized edema or mass effect
- T1 C+ (Gd): aforementioned lesions are non-enhancing
- T2/FLAIR: aforementioned lesions are hyperintense
- DWI: lesions have high diffusion signal
Treatment and prognosis
Treatment is largely supportive, often patients may require ICU admission for ventilation due to respiratory compromise. Antiviral therapy with ribavirin has been trialled, although its benefit is uncertain 2. Public health measures such as pig culling and banning the importation of infected pigs is also important 2.
The condition can be rapidly fatal progressing from the onset of symptoms to death on average in 6 days 6. In one study mortality was 32%, whilst 14% had lasting neurological deficit; only 50% experienced complete recovery 2. In survivors, lesions on follow-up MRI have been noted to resolve or diminish over time 4.
History and etymology
The virus is named after the Kampung Sungai Nipah village in Malaysia where the first outbreak occurred in 1998-1999 2.
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