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Mild encephalitis/encephalopathy with reversible splenial lesion (MERS) due to dengue virus

Fong CY, Khine MM, Peter AB, Lim WK, Rozalli FI, Rahmat K

J Clin Neurosci, 2017 Feb;36:73-75.
PMID: 27887978 DOI: 10.1016/j.jocn.2016.10.050

A 14-year-old girl presented with encephalopathy, delirium and ophthalmoplegia following a 3day history of high-grade fever. Brain MRI on day 6 of illness showed diffusion restricted ovoid lesion in the splenium of corpus callosum. Dengue virus encephalitis was diagnosed with positive PCR for dengue virus type-2 in both serum and cerebrospinal fluid. She made a complete recovery from day 10 of illness. Repeat brain MRI on day 12 of illness showed resolution of the splenial lesion. Serial diffusion tensor imaging (DTI) showed normal fractional anisotropy values on resolution of splenial lesion indicating that MERS was likely due to transient interstitial oedema with preservation of white matter tracts. This is the first reported case of MERS following dengue virus infection. It highlights the usefulness of performing serial DTI in understanding the underlying pathogenesis of MERS. Our case report widens the neurological manifestations associated with dengue infection and reiterates that patients with MERS should be managed supportively as the splenial white matter tracts are reversibly involved in MERS.

Matched MeSH terms: Encephalitis, Viral/etiology
Update: outbreak of Nipah virus--Malaysia and Singapore, 1999

Centers for Disease Control and Prevention (CDC)

MMWR Morb Mortal Wkly Rep, 1999 Apr 30;48(16):335-7.
PMID: 10366143

During March 1999, health officials in Malaysia and Singapore, in collaboration with Australian researchers and CDC, investigated reports of febrile encephalitic and respiratory illnesses among workers who had exposure to pigs. A previously unrecognized paramyxovirus (formerly known as Hendra-like virus), now called Nipah virus, was implicated by laboratory testing in many of these cases. Febrile encephalitis continues to be reported in Malaysia but has decreased coincident with mass culling of pigs in outbreak areas. No new cases of febrile illness associated with Nipah virus infection have been identified in Singapore since March 19, 1999, when abattoirs were closed. This report summarizes interim findings from ongoing epidemiologic and laboratory investigations in Malaysia and Singapore.

Matched MeSH terms: Encephalitis, Viral/etiology
Organ- and endotheliotropism of Nipah virus infections in vivo and in vitro

Maisner A, Neufeld J, Weingartl H

Thromb. Haemost., 2009 Dec;102(6):1014-23.
PMID: 19967130 DOI: 10.1160/TH09-05-0310

Nipah virus (NiV) is a highly pathogenic paramyxovirus that was first isolated in 1999 during an outbreak in Malaysia. In contrast to other paramyxoviruses NiV infects many mammalian species. Because of its zoonotic potential, the high pathogenicity and the lack of therapeutic treatment, NiV was classified as a biosafety level 4 pathogen. In humans NiV causes a severe acute encephalitis whereas in some animal hosts respiratory symptoms are predominantly observed. Despite the differences in the clinical outcome, microvascular endothelial cell damage predominantly underlies the pathological changes in NiV infections in all susceptible host species. NiV generally induces a pronounced vasculitis which is primarily characterised by endothelial cell necrosis and inflammatory cell infiltration. For future developments of specific antiviral therapies or vaccines, a detailed understanding of the molecular basis of NiV pathogenesis is required. This article reviews the current knowledge about natural and experimental infections in different mammals, focusing on the main organ and cell tropism in vivo, and summarises some recent studies in cell culture on the role of ephrin-B2 and -B3 receptors in NiV infection of endothelial cells.

Matched MeSH terms: Encephalitis, Viral/etiology
Fulltext Anthropogenic deforestation, El Niño and the emergence of Nipah virus in Malaysia

Chua KB, Chua BH, Wang CW

Malays J Pathol, 2002 Jun;24(1):15-21.
PMID: 16329551

In late 1998, a novel paramyxovirus named Nipah virus, emerged in Malaysia, causing fatal disease in domestic pigs and humans with substantial economic loss to the local pig industry. Pteropid fruitbats have since been identified as a natural reservoir host. Over the last two decades, the forest habitat of these bats in Southeast Asia has been substantially reduced by deforestation for pulpwood and industrial plantation. In 1997/1998, slash-and-burn deforestation resulted in the formation of a severe haze that blanketed much of Southeast Asia in the months directly preceding the Nipah virus disease outbreak. This was exacerbated by a drought driven by the severe 1997-1998 El Niño Southern Oscillation (ENSO) event. We present data suggesting that this series of events led to a reduction in the availability of flowering and fruiting forest trees for foraging by fruitbats and culminated in unprecedented encroachment of fruitbats into cultivated fruit orchards in 1997/1998. These anthropogenic events, coupled with the location of piggeries in orchards and the design of pigsties allowed transmission of a novel paramyxovirus from its reservoir host to the domestic pig and ultimately to the human population.

Matched MeSH terms: Encephalitis, Viral/etiology
Trailing a virus

Gibbs WW

Sci. Am., 1999 Aug;281(2):80-7.
PMID: 10443039
Matched MeSH terms: Encephalitis, Viral/etiology*
In enterovirus 71 encephalitis with cardio-respiratory compromise, elevated interleukin 1β, interleukin 1 receptor antagonist, and granulocyte colony-stimulating factor levels are markers of poor prognosis

Griffiths MJ, Ooi MH, Wong SC, Mohan A, Podin Y, Perera D, et al.

J Infect Dis, 2012 Sep 15;206(6):881-92.
PMID: 22829643 DOI: 10.1093/infdis/jis446

BACKGROUND: Enterovirus 71 (EV71) causes large outbreaks of hand, foot, and mouth disease (HFMD), with severe neurological complications and cardio-respiratory compromise, but the pathogenesis is poorly understood.
METHODS: We measured levels of 30 chemokines and cytokines in serum and cerebrospinal fluid (CSF) samples from Malaysian children hospitalized with EV71 infection (n = 88), comprising uncomplicated HFMD (n = 47), meningitis (n = 8), acute flaccid paralysis (n = 1), encephalitis (n = 21), and encephalitis with cardiorespiratory compromise (n = 11). Four of the latter patients died.
RESULTS: Both pro-inflammatory and anti-inflammatory mediator levels were elevated, with different patterns of mediator abundance in the CSF and vascular compartments. Serum concentrations of interleukin 1β (IL-1β), interleukin 1 receptor antagonist (IL-1Ra), and granulocyte colony-stimulating factor (G-CSF) were raised significantly in patients who developed cardio-respiratory compromise (P = .013, P = .004, and P < .001, respectively). Serum IL-1Ra and G-CSF levels were also significantly elevated in patients who died, with a serum G-CSF to interleukin 5 ratio of >100 at admission being the most accurate prognostic marker for death (P < .001; accuracy, 85.5%; sensitivity, 100%; specificity, 84.7%).
CONCLUSIONS: Given that IL-1β has a negative inotropic action on the heart, and that both its natural antagonist, IL-1Ra, and G-CSF are being assessed as treatments for acute cardiac impairment, the findings suggest we have identified functional markers of EV71-related cardiac dysfunction and potential treatment options.

Matched MeSH terms: Encephalitis, Viral/etiology*