Henipavirus

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(Redirected from Hendra virus)
Henipaviruses
Virus classification
Group:Group V ((-)ssRNA)
Order:Mononegavirales
Family:Paramyxoviridae
Genus:Henipavirus
Species

Hendravirus
Nipahvirus

Henipavirus is a genus of the family Paramyxoviridae, order Mononegavirales containing two members, Hendravirus (originally Equine morbillivirus, EBV) and Nipahvirus. The name is actually a combination of the two names. The Henipaviruses are characterised by their large size (18.2 kilobases; Wang et al., 2001), their natural occurrence in Pteropid fruit bats, and their recent emergence as zoonotic pathogens capable of causing illness and death in domestic animals and humans.

Contents

Hendra virus

Hendra virus was discovered in 1994 when it caused the deaths of thirteen horses, and a trainer at a training complex in Hendra, a suburb of Brisbane, Australia. A stable hand also fell ill, but recovered.

A second outbreak occurred in Mackay, 1000km north of Brisbane resulting in the death of two horses and their owner (Field et al., 2001).

Two more incidents, in Cairns in 1999 and Townsville in December 2004, each resulted in the death of one horse. A vet involved in autopsy of the horse from the 2004 incident developed a Hendra-related illness soon after and recovered. The timing of incidents suggests a seasonal pattern of outbreaks possibly related to the seasonality of fruit bat birthing, as Hendra virus has been isolated from foetal tissues and fluids (Halpin et al, 2000).

Symptoms of infection include respiratory illness and encephalitis. The route of transmission from bats to horses and humans is unknown, however, as there is no evidence that Hendra virus can be transmitted directly from bats to humans, it is believed that human infection occurs only via exposure to an intermediate host.

Nipah virus

Nipah virus was identified in 1999 when it caused an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia, resulting in 105 human deaths and the culling of one million pigs (Field et al., 2001). In Singapore, 11 cases including one death occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms.

Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus.

In human, the infection presents as fever, headache, drowsiness. The patients often have previous contact with sick animals, such as pigs or dogs. Cough, abdominal pain, nausea, vomiting, weakness and problem with swallowing and blurred vision are relatively common. About a quarter of the patients would have seizure. About 60% of the patients would become comatose and might need mechanical ventilation. In patients with severe disease, their conscious state would deteriorate, and later on, develop severe hypertension, very fast heart rate, and very high temperature. About 30% - 40% of the patients died, often of severe, irreversible low blood pressure that is not responsive to any treatment.

Nipah virus is also known to cause relapse encephalitis. In the initial Malaysian outbreak, a patient presented with relapse encephalitis some 53 months after his initial infection. There is no definitive treatment for Nipah encephalitis, apart from supportive measures, such as mechanical ventilation and prevention of secondary infection. Ribavirin, an antiviral drug, was tested in the Malaysian outbreak and the results were encouraging, though further studies are still needed.

Four more outbreaks of Nipah virus have occurred since 1998, all of them in Bangladesh. As with Hendra virus, the timing of the outbreaks indicates a seasonal effect.

  • 2001 April – May, Meherpur district: 13 cases with nine fatalities (69% mortality) (Hsu et al, 2004).
  • 2003 January, Naogaon district: 12 cases with eight fatalities (67% mortality) (Hsu et al, 2004).
  • 2004 January – February, Manikganj and Rajbari provinces: 42 cases with 14 fatalities (33% mortality).
  • 2004 19 February – 16 April, Faridpur district: 36 cases with 27 fatalities (75% mortality). Epidemiological evidence strongly suggests that this outbreak involved person-to-person transmission of Nipah virus, which had not previously been confirmed in humans. 92% of cases involved close contact with at least one other person infected with Nipah virus. Two cases involved a single short exposure to an ill patient, including a rickshaw driver who transported a patient to hospital. In addition, at least six cases involved acute respiratory distress syndrome which has not been reported previously for Nipah virus illness in humans. This symptom is likely to have assisted human-to-human transmission through large droplet dispersal.
  • 2005 January, Tangail district: 32 cases with 12 fatalities (38% mortality). The virus may have been contracted from drinking palm fruit juice contaminated by fruit bat droppings or saliva.

In addition to these confirmed cases, a suspected outbreak of encephalitis in Siliguri, India occurred in February-March 2001. The official diagnosis of measles was not supported by the clinical or epidemiological evidence, and later testing of samples by the Centers for Disease Control and Prevention in the USA confirmed the presence of Nipah virus (Kumar, 2003).

Nipah virus has been isolated from Pteropid bats in Cambodia (Reynes et al, 2005). The Cambodian strain shows 98% identity with the virus causing the 1998 outbreak. No infection of humans or other species have been observed in Cambodia.

References

External links

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