THE MERCK VETERINARY MANUAL
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Akabane Virus Infection

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Akabane is an insect-transmitted virus that causes congenital abnormalities of the CNS in ruminants. Disease due to Akabane virus has been recognized in Australia, Israel, Japan, and Korea; antibodies to it have been found in a number of countries in southeast Asia, the Middle East, and Africa. The disease affects fetuses of cattle, sheep, and goats. Asymptomatic infection has been demonstrated serologically in horses, buffalo, and deer (but not in humans or pigs) in endemic areas.

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.

Akabane virus is common in many tropical and subtropical areas between ∼35°N and 35°S. In these endemic areas, herbivores are bitten by the vectors, become infected at an early age, and develop a long-lasting immunity by the time of breeding; thus, congenital abnormalities are seldom seen. However, under favorable environmental conditions such as an extended humid summer, the vector (and hence the virus) may spread beyond its usual range into new areas, and outbreaks of congenital infection may be expected. These outbreaks usually occur at the northern or southern limits of the vector distribution or in areas of higher altitude. Similarly, pregnant ruminants from virus- and vector-free areas moved to virus-infected areas are at risk.

The incidence of Akabane virus-induced disease is influenced by the time of gestation at which infection occurs and also by the strain of virus. Infections in cattle during the last 3 mo of pregnancy result in a relatively low incidence of disease (5–10% of calves are affected). The peak incidence is seen after infection in the third and fourth months, when up to 40% of calves may be born with defects. Some strains of Akabane virus produce a very low incidence of abnormalities (<20%) even at the most susceptible stages of gestation, whereas the most severe can cause disease in up to 80% of infected animals.

In sheep and goats, disease is observed but the distinct sequential manifestation of different abnormalities seen in cattle does not occur due to the shorter period of gestation and the shorter period of susceptibility. Most abnormalities develop following infection between 28–56 days of gestation. Few, if any, abnormalities are observed after infection at other times. However, it is not known whether infection in large or small ruminants very early in gestation results in a lethal infection, with abortion of the fetus.

The clinical signs and pathology depend on the species of animal and time of infection. In a herd of cattle with an extended or year-round calving period, the full range of abnor-malities may be seen. The most severe defects are seen after susceptible cows have been infected between ~80–150 days of gestation; however, calves can be affected at most times after the first 2 mo of gestation. 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 incoordinated and on necropsy show a disseminated encephalomyelitis. Those infected earlier (120–180 days of gestation) have rigid fixation of limbs, usually in flexion (arthrogryposis), and sometimes also torticollis, kyphosis, and scoliosis with associated neurogenic muscle atrophy due to loss of spinal motor neurons. These abnormalities usually cause dystocia, and can result in severe obstetric complications, sometimes resulting in infertility and even death of cows. The first calves born with arthrogryposis are less severely affected than those born during the next 4–6 wk. Initially only 1–2 joints may be affected on a single limb, but later cases can have severe fixation of multiple joints on several or all limbs. Calves infected at 80–120 days of gestation are usually born alive and, if able to stand, walk poorly and are depressed and blind. These calves have varying degrees of cavitation of cerebral hemispheres, ranging from porencephaly to severe hydranencephaly. The latter is common, especially among those infected in the earlier stages of pregnancy. Some calves may be affected with both arthrogryposis and hydranencephaly.

Calves with severe hydranencephaly may be aborted in midgestation. A useful differential diagnostic feature is the virtual absence of either gross or histologic lesions in the cerebellum, distinguishing Akabane virus infection from other teratogenic viruses such as bovine viral diarrhea virus (BVDV).

In small ruminants, the lesions of arthrogryposis and hydranencephaly are often seen concurrently and are common in the same animals. In lambs and kids, a range of other defects may occur, including pulmonary hypoplasia and hypoplasia of the spinal cord. Most Akabane-infected lambs or kids are stillborn or die soon after birth. Abortions are also seen.

Akabane virus-induced congenital abnormalities (especially arthrogryposis and hydranencephaly) have been suspected in horses, but laboratory confirmation has been inconclusive.

A presumptive diagnosis can be made on the gross CNS lesions, but the disease must be differentiated from other infectious and genetic conditions. Infection can be confirmed by testing sera or body fluids (eg, pericardial or pleural fluid) from unsuckled, affected offspring and their dams for antibodies against Akabane virus. While the detection of antibody in maternal serum does not confirm Akabane as an etiologic agent, its absence is definitive for exclusion.

Other vectorborne viruses (and also nonvectorborne viruses such as BVDV) can cause congenital defects identical to those of Akabane virus. Aino virus, a relative of Akabane, is found in Australia, Japan, and several other countries where Akabane virus is found and has been an infrequent cause of disease in cattle. In Japan, Chuzan virus, a reovirus, is transmitted by Culicoides oxystoma and causes congenital infection in calves similar to Akabane virus. In the USA, Cache Valley virus, another vectorborne bunyavirus unrelated to Akabane virus, has been associated with congenital defects in sheep and perhaps cattle in some states.

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 nonendemic to endemic areas should be done well before first breeding. Effective vaccines are available in Japan.

Last full review/revision March 2012 by Peter D. Kirkland, BVSc, PhD

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