The author provides an account of the discovery of a previously undescribed disease of horses and a description of the studies involved in determining the aetiology of the disease. The causative virus, now named Hendra virus (HeV), is the reference virus for a proposed new genus within the virus family Paramyxoviridae. The virus is a lethal zoonotic agent able to cause natural disease in humans and horses and experimentally induced disease in cats, guinea-pigs and mice. The virus also naturally infects species of the family Megachiroptera, mainly subclinically, and such animals are the natural host of HeV. The virus appears to transmit readily between species of Megachiroptera, but not readily between horses under natural and experimental conditions, or from horses to humans. The method of transmission from bats to horses is not known. Three incidents of HeV disease in horses have been recorded in Australia--two in 1994 which caused the death of two humans and fifteen horses and one in 1999 which involved the death of a single horse. Hendra virus is related to Nipah virus, the virus that caused disease and mortality in humans, pigs, dogs and cats in Malaysia during 1998 and 1999.
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.