Displaying publications 1 - 20 of 39 in total

Abstract:
Sort:
  1. Fulltext Nipah virus among military personnel involved in pig culling during an outbreak of encephalitis in Malaysia, 1998-1999
    Ali R, Mounts AW, Parashar UD, Sahani M, Lye MS, Isa MM, et al.
    Emerg Infect Dis, 2001 Jul-Aug;7(4):759-61.
    PMID: 11592256
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  2. Risk factors for Nipah virus transmission, Port Dickson, Negeri Sembilan, Malaysia: results from a hospital-based case-control study
    Amal NM, Lye MS, Ksiazek TG, Kitsutani PD, Hanjeet KS, Kamaluddin MA, et al.
    Southeast Asian J. Trop. Med. Public Health, 2000 Jun;31(2):301-6.
    PMID: 11127330
    A hospital-based case-control study of viral encephalitis was carried out at Port Dickson Hospital, in the state of Negeri Sembilan, Malaysia. Between March and May 1999, 69 clinically diagnosed viral encephalitis cases and 31 controls were interviewed. Job histories on pig farming activities were assessed by a group of epidemiologists and veterinary surgeons. Results show that among clinical cases of viral encephalitis, 52 (75.4%) cases were diagnosed to have Nipah virus infection based on positive serology for antibodies to the cross-reacting Hendra virus antigen. The Nipah virus encephalitis was significantly associated with a history of working in pig farms (p < 0.001, OR = 196.0, 95% CI = 20.4-4741.6), history of contact with animals (p < 0.001, OR = 38.3, 95% CI = 8.2-209.0) and with history of direct contact with pigs (p = 0.002, OR = 34.4, 95% CI = 2.6-1,024.4). The Nipah virus infection was also significantly associated with history of feeding/cleaning pigs (p < 0.001, OR = 102, 95% CI = 11.9-2,271.5). These results provide evidence that involvement in pig farming activities is significantly associated with the risk of getting Nipah virus infection. They are potential risk factors for Nipah virus transmission in the major pig-producing area of Bukit Pelandok, Port Dickson Negeri Sembilan.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  3. 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*
  4. Update on the new virus in Malaysia
    Caplan CE
    CMAJ, 1999 Jun 15;160(12):1697.
    PMID: 10410627
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  5. Fulltext Japanese encephalitis virus is an important cause of encephalitis among children in Penang
    Cardosa MJ, Hooi TP, Kaur P
    Southeast Asian J. Trop. Med. Public Health, 1995 Jun;26(2):272-5.
    PMID: 8629059
    This study was carried out to determine if Japanese encephalitis virus is an important causative agent of viral encephalitis among pediatric admissions in Penang, Malaysia. 195 children with CNS symptoms and 482 children with non-specific febrile illness admitted into the Pediatric Ward of Penang Hospital during a 16 month period were entered into the study. The presence in serum of cerebrospinal fluid (csf) of Japanese encephalitis virus (JEV) specific IgM was determined by an IgM capture ELISA and cytomegalovirus (CMV) specific IgM was determined using a commercially available kit (Behringwerke AG). It was determined that 5 of 13 children with a discharge diagnosis of viral encephalitis had JEV specific IgM in csf, indicating that 38.5% of the viral encephalitis cases was due to JEV. One of the non-JEV cases was found to have mumps virus specific IgM in csf, while no etiology was determined for the other cases. It was also determined that 4 of the 195 (2.1%) cases with CNS symptoms had IgM to CMV, suggesting CMV may be an agent of encephalopathy in children in Penang. Other viruses found to be associated with CNS symptoms in children admitted into our study were measles and herpes simplex virus. A viral etiology was confirmed for 13 or the 195 cases (6.7%). We also screened 482 non-specific febrile cases for IgM to JEV and to dengue viruses and found that 2 (0.4%) had IgM specific for JEV and 9 (1.9%) had IgM specific for dengue virus.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  6. 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/epidemiology*
  7. 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*
  8. 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*
  9. Nipah encephalitis outbreak in Malaysia, clinical features in patients from Seremban
    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/epidemiology*
  10. 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*
  11. Fulltext Epidemiology, surveillance and control of Nipah virus infections in Malaysia
    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*
  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. 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*
  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. 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
  16. Fulltext New virus is identified in Malaysia epidemic
    Easton A
    BMJ, 1999 May 08;318(7193):1232.
    PMID: 10231244
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  17. 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
  18. Nipah-virus encephalitis--investigation of a new infection
    Farrar JJ
    Lancet, 1999 Oct 9;354(9186):1222-3.
    PMID: 10520625
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  19. Trailing a virus
    Gibbs WW
    Sci. Am., 1999 Aug;281(2):80-7.
    PMID: 10443039
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  20. 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
Related Terms
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links