Nipah Virus Infection of Pigs, Dogs, Rats, Goats, Horses & Humans 
In the Nipah virus epidemic, which began in October 1998, 258 people (mostly pig farm workers) developed encephalitis and 104 died. One million pigs were slaughtered to control the virus. Outbreaks in Bangladesh in 2004 also spread to humans. Fruit bats are an important wildlife reservoir of infection. The virus affects rats, cats, dogs and horses as well as swine

Nipah Virus Infection of Pigs, Dogs, Rats, Goats, Horses & Humans

*New Monoclonal Antibody treatment for Hendra & Nipah virus infections: November 2009

Investigation of the Nipah Virus Outbreaks in Malaysia in 2006
Film of the Investigators & Human & Swine Illness cases
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*The Big Nipah Virus Epidemic of Pigs & Pig Farm Workers in Malaysia: Video News Story
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*Hendra & Nipah virus vaccination - Vaccine Research: Progress

Virologists Discuss Hendra Virus & Flying Fox Fruit bats as Vectors

Hendravirus & Nipahvirus are Related...
Both are classified as members of the Henipavirus genus of the virus family Paramyxoviridae of the Order Mononegavirales. Natural wildlife hosts of Henipa viruses are Pteropid fruit bats (flying foxes). Both viruses are zoonotic pathogens causing disease and death in domestic animals and humans. Nipahvirus primarily affects pigs and humans, Hendravirus mainly infects horses and people.

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Nipah Virus Infection of Abattoir Workers

In March 1999 four abattoir personnel in Singapore developed encephalitis. The abattoir had imported pigs from a Malaysian farm infected with Nipah virus. Both Singapore abattoirs were immediately closed and all workers checked for fever, respiratory or neurological symptoms. Eleven men were found to have acute infection with Nipah virus as indicated by IgM antibodies in their serum. One man died and Nipah virus was identified in CSF and tissue by reverse transcriptase PCR. MRI scans of eight patients revealed focal areas of increased signal intensity in the white matter of the cerebral cortex. The Singapore virus strain is slightly different from the Malaysian strain.



Porcine virus risks: Asia, Far East & Oceania

  Veterinary experts at the 21st Conference of the Regional Commission for Asia, the Far East and Oceania of the International Office of Epizootics (OIE) have reviewed the risks to pigs from epidemic diseases. OIE is the international body to which national chief veterinary officers report outbreaks of serious infectious diseases. The conference was held in Taipei from 23 to 26 November and opened by the Honourable Dr Tso-Kwei Peng, Chairman of the Council of Agriculture of the Executive Yuan of Taipei China.

Nipah virus epidemic ended - claim

  Experts reported that the Nipah virus epidemic which began in the Malaysian Peninsula in October 1998 was now over and risk of spread to other countries is very low. More than one million pigs were slaughtered before the epidemic was brought under control. By that time more than one hundred people who had come into contact with infected pigs has died from encephalitis. Serological surveys indicate that a fruit-eating bat of the Pteropid genus is probably a reservoir of the virus (which can also infect dogs, cats, rats and horses). Some infected pigs show no signs, but others become quite ill with a variety of respiratory and neurological symptoms such as coughing, fever, respiratory distress, off food, trembling, head pressing, spasms, leg weakness, abortion, stillbirths, death.


  Other pig diseases of concern in the region are foot and mouth disease (FMD), swine vesicular disease (SVD) and classical swine fever (CSF). FMD is the most worrying disease because of the severe impact of new strains of the virus on cattle and pig production. Countries remaining free from FMD are Australia, Indonesia, Japan, the Republic of Korea, New Caledonia, New Zealand, Singapore and Vanuatu.



History of NIPAH virus: The Malaysian Epidemic of a Hendra-like Virus Infection

Report by Dr. Francis K.S. Ng, B.Vet.Med., Technical Service Manager, Great Wall Nutrition Technologies, Johore, Malaysia
Sources: Newsletter of Veterinary Association Malaysia (VAM) and notes taken by Dr. Ng during the epidemic conference held in Shah Alam, Malaysia, on 3 April 1999.

Japanese Encephalitis & Hendra-like virus in Malaysian Pigs

  The disease episode has been hypothesised to arise initially from two equine mortalities in Ampang in 1997. Subsequently, in 1998, mild disease in swine followed by mortalities in man in Ampang/Ulu Piah pig farms were reported. A similar disease in pigs and mortalities in man was reported in Sikamat/Sg. Nipah/Bukit Pelanduk from 1998. As at 31 March 1999, 71 people have died of viral encephalitis. Investigations have shown that Japanese Encephalitis (JE) and a Hendra-like virus have been implicated. Eleven of 15 blood samples from abattoir workers in Singapore tested Hendra-like positive. It has been proposed that the Hendra-virus disease in man be called "Nipah Encephalitis".

Investigation of Nipah Virus Outbreaks & Other Emerging Zoonotic Diseases
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Clinical Signs Observed in Swine in Affected Areas

The following signs may occur singly or in combination in pigs:-


The Nipah control area in Malaysia resumed pig farming in August 2001
The Malaysian government lifted the ban on pig farming in what was once the Malaysia's biggest pig producing region - Bukit Pelanduk, Negri Sembilan. Nipah virus killed over a hundred 100 people there, two years before.
Announcing the lifting of the ban, the Agriculture Minister said that the alternative was to incur great expense importing pork to meat the high domestic consumption. However, pig farmers would have to follow strict hygiene rules when they re-commence production. Poor hygiene and outdated production systems were blamed for the Nipah virus epidemic.


History of Hendra Virus

  In 1994-5 two people and fifteen horses died in Queensland, Australia as a result of infection with a new virus. This year (January 1999) another horse died of the disease near Cairns, Australia.

A research team at CSIRO Australian Animal Health Laboratory (AAHL) isolated and identified the causal virus. Virion structure was characteristic of Paramyxoviridae family viruses although none of them had previously been known to cause serious disease in both horses and humans.

The new virus was most closely related to a group known as morbilliviruses, which contains the viruses causing measles, rinderpest and canine distemper. It was initially named equine morbillivirus, but subsequent genetic analysis led to re-classification in a new genus within the Paramyxoviridae and it has been re-named Hendra virus, after the Brisbane suburb in which the first outbreak occurred.

Fruit bats are wildlife reservoir

Paramyxoviruses tend to be host-specific and Hendra virus is unusual in affecting more than one species. Fruit bats (flying foxes) are the natural hosts of the virus - they can be carriers without becoming appreciably ill. Approximately 25% of the bats have antibodies to Hendra virus.

After spreading to people or horses, Hendra is more pathogenic. Horses can develop fever, respiratory difficulty and a blood-tinged foamy discharge from the nose and mouth - the virus damages blood vessels. It also induces pulmonary oedema - the lung fill with fluid. Like the related viruses of canine distemper and measles, Hendra virus can also cause brain lesions.

Other species affected
Cats and guinea pigs have been susceptible to infection in laboratory investigations, and can suffer severe disease. Fruit bats and rabbits have also been infected in the laboratory, but do not become ill. Dogs, chickens, rat and mice could not be infected.

Epidemiology (mode of spread)
Hendra virus is not very contagious. Horses can be infected by eating contaminated feedstuffs e.g. after virus contamination from cat urine. Infected horses and guinea pigs can also excrete the virus in their urine. Airborne spread does not seem to occur.


Hendra Virus - Virology

    • Genome
        • single stranded RNA virus
        • genomic nucleic acid mostly negative sense
        • positive sense template strands occur
        • Genome monopartite, 15200-15900 nucleotides long
    • Morphology
        • Virions enveloped
        • pleomorphic and filamentous forms occur
        • spherical, or filamentous
        • (60-) 150-200 (-300) nm in diameter
        • 10000-10040 nm long
        • Surface projections of envelope distinct
        • spikes (of haemagglutinin-neuraminidase (HN)
        • fusion (F) glycoproteins 8-20 nm long spaced 6-10 nm apart
        • Capsids filamentous; nucleocapsids 13-18 nm in diameter
        • Symmetry helical, pitch of helix 5.5-7 nm



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