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The emergence of Nipah virus, a highly pathogenic paramyxovirus

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
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/mortality
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/mortality
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: Encephalitis, Viral/mortality
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/mortality
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/mortality
Clinical and pathological manifestations of human henipavirus infection

Wong KT, Tan CT

Curr. Top. Microbiol. Immunol., 2012;359:95-104.
PMID: 22427144 DOI: 10.1007/82_2012_205

The clinicopathological features of human Nipah virus and Hendra virus infections appear to be similar. The clinical manifestations may be mild, but if severe, includes acute encephalitic and pulmonary syndromes with a high mortality. The pathological features in human acute henipavirus infections comprise vasculopathy (vasculitis, endothelial multinucleated syncytia, thrombosis), microinfarcts and parenchymal cell infection in the central nervous system, lung, kidney and other major organs. Viral inclusions, antigens, nucleocapsids and RNA are readily demonstrated in blood vessel wall and numerous types of parenchymal cells. Relapsing henipavirus encephalitis is a rare complication reported in less than 10% of survivors of the acute infection and appears to be distinct from the acute encephalitic syndrome. Pathological evidence suggests viral recrudescence confined to the central nervous system as the cause.

Matched MeSH terms: Encephalitis, Viral/mortality
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/mortality