Also known as: Equine Morbillivirus Pneumonia
Introduction
Hendra virus is a morbillivirus of the family paramyxoviridae. The virus causes equine morbillivirus pneumonia, which is an acute viral respiratory infection of horses.
Hendra virus is a large, pleomorphic enveloped RNA virus. It is antigenically related to Nipah virus, with which it shares ~90% amino acid homology. Both viruses have been classified in a new genus, Henipavirus, in the subfamily Paramyxovirinae, family Paramyxoviridae.
Disease caused by Hendra virus has been reported only in horses and humans and outbreaks have been infrequent and have only occurred in Australia. Research has shown that flying foxes, or fruit bats in Australia and Papua New Guinea have a high prevalence of neutralizing antibodies to Hendra virus. These are considered to be the natural reservoir of the virus.
Transmission of the disease is unknown, but the small number of sporadic outbreaks indicate transmission is by chance and can be due to horses eating or drinking material infected with fruit bat excrement. Transmission between infected and non-infected horses occurs infrequently. The disease can be transmitted to humans and is therefore zoonotic. It has caused death in humans and care should be taken when performing a physical examination or necropsy on a horse considered to have the condition.
Clinical Signs
Signs include pyrexia of up to 410C, anorexia, depression, increased respiratory and heart rates, respiratory distress, and a mortality rate of around 60 - 70% of animals infected. Other clinical signs include jaundice, facial oedema and oedema of the limbs and prepuce, frothy nasal discharge and some neurological signs such as ataxia, head pressing and muscle fasciculations.
Pathology
The principal lesions found on necropsy include oedema and congestion of the lungs and marked dilatation of the subpleural lymphatics. The airways are found to be filled with thick froth, which is often blood-tinged.
Microscopically, the primary lesions are those of an acute interstitial pneumonia. Severe vascular damage, haemorrhage, thrombosis of capillaries, necrosis of alveolar walls, and alveolar macrophages are evident in the lungs. The presence of large endothelial syncytial cells is characteristic of infection and are most prominent in the pulmonary capillaries and arterioles.
Diagnosis
Clinical signs, history and signalment can be suggestive of the disease.
Confirmation of the diagnosis is based on laboratory examination on samples of lung, kidney, spleen, liver, lymph nodes and brain, by PCR or virus isolation.
Serologic confirmation of infection is based on testing acute and convalescent sera collected 3-4 wk apart, either in a neutralization or a validated ELISA.
Histopathologial examination can also be performed if a comprehensive range of tissue samples are collected. Presence of the characteristic vascular lesions is highly suggestive of the infection; specificity of the lesions can be confirmed by immunochemical labeling with Hendra virus reference antiserum.
Differentials to be excluded include African horse sickness and other causes of sudden death such as botulism, anthrax and toxins.
Treatment
There is no specific antiviral treatment and no vaccine for the disease caused by Hendra virus.
Due to poor knowledge of transmission of the virus and its sporadic occurrence, few control measures have been put into place for what to do when an outbreak occurs. Control measures include slaughtering all horses known to be infected and implementing a movement ban in that area.
References
Bridger, J and Russell, P (2007) Virology Study Guide, Royal Veterinary College.
Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders.
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