AKABANE DISEASE



Akabane disease is a viral condition affecting sheep, goats, and cattle. It is caused by the Akabane orthobunyavirus during early pregnancy and manifests as congenital arthrogryposis (joint immobility), hydranencephaly (absence of cerebral hemispheres), abortion, premature birth, and stillbirth. The virulence of Akabane virus strains is variable. While many strains affect unborn ruminants, some can cause neurological disorders (encephalomyelitis) in adults.

ETIOLOGY

The causative agent is the Akabane orthobunyavirus, belonging to the genus Orthobunyavirus within the family Peribunyaviridae, order Bunyavirales. Serologically, it is classified within the Simbu serogroup. Genetic segment reassortment can occur among viruses in this serogroup. The virus can be propagated in suckling mice via intracerebral inoculation and in embryonated chicken eggs. In vitro, susceptible cell cultures include those derived from hamster, porcine, and monkey lungs, as well as Vero, BHK, and MDBK cell lines.

EPIDEMIOLOGY



The disease exhibits a seasonal occurrence. It was first identified in Australia in 1955 and has since been reported in Asia, Africa, the Middle East, Australia, and Turkey. Virus strains causing encephalomyelitis in cattle and calves circulate in Japan, Taiwan, and Korea. In the autumn of 2015, an outbreak in the Southeastern Anatolia region of Turkey led to significant abortion storms in sheep, resulting in substantial economic losses. Although more prevalent in cattle, the disease also affects sheep.

Simbu serogroup viruses are transmitted among cattle, sheep, and goats exclusively through insect vectors (Culicoides midges). Transmission via direct contact, infected tissues, feces, or exudates has not been reported. Following the bite of an infected midge, pregnant cows become infected without showing clinical signs. The virus crosses the placenta, infecting the fetus and leading to congenital defects. The infection presents as abortion, premature births, hydranencephaly, and arthrogryposis. Young animals possess maternal antibodies and are resistant to the disease. Akabane antibodies have been detected in water buffalo, pigs, camels, horses, and donkeys, although the pathogenicity of the virus in these species is not well-documented.

The reservoirs for the disease are infected cattle and insect vectors. Viral replication occurs in both cattle and midges. Akabane disease emerges seasonally and is geographically restricted. The timing and location of fetal infection during early gestation are linked to the seasonal activity of the vectors. The disease may disappear and re-emerge at 5-10 year intervals, correlating with fluctuations in vector and susceptible host populations. Consequently, preventive measures are necessary in enzootic areas, particularly during dry years.

PATHOGENESIS

In natural infections, a viremic period (1-6 days) begins at least 3-4 days after viral entry. The initial antibodies appear 4-5 days post-viremia and subsequently increase. Pregnant cows, sheep, and goats infected with the virus typically do not show clinical symptoms. However, some virus strains have been reported to cause encephalomyelitis and neurological signs in adult animals. The virus crosses the placenta in pregnant cows, reaches the fetus, and localizes in the nervous system, leading to anomalies. A persistent infection is not established. The specific abnormalities that develop depend on the fetal age, developmental stage, and the neurotropism and pathogenicity of the virus.

Primary fetal infection results in encephalomyelitis and polymyositis. Severely affected fetuses may die and be aborted. Secondary lesions develop as a consequence of primary central nervous system (CNS) damage. For instance, arthrogryposis arises secondary to primary CNS disorders. These fetuses may be born at term, prematurely, or stillborn. Calves infected during the 3rd to 4th month of gestation develop hydranencephaly, while those infected around the 6th month develop arthrogryposis. Infected calves can be categorized into three groups: Group 1 exhibits only arthrogryposis; Group 2 shows both arthrogryposis and hydranencephaly; and Group 3 presents with hydranencephaly alone.

CLINICAL FINDINGS

Overt clinical signs are generally absent in adult animals, although viremia occurs 1-6 days post-infection. Antibodies against the Akabane virus can be detected 4-6 days after the viremic phase. Infection of pregnant animals during the initial months of gestation results in often inapparent fetal infection.

Congenital Akabane disease is characterized by seasonal, sporadic abortions, stillbirths, premature births, and deformed or anomalous bovine, ovine, and caprine fetuses and newborns. If infection occurs during the first trimester, extensive fetal damage is observed. If the infection happens later in gestation, central nervous system damage may be less severe, but alterations in movement may be apparent in newborns or young animals.

Fetal deformities develop. If severe, they typically result in stillbirth, with limbs locked in extension or flexion. Survivors often exhibit central nervous system degeneration and muscle lesions secondary to prolonged recumbency. Torticollis, scoliosis (spinal deviation), kyphosis (hunchback), and arthrogryposis (outward deformation of the thorax and spine) may be present concurrently. CNS lesions manifest as blindness, nystagmus (abnormal eye movements), deafness, depression, slow feeding, paralysis, and incoordination. Arthrogryposis and hydranencephaly, either alone or in combination, are present in fetuses and newborns. These lesions are associated with damage to the innervation of muscles stimulated by the CNS.

IMMUNITY

Infected animals develop neutralizing, precipitating, and hemagglutination-inhibiting antibodies. In cattle, these antibodies can be detected between 7-14 days following infection. Calves and lambs acquire maternal antibodies via colostrum. Neutralizing antibodies can be detected in lambs for up to 4 months and in calves for up to 6 months.

LABORATORY SAMPLE SUBMISSION

For virus isolation, samples such as placenta, cotyledons, fetal muscle, cerebrospinal fluid, and fetal nerve tissue should be collected and sent to the laboratory under an unbroken cold chain as quickly as possible. Otherwise, virus detection may fail. For serological diagnosis, fetal or pre-colostral serum, along with serum from adult animals in the same herd, should be obtained. For histopathology, samples of spleen, liver, lung, kidney, heart, lymph nodes, infected muscle, spinal cord, and brain should be preserved in 10% formalin and shipped to the laboratory swiftly without breaking the cold chain.

DIAGNOSIS

A presumptive field diagnosis of Akabane disease can be made based on clinical presentation, pathological lesions, and epidemiology. A sudden onset of abortions, and the delivery of mummified, premature, or stillborn offspring with hydranencephaly and arthrogryposis are suggestive. The disease may appear in previously unaffected herds. Historical data indicate a higher prevalence in animals infected during the first trimester, coinciding with peak vector activity. Aborted material contains the virus and can be isolated by inoculation into tissue cultures.

Diagnostic methods for detecting the agent or antibodies include the micronutralization test, immunofluorescence assay, RT-PCR, real-time RT-PCR, and ELISA.

Fetal losses and deformities can also arise from various nutritional, genetic, toxic, and infectious diseases, which must be differentiated from Akabane infection. Distinguishing hydranencephaly lesions from those of Bluetongue infection is particularly challenging. Bovine Viral Diarrhea (BVD) virus can cause cerebellar dysplasia in calves. Border disease can also result in the birth of underdeveloped, excessively hairy, tremulous offspring with bone defects. Akabane disease must be distinguished from these conditions as well.

PREVENTION AND CONTROL

No treatment exists for the disease, as affected animals have little chance of survival. Control strategies primarily focus on managing the vector midge population. Relocating animals to areas free of midges during seasons of high vector activity is crucial for prevention. Vaccination prior to the breeding season is reported as an effective control measure.

VACCINATION

Akabane vaccines are available in some countries and are effective in preventing fetal deaths. In Japan, both formalin-inactivated vaccines adsorbed to aluminum phosphate gel and live-attenuated vaccines have been developed. These vaccines help elevate antibody levels capable of neutralizing the virus before it can reach the fetus in cows or sheep. Vaccination should be administered prior to potential exposure to infected vectors.


Tag:

  • Akabane Disease

  • Akabane Virus

  • Orthobunyavirus

  • Veterinary Medicine

  • Livestock Diseases

  • Cattle Diseases

  • Sheep and Goat Diseases

  • Congenital Defects

  • Arthrogryposis

  • Hydranencephaly

  • Abortion Storm

  • Stillbirth

  • Vector-Borne Disease

  • Culicoides Midge

  • Simbu Serogroup

  • Ruminants

  • Veterinary Virology

  • Epidemiology

  • Vaccine

  • Disease Prevention

  • Neuropathic Disorder