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Akabane virus infection

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Akabane virus infection

Summary

  • Last modified
  • 12 July 2017
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Akabane virus infection
  • Pathogens
  • Akabane virus
  • Overview
  • Akabane virus (AKA virus) is a Culicoides transmitted teratogenic virus, which infects bovine, ovine and caprine fetuses in utero causing congenital arthrogryposis and hydranencephaly (A-H) and, less frequent...

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Pictures

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PictureTitleCaptionCopyright
Arthrogryposis the most frequently observed lesion in Akabane virus infection.
TitlePathology
CaptionArthrogryposis the most frequently observed lesion in Akabane virus infection.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Arthrogryposis the most frequently observed lesion in Akabane virus infection.
PathologyArthrogryposis the most frequently observed lesion in Akabane virus infection.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Hydranencephaly in Akabane virus infection.
TitlePathology
CaptionHydranencephaly in Akabane virus infection.
Copyright©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)
Hydranencephaly in Akabane virus infection.
PathologyHydranencephaly in Akabane virus infection.©USDA-2002/Foreign Animal Diseases Training Set/USDA-Animal and Plant Health Inspection Service (APHIS)

Identity

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Preferred Scientific Name

  • Akabane virus infection

International Common Names

  • English: A-H syndrome; akabane disease in ruminants; blind calf syndrome; congenital arthrogryposis (AG) and hydranencephaly (HE) syndrome; congenital articular rigidity; encephalomyelitis in cattle; hydranencephaly with or without cerebellar lesions in ruminants; myopathy associated with congenital articular rigidity

English acronym

  • CAR

Pathogen/s

Top of page Akabane virus

Overview

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Akabane virus (AKA virus) is a Culicoides transmitted teratogenic virus, which infects bovine, ovine and caprine fetuses in utero causing congenital arthrogryposis and hydranencephaly (A-H) and, less frequently, congenital polioencephalomyelitis and rarely, acute encephalitis in both young calves and adult cattle (Walton, 1992). It is one of about 25, related Simbu serogroup viruses (Family: Bunyaviridae, genus orthobunyavirus) including previously unrecognized viruses such as Schmallenberg virus in Europe (Hoffmann et al., 2012). Only a small number of the Simbu viruses have been associated with disease in animals.

Akabane virus has a relatively narrow host distribution. Antibody to AKA virus is extremely common in cattle, buffalo (Syncerus caffer and Bubalus bubalis), camels and small domestic ruminants in many tropical and temperate regions throughout the world. Horses, zebra and many of the wild ruminant species in Africa (wildebeest, kongoni, waterbuck, topi, eland, bushbuck, Impala, Grants gazelle and Thomson’s gazelle), show evidence of infection with AKA virus. Throughout much of its range however, where most cattle become infected with AKA before they reach breeding age, there is no evidence of any pathology in the known hosts. There is evidence to show that AKA virus activity occurs in a wide range of tropical, subtropical and temperate ecological zones in Africa and Asia as determined by the availability of suitable habitat for its insect vectors. Thus, although it may have only been studied in a small number of countries, the ecology of the virus would suggest that it is probably more widespread than recognised. As AKA virus is predominantly a fetal pathogen, disease is not an indicator for its distribution due to high levels of immunity in animals prior to reaching reproductive maturity. Serological surveys are required to identify its distribution.

The clinical congenital A-H syndrome due to AKA virus has a limited geographical distribution. Outbreaks are most commonly observed at the limits of the range of the vector, where periodic extensions occur, beyond where it is known to be endemic and where the ruminant hosts are susceptible or where the vectors are usually scarce or have only a brief and irregular period of seasonal activity. Reduction in the vector distribution in endemic areas under the influence of adverse climatic conditions such as drought can create susceptible generations of cattle that experience disease when the usual level of vector activity resumes. Disease is also observed when susceptible pregnant animals are introduced into endemic areas during the vector season.

Host Animals

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Animal nameContextLife stageSystem
Bos indicus (zebu)Domesticated hostCattle & Buffaloes: Calf|Cattle & Buffaloes/Heifer|Cattle & Buffaloes/Cow
Bos taurus (cattle)Domesticated hostCattle & Buffaloes: Calf|Cattle & Buffaloes/Heifer|Cattle & Buffaloes/Cow
Capra hircus (goats)Domesticated hostSheep & Goats: Lamb|Sheep & Goats/Gimmer|Sheep & Goats/Mature female
Ovis aries (sheep)Domesticated hostSheep & Goats: Lamb|Sheep & Goats/Gimmer|Sheep & Goats/Mature female
Sus scrofa (pigs)Domesticated host

Hosts/Species Affected

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The mammalian hosts in which pathological changes have been detected in fetuses, appear to be only cattle, sheep and goats (Della Porta et al., 1977; Jennings and Mellor, 1989; Kirkland et al., 1988). There are no reports describing similar fetal lesions which might be due to AKA virus in buffalo (Cape nor water), wild ruminants, Camelidae or Equidae. This may be a result of high levels of immunity in endemic areas or due to a lack of recognition. They may, however, all be important amplifying hosts for the virus in regions in which they occur. There has been evidence of infection in pigs in SE Asia but disease has not been described (Huang et al., 2003).

Systems Affected

Top of page bone, foot diseases and lameness in large ruminants
bone, foot diseases and lameness in small ruminants
nervous system diseases of large ruminants
nervous system diseases of small ruminants
reproductive diseases of large ruminants
reproductive diseases of small ruminants

Distribution

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Although the main vectors of AKA virus are Culicoides midges, AKA virus was first isolated from mosquitoes (Aedes vexans and Culex tritaeniorhynchus) in Akabane, Japan, in 1959 where large disease outbreaks have been described. AKA virus has also been isolated from a pool of Anopheles funestus mosquitoes in a coastal forest region of Kenya (Metselaar and Robin, 1976) and the virus is believed to be widespread on the African continent. A disease problem and the associated fetal pathology occurs periodically in Israel (Markusfeld and Mayer, 1971; Brenner, 2004a,b). The virus is widespread in northern and eastern Australia (Cybinski et al., 1978) and disease outbreaks have occurred intermittently (Della Porta et al., 1977; Shepherd et al., 1978; Jagoe et al., 1993). The virus is also present in Korea, Taiwan and other countries in the Southwest Pacific region, the Arabian peninsula, and in Turkey and Cyprus (Anon,1999a; Inaba and Matumoto, 1990).

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

IsraelPresentAnon., 1999a; Brenner et al., 2004a; Brenner et al., 2004b; Stram et al., 2004a; Zentis et al., 2012
JapanPresentAnon., 1999a; OYA et al., 1961, June; Sakai et al., 1998; Kono et al., 2008; Kamata et al., 2009
Korea, Republic ofPresentLee et al., 2002; Oem et al., 2012
TaiwanPresentLiao et al., 1996
TurkeyPresentAnon., 1999a

Africa

KenyaPresentAnon., 1999a
South AfricaPresentAnon., 1999a

Oceania

AustraliaPresentAnon., 1999a; CYBINSKI et al., 1978; Jagoe et al., 1993

Pathology

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The range of gross and histopathological changes that are observed in ruminants vary with the species (related to the length of gestation) and the time of gestation at which infection occurs. In cattle, there is a distinct suggestion of individual changes while in sheep and goats, multiple abnormalities can be observed in the same animal.

Calves that are infected late in gestation or sometimes soon after birth show acute neurological signs including a flaccid paralysis and have histological lesions of a non-suppurative polio-encephalomyelitis (Hartley et al., 1977; Kirkland et al., 1988).

In calves with arthrogryposis (AG), following infection between 5-6 months of gestation, apart from the fixation or severely restricted range of movement of joints, there are few other grossly detectable changes. These changes are largely due to degenerative changes in muscles and tendons arising from a neurogenic dystrophy. Microscopically there are severe degenerative changes in the motor horns of the spinal cord (Hartley et al., 1977; Kirkland et al., 1988). In some cases, degenerative changes are also apparent in the skeletal muscle.

When calves are stillborn or show behavioural changes, grossly apparent defects are likely to be apparent in the brain. These changes are the outcome of infection in the 3rd and 4th months of pregnancy and can vary from small cystic lesions to the virtual absence of the cerebral hemispheres and replacement with fluid filled meningeal sacs (hydranencephaly; HE) (Whittem, 1957; Shepherd et al., 1978; Hartley et al., 1997; Kirkland et al., 1988). There are few microscopic changes and histopathology is of minimal diagnostic value. There will be an absence of large areas of brain surrounded by tissues with relatively normal architecture. In cattle, the cerebellum is rarely, if ever, affected.

If a fresh aborted fetus is found, depending on the age of the fetus and time since it was infected, gross lesions may not be apparent. A range of acute necrotic, degenerative changes and perhaps a mild to moderate non-suppurative encephalomyelitis suggestive of a viral infection may be detected. The lesions can be detected in all parts of the CNS, with perivascular cuffing, neuronal degeneration and cavitation of the brain and neuronal degeneration in the motor neurones of the spinal cord. Muscular dystrophy may also be observed.

In sheep and goats, there can be varying combinations of gross and histological lesions observed in the same animal. As well as the abnormalities of the central nervous and musculoskeletal systems, developmental changes may sometimes be observed and include hypoplasia of the lungs and thymus.

Diagnosis

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Clinical Diagnosis

Akabane infection may be suspected when there is an increase in cases of neurological disease in newborn calves in late summer-autumn. Although adult animals do not normally exhibit clinical signs, the Japanese Iriki strain and some other virulent AKAV strains may cause acute encephalitis following postnatal infection, even at times in adult animals (Lee et al., 2002; Kamata et al., 2009; Oem at al., 2012; Zentis et al., 2012). Cases of acute encephalitis may soon be followed by a sudden increase in the rate of abortions and large numbers of aborted, mummified, premature or stillborn fetuses with AG and HE or other malformations. Fetuses are badly deformed, many dead at birth and in AG cases, the limbs are locked in position. Infected live-born young may exhibit CNS and muscular degeneration, which prevents them from standing and suckling. Calves with HE may survive for some months if hand-reared. AG may be accompanied by torticollis, cervical scoliosis, brachygnathism and kyphosis. Lesions of HE are expressed clinically as blindness, nystagmus, microphthalmia, deafness, dullness, slow suckling or dysphagia, paralysis and ataxia. The presence of gross lesions in the CNS can aid in diagnosis while histological changes in the motor neurones of the spinal cord are suggestive. There may also be muscular lesions.

The seasonal clustering of the concurrent birth of large numbers of sheep or goats with congenital defects and with highly suggestive gross pathology also increases suspicion. These cases would be expected to occur during the late winter and spring months.

 

Differential Diagnosis

When there is an outbreak of abortions and still births involving congenitally deformed ruminants, apart from AKAV, other vector borne viruses that must be excluded are other orthobunyaviruses such as Aino and Schmallenberg. When there is a small number of cases, other viral infections such as bovine viral diarrhoea virus (BVDV) and genetic diseases should also be excluded. In cattle, the cerebellum is rarely, if ever, affected following AKAV infection, a useful differential feature to distinguish from other congenital infections such as BVDV.

Similar fetal abnormalities in sheep or goats may be caused by vaccination with a modified live vaccine strain (the Smithburn neurotropic strain) of Rift Valley fever virus, which is widely used as a vaccine in Africa. However, there are not usually as many cases as seen  in epidemics of AKA disease. A history of vaccination during the first trimester of pregnancy should prompt investigations as to whether a vaccine may have been the cause. The differential diagnosis for neurological signs or behavioural changes can also include sheep associated malignant catarrhal fever (SA-MCF), transmissible spongiform encephalitis (TSE) and listeriosis.

 

Laboratory Diagnosis

Confirmation of AKA virus infection must be guided by an understanding of the pathogenesis of this disease and the biology of AKAV infection of the dam. As a disease predominantly of the fetus, the emphasis is on confirmation of infection in unsuckled ruminant neonates, stillborn or aborted fetuses. The capacity of the ruminant neonate to develop a strong immune response by full term provides an important approach to diagnosis. Infected bovine fetuses develop antibodies at from about 70 days of gestation (Inaba and Matumoto, 1990). The detection of AKAV specific antibody in either serum or body fluids (e.g. pericardial or pleural) is considered to be diagnostic. To guide such an approach, prior to testing for virus-specific antibodies, there is considerable value in testing for total IgG levels in these fluids. An elevated level of IgG can then be followed by specific antibody tests for AKAV or for other viruses (e.g. for other orthobunya viruses or BVDV). There are several different serological tests available to detect AKAV specific antibodies but those most frequently used are the VNT and ELISA. Tests such as the AGID and IFAT are more broadly reactive and have lower sensitivity but can still detect fetal antibodies to AKAV and closely related viruses.

In the absence of an elevated IgG level, efforts can be directed at virus detection by either virus isolation or PCR. However, the possibility that the case is not due to an infectious aetiology should be first considered and excluded. Virus detection is also much more likely to be successful in fetuses that are aborted in mid-gestation and soon after infection. Although virus isolation can be successful, there are considerable advantages in using PCR due to the higher sensitivity and the capacity to detect residual RNA that may be present in fetal tissues long after the virus is no longer infectious. Both conventional and real time PCR assays are available (Akashi et al., 1999; Stram et al., 2004b). Although viral RNA can be detected in a range of internal organs (especially spleen, lymph nodes and thymus), the brain and spinal cord remain tissues of choice. Residual RNA can also be detected from fetal fluids and the placentome. Virus isolation can be attempted from the placenta (caruncle) of the dam and fetal membranes (placentome) or chorio allantoic fluids, fetal blood, muscle or nervous tissue of affected fetuses, especially when aborted. Virus isolation may be attempted using a range of cell cultures but those derived from hamsters (eg BHK21, Hm Lu-1) and monkeys (Vero, CV-1) are preferred. There can also be an increased isolation rate by first inoculating insect cell cultures (eg C6/36 cells) with tissue homogenates and fluids.

Due to the extremely short duration of viraemia in the dam (lasting about 3-5 days) there is little point in attempting virus detection on maternal blood or on animals thought to have been infected postnatally and are showing signs of an acute encephalitis. Adult animals rapidly produce antibodies to AKAV and are invariably seropositive by about 14 days after infection and will persist for several years in the absence of further exposure. Therefore maternal serology is of little use to confirm fetal infections due to AKAV but a negative result is convincing for exclusion purposes.

List of Symptoms/Signs

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SignLife StagesType
Acoustic Signs / Deafness Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
Digestive Signs / Cleft palate or lip Sign
Digestive Signs / Malformation of jaw, brachygnathia, prognathia Sign
General Signs / Ataxia, incoordination, staggering, falling Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Generalized weakness, paresis, paralysis Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Kyphosis, arched back Sign
General Signs / Lordosis, ventral curvature of back Sign
General Signs / Opisthotonus Sign
General Signs / Scoliosis, lateral deviation of back Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Sign
General Signs / Torticollis, twisted neck Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
Musculoskeletal Signs / Abnormal forelimb curvature, angulation, deviation Sign
Musculoskeletal Signs / Abnormal hindlimb curvature, angulation, deviation Sign
Musculoskeletal Signs / Ankylosis, arthrogryposis decreased joint mobility in birds Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Diagnosis
Musculoskeletal Signs / Contracture fore limb, leg Cattle & Buffaloes:Calf Sign
Musculoskeletal Signs / Contracture hind limb, leg Cattle & Buffaloes:Calf Sign
Musculoskeletal Signs / Decreased mobility of forelimb joint, arthrogryposis front leg Sign
Musculoskeletal Signs / Decreased mobility of forelimb joint, arthrogryposis front leg Sign
Musculoskeletal Signs / Decreased mobility of hindlimb joint, arthrogryposis rear leg Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Diagnosis
Nervous Signs / Abnormal behavior, aggression, changing habits Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Sign
Nervous Signs / Excitement, delirium, mania Sign
Nervous Signs / Hyperesthesia, irritable, hyperactive Sign
Nervous Signs / Tremor Sign
Nervous Signs / Tremor Sign
Ophthalmology Signs / Blindness Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Sign
Ophthalmology Signs / Exophthalmos, eyes protruding, proptosis Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Ophthalmology Signs / Nystagmus Sign
Ophthalmology Signs / Nystagmus Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Cattle & Buffaloes:Calf,Sheep & Goats:Lamb Diagnosis
Reproductive Signs / Agalactia, decreased, absent milk production Sign
Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus Sign
Reproductive Signs / Female infertility, repeat breeder Sign
Reproductive Signs / Small litter size Sign
Respiratory Signs / Change in voice, vocal strength Sign

Disease Course

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Following attack by biting midges, the virus rapidly multiplies and if a susceptible pregnant female is infected, the virus is rapidly spread to the fetus by transplacental passage. Adults do not show a febrile response and are only viraemic for 3-5 days. With the exception of acute infections that occasionally lead to encephalitis, the pathogenesis is dependent on the stage of development at which the fetus is infected. There is no evidence that infection prior to about 70 days of pregnancy has any adverse effect in cattle (Kirkland et al., 1988). A succession of fetal defects is induced following infection of cattle between about 70-180 days of gestation. In sheep and goats, the most susceptible period is 28-36 days with few abnormalities observed after exposure at about 60 days.

Both the severity and incidence of these abnormalities is highest following infection at the earliest stages of pregnancy. Up to 50% of bovine fetuses can be affected with some strains of AKAV (Jagoe et al., 1993) and in experimentally infected sheep, this can rise as high as 80% with some virus strains.

Clinical manifestations of AKA infection do not usually become apparent until either abortion or birth occurs. In a herd in which cattle are infected at a wide range of stages of pregnancy, the type of abnormalities observed are initially those seen following infection in late gestation and naturally progress to the outcome of early fetal infection. Initially there are mild cases of AG in which there is only fixation of 1-2 joints on a single limb but later, as a result of infection around 120-150 days of gestation, there are severe defects involving multiple joints on all limbs (Kirkland et al., 1988). Finally, calves that are affected by HE are born – the product of infection from 70-120 days of pregnancy. They may be dead or survive with careful nursing but show signs of profound CNS damage. Aborted calves may have any abnormality depending on when they have been expelled relative to the time of infection but HE most frequently leads to spontaneous abortion. In sheep and goats, due to the shorter gestation, offspring are likely to be born or aborted with a mixture of defects - both severe AG and HE can be seen in the same animal.

Epidemiology

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Culicoides midges appear to be the major vectors of Akabane virus. The virus does not appear to replicate in mosquitoes (Mellor et al., 2000) although many isolates have been made from mosquitoes, perhaps as a result of a blood meal from infected cattle. Suspected primary vectors include Culicoides brevitarsis in Australia (Jagoe et al., 1993), Culicoides oxystoma in Japan (Sakai et al., 1998) and C. imicola in Israel (Braverman et al., 2008; Stram et al., 2004a). There are many bovine and ovine feeding midges in Africa, such as C. imicola, C. shultzei and C. milnei.

Monitoring groups of sentinel cattle in Kenya over an 8-year period showed that seroconversions to AKA virus occurred every year. This continuous challenge by AKA virus resulted in a situation where most animals of 4 to 6 years of age were seropositive to the virus. Approximately 85-95% were positive when they had attained breeding age. No fetal abnormalities, which may have been due to AKA virus were encountered in this period (Davies and Jessett, 1985). Due to the lack of disease postnatally, most virus infections remain unnoticed and the virus is maintained by an ongoing vector-host-vector cycle with no overt manifestation of disease. Similar results have been obtained in the Sudan. The annual emergence of infected vectors in this situation suggests that Culicoides are involved. Bluetongue is also active every year in this location but the mosquito-borne viruses such as Rift Valley fever are not evident, often for many years. Similar observations have been made in Australia where very high levels of immunity to AKA virus are achieved in the first year of life, similar transmission patterns to bluetongue virus are observed and there is little or no similarity to the spread of the mosquito borne bovine ephemeral fever virus.

Impact: Economic

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Akabane virus causes sporadic epidemics that result in considerable damage due to reproductive failure and death of new-born calves (Anon., 1999a). Damage to the reproductive tract in periparturient dams may increase mortality due to dystocia or increased culling rates (Zentis et al., 2012). Epidemics in Japan have been estimated to cause losses of US $20 million (Inaba and Matumoto, 1990).

Zoonoses and Food Safety

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AKA virus has no human health implications. However, one of the known Simbu serogroup viruses, Oropouche virus (a Culicoides transmitted virus) (Hart et al., 2009), has been involved in a large scale febrile epidemic in humans in South America. Food safety is not an issue as neither virus propagation nor viral contamination occurs in the food chain for animal or human consumption.

Prevention and Control

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The main form of prophylaxis is vaccination. Inactivated vaccines have been developed for Akabane virus cultured on hamster lung cell cultures and these are used in Japan and Australia (Anon., 1999a; Inaba and Matumoto, 1990). The time of vaccination should be geared to ensure maximum protection when the peak incidence of the arthropod vectors is expected. In the tropical sub-tropical global belt, in late spring or early summer is probably optimal. A live vaccine has also been developed (Inaba and Matumoto, 1990). A novel trivalent vaccine for the teratogenic Aino, Akabane and Chuzan viruses has been developed in Korea (Kim et al., 2011). Due to the very high attack rates of Culicoides, while vector control by the use of insecticides and habitat modification may reduce insect numbers, it is not considered that these are sufficiently effective to prevent the occurrence of disease.

References

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Akashi H; Onuma S; Nagano H; Ohta M; Fukutomi T, 1999. Detection and differentiation of Aino and Akabane Simbu serogroup bunyaviruses by nested polymerase chain reaction. Archives of Virology, 144(11):2101-2109; 18 ref.

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Braverman Y; Chizov-Ginzburg A; Friger M; Mumcuoglu KY, 2008. Nocturnal activity of Culicoides imicola Kieffer (Diptera: Ceratopogonidae) in Israel. Russian Entomological Journal, 17(1):37-39.

Brenner J; Tsuda T; Yadin H; Chai D; Stram Y; Kato T, 2004. Serological and clinical evidence of a teratogenic Simbu serogroup virus infection of cattle in Israel, 2001-2003. Veterinaria Italiana [Proceedings of the Third International Symposium on Bluetongue, Taormina, Italy, 26-29 October 2003. Part I.], 40(3):119-123.

Brenner J; Tsuda T; Yadin H; Kato T, 2004. Serological evidence of Akabane virus infection in Northern Israel in 2001. Journal of Veterinary Medical Science, 66(4):441-443.

CYBINSKI DH; STGEORGE TD; PAULL NI, 1978. Antibodies to Akabane virus in Australia. Australian Veterinary Journal, 54(1):1-3.

Davies G; Jessett DM, 1985. A study of the host range and distribution of antibody to Akabane virus (genus bunyavirus, family Bunyaviridae) in Kenya. Journal of Hygiene, 95(1):191-196.

Della Porta AJ et al., 1977. Akabane disease, isolation of the virus from naturally infected ovine foetuses. Australian Veterinary Journal, 53: 51-52.

Hart TJ; Kohl A; Elliott RM, 2009. Role of the NSs protein in the zoonotic capacity of orthobunyaviruses. Zoonoses and Public Health [Emerging zoonoses: recent advances and future challenges. Outcome of the 5th International Conference on Emerging Zoonoses, Limassol, Cyprus, November 2007.], 56(6/7):285-296. http://www.blackwell-synergy.com/loi/jvb

Hartley WJ; Saram WGDe; Della-Porta AJ; Snowdon WA; Shepherd NC, 1977. Pathology of congenital bovine epizootic arthrogryposis and hydranencephaly and its relationship to Akabane virus. Australian Veterinary Journal, 53(7):319-325.

Hoffmann B; Scheuch M; Höper D; Jungblut R; Holsteg M; Schirrmeier H; Eschbaumer M; Goller KV; Wernike K; Fischer M; Breithaupt A; Mettenleiter TC; Beer M, 2012. Novel orthobunyavirus in cattle, Europe, 2011. Emerging Infectious Diseases, 18(3):469-472. http://wwwnc.cdc.gov/eid/article/18/3/pdfs/11-1905.pdf

Huang ChinCheng; Huang TienShine; Deng MingChung; Jong MingHwa; Lin ShihYuh, 2003. Natural infections of pigs with akabane virus. Veterinary Microbiology, 94(1):1-11.

Inaba Y; Matumoto M, 1990. Akabane virus. Virus infections of ruminants., 467-480; 85 ref.

Jagoe S; Kirkland PD; Harper PAW, 1993. An outbreak of Akabane virus-induced abnormalities in calves after agistment in an endemic region. Australian Veterinary Journal, 70(2):56-58; 7 ref.

Jennings DM; Mellor PS, 1989. Culicoides:biological vectors of Akabane virus. Vet. Microb., 21:125-131.

Kamata H; Inai K; Maeda K; Nishimura T; Arita S; Tsuda T; Sato M, 2009. Encephalomyelitis of cattle caused by Akabane virus in southern Japan in 2006. Journal of Comparative Pathology, 140(2/3):187-193. http://www.sciencedirect.com/science/journal/00219975

Kim YeonHee; Kweon ChangHee; Tark DongSeob; Lim SeongIn; Yang DongKun; Hyun BangHun; Song JaeYoung; Hur Won; Park SeChang, 2011. Development of inactivated trivalent vaccine for the teratogenic Aino, Akabane and Chuzan viruses. Biologicals, 39(3):152-157. http://www.sciencedirect.com/science/journal/10451056

Kirkland PD; Barry RD; Harper PAW; Zelski RZ, 1988. The development of Akabane virus-induced congenital abnormalities in cattle. Veterinary Record, 122(24):582-586.

Kono R; Hirata M; Kaji M; Goto Y; Ikeda S; Yanase T; Kato T; Tanaka S; Tsutsui T; Imada T; Yamakawa M, 2008. Bovine epizootic encephalomyelitis caused by Akabane virus in southern Japan. BMC Veterinary Research, 4(20):(13 June 2008). http://www.biomedcentral.com/1746-6148/4/20

Lee JK; Park JS; Choi JH; Park BK; Lee BC; Hwang WS; Kim JH; Jean YH; Haritani M; Yoo HS; Kim DY, 2002. Encephalomyelitis associated with Akabane virus infection in adult cows. Veterinary Pathology, 39(2):269-273.

Levin A; Rubinstein-Guini M; Kuznetzova L; Stram Y, 2008. Cleavage of Akabane virus S RNA in the brain of infected ruminants. Virus Genes, 36(2):375-381. http://springerlink.metapress.com/link.asp?id=103010

Liao YK; Lu YS; Goto Y; Inaba Y, 1996. The isolation of Akabane virus (Iriki strain) from calves in Taiwan. Journal of Basic Microbiology, 36(1):33-39.

Markusfeld O; Mayer E, 1971. An arthrogryposis and hydranencephaly syndrome in calves in Israel, 1969/70. Epidemiological and clinical aspects. Refuah Veterinarith, 28(No.2):51-61.

Mellor PS; Boorman J; Baylis M, 2000. Culicoides biting midges: their role as arbovirus vectors. Annual Review of Entomology, 45:307-340; 213 ref.

Metselaar D; Robin Y, 1976. Akabane virus isolated in Kenya. Veterinary Record, 99: 86.

Oem JK; Lee KH; Kim HR; Bae YC; Chung JY; Lee OS; Roh IS, 2012. Bovine epizootic encephalomyelitis caused by Akabane virus infection in Korea. Journal of Comparative Pathology, 147(2/3):101-105. http://www.sciencedirect.com/science/journal/00219975

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