Displaying all 18 publications

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  1. A novel approach for collecting samples from fruit bats for isolation of infectious agents
    Chua KB
    Microbes Infect., 2003 May;5(6):487-90.
    PMID: 12758277
    During the outbreak of Nipah virus encephalitis involving pigs and humans in peninsular Malaysia in 1998/1999, a conventional approach was initially undertaken to collect specimens from fruit bats by mist-netting and shooting, as an integral part of wildlife surveillance of the natural reservoir host of Nipah virus. This study describes a novel method of collecting fruit bats' urine samples using plastic sheets for isolation of Nipah virus. This novel approach resulted in the isolation of several other known and unidentified infectious agents besides Nipah virus.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  2. Nipah virus infection in bats (order Chiroptera) in peninsular Malaysia
    Yob JM, Field H, Rashdi AM, Morrissy C, van der Heide B, Rota P, et al.
    Emerg Infect Dis, 2001 May-Jun;7(3):439-41.
    PMID: 11384522
    Nipah virus, family Paramyxoviridae, caused disease in pigs and humans in peninsular Malaysia in 1998-99. Because Nipah virus appears closely related to Hendra virus, wildlife surveillance focused primarily on pteropid bats (suborder Megachiroptera), a natural host of Hendra virus in Australia. We collected 324 bats from 14 species on peninsular Malaysia. Neutralizing antibodies to Nipah virus were demonstrated in five species, suggesting widespread infection in bat populations in peninsular Malaysia.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  3. Nipah-virus encephalitis--investigation of a new infection
    Farrar JJ
    Lancet, 1999 Oct 9;354(9186):1222-3.
    PMID: 10520625
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  4. Fulltext Novel Alphacoronaviruses and Paramyxoviruses Cocirculate with Type 1 and Severe Acute Respiratory System (SARS)-Related Betacoronaviruses in Synanthropic Bats of Luxembourg
    Pauly M, Pir JB, Loesch C, Sausy A, Snoeck CJ, Hübschen JM, et al.
    Appl Environ Microbiol, 2017 09 15;83(18).
    PMID: 28710271 DOI: 10.1128/AEM.01326-17
    Several infectious disease outbreaks with high mortality in humans have been attributed to viruses that are thought to have evolved from bat viruses. In this study from Luxembourg, the genetic diversity and epidemiology of paramyxoviruses and coronaviruses shed by the bat species Rhinolophus ferrumequinum and Myotis emarginatus were evaluated. Feces collection (n = 624) was performed longitudinally in a mixed-species colony in 2015 and 2016. In addition, feces (n = 254) were collected cross-sectionally from six Myotis emarginatus colonies in 2016. By use of degenerate primers in a nested format, overall prevalences of 1.1% (10/878) and 4.9% (43/878) were determined for paramyxoviruses and coronaviruses. Sequences of the partial RNA-dependent RNA polymerase and spike glycoprotein genes of coronaviruses, as well as sequences of the partial L gene of paramyxoviruses, were obtained. Novel paramyxovirus and Alphacoronavirus strains were identified in different Myotis emarginatus colonies, and severe acute respiratory syndrome (SARS)-related Betacoronavirus strains were shed by Rhinolophus ferrumequinum Logistic regression revealed that the level of Alphacoronavirus shedding was highest in July (odds ratio, 2.8; P < 0.01), probably due to periparturient stress. Phylogenetic analyses point to close virus-host coevolution, and the high genetic similarity of the study strains suggests that the Myotis emarginatus colonies in Luxembourg are socially connected. Most interestingly, we show that bats also host Betacoronavirus1 strains. The high similarity of the spike gene sequences of these viruses with mammalian Betacoronavirus 1 strains may be of concern. Both the SARS-related and Betacoronavirus 1 strains detected in bats in Luxembourg may cross the species barrier after a host adaptation process.IMPORTANCE Bats are a natural reservoir of a number of zoonotic pathogens. Several severe outbreaks in humans (e.g., a Nipah virus outbreak in Malaysia in 1998, and the almost global spread of severe acute respiratory syndrome in 2003) have been caused by bat-borne viruses that were transmitted to humans mostly after virus adaptation (e.g., in intermediate animal hosts). Despite the indigenousness of bat species that host viruses with suspected zoonotic potential and despite the zoonotic transmission of European bat 1 lyssavirus in Luxembourg, knowledge about the diversity and epidemiology of bat viruses remains limited in this country. Moreover, in contrast to other European countries, bat viruses are currently not included in the national surveillance activities of this land-locked country. We suggest that this gap in disease surveillance should be addressed, since we show here that synanthropic bats host viruses that may be able to cross the species barrier.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  5. Isolation of Nipah virus from Malaysian Island flying-foxes
    Chua KB, Koh CL, Hooi PS, Wee KF, Khong JH, Chua BH, et al.
    Microbes Infect., 2002 Feb;4(2):145-51.
    PMID: 11880045
    In late 1998, Nipah virus emerged in peninsular Malaysia and caused fatal disease in domestic pigs and humans and substantial economic loss to the local pig industry. Surveillance of wildlife species during the outbreak showed neutralizing antibodies to Nipah virus mainly in Island flying-foxes (Pteropus hypomelanus) and Malayan flying-foxes (Pteropus vampyrus) but no virus reactive with anti-Nipah virus antibodies was isolated. We adopted a novel approach of collecting urine from these Island flying-foxes and swabs of their partially eaten fruits. Three viral isolates (two from urine and one from a partially eaten fruit swab) that caused Nipah virus-like syncytial cytopathic effect in Vero cells and stained strongly with Nipah- and Hendra-specific antibodies were isolated. Molecular sequencing and analysis of the 11,200-nucleotide fragment representing the beginning of the nucleocapsid gene to the end of the glycoprotein gene of one isolate confirmed the isolate to be Nipah virus with a sequence deviation of five to six nucleotides from Nipah virus isolated from humans. The isolation of Nipah virus from the Island flying-fox corroborates the serological evidence that it is one of the natural hosts of the virus.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  6. Fatal encephalitis due to Nipah virus among pig-farmers in Malaysia
    Chua KB, Goh KJ, Wong KT, Kamarulzaman A, Tan PS, Ksiazek TG, et al.
    Lancet, 1999 Oct 9;354(9186):1257-9.
    PMID: 10520635
    Between February and April, 1999, an outbreak of viral encephalitis occurred among pig-farmers in Malaysia. We report findings for the first three patients who died.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  7. Diagnosis of nipah virus encephalitis by electron microscopy of cerebrospinal fluid
    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: Paramyxovirinae/isolation & purification*
  8. A rapid immune plaque assay for the detection of Hendra and Nipah viruses and anti-virus antibodies
    Crameri G, Wang LF, Morrissy C, White J, Eaton BT
    J Virol Methods, 2002 Jan;99(1-2):41-51.
    PMID: 11684302
    Rapid immune plaque assays have been developed to quantify biohazard level 4 agents Hendra and Nipah viruses and detect neutralising antibodies to both viruses. The methods rely on the fact that both viruses rapidly generate large syncytia in monolayers of Vero cells within 24 h and that monospecific antiserum to the Hendra virus phosphoprotein (P) detects that protein in both Hendra and Nipah virus-induced syncytia after methanol fixation of virus-infected cells. The P protein is a constituent of the ribonucleoprotein core of the viruses and a component of the viral RNA-dependent RNA polymerase and is made in significant amounts in infected cells. In the immune plaque assay, anti-P antibody is localised by an alkaline phosphatase-linked second antibody and the Western blot substrates 5-bromo-4-chloro-3-indolyl phosphate and p-nitro blue tetrazolium. A modification of the rapid immune plaque assay was also used to detect antibodies to Nipah virus in a panel of porcine field sera from Malaysia and the results showed good agreement between the immune plaque assay and a traditional serum neutralisation test. After methanol fixation, plates can be stored for up to 7 months and may be used in the immune plaque assay to complement the enzyme-linked immunosorbent assay screening of sera for antibodies to Nipah virus. At present, all enzyme-linked immunosorbent assay positive sera are subject to confirmatory serum neutralisation tests. Use of the immune plaque assay may reduce the number of sera requiring confirmatory neutralisation testing for Nipah virus antibodies under biohazard level 4 conditions by identifying those that generate false positive in the enzyme-linked immunosorbent assay.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  9. 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: Paramyxovirinae/isolation & purification
  10. Treatment of acute Nipah encephalitis with ribavirin
    Chong HT, Kamarulzaman A, Tan CT, Goh KJ, Thayaparan T, Kunjapan SR, et al.
    Ann Neurol, 2001 Jun;49(6):810-3.
    PMID: 11409437
    Nipah virus, a newly identified paramyxovirus caused a severe outbreak of encephalitis in Malaysia with high fatalities. We report an open-label trial of ribavirin in 140 patients, with 54 patients who were managed prior to the availability of ribavirin or refused treatment as control. There were 45 deaths (32%) in the ribavirin arm; 29 deaths (54%) occurred in the control arm. This represents a 36% reduction in mortality (p = 0.011). There was no associated serious side effect. This study suggests that ribavirin is able to reduce the mortality of acute Nipah encephalitis.
    Matched MeSH terms: Paramyxovirinae/isolation & purification
  11. 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: Paramyxovirinae/isolation & purification*
  12. 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: Paramyxovirinae/isolation & purification*
  13. [Emergence of transmissible disorders, a continuous process--a new type of viral meningoencephalitis]
    Ivan A, Indrei LL
    Rev Med Chir Soc Med Nat Iasi, 2000 Apr-Jun;104(2):51-5.
    PMID: 12089991
    In the interval 1994-1999, in Australia, Malaysia and Singapore, epizootic and epidemiological episodes of meningoencephalitis and severe acute respiratory syndromes were reported. Highly lethal in horses, swine and humans, the episodes were proved to be caused by the "new" viruses Hendra (HeV) and Nipah (NiV). At the same time three "new" viral agents have been isolated: Lyssavirus, Menanglevirus and Tupaia paramyxovirus. The intense contemporary circulation of people, animals and food products together with changes in human ecosystem favor new relations between humans and the "natural reservoirs" of biologic agents with a pathogenic potential for domestic and peridomestic animals and humans.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  14. A cohort study of health care workers to assess nosocomial transmissibility of Nipah virus, Malaysia, 1999
    Mounts AW, Kaur H, Parashar UD, Ksiazek TG, Cannon D, Arokiasamy JT, et al.
    J Infect Dis, 2001 Mar 1;183(5):810-3.
    PMID: 11181159 DOI: 10.1086/318822
    During 1998-1999, an outbreak of Nipah virus encephalitis occurred in Malaysia. To assess the possibility of nosocomial transmission, 338 health care workers (HCWs) exposed and 288 HCWs unexposed to outbreak-related patients were surveyed, and their serum samples were tested for anti-Nipah virus antibody. Needlestick injuries were reported by 12 (3%) HCWs, mucosal surface exposure to body fluids by 39 (11%), and skin exposure to body fluids by 89 (25%). No encephalitis occurred in either group. Three exposed and no unexposed HCWs tested positive by EIA for IgG antibodies. It is likely that these 3 were false positives; no IgM response occurred, and the serum samples were negative for anti-Nipah virus neutralizing antibodies. The risk of nosocomial transmission of Nipah virus appears to be low; however, given the high case-fatality rate and the presence of virus in respiratory secretions and urine of some patients, standard and droplet infection-control practices should be maintained with these patients.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
  15. 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: Paramyxovirinae/isolation & purification*
  16. 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: Paramyxovirinae/isolation & purification
  17. Experimental Nipah virus infection in pigs and cats
    Middleton DJ, Westbury HA, Morrissy CJ, van der Heide BM, Russell GM, Braun MA, et al.
    J Comp Pathol, 2002 Feb-Apr;126(2-3):124-36.
    PMID: 11945001 DOI: 10.1053/jcpa.2001.0532
    A human isolate of Nipah virus from an outbreak of febrile encephalitis in Malaysia that coincided with a field outbreak of disease in pigs was used to infect eight 6-week-old pigs orally or subcutaneously and two cats oronasally. In pigs, the virus induced a respiratory and neurological syndrome consistent with that observed in the Malaysian pigs. Not all the pigs showed clinical signs, but Nipah virus was recovered from the nose and oropharynx of both clinically and sub-clinically infected animals. Natural infection of in-contact pigs, which was readily demonstrated, appeared to be acute and self-limiting. Subclinical infections occurred in both inoculated and in-contact pigs. Respiratory and neurological disease was also produced in the cats, with recovery of virus from urine as well as from the oropharynx. The clinical and pathological syndrome induced by Nipah virus in cats was comparable with that associated with Hendra virus infection in this species, except that in fatal infection with Nipah virus there was extensive inflammation of the respiratory epithelium, associated with the presence of viral antigen. Viral shedding via the nasopharynx, as observed in pigs and cats in the present study, was not a regular feature of earlier reports of experimental Hendra virus infection in cats and horses. The findings indicate the possibility of field transmission of Nipah virus between pigs via respiratory and oropharyngeal secretions.
    Matched MeSH terms: Paramyxovirinae/isolation & purification
  18. Nipah virus infection: pathology and pathogenesis of an emerging paramyxoviral zoonosis
    Wong KT, Shieh WJ, Kumar S, Norain K, Abdullah W, Guarner J, et al.
    Am J Pathol, 2002 Dec;161(6):2153-67.
    PMID: 12466131
    In 1998, an outbreak of acute encephalitis with high mortality rates among pig handlers in Malaysia led to the discovery of a novel paramyxovirus named Nipah virus. A multidisciplinary investigation that included epidemiology, microbiology, molecular biology, and pathology was pivotal in the discovery of this new human infection. Clinical and autopsy findings were derived from a series of 32 fatal human cases of Nipah virus infection. Diagnosis was established in all cases by a combination of immunohistochemistry (IHC) and serology. Routine histological stains, IHC, and electron microscopy were used to examine autopsy tissues. The main histopathological findings included a systemic vasculitis with extensive thrombosis and parenchymal necrosis, particularly in the central nervous system. Endothelial cell damage, necrosis, and syncytial giant cell formation were seen in affected vessels. Characteristic viral inclusions were seen by light and electron microscopy. IHC analysis showed widespread presence of Nipah virus antigens in endothelial and smooth muscle cells of blood vessels. Abundant viral antigens were also seen in various parenchymal cells, particularly in neurons. Infection of endothelial cells and neurons as well as vasculitis and thrombosis seem to be critical to the pathogenesis of this new human disease.
    Matched MeSH terms: Paramyxovirinae/isolation & purification*
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