Akabane virus

From Cow
Electron microscopy of Akabane virus
Arthrogryposis in a newborn calf infected in utero with Akabane virus
Comparison of diseases (left) and normal brain of Akabane-infected cattle
Histopathology of a cow which died from Akabane viral infection. Note the perivascular infiltration of mononuclear cells and glial nodules in the formatio reticularis of cerebellopontine[1]

Bovine epizootic encephalomyelitis is an arthropod-borne viral disease that causes neurological disease in cattle in Australia, Japan, Korea, and Israel[2].

The virus is well known as a teratogenic pathogen that induces abortions, stillbirths, premature births and congenital abnormalities with arthrogryposis-hydranencephaly syndrome.


The causal agent, Akabane virus, is a member of the Simbu serogroup of the family Bunyaviridae. It is spread by biting midges (Culicoides spp) in Australia, Japan, and Kenya.

Cattle in endemic regions are often exposed from a young age and develop long-lasting immunity. Disease is usually associated with the virus spreading to immunologically-naive cattle that have no prior exposure to the virus. In utero infections of pregnant cows is common during outbreaks.

Clinical signs

Clinical signs usually manifest initially with locomotor ataxia, ataxia, tremor and hypersensitivity[3].

Abortions are not uncommonly reported. Calves infected late in pregnancy may be born alive but unable to stand and may have a flaccid paralysis of the limbs, or may be uncoordinated and on necropsy show a disseminated encephalomyelitis. Some calves may be affected with both arthrogryposis and hydranencephaly.

Postmortem changes observed in dead cattle include non-suppurative encephalomyelitis of the brain and spinal cord.


Presumptive diagnosis can be made on clinical signs an supportive evidence found during postmortem of dead cattle.

Histopathological changes include perivascular cuffing of lymphocytes and macrophages and diffuse gliosis in the cerebrum with degeneration and/or necrosis of neurons with vacuolation of the neuropil in the brainstem. Neuronal necrosis and neuronophagia are often noted in the ventral horn of the spinal cord[4].

Confirmation of Akabane viral infection requires ELISA or PCR testing[5].

Differential diagnosis would include other neurological disease processes such as Sporadic bovine encephalomyelitis, Bovine viral diarrhea virus (BVDV) as well as other arthropod-borne viruses such as Aino virus and Chuzan virus.


There is no specific treatment for affected animals. Measures should be directed at the prevention of infection of susceptible animals with Akabane virus during pregnancy. Introduction of stock from non-endemic to endemic areas should be done well before first breeding.

Trivalent vaccines have been developed which are reportedly effective at minimizing outbreaks in cattle[6]. In calves, maternal antibodies against Akabane wane after 4 months and vaccinations are recommended at this age[7].


  1. Kono R et al (2008) Bovine epizootic encephalomyelitis caused by Akabane virus in southern Japan. BMC Vet Res 4:20
  2. Charles JA (1994) Akabane virus. Vet Clin North Am Food Anim Pract 10(3):525-546
  3. Oem JK et al (2012) Bovine Epizootic Encephalomyelitis caused by Akabane Virus Infection in Korea. J Comp Pathol 147(2-3):101-105
  4. Kamata H et al (2009) Encephalomyelitis of cattle caused by Akabane virus in southern Japan in 2006. J Comp Pathol 140(2-3):187-193
  5. Kessell A et al (2011) Neurological diseases of ruminant livestock in Australia. IV: viral infections. Aust Vet J 89(9):331-337
  6. Kim YH et al (2011) Development of inactivated trivalent vaccine for the teratogenic Aino, Akabane and Chuzan viruses. Biologicals 39(3):152-157
  7. Tsutsui T et al (2009) Duration of maternally derived antibodies against Akabane virus in calves: survival analysis. J Vet Med Sci 71(7):913-918