Hendra virus

From Horse
Electron-micrograph of HeV

Hendra virus (HeV; formerly called equine morbillivirus) is a zoonotic virus of the Paramyxoviridae family transmitted by the fruit bat (Pteropus spp).

Hendra virus is the prototype species of a new genus Henipavirus within the subfamily Paramyxovirinae. The viral agent is endemic in specific species of fruit bats (also called flying foxes), and close contact with these bats is suspected to have facilitated transfer of the HeV to horses. Horses are infected by oronasal routes and excrete HeV in urine, saliva, and respiratory secretions.

Hendra virus was first isolated in horses and humans in Australia in 1994[1].

Human HeV infection has so far only resulted from close contact with the blood, body fluids, and tissues of infected horses, resulting in clinical symptoms that range from from mild to fatal. Although bats appear to be unaffected by HeV there is a high case-fatality rate in both humans and horses and spill-over events from bats to horses are occurring with increasing regularity[2].

Infected horses develop severe and often fatal respiratory disease, characterized by dyspnea, vascular endothelial damage, and pulmonary edema. Depression, anorexia, fever, respiratory difficulty, ataxia, tachycardia, and frothy, nasal discharge are common clinical signs[3].

The case fatality rate is about 50% and sub-clinical infections may be common. The course of the disease is short; death may occur within 1-3 days. Clinical recovery occurs occasionally.

The principal gross lesions are severe edema and congestion of the lungs and marked dilatation of the subpleural lymphatics. The airways are filled with thick froth, which is often blood-tinged. Additional lesions seen in some affected horses include increased pleural and pericardial fluids, congestion of lymph nodes, hemorrhages in various organs, and slight jaundice.

Microscopically, the primary lesions are those of an acute interstitial pneumonia. Severe vascular damage, with serofibrinous alveolar edema, hemorrhage, thrombosis of capillaries, necrosis of alveolar walls, and alveolar macrophages are evident in the lungs. Widespread fibrinoid degeneration of small blood vessels is seen in many organs, including the lungs, heart, kidneys, spleen, lymph nodes, meninges, alimentary tract, skeletal muscle, and bladder.

The presence of large endothelial syncytial cells is characteristic of infection. Although most prominent in pulmonary capillaries and arterioles, these cells are also observed in other organs (lymph nodes, spleen, heart, stomach, kidneys, and brain). Antigen specific for Hendra virus can be demonstrated in the vascular lesions and along alveolar walls by immunohistochemical staining. Intracytoplasmic viral inclusion bodies can be seen in infected endothelial cells by electron but not light microscopy. Lesions of nonsuppurative meningitis or meningoencephalitis, including perivascular cuffing, neuronal degeneration, and focal gliosis, have been observed in some infected horses.

Hendra virus infection should be considered in horses that die after a short febrile illness with prominent necropsy findings of severe interstitial pneumonia with marked distention of the subpleural lymphatics.

Diagnosis is based on immunohistochemistry and PCR isolation of viral particles within lung, kidney, spleen, liver, lymph nodes and brain.

A differential diagnosis would include African horse sickness, anthrax, botulism, certain bacterial infections (e.g., pasteurellosis, equine influenza, peracute equine herpesvirus 1 infection), and plant or chemical poisoning.

There is no specific antiviral treatment but a vaccine has been recently launched in Australia.

References

  1. Murray K et al (1995) A morbillivirus that caused fatal disease in horses and humans. Science 268(5207):94–97
  2. Smith I et al (2011) Identifying Hendra virus diversity in pteropid bats. PLoS ONE 6(9):e25275
  3. Merck Veterinary Manual