Displaying publications 1 - 20 of 68 in total

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  1. Lu XF, Wang ZG, Wang BY
    Zhonghua Liu Xing Bing Xue Za Zhi, 2004 Jun;25(6):541-3.
    PMID: 15231143
    Matched MeSH terms: Encephalitis, Viral/epidemiology*; Encephalitis, Viral/transmission; Encephalitis, Viral/virology
  2. Easton A
    BMJ, 1999 May 08;318(7193):1232.
    PMID: 10231244
    Matched MeSH terms: Encephalitis, Viral/epidemiology*; Encephalitis, Viral/transmission; Encephalitis, Viral/veterinary; Encephalitis, Viral/virology
  3. 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; Encephalitis, Viral/pathology
  4. Wong KT
    Acta Neuropathol, 2010 Sep;120(3):317-25.
    PMID: 20652579 DOI: 10.1007/s00401-010-0720-z
    In the last few decades, there is an increasing emergence and re-emergence of viruses, such as West Nile virus, Enterovirus 71 and henipaviruses that cause epidemic viral encephalitis and other central nervous system (CNS) manifestations. The mortality and morbidity associated with these outbreaks are significant and frequently severe. While aspects of epidemiology, basic virology, etc., may be known, the pathology and pathogenesis are often less so, partly due to a lack of interest among pathologists or because many of these infections are considered "third world" diseases. In the study of epidemic viral encephalitis, the pathologist's role in unravelling the pathology and pathogenesis is critical. The novel henipavirus infection is a good example. The newly created genus Henipavirus within the family Paramyxoviridae consists of two viruses, viz., Hendra virus and Nipah virus. These two viruses emerged in Australia and Asia, respectively, to cause severe encephalitides in humans and animals. Studies show that the pathological features of the acute encephalitis caused by henipaviruses are similar and a unique dual pathogenetic mechanism of vasculitis-induced microinfarction and parenchymal cell infection in the CNS (mainly neurons) and other organs causes severe tissue damage. Both viruses can cause relapsing encephalitis months and years after the acute infection due to a true recurrent infection as evidenced by the presence of virus in infected cells. Future emerging viral encephalitides will no doubt continue to pose considerable challenges to the neuropathologist, and as the West Nile virus outbreak demonstrates, even economically advanced nations are not spared.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*; Encephalitis, Viral/pathology*
  5. Looi LM, Chua KB
    Malays J Pathol, 2007 Dec;29(2):63-7.
    PMID: 19108397 MyJurnal
    The Nipah virus outbreak in Malaysia (September 1998 to May 1999) resulted in 265 cases of acute encephalitis with 105 deaths, and near collapse of the billion-dollar pig-farming industry. Because it was initially attributed to Japanese encephalitis, early control measures were ineffective, and the outbreak spread to other parts of Malaysia and nearby Singapore. The isolation of the novel aetiological agent, the Nipah virus (NiV), from the cerebrospinal fluid of an outbreak victim was the turning point which led to outbreak control 2 months later. Together with the Hendra virus, NiV is now recognised as a new genus, Henipavirus (Hendra + Nipah), in the Paramyxoviridae family. Efforts of the local and international scientific community have since elucidated the epidemiology, clinico-pathophysiology and pathogenesis of this new disease. Humans contracted the infection from close contact with infected pigs, and formed the basis for pig-culling that eventually stopped the outbreak. NiV targeted medium-sized and small blood vessels resulting in endothelial multinucleated syncytia and fibrinoid necrosis. Autopsies revealed disseminated cerebral microinfarctions resulting from vasculitis-induced thrombosis and direct neuronal involvement. The discovery of NiV in the urine and saliva of Malaysian Island flying foxes (Pteropus hypomelanus and Petropus vampyrus) implicated these as natural reservoir hosts of NiV. It is probable that initial transmission of NiV from bats to pigs occurred in late 1997/early 1998 through contamination of pig swill by bat excretions, as a result of migration of these forest fruitbats to cultivated orchards and pig-farms, driven by fruiting failure of forest trees during the El Nino-related drought and anthropogenic fires in Indonesia in 1997-1998. This outbreak emphasizes the need for sharing information of any unusual illnesses in animals and humans, an open-minded approach and close collaboration and co-ordination between the medical profession, veterinarians and wildlife specialists in the investigation of such illnesses. Environmental mismanagement (such as deforestation and haze) has far-reaching effects, including encroachment of wildlife into human habitats and the introduction of zoonotic infections into domestic animals and humans.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*; Encephalitis, Viral/pathology; Encephalitis, Viral/transmission
  6. Lo MK, Rota PA
    J Clin Virol, 2008 Dec;43(4):396-400.
    PMID: 18835214 DOI: 10.1016/j.jcv.2008.08.007
    Nipah virus first emerged in Malaysia and Singapore between 1998 and 1999, causing severe febrile encephalitis in humans with a mortality rate of close to 40%. In addition, a significant portion of those recovering from acute infection had relapse encephalitis and long-term neurological defects. Since its initial outbreak, there have been numerous outbreaks in Bangladesh and India, in which the mortality rate rose to approximately 70%. These subsequent outbreaks were distinct from the initial outbreak, both in their epidemiology and in their clinical presentations. Recent developments in diagnostics may expedite disease diagnosis and outbreak containment, while progress in understanding the molecular biology of Nipah virus could lead to novel therapeutics and vaccines for this deadly pathogen.
    Matched MeSH terms: Encephalitis, Viral/mortality; Encephalitis, Viral/epidemiology*; Encephalitis, Viral/virology
  7. Wong SC, Ooi MH, Wong MN, Tio PH, Solomon T, Cardosa MJ
    J Neurol Neurosurg Psychiatry, 2001 Oct;71(4):552-4.
    PMID: 11561048
    Nipah virus is a newly discovered paramyxovirus transmitted directly from pigs to humans. During a large encephalitis outbreak in Malaysia and Singapore in 1998-9, most patients presented acutely. A 12 year old child is described who developed encephalitis 4 months after exposure to the virus. She was diagnosed by a new indirect IgG enzyme linked immunosorbent assay (ELISA), which is also described. The late presentation and IgG subclass responses had similarities to subacute sclerosing panencephalitis. Nipah virus should be considered in patients with encephalitis even months after their possible exposure.
    Matched MeSH terms: Encephalitis, Viral/diagnosis; Encephalitis, Viral/immunology*; Encephalitis, Viral/transmission
  8. Farrar JJ
    Lancet, 1999 Oct 9;354(9186):1222-3.
    PMID: 10520625
    Matched MeSH terms: Encephalitis, Viral/diagnosis; Encephalitis, Viral/mortality; Encephalitis, Viral/epidemiology*
  9. Tan CT, Wong KT
    Ann Acad Med Singap, 2003 Jan;32(1):112-7.
    PMID: 12625108
    INTRODUCTION: Between September 1998 and June 1999, there was a severe outbreak of viral encephalitis among the pig farm workers in Malaysia.

    METHODS: This is a review of the published literature related to the outbreak with the focus on human diseases.

    RESULTS: The encephalitis was caused by a newly discovered paramyxovirus related to Hendra virus, later named Nipah virus. There were 265 patients with acute encephalitis. The disease is thought to spread from pig to man through close contact. The risk of human-to-human spread is thought to below. The disease affected mainly adult Chinese males, half of whom had affected family members. The disease presented mainly as acute encephalitis with a short incubation period of less than two weeks, with the main symptoms of fever, headache, and giddiness followed by coma. Distinctive clinical signs include segmental myoclonus, areflexia and hypotonia, hypertension, and tachycardia. Initial cerebrospinal fluid was abnormal in 75% of patients. Serology was helpful in confirming the diagnosis. Magnetic resonance imaging showed distinctive changes of multiple, discrete, and small high signal lesions, best seen with fluid-attenuated inversion recovery (FLAIR) sequences. Mortality was high at 40% and death was probably due to severe brainstem involvement. The main necropsy finding in acute encephalitis was that of disseminated microinfarction associated with vasculitis and direct neuronal involvement. Ribavirin was able to reduce the mortality by 36%. Relapse encephalitis was seen in 7.5% of those who recovered from acute encephalitis, and late-onset encephalitis in 3.4% of those with initial non-encephalitic or asymptomatic diseases. The mean interval between initial illness and the onset of the complication was 8.4 months. The relapse and late-onset encephalitis which manifested as focal encephalitis arose from recurrent infection.

    CONCLUSION: Nipah virus, a recently discovered paramyxovirus, causes a unique encephalitis with high mortality as well as relapse and late-onset encephalitis. The infection is mainly spread from pigs to man.

    Matched MeSH terms: Encephalitis, Viral/epidemiology*; Encephalitis, Viral/transmission; Encephalitis, Viral/virology*
  10. Caplan CE
    CMAJ, 1999 Jun 15;160(12):1697.
    PMID: 10410627
    Matched MeSH terms: Encephalitis, Viral/epidemiology; Encephalitis, Viral/transmission; Encephalitis, Viral/virology*
  11. Chong HT, Kunjapan SR, Thayaparan T, Tong J, Petharunam V, Jusoh MR, et al.
    Can J Neurol Sci, 2002 Feb;29(1):83-7.
    PMID: 11858542
    BACKGROUND: An outbreak of viral encephalitis occurred among pig industry workers in Malaysia in September 1998 to April 1999. The encephalitis was attributed to a new paramyxovirus, Nipah virus. This is a description of the clinical features of 103 patients treated in the Seremban Hospital with characterization of the prognostic factors.

    METHODS: Clinical case records and laboratory investigations were reviewed. The case definition was: patients from the outbreak area, direct contact or in close proximity with pigs, clinical or CSF features of encephalitis.

    RESULTS: The mean age was 38 years, 89% were male, 58% were ethnic Chinese, 78% were pig farm owners or hired workers. The mean incubation period was 10 days. The patients typically presented with nonspecific systemic symptoms of fever, headache, myalgia and sore throat. Seizures and focal neurological signs were seen in 16% and 5% respectively. In the more severe cases, this was followed by drowsiness and deteriorating consciousness requiring ventilation in 61%. Autonomic disturbances and myoclonic jerks were common features. The mortality was high at 41%. Systolic hypertension, tachycardia and high fever were associated with poor outcome. On the other hand, 40% recovered fully. As for the other 19%, the residual neurological signs were mostly mild.

    CONCLUSION: Nipah virus caused an encephalitis illness with short incubation period and high mortality. The prognosis for the survivors was good.

    Matched MeSH terms: Encephalitis, Viral/diagnosis*; Encephalitis, Viral/ethnology; Encephalitis, Viral/mortality; Encephalitis, Viral/epidemiology*
  12. Sarji SA, Abdullah BJ, Goh KJ, Tan CT, Wong KT
    AJR Am J Roentgenol, 2000 Aug;175(2):437-42.
    PMID: 10915690
    The newly discovered Nipah virus causes an acute febrile encephalitic illness in humans that is associated with a high mortality. The purpose of this study is to describe the MR imaging findings of Nipah encephalitis.
    Matched MeSH terms: Encephalitis, Viral/pathology*
  13. Chua KB
    Malays J Pathol, 2010 Dec;32(2):69-73.
    PMID: 21329176 MyJurnal
    The outbreak of Nipah virus, affecting pigs and pig-farm workers, was first noted in September 1998 in the north-western part of peninsular Malaysia. By March 1999, the outbreak had spread to other pig-farming areas of the country, inclusive of the neighbouring country, Singapore. A total of 283 human cases of viral encephalitis with 109 deaths were recorded in Malaysia from 29 September 1998 to December 1999. During the outbreak period, a number of surveillances under three broad groups; Surveillance in Human Health Sector, Surveillance in Animal Health Sector, and Surveillance for the Reservoir Hosts, were carried out to determine the prevalence, risk of virus infections and transmission in human and swine populations as well as the source and reservoir hosts of Nipah virus. Surveillance data showed that the virus spread rapidly among pigs within infected farms and transmission was attributed to direct contact with infective excretions and secretions. The spread of the virus among pig farms within and between states of peninsular Malaysia was due to movement of pigs. The transmission of the virus to humans was through close contact with infected pigs. Human to human transmission was considered a rare event though the Nipah virus could be isolated from saliva, urine, nasal and pharyngeal secretions of patients. Field investigations identified fruitbats of the Pteropid species as the natural reservoir hosts of the viruses. The outbreak was effectively brought under control following the discovery of the virus and institution of correct control measures through a combined effort of multi-ministerial and multidisciplinary teams working in close co-operation and collaboration with other international agencies.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*; Encephalitis, Viral/transmission; Encephalitis, Viral/virology
  14. Tan CT, Goh KJ, Wong KT, Sarji SA, Chua KB, Chew NK, et al.
    Ann Neurol, 2002 Jun;51(6):703-8.
    PMID: 12112075
    An outbreak of infection with the Nipah virus, a novel paramyxovirus, occurred among pig farmers between September 1998 and June 1999 in Malaysia, involving 265 patients with 105 fatalities. This is a follow-up study 24 months after the outbreak. Twelve survivors (7.5%) of acute encephalitis had recurrent neurological disease (relapsed encephalitis). Of those who initially had acute nonencephalitic or asymptomatic infection, 10 patients (3.4%) had late-onset encephalitis. The mean interval between the first neurological episode and the time of initial infection was 8.4 months. Three patients had a second neurological episode. The onset of the relapsed or late-onset encephalitis was usually acute. Common clinical features were fever, headache, seizures, and focal neurological signs. Four of the 22 relapsed and late-onset encephalitis patients (18%) died. Magnetic resonance imaging typically showed patchy areas of confluent cortical lesions. Serial single-photon emission computed tomography showed the evolution of focal hyperperfusion to hypoperfusion in the corresponding areas. Necropsy of 2 patients showed changes of focal encephalitis with positive immunolocalization for Nipah virus antigens but no evidence of perivenous demyelination. We concluded that a unique relapsing and remitting encephalitis or late-onset encephalitis may result as a complication of persistent Nipah virus infection in the central nervous system.
    Matched MeSH terms: Encephalitis, Viral/pathology; Encephalitis, Viral/physiopathology*; Encephalitis, Viral/prevention & control
  15. Chow VT, Tambyah PA, Yeo WM, Phoon MC, Howe J
    J Clin Virol, 2000 Dec;19(3):143-7.
    PMID: 11090749
    BACKGROUND: between 1998 and 1999, an outbreak of potentially fatal viral encephalitis erupted among pig farm workers in West Malaysia, and later spread to Singapore where abattoir workers were afflicted. Although Japanese encephalitis virus was initially suspected, the predominant aetiologic agent was subsequently confirmed to be Nipah virus, a novel paramyxovirus related to but distinct from Hendra virus.

    OBJECTIVE: to describe a case of Nipah virus encephalitis in a pig farm worker from Malaysia.

    STUDY DESIGN: the clinical, laboratory and radiological findings of this patient were scrutinized. Special emphasis was placed on the electron microscopic analysis of the cerebrospinal fluid (CSF) specimen from this patient.

    RESULTS: the neurological deficits indicative of cerebellar involvement were supported by the magnetic resonance imaging that showed prominent cerebellar and brainstem lesions. CSF examination provided further evidence of viral encephalitis. Complement fixation and/or RT-PCR assays were negative for Japanese encephalitis, herpes simplex, measles and mumps viruses. ELISA for detecting IgM and IgG antibodies against Hendra viral antigens were equivocal for the CSF specimen, and tested initially negative for the first serum sample but subsequently positive for the repeat serum sample. Transmission electron microscopy of negatively-stained preparations of CSF revealed enveloped virus-like structures fringed with surface projections as well as nucleocapsids with distinctive helical and herringbone patterns, features consistent with those of other paramyxoviruses, including Hendra virus.

    CONCLUSION: this case report reiterates the relevant and feasible role of diagnostic electron microscopy for identifying and/or classifying novel or emerging viral pathogens for which sufficiently specific and sensitive tests are lacking.

    Matched MeSH terms: Encephalitis, Viral/blood; Encephalitis, Viral/diagnosis*; Encephalitis, Viral/virology
  16. Ong KC, Wong KT
    Brain Pathol, 2015 Sep;25(5):605-13.
    PMID: 26276024 DOI: 10.1111/bpa.12278
    The genus Henipavirus within the family Paramyxoviridae includes the Hendra virus (HeV) and Nipah virus (NiV) which were discovered in the 1990s in Australia and Malaysia, respectively, after emerging to cause severe and often fatal outbreaks in humans and animals. While HeV is confined to Australia, more recent NiV outbreaks have been reported in Bangladesh, India and the Philippines. The clinical manifestations of both henipaviruses in humans appear similar, with a predominance of an acute encephalitic syndrome. Likewise, the pathological features are similar and characterized by disseminated, multi-organ vasculopathy comprising endothelial infection/ulceration, vasculitis, vasculitis-induced thrombosis/occlusion, parenchymal ischemia/microinfarction, and parenchymal cell infection in the central nervous system (CNS), lung, kidney and other major organs. This unique dual pathogenetic mechanism of vasculitis-induced microinfarction and neuronal infection causes severe tissue damage in the CNS. Both viruses can also cause relapsing encephalitis months and years after the acute infection. Many animal models studied to date have largely confirmed the pathology of henipavirus infection, and provided the means to test new therapeutic agents and vaccines. As the bat is the natural host of henipaviruses and has worldwide distribution, spillover events into human populations are expected to occur in the future.
    Matched MeSH terms: Encephalitis, Viral/diagnosis*; Encephalitis, Viral/pathology; Encephalitis, Viral/therapy
  17. Matlani M, Chakravarti A, Rawal A, Kashyap B, Gurtoo A
    Trop Doct, 2009 Apr;39(2):115-6.
    PMID: 19299303 DOI: 10.1258/td.2008.080257
    As well as dengue fever (DF) and dengue haemorrhagic fever-dengue shock syndrome (DHF/DSS), other atypical manifestations of dengue virus infection have also been reported. The frequency of CNS involvement in dengue remains unknown, although isolated cases with neurological manifestations have been reported in Southeast Asia, Malaysia, Burma, Puerto Rico and India. We present two cases of encephalitis associated with DF and DHF from New Delhi, India.
    Matched MeSH terms: Encephalitis, Viral/diagnosis*; Encephalitis, Viral/virology
  18. Ternhag A, Penttinen P
    Lakartidningen, 2005 Apr;102(14):1046-7.
    PMID: 15892474
    Matched MeSH terms: Encephalitis, Viral/transmission; Encephalitis, Viral/virology
  19. Marra CM
    Semin Neurol, 2000;20(3):323-7.
    PMID: 11051296
    As the 21st century begins, several outbreaks of encephalitis have been reported. An examination of these outbreaks brings into focus important epidemiological developments. Specifically, urbanization and encroachment on natural environments, the ease of world travel, and global trade can lead to spread of vectors and viruses from the developing world to the developed world. This review focuses on two recent epidemics of encephalitis: West Nile virus encephalitis in the eastern United States and Nipah virus encephalitis in Malaysia and Singapore. These examples demonstrate spread of a known viral agent from an endemic area to an area in which it had not previously been found and identification of a new viral agent. Infectious diseases in the developed world once considered "exotic" are now potential threats to all patients.
    Matched MeSH terms: Encephalitis, Viral/diagnosis*; Encephalitis, Viral/epidemiology*
  20. Okabe N, Morita K
    Uirusu, 2000 Jun;50(1):27-33.
    PMID: 10998976
    Matched MeSH terms: Encephalitis, Viral/epidemiology*; Encephalitis, Viral/transmission
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