Akabane disease

Akabane virus is an arbovirus and a member of the Simbu serogroup in the family Peribunyaviridae, genus Orthobunyavirus, family Bunyavirus.

Akabane virus is common in many tropical and subtropical areas in the Eastern Hemisphere, including parts of Asia, Africa, the Middle East and Australia. The disease has been recorded in Japan, Korea, Taiwan, Australia, Israel and Turkey.

The distribution of Akabane virus in Australia depends on the seasonal distribution of Culicoides brevitarsis (a biting midge) that transmits the virus.

Within Australia, Akabane virus occurs in the Kimberley region of Western Australia, the top half of the Northern Territory and throughout most of Queensland. With seasonal variation, Akabane virus also extends to the far southern eastern seaboard of New South Wales and adjacent hinterlands.

• ruminants
• other ungulates, including horses and pigs
• Culicoides brevitarsis (a biting midge)

In Australia, Akabane virus is transmitted by the biting midge Culicoides brevitarsis. Akabane virus is not transmitted between animals by direct contact.

The presence of virus in the blood usually occurs 1 to 6 days after infection, during which Akabane virus is transmitted across the placenta to the foetus. Disease due to infection of the foetus does not become evident until the animal is either born or aborted.

In endemic areas, susceptible animals become infected early in life and immune before reaching breeding age.

The disease occurs when non-immune pregnant animals are infected. This usually occurs when either:

• infected midges extend their geographic range to infect immunologically naïve animals
• non-immune pregnant animals are moved to Akabane-affected areas.

While animals that are pregnant when infected usually recover, the offspring is usually lost.

Natural infection produces lifelong immunity unless infected as a foetus before immunity is reached.

Ruminants do not become long-term carriers of Akabane virus.

Clinical signs only occur when non-immune animals are infected while pregnant.

Clinical signs include:

• late-term abortions and stillbirths
• congenital disease including; arthrogryposis (fixed contracted joints), hydranencephaly (part of the brain being absent), torticollis, scoliosis, kyphosis and spina bifida.

Clinical signs reflect the stage of foetal development at which Akabane virus infection occurs. As a result, outbreaks often occur as a series of overlapping syndromes.

1. increased abortions and stillbirths
2. arthrogryposis occurs some months later at the peak of the outbreak
3. hydranencephaly occurs late in the epizootic.

Limb deformities due to arthrogryposis may lead to difficult labour and possible death.

Calves with hydranencephaly show ataxia, blindness and have a poor or absent sucking reflex.

Economic loss due to:

• reproductive failure in non-immune animals
• market access restrictions that impact
  • live animal exports
  • semen and embryo testing.

Access to markets is dependent on recognition of NAMP vector-free regions.

• Movement of infected Culicoides brevitarsis beyond the normal geographic range.

All year round, during pregnancy with seasonal peaks when vector numbers increase due to factors such as rainfall.

Producers should monitor cattle, sheep and goats for signs consistent with Akabane disease (see symptoms).

Serological tests to determine immune status can inform herd management.

The National Arbovirus Monitoring Program monitors the distribution of Akabane virus in Australia.

Vaccines are not commercially available in Australia.

Movement of female breed stock into an endemic area at least 2 months prior to mating is likely to lead to protective immunity being established prior to pregnancy. The time required for most animals to develop immunity will vary depending on the number of infector vectors present.

Once the disease is observed, remedial action is ineffective as all remaining foetuses are likely to be infected.

There is no treatment for Akabane-affected offspring.