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  1. Nipah virus outbreak in Malaysia
    Chua KB
    J Clin Virol, 2003 Apr;26(3):265-75.
    PMID: 12637075
    Nipah virus, a novel paramyxovirus, closely related to Hendra virus emerged in northern part of Peninsular Malaysia in 1998. The virus caused an outbreak of severe febrile encephalitis in humans with a high mortality rate, whereas, in pigs, encephalitis and respiratory diseases but with a relatively low mortality rate. The outbreak subsequently spread to various regions of the country and Singapore in the south due to the movement of infected pigs. Nipah virus caused systemic infections in humans, pigs and other mammals. Histopathological and radiological findings were characteristic of the disease. Fruitbats of Pteropid species were identified as the natural reservoir hosts. Evidence suggested that climatic and anthropogenic driven ecological changes coupled with the location of piggeries in orchard and the design of pigsties allowed the spill-over of this novel paramyxovirus from its reservoir host into the domestic pigs and ultimately to humans and other animals.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  2. Emerging and re-emerging epidemic encephalitis: a tale of two viruses
    Wong KT
    Neuropathol. Appl. Neurobiol., 2000 Aug;26(4):313-8.
    PMID: 10931364
    Two major epidemics of viral encephalitis occurred in Asia in 1997 and 1998. The first was a re-emergence of neurovirulent strains of enterovirus 71, which caused severe encephalomyelitis in children in Malaysia, Taiwan and Japan, on a background of hand, foot and mouth disease. Necropsy studies of patients who died of enterovirus 71 infection showed severe perivascular cuffing, parenchymal inflammation and neuronophagia in the spinal cord, brainstem and diencephalon, and in focal areas in the cerebellum and cerebrum. Although no viral inclusions were detected, immunohistochemistry showed viral antigen in the neuronal cytoplasm. Inflammation was often more extensive than neuronal infection, suggesting that other factors, in addition to direct viral cytolysis, may be involved in tissue damage. The second epidemic of viral encephalitis was the result of a novel paramyxovirus called Nipah, which mainly involved pig handlers in Malaysia and Singapore. Pathological evidence suggested that the endothelium of small blood vessels in the central nervous system was particularly susceptible to infection. This led to disseminated endothelial damage and syncytium formation, vasculitis, thrombosis, ischaemia and microinfarction. However, there was also evidence of neuronal infection by the virus and this may also have contributed to the neurological dysfunction in Nipah encephalitis. Some patients who seemed to recover from the acute symptoms have been re-admitted with clinical findings suggestive of relapsing encephalitis. As these two epidemics indicate, the emergence and re-emergence of viral encephalitides continue to pose considerable challenges to the neuropathologist, in establishing the diagnosis and unravelling the pathogenesis of the neurological disease.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  3. Fulltext Nipah virus: a recently emergent deadly paramyxovirus
    Chua KB, Bellini WJ, Rota PA, Harcourt BH, Tamin A, Lam SK, et al.
    Science, 2000 May 26;288(5470):1432-5.
    PMID: 10827955
    A paramyxovirus virus termed Nipah virus has been identified as the etiologic agent of an outbreak of severe encephalitis in people with close contact exposure to pigs in Malaysia and Singapore. The outbreak was first noted in late September 1998 and by mid-June 1999, more than 265 encephalitis cases, including 105 deaths, had been reported in Malaysia, and 11 cases of encephalitis or respiratory illness with one death had been reported in Singapore. Electron microscopic, serologic, and genetic studies indicate that this virus belongs to the family Paramyxoviridae and is most closely related to the recently discovered Hendra virus. We suggest that these two viruses are representative of a new genus within the family Paramyxoviridae. Like Hendra virus, Nipah virus is unusual among the paramyxoviruses in its ability to infect and cause potentially fatal disease in a number of host species, including humans.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  4. Emerging zoonotic encephalitis viruses: lessons from Southeast Asia and Oceania
    Mackenzie JS
    J Neurovirol, 2005 Oct;11(5):434-40.
    PMID: 16287684
    The last decade of the 20th Century saw the introduction of an unprecedented number of encephalitic viruses emerge or spread in the Southeast Asian and Western Pacific regions (Mackenzie et al, 2001; Solomon, 2003a). Most of these viruses are zoonotic, either being arthropod-borne viruses or bat-borne viruses. Thus Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, has spread through the Indonesian archipelago to Papua New Guinea (PNG) and to the islands of the Torres Strait of northern Australia, to Pakistan, and to new areas in the Indian subcontinent; a strain of tick-borne encephalitis virus (TBEV) was described for the first time in Hokkaido, Japan; and a novel mosquito-borne alphavirus, Me Tri virus, was described from Vietnam. Three novel bat-borne viruses emerged in Australia and Malaysia; two, Hendra and Nipah viruses, represent the first examples of a new genus in the family Paramyxoviridae, the genus Henipaviruses, and the third, Australian bat lyssavirus (ABLV) is new lyssavirus closely related to classical rabies virus. These viruses will form the body of this brief review.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  5. 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/epidemiology
  6. Risk factors for Nipah virus infection among abattoir workers in Singapore
    Chew MH, Arguin PM, Shay DK, Goh KT, Rollin PE, Shieh WJ, et al.
    J Infect Dis, 2000 May;181(5):1760-3.
    PMID: 10823780
    During 10-19 March 1999, 11 workers in 1 of 2 Singaporean abattoirs developed Nipah-virus associated encephalitis or pneumonia, resulting in 1 fatality. A case-control study was conducted to determine occupational risk factors for infection. Case patients were abattoir A workers who had anti-Nipah IgM antibodies; control subjects were randomly selected abattoir A workers who tested negative for anti-Nipah IgM. All 13 case patients versus 26 (63%) of 41 control subjects reported contact with live pigs (P=.01). Swine importation from Malaysian states concurrently experiencing a Nipah virus outbreak was banned on 3 March 1999; on 19 March 1999, importation of Malaysian pigs was banned, and abattoirs were closed. No unusual illnesses among pigs processed during February-March were reported. Contact with live pigs appeared to be the most important risk factor for human Nipah virus infection. Direct contact with live, potentially infected pigs should be minimized to prevent transmission of this potentially fatal zoonosis to humans.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  7. Case-control study of risk factors for human infection with a new zoonotic paramyxovirus, Nipah virus, during a 1998-1999 outbreak of severe encephalitis in Malaysia
    Parashar UD, Sunn LM, Ong F, Mounts AW, Arif MT, Ksiazek TG, et al.
    J Infect Dis, 2000 May;181(5):1755-9.
    PMID: 10823779
    An outbreak of encephalitis affecting 265 patients (105 fatally) occurred during 1998-1999 in Malaysia and was linked to a new paramyxovirus, Nipah, that infected pigs, humans, dogs, and cats. Most patients were pig farmers. Clinically undetected Nipah infection was noted in 10 (6%) of 166 community-farm controls (persons from farms without reported encephalitis patients) and 20 (11%) of 178 case-farm controls (persons from farms with encephalitis patients). Case patients (persons with Nipah infection) were more likely than community-farm controls to report increased numbers of sick/dying pigs on the farm (59% vs. 24%, P=.001) and were more likely than case-farm controls to perform activities requiring direct contact with pigs (86% vs. 50%, P=.005). Only 8% of case patients reported no contact with pigs. The outbreak stopped after pigs in the affected areas were slaughtered and buried. Direct, close contact with pigs was the primary source of human Nipah infection, but other sources, such as infected dogs and cats, cannot be excluded.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  8. Nipah virus-associated encephalitis outbreak, Siliguri, India
    Chadha MS, Comer JA, Lowe L, Rota PA, Rollin PE, Bellini WJ, et al.
    Emerg Infect Dis, 2006 Feb;12(2):235-40.
    PMID: 16494748
    During January and February 2001, an outbreak of febrile illness associated with altered sensorium was observed in Siliguri, West Bengal, India. Laboratory investigations at the time of the outbreak did not identify an infectious agent. Because Siliguri is in close proximity to Bangladesh, where outbreaks of Nipah virus (NiV) infection were recently described, clinical material obtained during the Siliguri outbreak was retrospectively analyzed for evidence of NiV infection. NiV-specific immunoglobulin M (IgM) and IgG antibodies were detected in 9 of 18 patients. Reverse transcription-polymerase chain reaction (RT-PCR) assays detected RNA from NiV in urine samples from 5 patients. Sequence analysis confirmed that the PCR products were derived from NiV RNA and suggested that the NiV from Siliguri was more closely related to NiV isolates from Bangladesh than to NiV isolates from Malaysia. NiV infection has not been previously detected in India.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  9. Introduction: Nipah virus--discovery and origin
    Chua KB
    Curr. Top. Microbiol. Immunol., 2012;359:1-9.
    PMID: 22782307 DOI: 10.1007/82_2012_218
    Until the Nipah outbreak in Malaysia in 1999, knowledge of human infections with the henipaviruses was limited to the small number of cases associated with the emergence of Hendra virus in Australia in 1994. The Nipah outbreak in Malaysia alerted the global public health community to the severe pathogenic potential and widespread distribution of these unique paramyxoviruses. This chapter briefly describes the initial discovery of Nipah virus and the challenges encountered during the initial identification and characterisation of the aetiological agent responsible for the outbreak of febrile encephalitis. The initial attempts to isolate Nipah virus from the bat reservoir host are also described.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  10. Fulltext Agricultural intensification, priming for persistence and the emergence of Nipah virus: a lethal bat-borne zoonosis
    Pulliam JR, Epstein JH, Dushoff J, Rahman SA, Bunning M, Jamaluddin AA, et al.
    J R Soc Interface, 2012 Jan 7;9(66):89-101.
    PMID: 21632614 DOI: 10.1098/rsif.2011.0223
    Emerging zoonoses threaten global health, yet the processes by which they emerge are complex and poorly understood. Nipah virus (NiV) is an important threat owing to its broad host and geographical range, high case fatality, potential for human-to-human transmission and lack of effective prevention or therapies. Here, we investigate the origin of the first identified outbreak of NiV encephalitis in Malaysia and Singapore. We analyse data on livestock production from the index site (a commercial pig farm in Malaysia) prior to and during the outbreak, on Malaysian agricultural production, and from surveys of NiV's wildlife reservoir (flying foxes). Our analyses suggest that repeated introduction of NiV from wildlife changed infection dynamics in pigs. Initial viral introduction produced an explosive epizootic that drove itself to extinction but primed the population for enzootic persistence upon reintroduction of the virus. The resultant within-farm persistence permitted regional spread and increased the number of human infections. This study refutes an earlier hypothesis that anomalous El Niño Southern Oscillation-related climatic conditions drove emergence and suggests that priming for persistence drove the emergence of a novel zoonotic pathogen. Thus, we provide empirical evidence for a causative mechanism previously proposed as a precursor to widespread infection with H5N1 avian influenza and other emerging pathogens.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  11. Epidemiology. Breaking the chain in Bangladesh
    Stone R
    Science, 2011 Mar 4;331(6021):1128-31.
    PMID: 21385693 DOI: 10.1126/science.331.6021.1128
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  12. 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/epidemiology
  13. From the Centers for Disease Control and Prevention. Outbreak of Hendra-like virus--Malaysia and Singapore, 1998-1999
    JAMA, 1999 May 19;281(19):1787-8.
    PMID: 10340348
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  14. The presence of Nipah virus in respiratory secretions and urine of patients during an outbreak of Nipah virus encephalitis in Malaysia
    Chua KB, Lam SK, Goh KJ, Hooi PS, Ksiazek TG, Kamarulzaman A, et al.
    J Infect, 2001 Jan;42(1):40-3.
    PMID: 11243752
    To study the excretion of Nipah virus in the upper respiratory secretions and urine of infected patients in relation to other clinical features.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  15. Encephalitis and retarded growth of chicks caused by Sitiawan virus, a new isolate belonging to the genus Flavivirus
    Kono Y, Tsukamoto K, Abd Hamid M, Darus A, Lian TC, Sam LS, et al.
    Am J Trop Med Hyg, 2001 5 19;63(1-2):94-101.
    PMID: 11358004
    A new virus named Sitiawan virus (SV) was isolated from sick broiler chicks in chicken embryos. The virus replicated well with cytopathogenic effect (CPE) in the chicken B-lymphocyte cell line LSCC-BK3. The virus was an enveloped RNA virus of approximately 41 nm in size with hemagglutinating activity (HA) to goose erythrocytes. It was cross-reactive with Japanese encephalitis virus (JEV), a member of flaviviruses by HA inhibition tests but not by cross-virus neutralization tests. The cDNA fragment of NS5 gene was amplified with primers corresponding to NS5 gene of flaviviruses. The nucleotide sequences were 92% homologous to Tembusu virus, a member of the mosquito-borne virus cluster of the genus Flavivirus. In cross-neutralization tests with Tembusu virus, antiserum to SV did not neutralize Tembusu virus, and antiserum to Tembusu virus neutralized more weakly to SV than against homologous virus. These results indicate that SV is a new virus which can be differentiated serologically from Tembusu virus but is otherwise similar with respect to nucleotide sequence. The virus causes encephalitis, growth retardation, and increased blood glucose levels in inoculated chicks.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  16. Emerging diseases. Malaysian researchers trace Nipah virus outbreak to bats
    Enserink M
    Science, 2000 Jul 28;289(5479):518-9.
    PMID: 10939954 DOI: 10.1126/science.289.5479.518
    Scientists are a step closer to unraveling a medical mystery that killed 105 people in Malaysia last year and destroyed the country's pig industry. The Nipah virus, which caused the disease, most likely originated in a native fruit bat species, Malaysian researchers reported here at a meeting last week. They say the findings will help Malaysian health authorities prevent future outbreaks of the Nipah virus. Others see the case as an argument for expanding research into infections that can leap the boundary between animals and humans.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  17. Fulltext Clinical features of Nipah virus encephalitis among pig farmers in Malaysia
    Goh KJ, Tan CT, Chew NK, Tan PS, Kamarulzaman A, Sarji SA, et al.
    N Engl J Med, 2000 Apr 27;342(17):1229-35.
    PMID: 10781618 DOI: 10.1056/NEJM200004273421701
    BACKGROUND: Between September 1998 and June 1999, there was an outbreak of severe viral encephalitis due to Nipah virus, a newly discovered paramyxovirus, in Malaysia.
    METHODS: We studied the clinical features of the patients with Nipah virus encephalitis who were admitted to a medical center in Kuala Lumpur. The case definition was based on epidemiologic, clinical, cerebrospinal fluid, and neuroimaging findings.
    RESULTS: Ninety-four patients with Nipah virus infection were seen from February to June 1999 (mean age, 37 years; ratio of male patients to female patients, 4.5 to 1). Ninety-three percent had had direct contact with pigs, usually in the two weeks before the onset of illness, suggesting that there was direct viral transmission from pigs to humans and a short incubation period. The main presenting features were fever, headache, dizziness, and vomiting. Fifty-two patients (55 percent) had a reduced level of consciousness and prominent brain-stem dysfunction. Distinctive clinical signs included segmental myoclonus, areflexia and hypotonia, hypertension, and tachycardia and thus suggest the involvement of the brain stem and the upper cervical spinal cord. The initial cerebrospinal fluid findings were abnormal in 75 percent of patients. Antibodies against Hendra virus were detected in serum or cerebrospinal fluid in 76 percent of 83 patients tested. Thirty patients (32 percent) died after rapid deterioration in their condition. An abnormal doll's-eye reflex and tachycardia were factors associated with a poor prognosis. Death was probably due to severe brain-stem involvement. Neurologic relapse occurred after initially mild disease in three patients. Fifty patients (53 percent) recovered fully, and 14 (15 percent) had persistent neurologic deficits.
    CONCLUSIONS: Nipah virus causes a severe, rapidly progressive encephalitis with a high mortality rate and features that suggest involvement of the brain stem. The infection is associated with recent contact with pigs.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  18. Trailing a virus
    Gibbs WW
    Sci. Am., 1999 Aug;281(2):80-7.
    PMID: 10443039
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  19. Nipah virus: an emergent paramyxovirus causing severe encephalitis in humans
    Bellini WJ, Harcourt BH, Bowden N, Rota PA
    J Neurovirol, 2005 Oct;11(5):481-7.
    PMID: 16287690
    Nipah virus is a recently emergent paramyxovirus that is capable of causing severe disease in both humans and animals. The first outbreak of Nipah virus occurred in Malaysia and Singapore in 1999 and, more recently, outbreaks were detected in Bangladesh. In humans, Nipah virus causes febrile encephalitis with respiratory syndrome that has a high mortality rate. The reservoir for Nipah virus is believed to be fruit bats, and humans are infected by contact with infected bats or by contact with an intermediate animal host such as pigs. Person to person spread of the virus has also been described. Nipah virus retains many of the genetic and biologic properties found in other paramyxoviruses, though it also has several unique characteristics. However, the virologic characteristics that allow the virus to cause severe disease over a broad host range, and the epidemiologic, environmental and virologic features that favor transmission to humans are unknown. This review summarizes what is known about the virology, epidemiology, pathology, diagnosis and control of this novel pathogen.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  20. Nipah viral encephalitis or Japanese encephalitis? MR findings in a new zoonotic disease
    Lim CC, Sitoh YY, Hui F, Lee KE, Ang BS, Lim E, et al.
    AJNR Am J Neuroradiol, 2000 Mar;21(3):455-61.
    PMID: 10730635
    BACKGROUND AND PURPOSE: An epidemic of suspected Japanese encephalitis occurred in Malaysia in 1998-1999 among pig farmers. In neighboring Singapore, an outbreak occurred among pig slaughterhouse workers. It was subsequently established that the causative agent in the outbreak was not the Japanese encephalitis virus but a previously unknown Hendra-like paramyxovirus named Nipah virus.

    METHODS: The brain MR images of eight patients with Nipah virus infection were reviewed. All patients tested negative for acute Japanese encephalitis virus. Seven patients had contrast-enhanced studies and six had diffusion-weighted examinations.

    RESULTS: All patients had multiple small bilateral foci of T2 prolongation within the subcortical and deep white matter. The periventricular region and corpus callosum were also involved. In addition to white matter disease, five patients had cortical lesions, three had brain stem involvement, and a single thalamic lesion was detected in one patient. All lesions were less than 1 cm in maximum diameter. In five patients, diffusion-weighted images showed increased signal. Four patients had leptomeningeal enhancement and four had enhancement of parenchymal lesions.

    CONCLUSION: The brain MR findings in patients infected with the newly discovered Nipah paramyxovirus are different from those of patients with Japanese encephalitis. In a zoonotic epidemic, this striking difference in the appearance and distribution of lesions is useful in differentiating these diseases. Diffusion-weighted imaging was advantageous in increasing lesion conspicuity.

    Matched MeSH terms: Encephalitis, Viral/epidemiology
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